KEMBAR78
Progress Test | PDF | Heart | Myocardial Infarction
0% found this document useful (0 votes)
17 views77 pages

Progress Test

Uploaded by

hellyeet310
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
0% found this document useful (0 votes)
17 views77 pages

Progress Test

Uploaded by

hellyeet310
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
You are on page 1/ 77

PROGRESS TEST

Topics in PT

Topic Question
Breast Management of breast infection
Breast pathology postpartum – management
Diagnosis of breast lump
Breast cancer screening
Diagnosis of breast lump
Diagnosis of breast mass
Cancer Diagnosis of neck lump
Histopathology of lung cancer
Diagnosis of lymphoma
Presentation of leukaemia
Presentation of intraabdominal malignancy
Genetic predisposition to cancer
Management of metastatic bone disease
Diagnosis of lung cancer
Cardiovascular Anatomy of coronary arteries
Diagnosis of vascular insufficiency
Diagnosis of congenital cardiac defect
Management of cardiac arrhythmias
Microbiology of endocarditis
Long QT interval
Adverse effects of cardiovascular medications
Management of arrhythmia
Pharmacology of anti-arrhythmic drugs and agents
Pathophysiology of myocarditis
Management of myocardial infarction
Managing peripheral vascular disease
Adverse effects of cardiovascular
Recognition of heart block
Acute coronary syndrome
Management of cardiac arrhythmia
Child Health Diagnosing abdominal pain in children
Itchy scalp in a child
Assessment of developmental delay
Recognition of normal puberty
Causes of eye disease in a child
Complications of viral illness in children
Hip pain in a child
Microbiology of chest infection in a child
Child development
Safe prescribing in children
Brain tumours in children
Diagnosis of psychiatric disorder in children
Dermatology Management of cellulitis
Managing eczema
Complications of eczema
Assessment of skin lesion
Recognising pre-malignant skin conditions
Diagnosis of skin lesion
Examination of psoriasis
Emergency Diagnosis of electrolyte abnormalities
Medicine and Diagnosis of malabsorption
Intensive Care Causes of weakness
Investigation of limb weakness
Burns
Complications of drug misuse
Managing the ischaemic leg
Management of status epilepticus
Management of acutely unwell patient
Diagnosis of acute chest pain
Clinical signs in chest disease
Management of anaphylaxis
Assessment of fracture risk
Resuscitation of the new-born
Investigation of stroke
Management of carbon monoxide poisoning
Management of hip fracture
Emergency management of clotting disorder
Management of stroke
Treatment of anaphylaxis
Managing diabetic emergencies
Diagnosis of chest pain
Antidotes for serious poisons
Pathophysiology of diabetic ketoacidosis
Management of severe acute asthma
Diagnosis of shocked patient
Recognition of electrolyte disturbance
Management of delirium
Hand injuries
Investigation of chest pain
Status epilepticus
Causes of delirium
Management of paracetamol overdose
Endocrine Investigation of thyroid disorder
Distinguishing types of diabetes mellitus
Managing type 2 diabetes
Cause of thyroid problems
Management of hyperthyroidism
Investigation of thyroid disease
Ear, Nose and Approach to mouth ulcers
Throat Ear conditions causing pain
Management of sore throat
Recognition of Koplik spots
Gastrointestinal Investigation of liver disease
Diagnosis of abdominal pain
Causes of mucus and blood in faeces
Diagnosis of acute abdomen
Differential diagnosis of diarrhoea and anaemia
Investigation of abdominal pain
Diagnosis of abdominal swelling
Bruising in obstructive jaundice
Gastrointestinal red flags
Causes of mucus and blood in faeces
Diagnosis of abdominal pain
Diagnosis of malnutrition
Adverse gastrointestinal effects of drugs
Managing chronic lung disease
Haematology Interpretation of viral serology
Management of anaemia
Infection Severe soft tissue infection
Management of bacteraemia
Management of ear infection
Diagnosis of infection in immunocompromised
Diagnosis of opportunistic infection
Medical Ethics Driving after a provoked seizure
and Law Safeguarding and capacity
Consent for surgical procedures
Safeguarding of vulnerable adults
Safeguarding of vulnerable adults
Medical aspects of fitness to drive
Recognition of non-accidental injury
Medicine of Management of obesity
older adult
Mental Health Management of depression
Diagnosis of psychiatric disorder
Treatment of ADHD
Diagnosis of psychiatric disorder
Acute psychiatric conditions
Management of psychiatric illness
Musculoskeletal Management of bone health
Treatment of arthritis
Investigation of muscle pain and rash
Diagnosis of foot pain
Symptoms of spinal disease
Features of arthritis
Biochemistry of gout
Diagnosis of upper back pain
Hyper-sclerotic disease of bone
Management of rheumatological conditions
Causes of muscle disease
Managing gait disorder
Causes of neck pain
Diagnosis of joint pain
Cases of hip pain
Complications of limb fracture
Investigation of joint swelling
Neurosciences Management of psychosis
Diagnosis of facial pain
Diagnosis of vertigo
Diagnosis of intracerebral vascular anomaly
Peripheral nerve compression
Causes of confusion
Causes of headaches
Anatomy of referred pain
Management of first seizures
Causes of delirium
Management of brainstem death
Diagnosis of meningitis
Differential diagnosis of foot drop
Investigation of tremor
Anatomy of brain lesions
Peripheral nerve lesions of the upper limb
Recognition of causes of weakness in shoulders
Obstetrics and Diagnosis of problems in labour
Gynaecology Management of pregnancy complications
Management of abnormal labour
Diagnosis of fetal malformations
Management of abnormal cervical smear
Diagnosis of post-partum problems
Pathology of ovarian disease
Complications of pregnancy
Diagnosis of abdominal pain in pregnancy
Ophthalmology Diagnosis of visual loss
Management of red eyes
Anatomy of eye
Central retinal vein occlusion
Palliative Care Management of terminal illness
Nutrition in swallowing disorders
Peri-op med and Peri-operative assessment
anaesthesia Preparation for elective surgery
Risks of surgery
Renal and Treatment of severe urinary tract infection
Urology Diagnosis of urinary symptoms
Management of renal failure
Urinalysis
Causes of acute kidney injury
Drug treatment of overactive bladder
Investigation of renal disease
Management of renal pain
Complications of renal failure
Respiratory Immunology of asthma
Management of severe acute asthma
Investigation of respiratory disease
Blood gas interpretation
Interpretation of chest X-ray
Microbiology of community acquired pneumonia
Investigation of occupational lung disease
Chest infection in an adult
Interpretation of respiratory physical signs
Interpreting arterial blood gas
Hereditary causes of lung disease
Investigation of breathlessness
Managing chronic lung disease
Sexual Health Diagnosis of a vulval swelling
Acute prostatitis
Prescribing contraception
Complications of venereal disease
Diagnosis of painful intercourse
Management of scrotal problems
Investigation of testicular swelling
Social, Pop. Interpreting clinical trial data
Health and Infectious disease and public health
Research Understanding clinical trials
Interpretation of clinical trial data
Others Postoperative management after fracture
Postoperative analgesia
Ankle pain side effects of medication
Medication adverse effects
Adverse drug interactions
Pharmacokinetics of stable state
Calculating dosage of medications
Management of warfarin
Mode of action of tranexamic acid
Postoperative complications
Diagnosis of genetic disease
Diagnosis of alcohol dependence
Management of alcohol abuse
Prescribing opioid medication
Mechanism of action of antibiotics
Adverse effects of medication
Drug interactions with alcohol
Management of worm infestation

Cardiology
Anatomy of coronary arteries
Diagnosis of vascular insufficiency

 Duplex ultrasound to check for chronic venous insufficiency (leg veins don’t allow blood to
flow back up to the heart
 Sx: swelling in the legs or ankles, tight feeling in calves or painful legs, pain when walking
that stops when you rest, varicose veins, leg ulcers that are hard to treat, restless leg
syndrome
 Tx: elevating the legs, compression stockings, aspirin for ulcers, radiofrequency ablation to
close the vein, sclerotherapy, vein stripping

Diagnosis of congenital cardiac defect

 Foetal echocardiography (a special type of ultrasound) – 18 to 22 weeks of pregnancy or


examination after birth (blue tinge to skin or cyanosis)
 New-born physical examination - checking the eyes, heart, hips and testicles
 Most common = ventricular septal defect
 Tetralogy of Fallot = (1) a hole between the 2 ventricles, (2) narrowing of the pulmonary
valve and main pulmonary artery, (3) enlarged aortic valve and opens from both ventricles
rather than from the left ventricle only, (4) muscular wall of the lower right chamber of the
heart is thicker than normal

Long QT interval syndrome

 Long QT syndrome – a heart rhythm that can cause fast, chaotic heartbeats
 Can be classified into acquired and congenital long QT syndrome (passed on my genetics or
caused by medications e.g. hypokalemia, hypocalcemia, hypomagnesemia)
 Risk fx: history of cardiac arrest, first-degree relative with long qt syndrome, using
medications that cause prolonged qt intervals, being female and on heart medication,
excessive vomiting or diarrhoea, eating disorders
 Sx: fainting, lightheadedness, heart palpitations, weakness or blurred vision
 Ix: ECG, family history, genetic testing
 Tx: Nadolol, propranolol, mexiletine; left cardiac sympathetic denervation surgery (removal
of sympathetic nerves); ICD

Adverse effects of cardiovascular medications

Management of arrhythmia

Pharmacology of anti-arrhythmic drugs and agents

Pathophysiology of myocarditis

 Inflammation of the myocardium with necrosis of cardiac myocytes


 Causes: virus – COVID-19, hep B and C, parvovirus, HSV; bacteria - staphylococcus,
streptococcus, bacterium that causes diphtheria, tick-borne bacterium responsible for lyme
disease; parasites, fungi; medications; chemicals
 Sx: chest pain, fatigue, SOB, rapid or irregular heartbeats
 Ix: ECG, CXR, echo, MRI, blood tests (FBC and antibodies)
 Tx: corticosteroids, heart medications for heart failure or arrhythmias, VAD, IV medications

Condition: Acute Aortic Aneurysm


Definition: A bulge or swelling in the aorta that can get bigger over time and rupture, causing life-
threatening bleeding.
Presentation:
Risk factors: all men aged 66 or over and all women aged 70 or over who have 1 or more of (1)
high BP, (2) COPD, (3) high cholesterol, (4) family history of AAA, (5) CVD, (6) history of smoking,
(7) European family origin
Symptoms: a pulsing sensation in the tummy, tummy pain that does not go away, lower back pain
that does not go away. If burst: Triad of abdo/ flank pain + palpable pulsatile mass + hypotension
Examination findings/Signs:
Investigations:
Bedside: -
Bloods: -
Imaging: Ultrasound → thin slice contrast-enhanced arterial-phase CT angiography
Management:
Patient Education/ Counselling/ Resources: education about changing diet and lifestyle; NHS AAA
screening programme
Conservative: small AAA (3cm to 4.4cm across) – ultrasound scan every 2 years; lifestyle changes
→ refer to regional vascular service to be seen within 12 weeks of diagnosis
medium AAA (4.5cm to 5.4cm) – ultrasound scans every 3 months; lifestyle changes → refer to
regional vascular service to be seen within 12 weeks of diagnosis
Medical: statin therapy, treat risk fx
Surgical: large AAA (5.5cm or more) – refer to regional vascular service seen in 2 weeks or
emergency transfer if needed → surgery to stop it getting bigger or bursting → endovascular
surgery, graft is inserted into a blood vessel in the groin and passed into the aorta; open surgery,
graft is placed in the aorta through a cut in your tummy
Small or medium AAAs that have grown by more than 1 cm over 12 months or having symptoms
linked to AAA that do not go away.
Miscellaneous:
Complications: Endovascular surgery – lower than open heart, leaky or slipping of graft, wound
infection, heavy bleeding from groin, blood clot, heart attack or stroke
Open surgery – wound infection, blood clot, heavy bleeding, heart attack, stroke, erectile
dysfunction, slipping of graft is less likely

Condition: Aortic Dissection

Definition: tear in the tunica intima of the aorta provoked by intramural bleeding, resulting in the
separation of the aortic wall layers and subsequent formation of a true lumen and a false lumen
with or without communication
Stanford classification: Type A – ascending aorta (2/3 cases); Type B – does not involve the
ascending aorta (1/3 cases)
DeBakey classification: Type I – aorta, aortic arch and descending aorta; Type II – ascending aorta
only, Type III – descending aorta distal to left subclavian
Presentation:
Risk factors: Hx of hypertension, smoking, raised cholesterol, pre-existing aortic diseases, aortic
valve disease, family history, hx of cardiac surgery, smoking, cocaine or amphetamine usage,
Marfan’s syndrome
Symptoms: sudden and sharp onset of chest pain radiating the to the chest or back; mild pain in
the chest, back or groin; “ripping or tearing”, unequal arm pressure/ pulse deficit
Examination findings/Signs:
Investigations:
Bedside: ECG (20% of patients with type A dissection have ECG evidence of acute ischaemia or
acute MI)
Bloods: -
Imaging: CXR to exclude aortic dissection; transthoracic ultrasound to provide indication of site
and extent of dissection; MRI to confirm diagnosis (best sensitivity and specificity)
Management:
Patient Education/ Counselling/ Resources:
Conservative: morphine
Medical: IV beta-blocker, manage hypertension (ACE inhibitors)
Surgical: type A – implantation of composite graft in ascending aorta, type B – thoracic
endovascular aortic repair (TEVAR) + optimal medical treatment
Miscellaneous:
Complications: hypotension due to cardiac tamponade or MI, aortic regurgitation, cardiac failure,
can involve coeliac artery which produces persistent abdominal pain, elevation of acute phase
proteins and increase of lactate dehydrogenase, syncope

Condition: ACS/ MI

Definition: a range of acute myocardial ischaemic states including ST-elevation and Non-ST
elevation ACS
Presentation:
Risk factors: increasing age, male, family hx, smoking, diabetes and impaired glucose tolerance,
hypertension, dyslipidaemia (raised LDL), reduced HDL, obesity, non-atherosclerotic causes
(coronary emboli from an infected cardiac valve, coronary occlusion, coronary artery spasm,
cocaine use, coronary trauma, hyperthyroidism, severe anaemia)
Symptoms: prolonged angina pain, limitation of daily activities, sweating, nausea, vomiting,
fainting, SOB and palpitations
If acute: pain in chest and other areas (jaw, back, arms) lasting longer than 15 mins, marked
sweating or breathlessness, nausea, vomiting, new onset chest pain with little or no exertion
Examination findings/Signs:
Investigations:
Bedside: 12 lead ECG (ST depression or elevation)
Bloods: troponin I and T in serum 3-6 hours after infarction, peak at 12-24 hours and remain
raised for up to 14 days; FBC (anticoagulants, blood glucose, renal function and electrolytes, CRP)
Imaging: echocardiography (demonstrates wall motion), CXR (complications of ischemia e.g.
pulmonary oedema) or explore alternative diagnoses e.g. pneumothorax, aortic aneurysm, CMR
(function and perfusion of scar tissue for myocarditis), GOLD STANDARD: coronary angiography to
check for coronary artery disease
Deviation:
LEAD I LEAD AVF AXIS
Positive Positive Normal (0 to +90 degrees)
Positive Negative Possible LAD
Is lead II positive?
Yes -> Normal (0 to -30 degrees)
No -> LAD (-30 to -90 degrees)
Negative Positive RAD (+90 to 180 degrees)
Negative Negative Extreme Axis Deviation (-90 to 180 degrees)
Management:
Patient Education/ Counselling/ Resources: lifestyle changes, management of hypertension if
present, statins, ACEi and BB.
Conservative: pain relief: GTN or IV opioid + antiemetic, single dose of aspirin unless person is
allergic, resting 12-lead ECG, assess O2 sats using pulse oximetry (94-98%)
Medical: STEMI = antiplatelet and anticoags (aspirin and ticagrelor) (do not offer dual antiplatelet
therapy to patients with chest pain before diagnosis of NSTEMI or unstable angina); consider
clopidogrel + aspirin if ongoing oral anticoag. Prasugrel + aspirin in adults with ACS having primary
or delayed PCI. Glycoprotein IIb/IIIa inhibitors should be considered as an adjunct to PCI for
patients at intermediate or higher risk who are not already receiving a glycoprotein inhibitor;
antithrombin therapy (fondaparinux to patients without high bleeding risk unless angiography is
planned within 24 hours of admission) (consider unfractionated heparin for patients with high
creatinine)
NSTEMI = aspirin and continue unless contraindicated + offer fondaparinux (anti-thrombin) unless
high bleeding risk or immediate angiography; consider unfractionated heparin if high creatinine →
GRACE score to measure risk → low risk → consider conservative mx without angiography + offer
ticagrelor with aspirin unless high bleeding risk; intermediate or high risk → angiography with
follow up PCI unless contraindications → offer prasugrel or ticagrelor with aspirin → assess left
ventricular function and assess for unstable angina
Surgical: Coronary angiography within 72 hours of first admission and no contraindications and
follow on PCI if indicated; CABG; stent
Others: Nitrates for ongoing pain while waiting, beta-blockers, calcium antagonists (non-
dihydropyridines), amlodipine (for patients with reduced EF), ACEi
Miscellaneous:
Complications:
 Cardiac arrest - This most commonly occurs due to patients developing ventricular
fibrillation and is the most common cause of death following a MI. Patients are managed
as per the ALS protocol with defibrillation.
 Cardiogenic shock - If a large part of the ventricular myocardium is damaged in the
infarction the ejection fraction of the heart may decrease to the point that the patient
develops cardiogenic shock. This is difficult to treat. Other causes of cardiogenic shock
include the 'mechanical' complications such as left ventricular free wall rupture as listed
below. Patients may require inotropic support and/or an intra-aortic balloon pump.
 Chronic heart failure - if the patient survives the acute phase their ventricular
myocardium may be dysfunctional resulting in chronic heart failure. Loop diuretics such as
furosemide will decrease fluid overload. Both ACE-inhibitors and beta-blockers have been
shown to improve the long-term prognosis of patients with chronic heart failure.
 Tachyarrhythmias - Ventricular fibrillation, as mentioned above, is the most common
cause of death following a MI. Other common arrhythmias including ventricular
tachycardia.
 Bradyarrhythmias - Atrioventricular block is more common following inferior myocardial
infarctions.
 Pericarditis - Pericarditis in the first 48 hours following a transmural MI is common (c. 10%
of patients). The pain is typical for pericarditis (worse on lying flat etc), a pericardial rub
may be heard and a pericardial effusion may be demonstrated with an echocardiogram.
 Dressler's syndrome tends to occur around 2-6 weeks following a MI. The underlying
pathophysiology is thought to be an autoimmune reaction against antigenic proteins
formed as the myocardium recovers. It is characterised by a combination of fever,
pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs.
 Left ventricular aneurysm - The ischaemic damage sustained may weaken the
myocardium resulting in aneurysm formation. This is typically associated with persistent
ST elevation and left ventricular failure. Thrombus may form within the aneurysm
increasing the risk of stroke. Patients are therefore anticoagulated.
 Left ventricular free wall rupture - This is seen in around 3% of MIs and occurs around 1-2
weeks afterwards. Patients present with acute heart failure secondary to cardiac
tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). Urgent
pericardiocentesis and thoracotomy are required.
 Ventricular septal defect - Rupture of the interventricular septum usually occurs in the
first week and is seen in around 1-2% of patients. Features: acute heart failure associated
with a pan-systolic murmur. An echocardiogram is diagnostic and will exclude acute mitral
regurgitation which presents in a similar fashion. Urgent surgical correction is needed.
 Acute mitral regurgitation - More common with infero-posterior infarction and may be
due to ischaemia or rupture of the papillary muscle. Acute hypotension and pulmonary
oedema may occur. An early-to-mid systolic murmur is typically heard. Patients are
treated with vasodilator therapy but often require emergency surgical repair.

Condition: Acute Congestive Heart Failure

Definition: Ability of the heart to maintain the circulation of blood is impaired as a result of a
structural or functional impairment of ventricular filling or ejection.
Presentation:
Risk factors:
Symptoms: Ankle swelling, tiredness, severe breathlessness, orthopnea, coughing (rarely
producing frothy, blood-stained sputum)
Examination findings/Signs: elevated jugular venous pressure, gallop rhythm, inspiratory crackles
at lung bases, wheeze
Investigations:
Bedside: history, clinical examination, bloods, ECG
Bloods: serum natriuretic peptides (NT-proBNP <400ngL) to rule out AHF
Imaging: CXR, transthoracic Doppler 2D for patients with new suspected AFH with raised NP levels
Management:
Patient Education/ Counselling/ Resources: obesity, contraception and pregnancy, driving, travel
Conservative:
Medical:
Surgical:
Miscellaneous:
Complications:

Condition: Chronic Congestive Heart Failure

Definition: Ability of the heart to maintain the circulation of blood is impaired as a result of a
structural or functional impairment of ventricular filling or ejection.
 HF-Ref = reduced LVEF < 35 – 40 % -> typically have systolic dysfunction due to ischaemic
heart disease, dilated cardiomyopathy, myocarditis, arrhythmias
 HF-Pef = preserved LVEF -> typically have diastolic dysfunction due to hypertrophic
obstructive cardiomyopathy, restrictive cardiomyopathy, cardiac tamponade, constrictive
pericarditis
 Urgent symptoms are often due to left ventricular failure resulting in pulmonary oedema
 Typically develop left-sided heart failure and may be due to increased left ventricular
afterload or increased left ventricular preload
 LV failure results in: pulmonary oedema (dyspnoea, orthopnoea, paroxysmal nocturnal
dyspnoea, bibasal fine crackles)
 RV failure results in: peripheral oedema, raised JVP, hepatomegaly, weight gain due to
fluid retention, anorexia
 High output heart failure due to increased metabolic needs: anaemia, paget’s disease,
pregnancy, thyrotoxicosis, thiamine deficiency (Wet beri-beri)
Presentation:
Risk factors: coronary artery disease including previous history of myocardial infarction,
hypertension, Afib and diabetes mellitus; drugs; alcohol; family history of heart failure or sudden
cardiac death under the age of 40 y/o.
Symptoms: breathlessness on exertion, orthopnea, nocturnal cough, paroxysmal nocturnal
dyspnoea); fluid retention (ankle swelling, bloated feeling, abdominal swelling, weight gain);
fatigue; light-headedness; history of syncope
Examination findings/Signs: tachycardia, heart murmurs, 3rd or 4th heart sounds (gallop rhythm),
raised jugular venous pressure, enlarged liver, tachypnoea, basal crepitations ad pleural effusions;
obesity
Investigations:
Bedside: 12 lead ECG, urine dipstick
Bloods: NT-proBNP (if above 2000pg/ML, refer urgently for specialist assessment and echo within
2 weeks; 400-2000 pg/Ml, refer for specialist assessment and echo within 6 weeks), urea and
electrolytes, estimated GFR, full blood count, iron studies (transferrin and ferritin), thyroid
function tests, LFTs, HbA1C, fasting lipids
Imaging: CXR
Management:
Patient Education/ Counselling/ Resources: discussion regarding advance care planning and
advance decisions, obesity, contraception and pregnancy, driving, travel
Conservative: Preserved EF - ensure drugs which may worsen HF are discontinued (CCB and BB) →
loop diuretic (furosemide) → refer to a specialist → consider antiplatelets for coronary heart
disease patients → consider statin therapy → ensure causes, comorbidities and precipitating
factors are managed → screen for depression and anxiety → refer to a supervised exercise-based
group rehab programme
Reduced EF – ensure drugs which may worsen HF are discontinued → ACEi (or ARB) if person has
diabetes or has signs of fluid overload (review faulty valve first if suspected) → BB (if person has
angina) → Spironolactone → Entresto (Sacubitril/ Valsartan) → refer to specialist if still
symptomatic → consider Ivabradine and cardiac resynchronisation therapy → consider
antiplatelets → consider statin → screen for depression and anxiety → refer to a supervised
exercise-based group rehab programme
Medical:
Surgical: ICD, CRT-P/ CRT-D (if symptomatic severe LVSD + EF<35% + LBBB), LVAD, transplant
Miscellaneous:
Complications:

Conditions: Pericarditis/ Acute Tamponade

Definition: accumulation of pericardial fluid, blood, pus or air within the pericardial space that
creates an increase in intra-pericardial pressure, restricting cardiac filling and decreasing cardiac
output
Causes: malignancy, acute MI and post-infarction (dressler’s syndrome), infective viral (HIV or
Coxsackie) or bacterial (TB), rheumatoid arthritis, dermatomyosistis, radiation therapy, chronic
kidney disease, haemorrhagic pericarditis, drugs (hydralazine, isoniazid), trauma, surgery
Presentation:
Risk factors:
Symptoms: Sharp, constant sternal pain relieved by sitting forward. Pain can radiate to left
shoulder/ left arm or into the abdomen. Worse when lying on the left side and on inspiration,
swallowing and coughing. Fever, cough, breathlessness, dysphagia, hoarseness.
Examination findings/Signs: Pericardial friction rub (high pitched scratching sound, best heard
over the left sternal border during expiration). Pulsus paradoxus (decrease in palpable pulse and
arterial systolic BP of 10mmHg on inspiration). Hypotension, muffled heart sounds and jugular
vein distention (Beck’s triad).
Investigations:
Bedside: ECG (sinus tachycardia, low-voltage QRS complex, PR segment depression, saddle
shaped ST elevations, widespread), transthoracic echo, FBC, cardiac catheterisation
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative: oxygen, bed rest with leg elevation, positive inotrope (dobutamine),
echocardiogram-guided pericardiocentesis
Medical: NSAIDS+ colchicine for idiopathic or viral pericarditis
Surgical: pericardiodesis (for recurrent tamponade + corticosteroids or tetracycline), pericardio-
peritoneal shunt, pericardiectomy
Miscellaneous:
Complications:

Condition: Infective endocarditis

Definition: infection involving the endocardial surface of the heart including vulvular structures,
chordae tendineae, sites of septal defects
 Strongest risk factor is a previous episode of endocarditis
 Types of patients: previously normal valves (most common = mitral valve), rheumatic
valve disease, prosthetic valve, congenital heart defects, intravenous drug users, has
recent piercings
 Causes: staph aureus (most common), strep viridans (commonly found in the mouth and
associated with poor dental hygience), staph epidermidis (common following prosthetic
valve surgery), strep bovis (colorectal cancer), non-infective (SLE) // negative culture:
coxiella brunetii, bartonella, Brucella, HACEK, prior antibiotic therapy
Presentation:
Risk factors: acquired valvular heart disease with stenosis or regurgitation, hypertrophic
cardiomyopathy, previous infective endocarditis, structural congenital heart dz, valve replacement
Symptoms: aching joints and muscles, chest pain, fatigue, flu-like symptoms, night sweats, SOB,
swelling in feet, legs or abdomen, weight loss, cardiac murmur
Examination findings/Signs:
Investigations:
Bedside:
Bloods: full blood count, C-reactive protein, blood cultures, ESR, rheumatoid factor
Imaging: ECG
Management:
Patient Education/ Counselling/ Resources:
Conservative:
Medical: antibiotic prophylaxis, unless patient is undergoing dental procedures or procedures for
the GI tract, genitourinary tract, respiratory tract
 Suspected: supportive care and empirical broad-spectrum antibiotic therapy, consider
surgery
 Staphylococci: flucloxacilllin; vancomycin + rifampicin if allergic to penicillin
 Streptococci: benzylpenicillin sodium (+ gentamicin if less sensitive); vancomycin +
gentamicin if allergic to penicillin
Enterococci: amoxicillin + gentamicin or benzylpenicillin sodium + gentamicin; vancomycin
+ gentamicin if penicillin allergic
Surgical:
Miscellaneous:
Complications:

Condition: Peripheral arterial disease

Definition: build-up of fatty deposits in the arteries that restrict blood supply to leg muscles
Presentation:
Risk factors: smoking, diabetes, hypertension, hypercholesterolaemia, age
Symptoms: intermittent claudication (painful ache which usually disappears after a few minutes’
rest), hair loss on legs and feet, numbness and weakness in legs, ulcers, blue tinge to legs, erectile
dysfunction, wasting of muscles
Examination findings/Signs:
Investigations:
Bedside: physical examination, ABPI
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources: lifestyle changes, smoking cessation, losing weight,
reduced alcohol consumption
Conservative:
Medical:
Surgical:
Miscellaneous:
Complications: coronary heart disease, stroke, heart attack, angina
*Critical limb ischaemia – blood flow to legs become severely restricted
Sx: severe burning pain in legs and feet even when resting, pale and dry skin, wounds and ulcers
on legs and feet, wasting of muscles, gangrene on toes
Tx: angioplasty, bypass graft, amputation

ENT
Approach to mouth ulcers

 Causes: mechanical trauma, infections, lesions, inflammatory conditions, nutritional


deficiencies (iron, folic acid, vitamin b12), GI disease, drug therapy
 Unexplained mouth ulcer of more than 3 weeks should be referred urgently to a specialist to
exclude oral cancer
 Treatment: corticosteroids (hydrocortisone tablets, beclomethasone dipropionate inhaler
and betamethasone tablets; topical anaesthetics (lidocaine hydrochloride), topical analgesics
(benzydamine hydrochloride) and topical antimicrobial agents (chlorhexidine), sodium
bicarbonate mouthwash to sooth ulcers

Ear conditions causing pain

 Meniere’s disease – condition of the inner ear that causes sudden attacks of:
o Cause is multi-factorial
o Sx: dizziness with vertigo, unsteadiness, tinnitus, hearing loss, pressure felt deep
inside the ear, nausea or vomiting; lasts commonly for 2-3 hours
o Ix: ENT specialist will check whether there is vertigo with at least 2 attacks lasting 20
minutes within a short space of time, fluctuating hearing loss and tinnitus
o Tx: prochlorperazine (relieves severe nausea and vomiting) and antihistamines;
betahistine to reduce the frequency and severity of attacks
 Otitis externa
o Caused by pseudomonas aeruginosa or staphylococcus aureus
o Tx: flucloxacillin or clarithromycin or ciprofloxacin (if pseudomonas suspected)
 Otitis media
o Commonly seen in children and is usually caused by viruses (RSV, rhinovirus,
adenovirus, influenza virus) or bacteria (haemophilus influenza, strep. Pneumoniae,
strep pyrogenes)
o Tx: amoxicillin, co-amoxiclav (if worsening symptoms despite 2-3 days of
antibacterial tx) or clarithromycin or erythromycin and consult microbiologist if
worsening symptoms

Management of sore throat

 Admit anyone with breathing difficulty or clinical dehydration


 If taking DMARD, withhold it and discuss with rheumatology unless WCC drops, then urgent
specialist referral
 If taking carbimazole, take urgent FBC
 If on chemotherapy or has a disease that decreases immune system, seek specialist referral
 If group A strep has been confirmed by rapid antigen testing, prescribe antibiotics and lower
the threshold if person is at risk of rheumatic fever (e.g. those with history of rheumatic
fever and those living in south Africa, astralia, maori and Philippines; vulnerable groups of
people being managed in primary care)
 Prescribe phenoxymethylpenicillin for severe cases
 If candida pharyngitis is suspected, prescribe nystatin for mild and moderate cases and
fluconazole if fungal infection is more widespread

Recognition of Koplik spots

Respiratory
Immunology of asthma
Blood gas interpretation

https://geekymedics.com/abg-interpretation/

Interpretation of chest X-ray

Chest infection in an adult

 Cause can be viral or bacterial – viral could lead to viral bronchitis


o Sx: chesty cough, wheezing and SOB, chest pain, high temp, headache, aching
muscles, tiredness (cough and mucus can last up to 3 weeks)
 Bronchitis is an infection of the main airways of the lungs, causing them to become irritated
and inflamed.
o Sx: acute – temporary inflammation of the airways that causes a cough and mucus
and can last up to 3 weeks; chronic – daily productive cough that lasts for 3 months
and for at least 2 years in a row

Interpretation of respiratory physical signs

Occupational Asthma

 Causes: isocyanates (most common cause, e.g. occupations such as spray painting and foam
moulding), platinum salts, soldering flux resin, flour, epoxy resins, glutaraldehyde

Hereditary causes of lung disease

 Cystic fibrosis – mutation in the CFTR gene, treated by the drug ivacaftor
 Alpha-1 antitrypsin deficiency – recessive inherited disorder which increases susceptibility to
the harmful effects of smoking, leading to severe emphysema at an early age
 Pulmonary embolism – mutation in the coagulation factor V gene (factor V Leiden mutation)
leads to increased risk of developing DVT
 Lung cancer – mutation of chromosome 15
 Pulmonary fibrosis – mutations of TERT, TERC and MUC5B gene
 Asthma and COPD – TNFa, TGFB1, MMP12, ADAM33

Managing chronic lung disease

Control of ventilation

 Respiratory centres:
o Medullary respiratory centre – ventral group controls forced voluntary expiration
and dorsal group controls inspiration; depressed by opiates
o Apneustic centre – lower pons; stimulates inspiration (activates and prolongs
inhalation); overridden by pneumotaxic control to end inspiration
o Pnuemotaxic centre – upper pons; inhibits inspiration at a certain point; fine tunes
the respiratory rate
 Chemoreceptors:
o Peripheral chemoreceptors: located in the bifurcation of carotid arteries and arch of
the aorta – respond to changes in reduced Po2, increased H+ and increased PCO2 in
arterial blood
o Central chemoreceptors: located in the medulla, respond to increased H+ in brain
interstitial fluid to increase ventilation (NOT influenced by O2 levels)
 Lung receptors:
o Stretch receptors: respond to lung stretching causing a reduced respiratory rate
o Irritant receptors: respond to smoke etc. causing bronchospasm
o J receptors

Condition: Acute Asthma

Definition: Condition in which the airways are narrowed and swollen and may produce excess
mucus. Progressive worsening of asthma symptoms (breathlessness, wheeze, cough and chest
tightness.
Presentation:
Risk factors:
Symptoms: agitation (hypoxia), exhaustion, cyanosis, use of accessory muscles at rest
Examination findings/Signs: moderate – PEFR more than 50-75% best or predicted and normal
speech, no features of acute asthma
Acute severe – PEFR 33-50% best or predicted or resp rate at least 25/min in people over 12 y/o,
inability to complete sentences in 1 breath, accessory muscle use
Life-threatening – PEFR less than 33% best or predicted or o2 sats of less than 92%, altered
consciousness, exhaustion, cardiac arrhythmia, hypotension, cyanosis, poor resp effort, confusion
Investigations:
Bedside: history (compliance with medication) and details of previous exacerbations → admit if
life-threatening with persisting symptoms after initial bronchodilator treatment (or have factors
that warrant a lower threshold for admission (poor treatment adherence, living alone, previous
severe asthma attack, psychological problems etc.)
Bloods: -
Imaging: -
Management:
Patient Education/ Counselling/ Resources: check peak expiratory flow, inhaler technique,
address preventable contributors, lifestyle changes, consider supply of oral corticosteroids, self-
management education
Conservative: controlled supplementary o2 to all people with hypoxia with a face mask, nasal
cannulae or venturi mask (94-98%)
Medical: short-acting beta-2 agonist- salbutamol→ inhaled corticosteroids (prednisolone/
methylprednisolone/ IV hydrocortisone) + monitor peak expiratory flow rate and O2 sats → ICS +
LTRA (leukotriene receptor antagonist (Montelukast) → add LABA (Stop montelukast after 8
weeks of no improvement)
If severe/life-threatening → manage in hospital → nebulised salbutamol → add nebuliser
ipratropium bromide → IV magnesium sulphate
If near fatal (PaCO2 >= 6kPa) → ICU referral → all measures as severe/life-threatening → IV
aminophylline → intubation and ventilation
Surgical:
Miscellaneous:
Complications: -

Condition: Pneumothorax

Definition: Collection of gas in the pleural space causing variable amounts of lung collapse on the
affected side. Primary (no underlying lung pathology) – asymptomatic; Secondary (lung disease
e.g. COPD/ asthma) – breathlessness out of proportion to size of pneumothorax
Causes: Chronic lung disease (asthma, COPD, CF, sarcoidosis), infection
Presentation:
Risk factors:
Symptoms: Primary – asymptomatic, dyspnoea, pleuritic chest pain; Secondary – sudden onset
breathlessness
Examination findings/Signs: Haemodynamic instability – hypoxia, hypotension, tachycardia
Investigations:
Bedside:
Bloods:
Imaging: CXR
Management:
Patient Education/ Counselling/ Resources:
Conservative: Primary → bilateral or haemodynamically unstable? → yes → proceed to chest
drain; no → pneumothorax > 2cm? Breathlessness? → yes → needle aspiration → success < 2cm?
breathing improved → discharge + review in OPD; no → 0-14 Fr chest drain, admit
Secondary → bilateral or haemodynamically unstable → yes proceed to chest drain; no →
pneumothorax > 2cm? breathlessness? → yes → 8-14 Fr chest drain + admit; no → pneumothorax
1-2cm → yes → needle aspiration → success < 1cm> → yes →admit + observe 24 hours; no → 8-
14 Fr chest drain, admit
Medical:
Surgical:
Miscellaneous:
Complications: Tension pneumothorax (medical emergency) – immediate decompression with
grey cannula into 2nd intercostal space, mid-clavicular line
Cause: intrapleural pressure > atmosphere pressure → impaired venous return and reduced CO
Associated with: ventilated patients on ICU, trauma, acute asthma/ COPD, blocked chest drains

Condition: Pneumonia

Definition: infection that inflames the air sacs in one or both lungs
Causes: most common CAP cause = S. pneumoniae, most common HAP cause = Pseudomonas
aeruginosa (E. coli, Klebsiella). Legionella causes severe pneumonia
o Haemophilus influenza – particularly common in patients with COPD
o Staphylococcus aureus – often occurs in patients following influenza infection
o Mycoplasma pneumoniae – presents with a dry cough and chest signs
o Legionella pneumophilia – seen secondary to infected air conditioning units
o Klebsiella pneumoniae – classically seen in alcoholics
o Pneumocystis juroveci – typically seen in patients with HIV, presents with a dry cough and
absence of chest signs
Presentation:
Risk factors:
Symptoms: chest pain, productive cough, fatigue, fever, sweating, malaise, difficulty breathing
Examination findings/Signs: severity of pneumonia is first assessed using the CRB65 or CURB65
score (Confusion, Urea, Respiratory rate, Blood pressure, Age >= 65)
 Low severity – CRB65 score 0 or CURB65 score 0 or 1
 Moderate severity – CRB65 score 1 or 2 or CURB65 score 2
 High severity – CRB65 score 3 or 4 or CURB65 score 3 to 5
Investigations:
Bedside: reassess if symptoms do not improve or worsen and consider non-bacterial causes such
as flu
Bloods: FBC (usually shows neutrophilia in bacterial infections), U&E, CRP; ABG
Imaging: CXR – look for consolidation and confirm whether patient meets the criteria for CAP

Management:
Patient Education/ Counselling/ Resources:
Conservative:
Medical: offer an antibiotic within 4 hours of diagnosis, consider sending a sputum sample if
severe symptoms (give oral antibiotics first line, review IV antibiotics by 48 hours and consider
switching to oral antibiotics if possible)
 Low severity – amoxicillin, no need to admit to hospital
o If allergic, give doxycycline, clarithromycin or erythromycin
 Moderate severity – amoxicillin, clarithromycin or erythromycin
 High severity – co-amoxiclav, clarithromycin, erythromycin
o If allergic, give levofloxacine
Surgical:
Miscellaneous:
Complications:

Condition: COPD and pulmonary hypertension

Definition: Combination of chronic bronchitis and emphysema (FEV1/FVC < 0.7)


Severity → mild >= 80%, very severe < 30%
 Chronic bronchitis
 Emphysema – including alpha-1 antitrypsin deficiency
 Asthma
 Bronchiectasis
Presentation:
Risk factors: usually older patients who are long-term smokers
Symptoms:
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative: COPD diagnosis → current smoker (smoking cessation immediately) → SABA or
SAMA → asthmatic features or features suggestive of steroid responsiveness (previous diagnosis
of asthma, high eosinophil count, variation in FEV1, diurnal variation in peak flow) → Yes → LABA
+ ICS (inhaled corticosteroid therapy); No → LABA+ LAMA → severe exacerbation or 2 moderate
exacerbations in 1 year? → triple therapy: LABA, LAMA, ICS;
Medical:
Surgical:
Miscellaneous:
Complications: Pulmonary hypertension – pulmonary artery pressure >=20mmHg not related to
underlying cause
Features: F>M; progressive exertional dyspnoea with lethargy; R-sided HF (raised JVP, peripheral
oedema, loud P2 +/- tricuspid regurg
Ix: Echocardiogram + pulmonary artery pressure
Mx: CCB, endothelin antagonist (bosentan), ultimately require heart-lung transplant
Tx: Current smoker? (cessation immediately) → optimisation of COPD medications → ABG: Po2 <
8.0 + features of Cor pulmonale → long term o2 therapy (cannot start if they are current
smokers!) → diuretics

Restrictive Lung Dz: drug-induced fibrosis – amiodarone, methotrexate; asbestosis; idiopathic


pulmonary fibrosis; silicosis; sarcoidosis; coal worker’s pneumoconiosis; NMD; polio; myasthenia
gravis; obesity

Condition: Bronchiectasis

Definition: permanent dilatation of the airways secondary to chronic infection or inflammation


Causes: Haemophilus influenza, pseudomonas aeruginosa, klebsiella spp., strep. Pneumoniae
Presentation:
Risk factors: having had a lung infection in the past, such as pneumonia or whooping cough that
damages the bronchi; aspergillosis; underlying problems with the immune system
Symptoms: coughing up yellow or green mucus, SOB, fatigue, fevers and chills, hemoptysis,
wheezing
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging: CXR, CT chest (tram-tracks and signet ring signs)
Management:
Patient Education/ Counselling/ Resources: physical training
Conservative:
Medical: antibiotics for exacerbations and long-term rotating antibiotics in severe cases,
bronchodilators, immunisations
Surgical: postural drainage
Miscellaneous:
Complications:

Condition: Lung cancer

Definition: Non-small cell (NSCLC) – squamous cell carcinoma, strongly linked to smoking;
adenocarcinoma is the most common NSCLC and most common lung cancer in non-smokers, most
common in smokers = squamous cell
Small cell (SCLC) – fast growing, often presents disseminated with many paraneoplastic
syndromes; often associated with SIADH, cushing’s and lambert-eaton syndrome
Presentation:
Risk factors: smoking, asbestos/ silica, family history
Symptoms: cough with blood, unplanned weight loss, progressive breathlessness
Examination findings/Signs: can present with ipsilateral elevation of the hemidiaphragm due to
compression of the phrenic nerve
Investigations:
Bedside:
Bloods:
Imaging: Referral for urgent CXR requires 2 or more or a smoking history and 1 of: cough, fatigue,
SOB, chest pain, weight loss, appetite loss
Referral for suspected cancer (2 week wait): CXR findings suggestive of lung cancer or age > 40
with unexplained haemoptysis
Management:
Patient Education/ Counselling/ Resources:
Conservative: CXR suspicious for Lung cancer → CT thorax → suspicion of neoplasm → biopsy
(endobrachial US) → NSCLC → surgical resection, adjuvant chemotherapy, radical radiotherapy,
systemic chemotherapy; SCLC → radical radiotherapy, systemic chemotherapy
Medical:
Surgical:
Miscellaneous:
Complications: widespread metastasis (brain, bone, liver, adrenal glands), hypercalcemia,
pathological fractures, side effects of chemoradiotherapy
Hypercalcemia (mild <3, severe > 3.5 mmol/l)
Fx: Acute → ECG changes, Osborn J waves, Short QT – VF; Chronic → renal stones, lethargy,
abdominal pain, polyuria, constipation, anxiety, psychosis
Tx: IV saline 0.9% 24 hours → IV zolendronate/ zolendronic acid (bisphosphonate) → recheck
serum calcium at day 2 and 4

Condition: Pulmonary embolism

Definition: Provoked or unprovoked


Presentation:
Risk factors: all malignancies
Symptoms: chest pain, worse on taking a deep breath, leg pain, SOB, low BP, cardiac arrest
Examination findings/Signs: ECG – sinus tachycardia; new complete or incomplete RBBB, right
ventricular strain pattern, atrial arrhythmias
Investigations:
Bedside: PE diagnosis → PE occurs after: surgery/ trauma in last 3 months; significant immobility
in the last 3 months; pregnancy; COCP; active cancer → provoked PE → no further Ix needed
No PE risk factors → Any symptoms consistent with cancer? → Yes → CT TAP (thorax, abdomen
and pelvis) → concern for Cancer? → no → consider thrombophilia screen (screen for anti-
phospholipid syndrome and hereditary thrombophilia); if no symptoms consistent with cancer →
bloods – FBC, U&E, clothing, physical exam, LFTs to look for cancer
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative: Haemodynamic instability? → yes → urgent thrombolysis; no →
Provoked PE → Cancer diagnosis? → yes → 6 months DOAC (Apixaban or rivaroxaban); no → 3
months DOAC
Unprovoked PE → 6 months DOAC
(Does not apply to patients who are pregnant; have poor renal function; are antiphospholipid
triple positive)
Medical:
Surgical:
Miscellaneous:
Related: Anti-phospholipid syndrome → recurrent miscarriages, prolonged APTT and
thrombocytopenia
R ventricular strain pattern → ST depression, T wave inversion V1-4 and II, III, AVF

Gastrointestinal

Condition: Acute liver failure

Definition: Liver loses the ability to regenerate or repair, so that decompensation occurs.
Causes: toxins (chronic alcohol abuse, paracetamol poisoning, illicit drugs, reye’s syndrome, drug
toxicity); infections (viral hepatitis, adenovirus, EBV, CMV); neoplastic (hepatocellular carcinoma);
Metabolic (Wilson’s disease, alpha-1-antitrypsin deficiency); pregnancy-related (acute fatty liver
of pregnancy); vascular (Budd-chiari syndrome-blockage of hepatic vein); others (autoimmune
liver disease)
Presentation:
Risk factors:
Symptoms: Hepatic encephalopathy, abnormal bleeding, ascites, jaundice
Examination findings/Signs: drowsiness or confusion, ascites, hepatomegaly, splenomegaly,
cerebral oedema, asterixis, palmar erythema
Investigations:
Bedside:
Bloods: FBC → iron-deficiency anaemia in 75% of patients with chronic liver disease,
thrombocytopenia, raised INR, raised transaminases, slightly raised alkaline phosphatase, raised
bilirubin, raised ammonia, raised creatinine, elevated lactate, low glucose. Viral serology →
infection. Specific tests → free copper in wilson’s disease and paracetamol levels
Imaging: Doppler ultrasound to check whether hepatic vein is patent (Budd-chiari syndrome) and
looking for carcinomas and ascites. Non-contrast CT or MRI to check hepatic anatomy. Imaging of
head for cerebral oedema, EEG for encephalopathy.
Management:
Patient Education/ Counselling/ Resources:
Conservative: IV NAC for paracetamol overdose; lactulose + neomycin to reduce ammonia
production; mannitol to reduce ICP
Medical: haemodialysis for acute kidney injury, give fresh-frozen plasma, platelet concentrates,
antifibrinolytic drugs, prothrombin complex and recombinant activated factor VII, IV glucose
Surgical: Liver transplant, artificial liver devices
Miscellaneous:
Complications: opportunistic infection, intracranial hypertension, oesophageal varices, sepsis,
respiratory failure, acute kidney injury.

Condition: Biliary obstruction

Definition: Yellow discolouration caused by an accumulation of bilirubin in tissue (> 35


micromol/L). Can be caused by pre-hepatic causes, hepatocellular disease, post-hepatic causes or
cholestasis
Pre-hepatic: Gilbert’s syndrome, haemolytic anaemias, thalassaemia, trauma, crigler-najjar
syndrome (diphosphate glycosyltransferase deficiency)
Hepatocellular: viral hep, leptospirosis, glandular fever, alcoholic hepatitis, autoimmune hepatitis,
drug-induced hepatitis, hepatotoxic chemicals (phosphorus, phenol), decompensated cirrhosis
Cholestasis: Dubin-johnson syndrome (autosomal recessive disorder by conjugated
hyperbilirubinemia), primary sclerosing cholangitis, common duct stone, bile duct strictures,
cancer of head of the pancreas, pancreatitis, tumour of the ampulla of vater
Presentation:
Risk factors: Ask about weight loss, recent travel history, alcohol consumption, drug abuse, blood
transfusions, education history (chlorpromazine, imipramine, isoniazid, MAOIs, oral contraceptive
pill, rifampicin, sulphonamides, salicylates), post medical history of hepatitis or biliary surgery;
occupational history; family history
Symptoms: Prodromal flu-like sx → viral hepatitis; sudden onset of jaundice with pain in healthy
patient→ gallstones; slow onset of painless jaundice with central abdominal ache, loss of appetite
and weight → carcinoma; pale stool and darkening of urine preceding jaundice → viral hepatitis
and obstructive jaundice
Examination findings/Signs: If liver is enlarged and tender → viral hepatitis; if liver edge is firm →
cirrhosis; if liver edge is irregular → malignancy; if gallbladder is palpable → probable that cause is
not a stone; if liver is smoothly enlarged → post hepatic obstructive jaundice; splenomegaly →
cirrhosis, haematological disorders
Investigations:
Bedside: LFT (raised unconjugated: Gilbert’s, haemolysis, mild chronic hepatitis, crigler-najjar
syndrome; raised conjugated: liver disease, pancreatic disease, dubin-johnson syndrome)
Prehaptic: normal LFT, elevated bilirubin
Hepatic: Increased AST and ALT, increased GGT and ALP at later stages, elevated bilirubin, albumin
and clotting factors (viral hepatitis, non-alcoholic fatty liver disease, alcohol related liver disease,
autoimmune hepatitis
Posthepatic: Increased GGT and ALP, elevated bilirubin (raised ALP → primary biliary cholangitis,
primary sclerosing cholangitis, biliary obstruction, liver congestion, bone disease (paget’s disease))
Mixed picture: cholestasis and hepatocyte damage due to cholangitis associated with stones in
the common bile duct
Bloods: prothrombin time (prolonged in vitamin K malabsorption), serum immunoglobulins (acute
hepatitis), alpha-1-antitrypsin levels (cirrhosis and emphysema), ferritin (haemochromatosis)
Imaging: abdominal ultrasound; no CBD stones but LFTs or bile duct dilatation on ultrasound, do a
MRCP
“Beads on a string” on ERCP → Primary sclerosing cholangitis
Management:
Patient Education/ Counselling/ Resources:
Conservative: arrange admission to secondary care if person with jaundice has any red flags
(hepatic encephalopathy → confusion, altered neuromuscular function; severe hepatic
dysfunction → bruising, purpura; GI bleed → hematemesis or melena; sepsis → fever,
hypotension, tachycardia; ascending cholangitis → fever, jaundice and right upper quadrant pain
(charcot’s triad), marked abdominal pain, suspected paracetamol overdose, weight loss
Medical:
Surgical: laparoscopic cholecystectomy and an ERCP
Miscellaneous:
Complications:

Condition: Cholecystitis

Definition: Inflammation of the gallbladder due to obstruction of the gallbladder neck or cystic
duct
Presentation:
Risk factors: gallstones 90-95% of the time (increasing age, female, obesity, low fibre diet); bile
stasis or thickening (sepsis, major surgery, extensive trauma, prolonged fasting or starvation)
Symptoms: sudden onset, constant, severe pain in the URQ lasting several hours; tenderness,
fever, severe steady pain that may radiate to the back, referred pain can be felt in the right
shoulder or interscapular region
Examination findings/Signs: murphy’s sign (inspiration is inhibited by pain on palpitation when
examiner’s hand is positioned along the costal margin), palpable mass (abscess), signs of sepsis
(mottled skin, fever, rigors, chills, SOB)
Investigations:
Bedside: monitor blood pressure, pulse and urine output
Bloods: WBC, CRP, serum amylase
Imaging: CT or MRI of abdomen, abdominal ultrasound (consider MRCP and endoscopic
ultrasound)
Management:
Patient Education/ Counselling/ Resources:
Conservative: Intravenous fluids, antibiotics, analgesia
Medical:
Surgical: cholecystectomy
Miscellaneous:
Complications:

Condition: Gallstones
Definition:
Presentation:
Risk factors:
Symptoms:
Disease Features Management
Biliary colic Colicky abdominal If imaging shows gallstones and history
pain, worse compatible then laparoscopic
postprandially, cholecystectomy
worse after fatty
foods
Acute Right upper Analgesics, no drinking or eating, IV fluid
cholecystiti quadrant pain → Imaging (USS) and cholecystectomy
s Fever (ideally within 48 hours of presentation)
Murphys sign on (2)
examination
Occasionally mildly
deranged LFT's
(especially if Mirizzi
syndrome)
NO JAUNDICE
Gallbladder Usually prodromal Imaging with USS +/- CT Scanning
abscess illness and right Ideally, surgery although subtotal
upper quadrant cholecystectomy may be needed if
pain Calot's triangle is hostile
Swinging pyrexia In unfit patients, percutaneous drainage
Patient may be may be considered
systemically unwell
Generalised
peritonism not
present
Cholangitis Patient severely Fluid resuscitation
septic and unwell Broad-spectrum intravenous antibiotics
Jaundice (ciprofloxacin, co-amoxiclav, co-
Right upper trimoxazole
quadrant pain Correct any coagulopathy
Early ERCP
Gallstone Patients may have Laparotomy and removal of the gallstone
ileus a history of from small bowel, the enterotomy must
previous be made proximal to the site of
cholecystitis and obstruction and not at the site of
known gallstones obstruction. The fistula between the
Small bowel gallbladder and duodenum should not be
obstruction (may interfered with.
be intermittent)
Acalculous Patients with
cholecystiti intercurrent illness
s (e.g. diabetes,
organ failure)
Patient of
systemically unwell
Gall bladder
inflammation in the
absence of stones
High fever

Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging: ultrasound + blood test for signs of infection
Management:
Patient Education/ Counselling/ Resources:
Conservative:
Medical:
Surgical: cholecystectomy via the laparoscopic route; during procedure, perform interoperative
cholangiography to confirm anatomy or to exclude CBD stones (laparoscopic ultrasound is easier
for stones)
Miscellaneous:
Complications:

Condition: Hepatitis

Definition:
Presentation:
Risk factors:
Symptoms:
Examination findings/Signs:
Investigations:
Bedside: abnormal liver function → (1) hepatitis picture AST/ALT raised → AST: ALT ratio >= 2:1 →
alcohol related (or else consider NAFLD, hep A,B,C,D,E, autoimmune hepatitis, ischaemic hepatitis,
drugs: TB medications, methotrexate, paracetamol)
(2) cholestatic picture bilirubin/ALP raised → RUQ pain → gallstone-related obstructive pathology
(or else pancreatic tumour, cholangiocarcinoma, primary biliary cholangitis, primary schlerosing
cholangitis, drugs: penicillin, sulfonylureas)
Bloods: blood labs
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative:
Medical: chronic hep B → refer to secondary care for management → interferon-alpha → anti-
viral therapy e.g. tenofovir or entecavir. Hep C → notify public health England → direct acting anti-
virals
Surgical:
Miscellaneous:
Complications:

Condition: Acute Pancreatitis


Definition: autodigestion of pancreatic tissue by the pancreatic enzymes, leading to necrosis
Causes: GET SMASHED – gallstones, ethanol, trauma, steroids, mumps, autoimmune, scorpion
venom, hypertriglyceridaemia/ hyperchylomicronaemia/ hypercalcaemia/ hypothermia, ERCP,
drugs (azathioprine, bendroflumethiazide, furosemide, pentamidine, steroids)
Presentation:
Risk factors:
Symptoms: severe epigastric pain that may radiate through to the back, vomiting, epigastric
tenderness, ileus and low-grade fever, Cullen’s sign (periumbilical discolouration) and flank
discolouration (grey-turner’s sign)
Examination findings/Signs:
Investigations:
Bedside:
Bloods: serum amylase (raised in 75% of patients), levels do not correlate with disease severity;
serum lipase (more sensitive and specific than serum amylase; longer half-life than amylase)
Imaging: diagnosis can be made without imaging if characteristic pain + amylase/ lipase > 3 times
normal level; early ultrasound imaging can be used to assess the aetiology as this may affect
management e.g. gallstones/ biliary obstruction; MRCP or EUS if underlying cause is unknown
Management:
Patient Education/ Counselling/ Resources:
Conservative: use scoring systems (ranson score, Glasgow score and APACHE II) to identify
severity of pancreatitis which may require intensive care (age > 55, hypocalcaemia,
hyperglycaemia, hypoxia, neutrophilia, elevated LDH and AST
Medical: resuscitation with intravenous fluids, supplemental o2, IV analgesia, IV antibiotics for
infected pancreatic necrosis and/or cholangitis
Surgical:
Miscellaneous:
Complications: peripancreatic fluid collections in or near pancreas, pseudocysts, pancreatic
abscess, haemorrhage

Condition: Chronic Pancreatitis

Definition: inflammatory condition that can affect both exocrine and endocrine functions of the
pancreas. Around 80% of cases are due to alcohol excess. Other causes: cystic fibrosis,
haemochromatosis; ductal obstruction – tumors, stones, structural abnormalities
Presentation:
Risk factors:
Symptoms: pain getting worse 15-30 mins following a meal, steatorrhoea, diabetes mellitus
(occurs more than 20 years after symptoms begin)
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging: abdominal x-ray shows pancreatic calcification in 30% of cases; CT is more sensitive at
detecting pancreatic calcification; faecal elastase
Management:
Patient Education/ Counselling/ Resources:
Conservative: Pancreatic enzyme supplements, analgesia
Medical:
Surgical:
Miscellaneous:
Complications:
Condition: Appendicitis

Definition: inflammation of the appendix


Presentation:
Risk factors:
Symptoms: abdominal pain at epigastric region that migrates to the right lower quadrant over 24-
48 hours, often worsened by movement, fever, general malaise, anorexia, nausea and vomiting,
constipation
Examination findings/Signs: facial flushing, dry tongue, low-grade fever, tenderness in the RLQ
over McBurney’s point, abdominal distension, guarding, rebound tenderness, percussion
tenderness (peritonitis), absent bowel sounds may indicate ileus or peritonitis associated with
perforation, palpable mass, Rovsing’s sign (palpitation of LLQ increases pain in RLQ)
Investigations:
Bedside:
Bloods: FBC (increased neutrophil), raised CRP, urine dipstick test (to exclude UTI), pregnancy test
(to exclude ectopic pregnancy)
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative: arrange emergency hospital admission if acute appendicitis is suspected.
Medical: IV fluid and antibiotics if acute appendicitis is uncomplicated
Surgical: gold standard = removal of appendix. If patient is experiencing persistent pain, do a
laparoscopy for alternative diagnosis
Miscellaneous:
Complications:

Condition: Inflammatory bowel disease

Definition: Ulcerative colitis or Crohn’s disease


Presentation:
Risk factors: family history of IBD, coeliac disease or colorectal cancer
Symptoms: UC → bloody diarrhoea for more than 6 weeks, faecal urgency, nocturnal defecation,
tenesmus (persistent, painful urge to pass stool even when rectum is empty), abdominal pain
(especially in left lower quadrant), weight loss, fatigue, malaise
Crohn’s disease → persistent diarrhoea (less likely to be bloody), faecal urgency, abdominal pain,
tenesmus, nocturnal diarrhoea, weight loss
Examination findings/Signs: UC → pallor, clubbing, mouth ulcers, abdominal distention,
tenderness, signs of malnutrition
Crohn’s disease → pallor, clubbing, abdominal tenderness or mass in lower quadrant, perianal
tenderness, signs of malnutrition
Investigations:
Bedside:
Bloods: UC → FBC (Anaemia due to blood loss, malabsorption, increased WBC); CRP; U&E, LFT;
thyroid function tests; serum ferritin, vitamin B12, folate, vitamin D; coeliac serology; stool
microscopy and culture including clostridium difficile (to exclude infective gastroenteritis)
Crohn’s disease → same
Imaging: UC → colonoscopy with biopsy; upper intestinal endoscopy for children and young
people (to differentiate crohn’s and UC as UC affects the entire colon whereas crohn’s affects any
part of the digestive tract from mouth to anus) Barium enema → loss of haustrations; superficial
ulceration, 'pseudopolyps', long standing disease: colon is narrow and short -'drainpipe colon'.
Histology → No inflammation beyond submucosa (unless fulminant disease) - inflammatory cell
infiltrate in lamina propria; neutrophils migrate through the walls of glands to form crypt
abscesses; depletion of goblet cells and mucin from gland epithelium; granulomas are infrequent
Crohn’s disease → Histology - Inflammation in all layers from mucosa to serosa; increased goblet
cells; granulomas
Management:
Patient Education/ Counselling/ Resources:
Conservative: UC → Signs of acute, severe disease? (>6 stools, frank blood, temperature, HR > 90,
anaemia, ESR > 30) →
Yes? → Admit + IV hydrocortisone → no improvement? → IV ciclosporin + surgical input →
infliximab
No? → (1) Proctitis, proctosigmoiditis, L sided colitis → topical aminosalicylate (salfasalazine) →
no improvement at 4 weeks? → oral aminosalicylate
→ (2) Pancolitis → topical + oral aminosalicylate → no improvement at 4 weeks → oral
corticosteroids
Crohn’s disease → glucocorticosteroid (prednisolone, IV hydrocortisone) → contraindicated? →
budesonide or aminosalicylate (do not use both for severe presentations) → add azathioprine or
mercaptopurine if there are 2 or more inflammatory exacerbations in a 12-month period →
contraindicated? → methotrexate + glucocorticosteroid → infliximab if severe and do not respond
to conventional therapy
Medical:
Surgical: ileocaecal resection, segmental small bowel resections, stricturoplasty, perianal fistulae,
perianal abscess
Miscellaneous:
Complications: UC → toxic megacolon – colonic dilatation + systemic toxicity with risk of bowel
perforation; “3-6-9” rule – 3cm small bowel, 6cm large bowel, 9cm caecum → Mx: IV
hydrocortisone, infliximab or surgery
Crohn’s disease → passing gas or faeces into the urine or vagina, partial or complete bowel
obstruction, perianal discharge of mucus or pus; small bowel cancer; colorectal cancer (less than
UC); osteoporosis

Condition: Gastro-oesophageal reflux disease

Definition: a condition where some of the acidic stomach contents come back up the oesophagus
towards the mouth
Presentation:
Risk factors:
Symptoms: heartburn, pain in the chest behind the breastbone, and can move up the breastbone,
unpleasant taste in mouth and swallowing problems
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative:
Medical: full-dose PPI for 4-8 weeks (Esomeprazole, lansoprazole, omeprazole) → if symptoms
continue to recur → offer PPI at lowest dose possible → offer self-management advice →
investigate Barrett’s oesophagus (risk factors: long duration of symptoms, increased frequency of
symptoms, previous oesophagitis, previous hiatus hernia, oesophageal stricture, male gender) →
laparoscopic fundoplication (a confirmed diagnosis of acid reflux that are responding to ppi but
who cannot tolerate acid suppression therapy)
Surgical:
Miscellaneous:
Complications: Barrett’s oesophagus → stratified squamous epithelium is replaced by columnar
epithelium (increases risk of oesophageal adenocarcinoma) → mainly asymptomatic
Other risk factors → male gender, smoking, central obesity
Diagnosis → endoscopy for upper GI symptoms such as dyspepsia
Management → endoscopic surveillance with biopsies, high dose PPI

Condition: Coeliac disease

Definition: a condition of the small bowel resulting in villous atrophy from ingestion of gluten in
the diet. Associated with other autoimmune conditions: type 1 diabetes, autoimmune thyroiditis
Presentation:
Risk factors:
Symptoms: persistent unexplained GI symptoms, fatigue, unexpected weight loss, unexplained
iron, B12 or folate deficiency, T1DM
Examination findings/Signs:
Investigations:
Bedside:
Bloods: Ensure eating gluten for 6 weeks before serological testing →
(1) IgA TTG → (+) endoscopy + duodenal biopsy; weakly (+) IgA EMA; (-) consider IgG EMA,
IgG TTG
(2) Serum IgA levels → refer to gastroenterology if clinical suspicion
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative: gluten free diet
Medical:
Surgical:
Miscellaneous:
Complications: Extra-intestinal manifestations: dermatitis herpetiformis, metabolic bone disorder
(osteomalacia), anaemia (iron deficiency, B12, folate), hyposplenism, T cell gastrointestinal
lymphoma

Condition: Irritable bowel syndrome

Definition: a chronic, relapsing, lifelong disorder of the lower GI recurring at least 1 day/week in
last 3 months.
Presentation:
Risk factors:
Symptoms: abdominal pain associated with a change in stool form and/ or frequency (diarrhoea
and constipation), bloating
Examination findings/Signs:
Investigations:
Bedside: if person has abdominal pain which is either related to defecation or associated with
altered stool frequency or appearance and has at least 2 of the following: 1. Alternative conditions
with symptoms have been excluded, passage of rectal mucus, symptoms worsened by eating,
abdominal bloating, altered stool passage
Bloods: FBC, EST, CRP, Coeliac serology
Imaging:
Management:
Patient Education/ Counselling/ Resources: psychological interventions if do not respond to
pharmacological Mx in 12 months; eat regular meals that are healthy and balanced, fibre
supplements, probiotics, fluid intake, regular exercise
Conservative:
Medical: bulk-forming laxative, linaclotide, loperamide for diarrhoea, antispasmodic for pain
(smooth muscle relaxants e.g. mebeverine hydrochloride, alverine citrate, peppermint oil),
TCA/SSRI for refractory abdominal pain
Surgical:
Miscellaneous:
Complications:

Condition: Peptic ulcer

Definition: Includes gastric or duodenal ulceration, which is a breach in the epithelium of the
gastric or duodenal mucosa. Common causes are NSAID use and H.pylori infection
Presentation:
Risk factors: smoking, alcohol consumption, stress, usage of drugs that increase risk of GI adverse
effects (anticoagulants, corticosteroids, SSRIs), has a serious co-morbidity (CVD, hypertension,
diabetes, renal or hepatic impairment)
Symptoms: upper abdominal pain, pain is worse after eating, nausea, indigestion, heartburn, loss
of appetite, weight loss and bloated feeling
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources: healthy eating, weight loss, avoid trigger foods,
eating smaller meals, eating evening meal 3-4 hours before going to bed, raise the head of the
bed, stop smoking, reduce alcohol
Conservative: stop drugs that induce peptic ulcers (NSAIDs, aspirin, bisphosphonates,
immunosuppressive agents, potassium chloride, SSRIs, recreational drugs)
Medical: H.pylori – amoxicillin and clarithromycin; PPI for ulcer associated with NSAID use (8
weeks); if unable to find cause – give PPI for 4 to 8 weeks
Follow-up: patients positive for H.pylori need a repeat endoscopy 6-8 weeks after treatment to
confirm ulcer healing. Review need for NSAIDs at least every 6 months and use on a limited, as
needed basis. Consider a COX-2 inhibitor instead of an NSAID and PPI or H2-receptor antagonist
for gastro-protection. If symptoms are persisting, check for patient adherence and other rare
causes.
Surgical:
Miscellaneous:
Complications:

Condition: Gastroenteritis
Definition: bacteria or virus causing diarrhoea and vomiting
Presentation:
Risk factors: dehydration risk factors like fluid intake, food intake, urinary output
Symptoms: sudden onset diarrhoea usually at least 3 times in 24 hours, blood or mucus in stool,
faecal urgency, nausea or sudden vomiting, fever or general malaise, abdominal pain or cramps,
headache, myalgia, bloating, flatulence, weight loss, malabsorption
Examination findings/Signs: ask about occupation, recent food intake, exposure to contaminated
water, foreign travel, recent contact with affected individuals, recent antibiotic, PPI use or hospital
admission (C.diff), ACE or diuretics (stop to reduce risk of dehydration and acute kidney injury)
Investigations:
Bedside: stool culture and sensitivity if person is unwell or immunocompromised, has bloody or
painful diarrhoea, has had recent antibiotic or PPI tx, recent hospital admission, suspected food
poisoning, has travelled abroad, prolonged diarrhoea, at risk of transmission of infection or was in
contact with an affected person or outbreak of diarrhoea
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources: advice person not to attend work or other social
settings until at least 48 hours after last episode of diarrhoea or vomiting, if cyrtosporidiosis or
giardiasis is suspected, person cannot go swimming for 2 weeks after last episode of diarrhoea ->
notify local health protection team of notifiable diseases (food poisoning: bacillus cereus,
campylobacter spp. Clostridium perfringens, cryptosporidium spp., entomoeba histolytica, e.coli,
salmonella spp. Giardia lamblia; haemolytic uraemic syndrome; infectious bloody diarrhoea;
enteric fever; cholera)
Conservative: emergency hospital admission if person is unwell and is showing signs of
dehydration -> encourage regular fluid intake (oral rehydration salts if at increased risk of
dehydration)
Medical: antidiarrhoeal, antiemetics, probiotics not routinely used and cannot be used if person
has blood or mucus in stools or high fever or is confirmed to have shigellosis or shiga toxin
producing E. coli 0157 infection
 Campylobacteriosis: clarithromycin if severe
 Amoebic dysentery: metronidazole and antiprotozoal drug diloxanide
 E. coli: if there is confirmed infection, 2 consecutive neg stool samples are needed for at
least 24 hours apart, once person is symptom free for at least 48 hours before they can
return to work - no antibiotic treatment available
 Giardiasis: tinidazole
 Salmonella: none
 Shigellosis: none unless severe, advice on safe sex if transmission is amongst men
Surgical:
Miscellaneous:
Complications:

Condition: Diverticular disease

Definition: herniation of colonic mucosa through the muscular wall of the colon, usually between
the taenia coli where vessels pierce the muscle to supply the mucosa (if asymptomatic →
diverticulosis)
Presentation:
Risk factors:
Symptoms: altered bowel habit, rectal bleeding, abdominal pain
Examination findings/Signs:
Investigations:
Bedside: colonoscopy
Bloods:
Imaging: CT cologram, barium enema, abdominal scan with oral and IV contrast will help to
identify whether acute inflammation is present
Management:
Patient Education/ Counselling/ Resources: increased dietary fibre intake
Conservative: antibiotics for mild attacks
Medical:
Surgical: recurrent episodes require hospitalisation and segmental resection. Hinchey IV
perforations (generalised faecal peritonitis) will require resection and a stoma – less severe
perforations may be managed by laparoscopic washout and drain insertion.
Miscellaneous:
Complications: diverticulitis, haemorrhage, development of fistula, perforation and faecal
peritonitis, perforation and development of abscess

Condition: Large bowel obstruction

Definition: passage of food, fluids and gas through large intestines become blocked
Causes: tumour (60% - esp. in distal colonic and rectal tumours), volvulus, diverticular disease
Presentation:
Risk factors:
Symptoms: absence of passing flatus or stool, abdominal pain or distention, nausea and vomiting
are late symptoms, peritonism may be present if there is associated bowel perforation
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging: abdominal x-ray (normal: 10-12cm for caecum, 8cm for ascending colon, 6.5cm for
recto-sigmoid); CT scan (good for identifying obstruction and aetiology of obstruction)
Management:
Patient Education/ Counselling/ Resources:
Conservative: NBM, IV fluids, nasogastric tube with free drainage for up to 72 hours
Medical: IV antibiotics can be given if perforation is suspected or surgery planned - Metronidazole
Surgical: if there is any overt peritonitis or evidence of bowel perforation → emergency surgery;
address underlying cause of obstruction → irrigation of abdominal cavity, resection of perforated
segment and ischaemic bowel
Sigmoid volvulus → untwist the sigmoid loop by passing a flatus tube alongside a sigmoidoscope
→ rapid recompression of distended colon for 24 hours → resection of colon (double-barrelled
colostomy
Miscellaneous:
Complications:

Conditions: Small bowel obstruction

Definition: passage of food, fluids and gas through the small intestines becomes blocked. Most
common cause is adhesions caused by previous surgery.
Presentation:
Risk factors:
Symptoms: diffuse, central abdominal pain; nausea and vomiting; constipation with complete
obstruction and lack of flatulence; abdominal distension; tinkling bowel sounds
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging: abdominal x-ray – distended small bowel loops with fluid levels (considered dilated if
small bowel is >3cm diameter; CT is more definitive
Management:
Patient Education/ Counselling/ Resources:
Conservative: Acutely unstable patient with imminent risk of death? → emergency laparotomy
mm; stable? → CT of abdomen and pelvis with IV contrast (if Egfr<30 then CT without contrast) →
bowel ischaemia, obstructive lesion, closed loop obstruction? → Yes? → emergency laparotomy;
No? → adhesional SBO → trial of conservative management (NG tube and IV fluids)
Medical:
Surgical:
Miscellaneous:
Complications:

Condition: Ischaemic colitis

Definition: inflammation in the large intestine or colon resulting from a lack of blood flow to that
area, usually because an artery is blocked or narrowed.
Presentation:
Risk factors:
Symptoms: abdominal pain, diarrhoea and/ or rectal bleeding in the presence of risk factors for
ischaemia – intermittent pain usually after eating
Examination findings/Signs:
Investigations:
Bedside: ECG
Bloods: FBC, U&E, LFT, CRP, coagulation screen, serum lactate
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative:
Medical:
Surgical: IRCI suspected (right-sided colitis)? -> CT mesenteric angiography -> Vascular occlusion ->
Yes? -> consider intravenous angiography to relieve vascular occlusion -> surgical review and
consider emergency surgical resection; No? -> Lower GI endoscopy
IRCI not suspected? -> CT abdomen and pelvis with intravenous contrast -> lower GI endoscopy ->
haemodynamic compromise complications? -> No? -> Trail conservative mx (IV antibiotics, fluids,
bowel rest)
Yes? -> surgical review and consider emergency surgical resection
Miscellaneous:
Complications:

Condition: Colorectal cancer

Definition: 90% are adenocarcinomas, 75% are distal to the splenic flexure, 25% are proximal
Presentation:
Risk factors: smoking, red meat consumption, low fibre diet; male, age, FHx, IBD; genetic: FAP,
HNPCC, Peutz-Jehgers syndrome
Symptoms: change in bowel habit, palpable mass, iron deficiency anaemia (red flag sx in males
and post-menopausal women >= 60), PR bleed, acute (obstruction or perforation)
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging: Colonoscopy or CT colonogram → staging CT thorax and referral for resection if needed
MRI → staging of rectal cancer
Management:
Patient Education/ Counselling/ Resources:
Conservative: Colon cancer → T4 → consideration for neoadjuvant treatment; T1-T3 → colonic
resection → T3+ or nodal disease → adjuvant chemotherapy
Rectal cancer → T3-4 → neoadjuvant treatment → colonic resection → T3+ or nodal disease →
adjuvant chemotherapy; T1-2 → transanal excision
Medical:
Surgical:
Right Left Sigmoid Anterior Abdominoperineal
hemicolectom hemicolectomy colectomy/ resection resection
y Hartmann’s
Indication Proximal colon Left colon up Sigmoid Rectal Rectal (tumour <
(tumour to the hindgut to sigmoid tumour > 5cm) from anal
location) 5cm from verge
anal verge
What is Ascending Descending Sigmoid Rectum, Rectum,
resected? colon and colon and colon sparing the sphincters and
caecum splenic flexure sphincters anus
Stoma No No Yes – if No Yes
likely? Hartmanns
Type of Ileostomy Colostomy Colostomy Colostomy Colostomy
stoma if
needed
Miscellaneous:
Complications:

Renal and Urology


Urinalysis

 Glucose – normal is to have no glucose in urine. Causes of glycosuria are diabetes, renal
tubular disease and some diabetic medications (SGLT2 inhibitors)
 Bilirubin – normal is to have no bilirubin. Causes of presence of bilirubin are increased levels
of conjugated bilirubin due to biliary obstruction
 Ketones – normal is to have no ketones. Presence of ketones is due to increased fatty acid
metabolism such as in diabetic ketoacidosis
 Specific gravity – low specific gravity is due to production of dilute urine such as diabetes
insipidus and acute tubular necrosis; high specific gravity is due to dehydration, glycosuria,
proteinuria (nephrotic syndrome)
 PH – low ph is due to starvation, diabetic ketoacidosis, metabolic acidosis (sepsis); high ph is
due to UTIs, metabolic alkalosis and medications (diuretics)
 Blood – absence of RBCs, haemoglobin and myoglobin is normal. Presence means UTI, renal
stones, injury to urinary tract, myoglobinuria, nephritic syndrome and malignancy of the UT
 Protein – absence is normal. Causes are nephrotic syndrome and chronic kidney disease
 Nitrites – absence is normal. Presence means UTIs (breakdown of gram-negative organisms)
 Urobilinogen – presence is normal. Increased levels can be caused by haemolysis
(haemolytic anaemia, malaria). Low levels can be caused by biliary obstruction
 Leukocyte esterase – enzyme produced by neutrophils so positive finding indicates presence
of WBCs in the urine. Cause can be due to a UTI.

Drug treatment of overactive bladder

 Non-surgical: lifestyle changes, pelvic floor muscle training, bladder training;


o For stress incontinence: duloxetine (SNRI)
o For urge incontinence: oxybutynin, tolterodine (Antimuscarinics)
o For nocturia: desmopressin

Condition: Acute kidney injury

Definition: abrupt loss of kidney function resulting in the retention of urea and other nitrogenous
waste products and in the dysregulation of extracellular volume and electrolytes
Causes: Prerenal (volume depletion e.g. haemorrhage, severe vomiting or diarrhoea, burns,
diuresis; cardiac failure, cirrhosis, nephrotic syndrome; hypotension (cardiogenic shock, sepsis,
anaphylaxis); cardiovascular (severe cardiac failure, arrhythmias); renal hypoperfusion (NSAIDs or
COX-2 inhibitors, ACE inhibitors))
Intrinsic renal: Glomerulonephritis, thrombosis, haemolytic uraemic syndrome, acute tubular
necrosis, nephrotoxins, acute interstitial nephritis due to drugs, infection or autoimmune diseases,
vasculitis, renal artery stenosis, renal vein thrombosis, eclampsia
Postrenal: calculus, blood clot, papillary necrosis, bladder tumour, radiation fibrosis, pelvic
malignancy, prostatic hypertrophy
Presentation:
Risk factors: age > 65 y/o, Egfr < 60, past history of AKI, co-existing illness (cardiac failure, liver
disease or diabetes), neurological impairment or disability, hypovolaemia, sepsis, use of iodinated
contrast agents in previous week, medication with nephrotoxic potential (NSAIDs, ACE inhibitors,
aminoglycosides, diuretics)
Symptoms: Rise in serum creatinine within 48 hours, 50% increase in serum creatinine within
preceding 7 days, fall in urine output to less than 0.5Ml/kg/hour; anuria/oliguria (acute anuria
suggest acute obstruction, acute glomerulonephritis or acute renal artery occlusion), gradual
diminution could be urethral stricture or bladder outlet obstruction; nausea, vomiting,
dehydration
Examination findings/Signs: Signs of infection or sepsis; acute or chronic heart failure fluid status
(dehydration or fluid overload); palpable bladder or abdominal mass; systemic disease (rashes)
Investigations:
Bedside: urinalysis (blood, nitrates, leukocytes, glucose and protein)
Bloods: FBC, U&Es and creatinine, disseminated intravascular coagulation associated with sepsis,
creatine kinase (+ myoglobinuria = rhabdomyolysis), CRP, raised antitreptolysin O and anti-DNase
B in streptococcal infection; hep B and C
Imaging: CXR (pulmonary oedema), abdominal x-ray, Doppler ultrasound for occlusion of renal
artery and veins, Magnetic resonance angiography
Management:
Patient Education/ Counselling/ Resources:
Conservative: stop nephrotoxic drugs → monitor creatinine, sodium, potassium, calcium,
phosphate, glucose
Medical: relief of urinary tract obstruction (papillary necrosis, tumours, strictures); acute tubule-
interstitial nephritis (high-dose corticosteroids) → refer to urologist if there is an obstructive cause
Surgical: angioplasty or stenting if acute renal artery stenosis
Dialysis → AEIOU
Acidosis, Electrolyte: hyperkalaemia, Intoxications, Oedema (pulmonary), Uraemia (hyperuraemia)
Miscellaneous:
Related: Chronic kidney disease
Risk factors: hypertension, diabetes, chronic NSAID use, prolonged AKI, untreated outflow
obstruction, cardiovascular disease
Progression: sustained decrease in Egfr over 12 months
Complications: anaemia, mineral and bone disorders, fluid overload, hyperkalaemia, acidosis,
osteodystrophy (polyathropathy, fractures, calcific skin lesions)

Condition: Chronic kidney disease

Definition: gradual decline of kidney function over >= 3 months


Causes:
 Hypertension (most common) -> hypertrophy or sclerosis of renal arteries ->
hypoperfusion -> growth factor secretion by macrophages -> mesangial cells regress to
mesoangioblasts, secrete extracellular matrix -> glomerulosclerosis, loss of function
 Diabetic nephropathy -> non-enzymatic glycosylation of efferent arterioles -> initial
hyperinflation -> mesangial cells secrete structural matrix -> nodular glomerulosclerosis
 (less common) -> glomerulonephritis, rheumatoid arthritis, HIV nephropathy, long term
NSAID use, polycystic kidney disease
Presentation:
Risk factors: family history, reflux nephropathy, other congenital kidney disorders
Symptoms: less advanced stages usually asymptomatic, oliguria (urine output < 400ml in 24
hours), peripheral oedema, uremic pruritus, excoriations, ulcerations, bleeding of GI, increased K+
(cardiac arrhythmias), fatigue, confusion, appetite loss
Examination findings/Signs: iron deficiency anaemia, metabolic acidosis, high Cr over months,
increased blood urea nitrogen: creatinine, decreasing GFR
 Decreased erythropoietin -> anaemia
 Decreased GFR -> hypertension
 Decreased vitamin D activation -> decreased intestinal absorption of Ca2+ ->
hypocalcaemia
Investigations:
Bedside:
Bloods:
Imaging: ultrasound to exclude polycystic kidney disease, renal artery stenosis, hydronephrosis
Management:
Patient Education/ Counselling/ Resources:
Conservative: dialysis, haemodialysis (remove excess waste products and fluids via artificial
kidney), peritoneal dialysis
Medical: ACE inhibitors, ARBs
Surgical: kidney transplant – patient at risk of developing Pneumocystis jiroveci pneumonia due to
suppressed immune system (opportunistic infection)
Miscellaneous:
Complications: renal osteodystrophy (increased risk of skeletal fractures, caused by secondary
hyperparathyroidism due to lack of vitamin D), renovascular hypertension, congestive heart
failure

Condition: Renal stones

Definition:
Presentation:
Risk factors:
Symptoms:
Examination findings/Signs:
Investigations:
Bedside: urine dipstick and culture, serum creatinine and electrolytes, FBC/ CRP, calcium/ urate
Bloods:
Imaging: non-contrast CT KUB for all patients; if uncertain, do CT KUB to exclude other diagnoses;
CT > ultrasound
Management:
Patient Education/ Counselling/ Resources:
Conservative: Initial mx – NSAID (be wary of CVD with diclofenac), offer IV paracetamol if NSAID is
contraindicated
Medical: DO NOT give antispasmodics
Surgical: stones < 5mm will pass spontaneously
Disease Option
Stone burden of less than 2cm in aggregate Lithotripsy
Stone burden of less than 2cm in pregnant Ureteroscopy
females
Complex renal calculi and staghorn calculi Percutaneous
nephrolithotomy
Ureteric calculi less than 5mm Manage expectantly
Miscellaneous:
Complications:

Condition: Testicular torsion

Definition: twisting of the spermatic cord causing blood flow to the testis to be blocked. Most
commonly seen in teenage boys aged 13-18 years.
 Extravaginal torsion predominates in utero and in neonates where twisting of the entire
cord including the processus vaginalis
 In older children and adults, testicular torsion is usually intravaginal where there is
twisting of the cord within the tunica vaginalis
Presentation:
Risk factors:
Symptoms: severe pain that develops quickly within a few hours, often much more quickly; pain
might be in the lower abdomen, nausea and vomiting (easing pain is not a good sign because pain
also eases as the testis starts to die)
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging: ultrasound
Management:
Patient Education/ Counselling/ Resources:
Conservative:
Medical:
Surgical: refer to urology or paediatric surgery -> immediate surgical detorsion and bilateral
orchidopexy (fixation of the testicle)
 Surgical repair within 4 hours to salvage the testicle and prevent atrophy
 Non-operative management by NSAIDs
Miscellaneous:
Complications:

Condition: Lower UTI

Definition: a bladder infection usually caused by bacteria travelling up the urethra from the
genitourinary tract
Presentation:
Risk factors:
Symptoms: burning with urination, increased urgency of urination, bloody urine, cloudy urine,
strong odour, pelvic pains
Examination findings/Signs:
Investigations:
Bedside:
 Non-pregnant women: Consider a back-up antibiotic prescription or immediate antibiotic
 Pregnant women, or man, or child or young person under 16 years old: send midstream
urine for culture and susceptibility for pregnant women and men. Send urine for culture
and susceptibility or dipstick in line with NICE guidelines for under 16s. Offer immediate
antibiotics
 Reassess at any time if symptoms worsen or do not improve in 48 hours of taking
antibiotics and refer to hospital if there are signs of sepsis
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative: paracetamol or ibuprofen for pain, advice drinking enough fluid to avoid
dehydration
Medical: Antibiotics; asymptomatic bacteriuria is treated in pregnant women because of risk
factor for pyelonephritis and premature delivery
For non-pregnant women aged 16 years and over:
 1st choice: Nitofurantoin 100mg or trimethoprim 200mg
 2nd choice: Nitrofurantoin 100mg, pivmecillinam 400mg, fosfomycin 3g
For children aged 3 months or over:
 1st choice: Trimethoprim 4mg/kg or nitrofurantoin 750 micrograms/kg
 2nd choice: nitrofurantoin or amoxicillin or cefalexin
For pregnant women aged 12 years and over:
 1st choice: nitrofurantoin 100mg (7 day course)
 2nd choice: amoxicillin, cefalexin, alternative second choice
 Choose from nitrofurantoin, amoxicillin or cefalexin for asymptomatic bacteriuria
For men aged 16 years and over:
 1st choice: trimethoprim 200mg, nitrofurantoin 100mg
 2nd choice: consider alternative diagnoses
Surgical:
Miscellaneous:
Complications:

Condition: Pyelonephritis

Definition: an infection of one or both kidneys caused by bacteria travelling up from the bladder
Presentation:
Risk factors: possesses abnormalities of the genitourinary tract or underlying disease such as
diabetes or immunosuppression
Symptoms:
Examination findings/Signs:
Investigations:
Bedside: send a midstream urine sample for culture and susceptibility testing for people aged 16
years and older
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative: advice paracetamol for pain or low-dose of a weak opioid such as codeine
Medical: narrow spectrum antibiotics
For non-pregnant women and men aged 16 years and older:
 1st choice of oral antibiotics: cafelexin 500mg or co-amoxiclav 500mg or trimethoprim
200mg or ciprofloxacin 500mg
 1st choice of IV antibiotics: co-amoxiclav 1.2g or cefuroxime 750mg, ceftriaxone 1 to 2g,
ciprofloxacin 400mg, gentamicin 5-7mg/kg, amikacin 15 mg/kg
For pregnant women aged 12 years and over:
 1st choice: cefalexin 500mg
 1st choice IV: cefuroxime 750mg
 2nd choice: cosult local microbiologist
For children and young people under 16 years old:
 1st choice: cefalexin, co-amoxiclav
 1st choice IV: co-amoxiclav, cefuroxime, ceftriaxone, gentamicin, amikacin
Surgical:
Miscellaneous:
Complications: refer to hospital if person has symptoms of a more serious illness or condition

Sexual Health
Diagnosis of a vulval swelling

 Most common symptom of vaginitis


 Causes= yeast (most common), pregnancy, uncontrolled diabetes, weakened immune
system, drugs (steroids, antibiotics, oral birth control pills); bacterial; trichomoniasis
 Bartholin’s cysts – usually occur in women in their 20s and the risk decreases with age

Acute prostatitis

 Sx: perineal, penile or rectal pain, acute urinary retention, low back pain on ejaculation,
tender and swollen prostate, (bacteraemia): rigors, myalgia, fever, tachycardia
 Ix: mid-stream urine to confirm UTI, FBC, physical examination and digital rectal
examination, screen for STIs
 Mx: ciprofloxacin or ofloxacin twice daily; trimethoprim if unsuitable. Levofloxacin or co-
trimoxazole twice daily if there is bacteriological evidence
o Take paracetamol for pain and drink enough fluids to avoid dehydration

Prescribing contraception

 Contraception available:
o Combined - COCP, combined transdermal patch, combined vaginal ring
o Progestogen only – POP, progestogen only implant, progestogen only injectable
o Intrauterine contraception – copper intrauterine device and levonorgestrel
intrauterine system
o Barrier methods – female, male condom, diaphragm, cup
o Sterilization methods – vasectomy for males, tubal occlusion for females
o Long acting reversible contraceptives – progesterone only injectable, progestogen
only implant, copper IUD
 Emergency contraception:
o Cu-IUD most effective – inserted within 5 days after the first unprotected sexual
intercourse or within 5 days of the earliest estimated date of ovulation
 If positive for STI – abstain and finish 1 week course of azithromycin
o Oral ulipristal actate 30mg tablet – delays ovulation after start of the LH surge (5
days). Licensed for use within 5 days after UPSI.
o Levonorgestrel – inhibits ovulation for 5 days until sperm is no longer viable.
Ineffective in the late follicular phase. Licensed for use within 72 hours after UPSI
 COCP and POP
o COCP – most common = microgynon amd brevinor
o Advantage: lighter menses, reduced risk of cancer of the ovary, uterus and colon,
reduced risk of functional ovarian cysts
o Disadvantage: BP may increase, breakthrough bleeding and spotting for first few
months, increased risk of venous thromboembolism, small risk of myocardial
infarctions and strokes, small increase risk of breast and cervical cancer
o Contraindications: BMI greater than 35, breast feeding, smoking over the age 35,
hypertension, history of venous thromboembolisms, prolonged immobility, diabetes
with complications, history of migraines with aura, breast cancer or primary liver
tumours

Management of syphilis

 IM benzathine penicillin, do not give doxycycline in pregnant women as it can cause affect
tooth and bone development in the baby
 May cause the harisch-herxheimer reaction (fever, rash and tachycardia) due to release of
endotoxins following bacterial death within a few hours of treatment

Endocrinology
Condition: Cushing’s syndrome
Definition: Hypercortisolism – pituitary gland releases too much ACTH which stimulates the
production and release of cortisol
Causes: ACTH dependent = increased/ inappropriately normal ACTH; pituitary adenoma (cushing’s
disease), ectopic ACTH secretion; exogenous corticosteroid use (e.g chronic asthma or rheumatoid
arthritis)
Differentials: metabolic syndrome, physical stress, malnutrition, alcoholism, depression and
pregnancy
Presentation:
Risk factors:
Symptoms: weight gain and more body fat on chest and tummy, but slim arms and legs; build-up
of fat on back of the neck; red, puffy face; skin that bruises easily, weakness in upper arms and
thighs, low libido and fertility problems
Examination findings/Signs: high BP, bone loss, hypokalaemia (cortisol can have a
mineralocorticoid effect → mimic aldosterone at Na+/K+ pumps)
Investigations:
Bedside: cushing’s syndrome not confirmed → exclude exogenous glucocorticoid exposure →
perform one of the following
(1) 24-hour urinary cortisol
(2) Overnight 1mg dexamethasone suppression test (low-dose)
(3) Salivary cortisol
→abnormal results? → Yes → exclude physiological causes → perform other tests from 3 above
not initially completed → abnormal result? → confirm diagnosis
No → unlikely cushing’s syndrome
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative: Cushing’s syndrome confirmed → serum midnight ACTH measurement → ACTH
inappropriately normal or raised → high-dose dexamethasone suppression test → cortisol
suppressed → Cushing’s syndrome → pituitary MRI; cortisol not suppressed → ectopic ACTH → CT
tap
ACTH low → ACTH independent cause → CT tap for adrenal adenoma
Medical: somatostatin analogues (ketoconazole, mitotane, metyrapone) – inhibits adrenal gland
from secreting cortisol; glucocorticoid receptor antagonists (mifepristone, relacorilant) – inhibits
glucocorticoid receptors from binding to cortisol
Surgical: transsphenoidal resection of pituitary adenoma; laparoscopic adrenalectomy; resection
of ACTH producing tumour, bilateral adrenalectomy
Miscellaneous:
Complications:

Condition: Addison’s disease

Definition: autoimmune destruction of the adrenal glands and primary cause of hypoadrenalism
(80% of cases). Causes a deficiency of aldosterone → Na+/K+ ATPase are less activated, causing
reduced renal potassium secretion → hyperkalaemia
Conn’s syndrome → hyperaldosteronism → activates Na+/K+ ATPase to move potassium into the
cell → hypokalaemia
Sx: female, young, resistant hypertension, hypokalaemia
Presentation:
Risk factors:
Symptoms: lethargy, weakness, anorexia, nausea and vomiting, weight loss; pyrexia, shock
Examination findings/Signs: very low cortisol, fatigue, syncope, hyperpigmentation, hypotension,
hypoglycaemia, hyponatraemia
Investigations:
Bedside: adrenal crisis is an emergency and has to be treated immediately
Bloods: serum cortisol levels (has diurnal variation where it’s highest in the early morning and
lowest late in the evening), U&E (sodium may be low and potassium high), blood glucose
(borderline or low), calcium (mild hypercalcaemia), FBC (anaemia or mild eosinophilia), LFT (raised
liver transaminases), thyroid function tests (raised TSH) – patients with addison’s often have an
underactive thyroid
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative: electrolyte supplementation
Medical: IV or IM hydrocortisone or fludrocortisone, children need higher fludrocortisone and
may need salt supplementation
Surgical:
Miscellaneous:
Complications: Can lead to adrenal crisis when there is low BP, low blood sugar and high blood
levels of potassium
Tx: IV or IM hydrocortisone or fludrocortisone, children need higher fludrocortisone and may need
salt supplementation

Condition: Hypothyroidism

Definition: thyroid gland does not produce enough thyroxine hormone (T4)
Causes: Hashimoto’s disease (immune system attacks the thyroid glands, common in people with
another immune system disorder e.g T1DM and vitiligo); side effect or complication of previous
treatment to the thyroid gland; lack of dietary iodine (most common cause of hypothyroidism in
the developing world); drugs (lithium, amiodarone, interferons); subacute thyroiditis (de
Quervain’s), Riedel thyroiditis
Presentation:
Risk factors:
Symptoms: tiredness, weight gain, constipation, muscle aches and weakness, loss of libido, carpal
tunnel syndrome, irregular periods, being sensitive to cold, lethargy, brittle hair and nails,
menorrhagia
Examination findings/Signs:
Investigations:
Bedside:
Bloods: Thyroid function test
 High TSH and low T4 = primary hypothyroidism e.g. Hashimoto’s
 Low TSH and low T4 = secondary hypothyroidism or sick euthyroid syndrome (common in
hospital inpatients)
 High TSH and normal T4 = high risk of having underactive thyroid in the future or patients
who are poorly compliant
Thyroid antibody test – help to diagnose or rule out autoimmune thyroid conditions e.g.
Hashimoto’s thyroiditis
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative:
Medical: levothyroxine (taken same time every day) – side effects of overdose are chest pain,
sweating, headaches, diarrhoea. Combination therapy of levothyroxine and triiodothyronine (T3)
should be avoided because it can cause AF, strokes, osteoporosis and fractures.
Surgical:
Miscellaneous:
Complications: high cholesterol, atherosclerosis -> angina and heart attack; goitre; pre-eclampsia,
birth defects, premature birth, stillbirth; myxoedema coma – confusion, hypothermia and
drowsiness

Condition: Hyperthyroidism

Definition:
Causes: most common cause in iodine-sufficient areas = Graves’ disease; toxic multinodular goitre
drugs e.g. amiodarone
Presentation:
Risk factors:
Symptoms: rapid-onset malaise, fever and thyroid pain; breathlessness, hoarse voice, dysphagia;
agitation; fatigue; heat intolerance; increased appetite with unintentional weight loss; polyuria;
reduced libido; palpitations, anxiety, tremor, oligomenorrhea
Examination findings/Signs: agitation, enlarged thyroid, muscle wasting, splenomegaly,
gynaecomastia
Investigations:
Bedside:
Bloods: TFT; TSH-receptor antibodies to distinguish cause of hyperthyroidism
 Low TSH and high T4 = primary hyperthyroidism e.g. Grave’s
 High TSH and high T4 = secondary hyperthyroidism
Imaging: thyroid ultrasound scan with Doppler to provide info on thyroid size, presence of
nodules and vascularization
Management:
Patient Education/ Counselling/ Resources:
Conservative: beta-blocker for adrenergic symptoms e.g. palpitations, tremors, tachycardia
Medical: antithyroid drug e.g. carbimazole or propylthiouracil (not first line as can cause liver
injury) – blocks thyroid peroxidase from coupling and iodinating tyrosine residues
Surgical: thyroidectomy or hemithyroidectomy if high risk of recurring hyperthyroidism
Miscellaneous:
Complications:

Condition: Diabetes Mellitus

Definition:
Presentation:
Risk factors:
Symptoms:
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative
Medical:
Surgical:
Miscellaneous:
Complications: Diabetic foot disease - occurs secondary to 2 factors: neuropathy – loss of
protective sensation, charcot’s arthropathy, dry skin; peripheral arterial disease – risk factor for
macro and microvascular ischaemia
Presentation – loss of sensation, absent foot pulses, reduced ABPI, intermittent claudication,
calluses, ulceration, cellulitis, osteomyelitis, gangrene

Orthopaedics/ Rheumatology
Investigation of ankylosing spondylitis

 Pelvic xray is gold standard to image the sacroiliac joints – sacroilliatis is one of the first signs
and inflammation often spreads to joints between the vertebrae

Condition: Osteoarthritis

Definition:
Presentation:
Risk factors: increasing age, female, obesity, developmental dysplasia of the hip
Symptoms: chronic history of groin ache following exercise and relieved by rest; red flag
suggesting different cause include rest pain, night pain and morning stiffness > 2 hours (LOSS –
loss of joint space, osteophytes, subchondral sclerosis, subchondral cysts)
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging: plain x-rays
Management:
Patient Education/ Counselling/ Resources:
Conservative: oral analgesia, intra-articular injections
Medical:
Surgical: hip replacement – arthroplasty (intrascapular), screw (extrascapular)
Miscellaneous:
Complications: venous thromboembolism, nerve injury, surgical site infection; leg length
discrepancy; posterior dislocation (internal rotation and shortening of affected leg); aseptic
loosening (prosthetic joint infection)

Condition: Rheumatoid arthritis

Definition: chronic, autoimmune, inflammatory arthritis


Presentation:
Risk factors:
Symptoms: symmetrical synovitis for > 6 weeks; pain in the small joints of the hands and feet
which improves with exercise; pain is worse in the morning
Examination findings/Signs:
Investigations:
Bedside:
Bloods: bloods for rheumatoid factor, anti-CCP and CRP/ESR
Imaging: x-ray shows bony erosions; boutonniere’s deformity, loss of joint space (LESS – loss of
joint space, erosions, soft tissue swelling, see through bones (osteopenia)
Management:
Patient Education/ Counselling/ Resources: lifestyle modifications – exercise, weight loss, dietary
advice
Conservative: Analgesia
Medical: Monotherapy with conventional DMARDs (disease modifying anti-rheumatic drug; e.g.
methotrexate, sulfasalazine; hydroxychloroquine; leflunomide) with bridging steroids
(prednisolone) until symptom control is manageable in an acute flare → if target is not met, titrate
up and try dual therapy → consider biological agents when DAS28 score > 5.1
Surgical:
Miscellaneous:
Rheumatological antibodies:

Complications: respiratory (pulmonary fibrosis, pleural effusion); ischaemic heart disease;


increased risk of infections; osteoporosis; keratoconjunctivitis sicca (most common);
stherosclerotic disorders

Condition: Septic joint

Definition: a hot swollen joint with a reduced range of movement → septic arthritis until proven
otherwise
Presentation:
Risk factors: high risk of gram negative if elderly, has recurrent UTIs, had recent abdominal
surgery or had previous gram negative bacteraemia
Symptoms: symptoms arise < 2 weeks, immunocompromised, one joint has symptoms out of
proportion to other affected joints, an obvious source of infection is present
Examination findings/Signs:
Investigations:
Bedside: Send fluid for 3C’s and G (cells, culture, crystals and gram stain) → empirical IV
antibiotics and repeat joint aspiration until dry (if sexually active add Gonococcal NAAT) →
bacterial growth on culture? → prolonged course of tailored antibiotics
If no? → purulent fluid with high WCC → re-aspirate joint
If no purulent fluid → consider other diagnosis
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative: IV antibiotics based on likely organism – staph aureus is most common
Medical: if staph aureus (gram-positive) → flucloxacillin
If gram-negative bacteria → cephalosporin
Surgical:
Miscellaneous:
Complications:

Condition: Gout

Definition: A crystal arthropathy, where negative birefringence monosodium urate crystals are
deposited in soft tissues
Presentation:
Risk factors: purine rich diet (shellfish, organ meats, alcohol, soft drinks), obesity, high ETOH
intake, diabetes chemotherapy/ malignancy and various genetic defects of purine metabolism
Symptoms:
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative: Acute attack → strong NSAID (naproxen) until 1-2 days after the attack has settled
with PPI gastric coverage OR prescribe colchicine for 5-7 days
Medical: urate lowering therapy (ULT) with allopurinol (1st line) or febuxostat (2nd line). Costart
with colchicine cover as allopurinol can trigger an acute flair
Surgical:
Miscellaneous:
Related: Psuedogout – a form of microcrystal synovitis caused by the deposition of calcium
pyrophosphate dehydrate crystals in the synovium.
Risk factors: Increasing age; if at younger age, they usually have some underlying risk factors:
haemochromatosis, hyperparathyroidism, low magnesium, low phosphate, acromegaly, wilson’s
disease
Symptoms: knee, wrist and shoulders most commonly affected; joint aspiration – birefringent
rhomboid-shaped crystals; x-rays show chondrocalcinosis linear calcification of the meniscus and
articular cartilage
Management: aspiration of joint fluid to exclude septic arthritis, NSAIDS or steroids

Condition: Lower limb fracture

Definition: fracture to any of the bones in the lower limb – tibia, fibula and talus
Presentation:
Risk factors:
Symptoms:
Examination findings/Signs: Pain on palpitation of the anatomical snuff box → scaphoid fracture
Strong, lateral blow to the knee → “unhappy triad” ACL, MCL and medical meniscus tears
Segond fracture (lateral tibial plateaux) → 75% associated with ACL rupture

Investigations:
Bedside:
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative: Ankle injury (excluding open fractures) → Ottawa rule
If yes to any of these questions, a fracture can’t be ruled out:
1. Inability to weight bear immediately after injury and in A&E
2. Pain on palpitation of lateral malleolus
3. Pain on palpitation of medial malleolus
→ if no → discharge with RICE
→ if yes → x ray AP, lateral and oblique
→ Unimalleolar → no evidence of ligamentous injury on x-ray → discharge with case and fracture
clinic follow up x-rays
→ evidence of ligamentous injury on x-ray or Bi or trimalleolar → UNSTABLE → closed reduction
(if joint is dislocated on x-ray) and refer for surgical fixation

Foot x-ray is required only if yes to any of these questions:


1. Pain on palpitation of navicular
2. Pain on palpitation of base of 5th metatarsal
3. Inability to bear weight immediately after injury and in A&E

Lateral malleolus → weber system → weber C requires surgery


Open fractures → Gustilo-anderson system → IV antibiotics +/- tetanus booster and remove gross
debris
1 - <1cm wide, typically clean
2 – 1-10 cm wide, typically some soiling
3a - >10cm wide, adequate tissue coverage for closure
3b - >10cm wide but inadequate soft tissue coverage for closure, requires a tissue flap
3c – any wound with a major vascular injury
Medical: bisphosphonates (e.g. alendronic acid) – inhibit osteoclast
Surgical:
Miscellaneous:
Complications:

Condition: Osteoporosis

Definition: low bone mass and structural deterioration of bone tissue, resulting in increased bone
fragility and increased susceptibility to fractures
Causes fractures at low impact: hip (neck of femur), vertebrae (compression fracture), wrist
(colles’ fracture – dinner fork deformity, fall on outstretched hand)
Presentation:
Risk factors: use of steroids, smoker/ high alcohol intake, low BMI, endocrine conditions, chronic
illnesses, alcohol intake > 14 units/ week
Symptoms:
Examination findings/Signs: DEXA scan at neck of femur < 2.5 standard deviations below the
mean peak mass
T-score = BMD (bone mineral density) compared to young adult
Z-score = BMD compared to age matched individual, scores of -2.5 should prompt further
investigation
Calculate Q fracture or FRAX score → arrange DEXA scan if high fracture risk or/ >50 years old with
history of fragility fracture/ intermediate risk + risk factors
Investigations:
Bedside:
Bloods:
Imaging: DEXA score of 0 to -2.5 (osteopenia) → lifestyle advice, regular exercise, reduce alcohol,
balanced diet, treat underlying causes → repeat DEXA at 2 years
<2.5 (osteoporosis) → bisphosphonates (oral) 10mg OD or 70 mg once weekly → replace vitamin
D and calcium if inadequate intake → treatment reviewed every 3-5 years; if not tolerated IV
bisphosphonates, denosumab (monoclonal antibody), raloxifene (SERM) and terparatide
(parathyroid hormone tx) can be used.
Management:
Patient Education/ Counselling/ Resources:
Conservative
Medical:
Surgical:
Miscellaneous:
Osteoporosis vs osteomalacia: Osteomalacia – marked softening of the bones most commonly
caused by vitamin D deficiency.
Paget’s disease – normal serum calcium and phosphate with elevated ALP
Osteoporosis Osteomalacia
Bone mass Reduced Normal
Bone mineral density Reduced Maybe reduced
Symptoms Asymptomatic, fractures, Asymptomatic, fractures,
bone pain bone pain
Patient demographic Post-menopausal women, People with little sun light
chronic steroid user older guy exposure causing
hypophosphatemia
Bloods Normal calcium, phosphate Reduced calcium, phosphate
and alkaline phosphase and vitamin and elevated
Alkaline phosphate,
parathyroid hormone
Treatment biphosphonates Vitamin D

Haematology
Condition: Haemophilia

Definition: X-linked recessive bleeding disorder – Haemophilia A and B


Haemophilia A – factor VIII deficiency
Haemophilia B – factor IX deficiency
Presentation:
Risk factors:
Symptoms: family history in males of bleeding, most common = haemarthrosis (bleeding into the
joints)
Examination findings/Signs:
Investigations:
Bedside:
Bloods: Prothrombin time – normal; APTT – increased; bleeding time – normal → do a factor VIII
and IX assay
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative
Medical: Severe and life-threatening e.g. intracranial haemorrhage → factor VIII concentrates
Haemarthrosis → assess → factor VIII concentrate
 Haemophilia A – regular injections of octocog alfa (Advate)-> engineered version of
clotting factor VIII. Side effects include an itchy skin rash and soreness at site of injection
 Haemophilia B – regular injections of nonacog alfa (Benefix) -> engineered version of
clotting factor IX. Side effects include headaches, altered taste, feeling sick, discomfort
and swelling at injection site
On-demand treatment
 Haemophilia A – octocog alfa or desmopressin (side effects: headaches, stomach pain,
nausea)
 Haemophilia B – nonacog alfa
Complications of haemophilia
 Developing inhibitors in the immune system which makes medicine less effective (treated
with immune tolerance induction (ITI) for people with severe haemophilia A; bypass
therapy or immunosuppressants are other options)
 Joint damage – joint bleeds can damage the cartilage and synovium (treated with a hip or
knee replacement)
Surgical:
Miscellaneous:
Other related diseases:
Disorder INR APTT PT Platelets Bleeding time
Haemophilia normal increased normal normal normal
Von Normal increased normal normal Increased
willebrand’s
disease
Disseminated increased increased increased low Increased
intravascular
coagulation
(DIC)
Liver cirrhosis increased increased normal low (with Increased
splenomegaly)
Menorrhagia, prolonged bleeding time → von-willebrand’s disease
Low platelets, low fibrinogen → DIC
Raised INR, low platelets and deranged LFTs → liver cirrhosis
*Normal INR = <1.1; INR of people taking warfarin for disorders like AF or a blood clot in the lef ot
lung = 2.0-3.0

Condition: Microcytic anaemia

Definition: Most common is iron deficiency anaemia and is a red flag symptom for colorectal
cancer.
Presentation:
Risk factors:
Symptoms:
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Serum Serum Transferrin Iron in Iron in MCV
ferritin TIBC sat marrow erythroblasts
IDA Reduced Increased Low None None Low
Thalassaemi Normal Normal Normal Present Present Very low
a
Sideroblastic Increased Decreased High- Increased Ring forms Low
anaemia normal
Anaemia of Increased Low- Low Present Absent Low-
chronic dz normal normal
Normocytic anaemia, reduced renal function → CKD-related anaemia (EPO)
Imaging: >=40-49 → unexplained weight loss, abdominal pain, rectal bleeding → colonoscopy;
none → consider alternative diagnosis
>= 50-59 → rectal bleeding → colonoscopy; no rectal bleeding → faecal occult blood test
>= 60 → colonoscopy
If pt has dyspepsia + IDA + >55 → urgent endoscopy to check for upper GI malignancy
Management:
Patient Education/ Counselling/ Resources:
Conservative:
Medical:
Surgical:
Miscellaneous:
Complications:

Condition: Macrocytic anaemia

Definition: a type of anaemia that causes unusually large red blood cells and low haemoglobin.
Most common is pernicious anaemia = megaloblastic anaemia which is caused when the bone
marrow produces structurally abnormal and immature megaloblasts due to deficiency of vitamin
b12 or folate. Other type is pernicious anaemia = immune system attacks the cells in your stomach
that produce intrinsic factors which means the body can’t absorb vitamin B12
Causes of vitamin b12 deficiency:
 Pernicious anaemia (most common)
 Drugs – colchicine, metformin, NO, PPI, H2-receptor antagonists
 Gastric causes – gastrectomy, congenital IF deficiency, zollinger-ellison syndrome
 Intestinal causes – malabsorption, crohn’s disease,
 Nutritional – malnutrition, vegan diet
Causes of folate deficiency:
 Dietary intake
 Drugs – alcohol, anticonvulsants, nitrofurantoin, sulfasalazine, methotrexate,
trimethoprim
 Excessive requirements in pregnancy, malignancy, blood disorders or malabsorption
 Excessive urinary secretion
 Liver disease
Presentation:
Risk factors:
Symptoms: dyspnoea, headache, indigestion, loss of appetite, palpitations, tachypnoea, visual
disturbances, weakness, lethargy. Onset of megaloblastic anaemia is usually insidious with
gradually progressive symptoms. Pernicious anaemia may develop gradually over several years
and symptoms may not appear until it is severe
Examination findings/Signs: anorexia, angular cheilosis, brown pigmentation affecting nail beds
and skill creases, congestive heart failure, glossitis, liver enlargement, mild jaundice, mild pyrexia,
tachycardia, weight loss
Investigations:
Bedside:
Bloods: FBC to determine MCV, haematocrit and haemoglobin levels and a blood film. Measure
serum cobalamin and folate levels to determine cause of anaemia. LFT, GGT, thyroid function
tests
 If vitamin B12 deficiency is found, serum anti-IF antibodies should be checked
 If folate levels are low and history suggests malabsorption, tests for anti-endomysial or
anti-transglutaminase antibodies should be done to exclude coeliac disease
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative:
Medical:
 Vitamin b12 deficient: seek specialist help from a neurologist and/or haematologist ->
administer hydroxocobalamin 1mg IM 3 times a week for 2 weeks -> maintenance dose
depends on whether deficiency is related to diet -> give dietary advice about foods high in
vitamin B12 (eggs, fortified foods, meat, milk, salmon)
 Folate deficient: check vitamin B12 levels in all people -> start oral folic acid 5mg daily ->
give dietary advice about foods high in folate (asparagus, broccoli, brown rice, chickpeas)
 Perform a FBC and reticulocyte count within 7-10 days of starting treatment (should
increase to above the normal range)
 After 8 weeks of treatment, measure iron and folate levels (MCV should be normal)
 No need to measure cobalamin levels as they will increase regardless of how effective it is
Surgical:
Miscellaneous:
Complications: refer to a gastroenterologist if malabsorption or IBD is suspected. Or if there is
suspicion of gastric cancer

Condition: HIV and Aids

Definition: retrovirus which infects human CD4 T cells and macrophages and is spread via body
fluids
 HIV 1: more common and prevalent
 HIV 2: less pathogenic and limited to west Africa
 AIDS = CD4 count <200cells/ microliter, which puts the individual at risk of opportunistic
infections
Presentation:
Risk factors:
Symptoms: mostly asymptomatic when person has HIV
Examination findings/Signs:
Investigations:
Bedside: full STI, hepatitis C, TB -> confirmed diagnosis if there are HIV antibodies and p24 antigen
Bloods: FBC, liver, renal and glucose testing (high viral load in the first 6 months but they can
spread the infection without knowing that they have the disease)
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative:
Medical: Antiretroviral therapy = to reduce the viral load to undetectable and improve HIV
morbidity and mortality
 3 drugs = 2 nucleoside reverse transcriptase inhibitors (NRTIs) and 1 further agent
 Adverse effects = hypersensitivity, lipodystrophy (redistribution of fat), lipoatrophy (loss
of fat), T2DM, hyperlipidaemia, Immune reconstitution inflammatory syndrome (IRIS) =
worsening of infection on commencement of ART
Surgical:
Miscellaneous:
Complications:

Dermatology
Management of cellulitis

 Causes: most common = streptococcus and streptococcus that can bypass the skin due to
injuries, infections after surgery. Other causes: long term skin conditions such as eczema or
psoriasis, foreign objects in the skin, bone infections
 Sx: acute onset of red, painful, hot, swollen and tender skin that spreads rapidly; fever,
malaise, nausea, shivering and rigors; obvious skin break and diffuse redness; blisters and
bullae; inflamed regional lymph nodes or lymphangitis
 Ix: swab for culture, ultrasonography (distinguishes non-purulent cellulitis from cellulitis with
underlying abscess and for identifying drainable fluid collection), skin biopsy, WBC, ESR, CRP
 Mx: high-dose oral antibiotic treatment (flucloxacilllin 500-1000mg 4 times daily for 5-7
days, clarithromycin, doxycycline)

Managing eczema

 Control pruritis – antihistamines, topical calcineurin inhibitors (tacrolimus ointment,


pimecrolimus cream)
 Immune suppression – topical (systemic corticosteroids), topical calcineurin inhibitors, oral
cyclosporine, dupilumab (IL-4 receptor antagonist)

Complications of eczema

 skin infections – staphylococcus aureus common commensal organism -> impetigo


 Viral skin infections – infected with HSV which normally causes cold sores -> causes eczema
herpeticum (areas of painful eczema, groups of fluid-filled blisters that break open and leave
small, shallow open sores, hot and shivery)
 Psychological effects

Examination of psoriasis

Condition: Skin Cancer

Definition: Neoplasm originating from melanocytes in the epidermis


Common types: superficial spreading (70%), nodular (15%). Lentigo (10%), amelanotic (8%)
Presentation:
Risk factors: prolonged sun exposure, sunbed use, Fitzpatrick skin type 1, freckles, moles, family
history, previous skin cancer, >50 years of age, xeroderma pigmentosum
Symptoms: ABCDE (Asymmetry, borders (irregular), colour, diameter (>7mm), exposed area/
elevated)
Major criteria (2 pts): change in size, irregular colour, irregular shape
Minor criteria (1 pt): diameter>7mm, inflammation, oozing, change in sensation
Suspicion is greater for lesions scoring 3 points or more, but also factor in family history of
melanoma, personal history of melanoma, immunosuppression, excessive UV exposure
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative
Medical:
Surgical: lesions suspicious of melanoma (> 3 points) → excision biopsy, Breslow >2mm → sentinel
lymph node biopsy → met screen → stage 4 → resect if possible, chemotherapy, metastectomy,
palliative input
Miscellaneous:
Complications:

Condition: Contact dermatitis

Definition: inflammation of skin after contact exposure to allergens/ irritants, most common form
= irritant contact dermatitis
Causes:
 Exposure to irritant – acute (strong irritant), chronic (recurring exposure to weak irritant)
 Detergents, surfactants, extreme ph, organic solvents, water (fat emulsion > defatting of
dermal lipid > cellular damage to epithelium > DNA damage, transepidermal water loss >
cytotoxic cell damage > cytokine release from keratinocytes > activation of innate
immunity
 Allergic contact dermatitis – poison ivy, oak or sumac; nickel, fragrances, dyes
Presentation:
Risk factors: age (highest risk are infants), body site exposure (more irritated at areas with thin
stratum corneum), occupation exposure
Symptoms: erythematous rash, vesicles, wheals, glaze, scaling, hyperkeratosis, fissuring, itching,
burning
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative: treat blistering (cold compress), retain moisture by using barrier cream e.g. zinc
oxide
 Irritant contact dermatitis: use mild acidic solutions e.g. acetic acid to neutralise alkali
irritants, emollients (aquaphor)
 Allergic contact dermatitis: phototherapy
Medical:
 Pruritus – calamine lotion
 Mild topical corticosteroid
 Oral antihistamine
 Allergic contact dermatitis – high potency topical corticosteroids orally, topical calcineurin
inhibitors (tacrolimus/ pimecrolimus), systemic immunosuppression (Azathioprine,
cyclosporine, mycophenolate mofetil)
Surgical:
Miscellaneous:
Complications:

Condition: Psoriasis

Definition: chronic dermatosis of skin, nails and joints caused by environmental factors and
genetic abnormalities of immune system (CD4+, TH1, TH17 and CD8 T cells collect in epidermis,
secreting cytokines and growth factors -> accelerates keratinocyte proliferation

Presentation:
Risk factors: skin abrasion, infection, drugs (lithium, beta blocker, chloroquine), psychological
stress
Symptoms: salmon pink plaques covered by silver-white scales found in any area of the body;
thickening and yellow-brown discoloration of the nail plate; severe itching, swelling and pain;
drop-like appearance associated with group A streptococcus
Examination findings/Signs: acanthosis (epidermis thickening), accumulation of neutrophils in
superficial epidermis and stratum corneum
Investigations:
Bedside:
Bloods: elevated inflammatory markers, negative rheumatoid factor, anti-cyclic citrullinated
peptide antibody (anti-CCP)
Imaging: for psoriatic arthritis -> xray (erosive changes and presence of new bone formation), MRI
(inflammation in adjacent bone marrow and soft tissues)
Management:
Patient Education/ Counselling/ Resources:
Conservative: coal tar (inhibits cellular mitotic proliferation), emollients, phototherapy
Medical: topical corticosteroids, vitamin D derivatives (calcipotriene, calcipotriol) limit
keratinocyte proliferation, anthralin (suppresses proliferation), combination therapy is most
effective (betamethasone dipropionate + calcipotreine), immunosuppressant (methotrexate,
cyclosporine), systemic retinoids (acitretin) inhibits pro-inflammatory cytokines, biologic therapy
(anti-TNF, T cells)
Surgical:
Miscellaneous:
Complications: psoriatic arthritis (inflammatory cells in joint tissue -> synoviocyte proliferation
 Sx: sausage digits, pain, red overlying area, swelling and hot to touch

Ophthalmology
PainLESS loss of vision

 Retinal artery occlusion: Internal carotid artery -> ophthalmic artery -> central retinal artery
 Retinal vein occlusion
 Retinal detachment
 Stroke/ TIA
 Vitreous Haemorrhage
PainFUL loss of vision
 Acute angle closure glaucoma
 Anterior uveitis
 Corneal ulcer
 GCA
 Optic neuritis

Visual field defects

 Left homonymous hemianopia means visual field defect to the left so the lesion is on the
right optic tract
 Homonymous quadrantanopias: PITS (parietal – inferior, temporal – superior)
 Incongruous defect (asymmetric visual field loss) - optic tract lesion, congruous defects –
optic radiation lesion or occipital cortex
 Examples:
o Homonymous hemianopia
 Incongruous defects: lesion of optic tract
 Congruous defects: lesion of optic radiation or occipital cortex
 Macula sparing: lesion of occipital cortex
o Homonymous quadrantanopia
 Superior: lesion of the inferior optic radiations in the temporal lobe
 Inferior: lesion of the superior optic radiations in the parietal lobe
o Bitemporal hemianopia
 Lesion of optic chiasm
 Upper quadrant defect > lower quadrant defect = inferior chiasmal
compression, commonly a pituitary tumour
 Lower quadrant defect > upper quadrant defect = superior chiasmal
compression, commonly a craniopharyngioma

Condition: Central retinal artery occlusion

Definition: blockage of blood to the retina of one eye (internal carotid artery -> ophthalmic artery
-> central retinal artery)
Causes:
 Ischaemic – carotid artery atherosclerosis or cardiogenic embolism (accounts for up to
20% of acute strokes -> emboli may arise from the heart, the extracranial arteries
including the aortic arch
 Vasculitic – giant cell arteritis/ temporal arteritis (form of vasculitis -> temporal arteries
which supply blood from the heart to the scalp become inflamed and constricted
Presentation:
Risk factors: Male, older adults, smoking, diabetes, hypertension, cholesterol
Symptoms: acute, severe, painless monocular vision loss, typically monocular; RAPD because
visual input is not sensed by the ischaemic retina (RAPD is a condition in which pupils respond
differently to light stimuli shone in one eye at a time due to unilateral or asymmetrical disease of
the retina or optic nerve)
Examination findings/Signs: Fundoscopy – ischaemic retinal whitening with cherry red spot in the
centre (if there is a pale retina without cherry red spot on -> ophthalmic artery occlusion)
Ischaemic Normal
Investigations:
Bedside:
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative: ocular massage
Medical: intra-arterial thrombolysis, Acetazolamide (carbonic anhydrase inhibitors that decrease
production of fluid inside the eye to reduce IOP)
Surgical: anterior chamber paracentesis to reduce intra-ocular pressure
Miscellaneous:
Complications:

Condition: Amaurosis Fugax

Definition: painless and temporary vision less lasting a few seconds to minutes. Often described
“like a curtain coming down”
Cause: ischaemia or vascular insufficiency, commonly carotid artery stenosis (hence different from
the central retinal artery occlusion) -> a strong predictive factor for future TIA/ stroke
Presentation:
Risk factors: people > 50 years with atherosclerotic risk factors e.g. DM, HTN, smoking and
hyperlipidaemia
Symptoms:
Examination findings/Signs:
Investigations:
Bedside: ECG
Bloods:
Imaging: CT/ MRI of brain, echo and carotid Doppler
Management:
Patient Education/ Counselling/ Resources:
Conservative:
Medical: aspirin + secondary prevention of cardiac and stroke risk factors
Surgical:
Miscellaneous:
Others:
Risk factors Presentation Direct Treatment
Fundoscopy
Retinal vein HTN Unilateral Flame and blot Pan-retinal
occlusion High cholesterol sudden painless haemorrhages photocoagulation
Smoking vision loss Macular oedema Anti-VEGF
Diabetes (reduce new
blood vessels or
oedema)
Retinal Severe myopia Unilateral Detached Vitrectomy
detachment Eye trauma painless vision portion appears Scleral buckling
loss corrugated or Pneumatic
Flashes and out of focus retinopexy
floaters
Stroke/TIA HTN Sudden vision Typically Thrombolysis if
High cholesterol field loss changes seen in ischaemic
Smoking Bilateral hypertensive BP control
Diabetes quadrantanopia retinopathy

Condition: Diabetic retinopathy

Definition: One of the consequences of poorly managed diabetes alongside nephropathy,


neuropathy and peripheral vascular disease. Eventually will progress onto maculopathy
Presentation:
Risk factors:
Symptoms: asymptomatic until advanced. Blurry vision, reduced acuity and floaters
Examination findings/Signs: *urgent ophthalmology review, ideally same day
Class Symptoms Features on fundoscopy
Pre-proliferative (mild) None Microaneurysms
Pre-proliferative (moderate) None Dot and blot haemorrhages, hard
exudates
Pre-proliferative (severe) None Large dot and blot haemorrhages,
cotton wool spots, venous beading
Proliferative * Floaters, reduced All of the above with new vessel
acuity formation
Diabetic maculopathy * Blurred vision, reduced All of the above with retinal
acuity thickening and macular leaking
Investigations:
Bedside:
Bloods:
Imaging:

Management:
Patient Education/ Counselling/ Resources: lifestyle and diet advice, pharmacological therapies,
stop smoking – improve diabetic control, blood pressure and lipid levels; prescription glasses/
lenses
Conservative:
Medical:
Surgical: laser photocoagulation when advanced
Miscellaneous:
Complications:

Condition: Macular Degeneration

Definition: progressive damage to the macula of the retina related to age


Presentation:
Risk factors: smoking, HTN, older age, BMI>30, high fat diet, lack of exercise, family history
Symptoms:
Examination findings/Signs:
Classification Definition
Early Small or medium sized drusen
Intermediate Large drusen, retinal pigment abnormalities on retina (black sports of
hypertrophy)
Late dry Dense or confluent drusen with advanced pigmentary changes. Central
visual loss
Late wet Choroidal neovascularisation, retinal proliferation, bleeding and leaking on
the retina, central visual loss, rapidly progressive
*Drusen = small yellow deposits of fatty proteins that accumulate under the retina
Investigations:
Bedside:
Bloods:
Imaging: fundoscopy
Management:
Patient Education/ Counselling/ Resources:
Conservative: supportive treatment
Medical: late stage wet MD – intravitreal injections of Anti-VEGF to slow the progression
Surgical:
Miscellaneous:
Complications:

Condition: Primary open-angle glaucoma

Definition: optic neuropathy associated with raised intraocular pressure


Presentation:
Risk factors:
Symptoms: symptomless for a long period, typically present following an ocular pressure
measurement during a routine examination by an optometrist
Examination findings/Signs: increased intraocular pressure, visual field defect, cupping of the
optic disc
Investigations:
Bedside: slit lamp examination to assess optic nerve and fundus, tonometry, central corneal
thickness measurement, assess risk of future visual impairment
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative:
Medical:
 1st line = prostaglandin analogue (PGA) eyedrop
 2nd line = beta-blocker (reduces aqueous production), carbonic anhydrase inhibitor or
sympathomimetic eyedrop (avoid if taking MAOI or TCA)
 If more advanced = surgery or laser treatment (trabeculectomy)
Surgical:
Miscellaneous:
Complications:

Emergency Medicine
Investigation of limb weakness

 Chemistry and urinalysis – elevated plasma muscle enzymes (creatine kinase, aldolase,
lactate dehydrogenase and aminotransferases) are highly suggestive of muscle disease
 Serologic tests – antinuclear antibodies, antibodies against extractable nuclear antigens if an
inflammatory myopathy is suspected
 Anti-neutrophil cytoplasmic antibody (ANCA), hep B and C and cryoglobulins if vasculitis is
suspected
 Nerve conduction and EMG studies – determine site of lesion
 MRI – useful in selecting a muscle for biopsy
 Muscle biopsy – determines the precise form of myopathy e.g. giant cell arteritis

Burns

 For superficial epidermal burns – topical emollients such as emulsifying ointment daily until
burn is no longer dry or itchy
 For superficial dermal burns – arrange appropriate wound cleaning, debridement
(hydrogels), blister management and wound dressing by qualified person. Assess for need of
tetanus prophylaxis. Check the would after 48 hours to check for signs of infection and
change the dressing. Change the dressing every 3-5 days. Advise to use emollient around 3-6
months to reduce the risk of hypertrophic scarring and use sunblock over affected skin for 1-
2 years to prevent irregular pigmentation
 Wound dressing – use non-adherent dressing such as paraffin gauze, silicone-coated nylon
dressing, polyurethane film or hydrocolloid dressing; the use secondary non-fibrous
absorbent dressing such as a dressing pad and secure with bandage. Once burn depth is
accurately estimated, frequency of dressing change may be reduced to minimise risk of
bacterial contamination and trauma to the wound
 Wound infection – cleaned with 0.9% sodium chloride or lukewarm tap water. Start oral
flucloxacillin or clarithromycin

Managing the ischaemic leg

 Sx: Pain (constantly present and persistent), Pulseless, Pallor, Power loss or paralysis,
Paraesthesia, Perishing with cold
o If ischaemia due to an embolus: onset is acute; limb appears white; vascular
examination in the other leg is usually normal
o If ischaemia due to thrombosis: onset is gradual; limb may not be as white and
severe
o Intermittent claudication: cramp like pain in muscle groups after walking a
predictable distance that is relieved by rest, usually occurs in the distal extremity
before the proximal extremity
o Chronic limb threatening ischaemia: chronic rest pain especially at night, reduced
capillary refill, skin changes e.g. ischaemic ulcers, gangrene, absent foot pulses
 Tx:
o Acute: endovascular therapies e.g. percutaneous catheter-directed thrombolytic
therapy, percutaneous mechanical thrombus extraction; surgical interventions e.g.
surgical thromboembolectomy, endarterectomy, bypass surgery
o Critical: refer to vascular team, manage pain
o Intermittent claudication: offer supervised exercise programme > refer consideration
for angioplasty or bypass surgery > consider naftidrofuryl oxalate

Management of acutely unwell patient

 A – airway (head tilt + chin lift)


 B – breathing (check O2 sats and look for chest expansion and signs of cyanosis, listen to the
chest and feel for chest expansion)
 C – circulation (temperature, capillary return, BP, heart sounds, feel pulse
 D – disability (AVPU, U is equivalent to <8 on GCS and patient requires intubation; check
pupils – do not use morphine for head injuries as it can alter papillary response; check
glucose)
 E – exposure (full examination, ECG, BP, give O2, fluids and get bloods – do not take blood
from a cannula)
 R – reassess
 P – plan (consider further investigations, call for assistance)
o Fluids: get 2 wide bore cannulas in ASAP, give saline or gelofusine (avoid potassium
until you have blood results back); if patient is in shock, give a fluid challenge
 If improved, patient is in non-cardiogenic shock and can continue to give
more fluids aim for systolic >90, and consider blood transfusion if patient is
still in shock (remember that Hb will be low due to dilution of the blood);
 If not improved, patient might be in cardiogenic shock – stop fluids, measure
urine output and give furosemide 20mg if BP is high

Assessment of fracture risk

 FRAX and QFracture – details of age, sex, height and weight, related conditions or are taking
steroids and how much you smoke or drink (steroids increases risk of fractures most); limit
to these tools are 90 yo for FRAX and 85 yo for QFracture)
 Bone scan – if you are aged under 40 years and thought to be at particularly high risk of
fracture or have been taking high doses of steroids

Resuscitation of the new-born

 If heart rate remains very slow or absent after 30 seconds of good quality ventilation, start
chest compressions and increase delivered inspired oxygen to 100%
 Provide 3 compressions to 1 ventilation at about 15 cycles every 30 seconds (use 2 handed
technique for compressions, re-evaluate response every 30 seconds)
 If heart rate remains very slow or absent, continue chest compressions but ensure airway is
secured
 Use umbilical venous access to administer adrenaline IV (20 micrograms of 1:10,000),
glucose (in prolonged resuscitation to reduce likelihood of hypoglycaemia), volume
replacement – group O Rh-negative blood or isotonic crystalloid (with suspected blood loss
or shock unresponsive to other resuscitative measures), sodium bicarbonate (may be
considered in a prolonged unresponsive resuscitation to reverse intracardiac acidosis)

Managing diabetic emergencies

Pathophysiology of diabetic ketoacidosis

Recognition of electrolyte disturbance

 Hypernatremia – dehydration, nausea, vomiting, fatigue, weakness, increased thirst, excess


urination (may be on diuretics or NSAIDs)
o Causes: dehydration, vomiting, diarrhoea, heatstroke; diabetes insipidus, renal
disease, sickle cell disease; conn’s syndrome, cushing’s syndrome
o Treat immediately with IV saline infusion if showing signs of shock such as
tachycardia or hypotension)
 Hyponaetremia – loss of appetite, nausea, vomiting, confusion, weakness, seizures, coma
o Causes: heart failure, chronic kidney disease, liver disease, treatment with thiazide
diuretics. Psydohyponatremia is a false low sodium reading that can be caused by
high levels of fats or proteins
o Treated with hypertonic saline, may be placed on fluid restriction, salt restriction
and treated with a diuretic
 Hyperkalemia – nausea, vomiting and diarrhea, muscle cramps, numbness, absence of
reflexes
o IV calcium to stabilise cardiac cells, insulin and albuterol inhalers to shift potassium
into cells, haemodialysis or loop diuretics to excrete potassium from body
 Hypokalemia – often asymptomatic, muscle weakness, cramping, cardiac arrhythmias
o Oral or IV potassium and magnesium
 Hypercalcemia – abdominal pain, constipation, kidney stones, extreme thirst, excessive
urination, nausea, altered mental status
 Hypercalcemia – abdominal pain, kidney stones, extreme thirst, excessive urination, nausea
and vomiting
o IV fluids and bisphosphonates if severe or associated with cancer
 Hypocalcemia – muscle cramping or twitching, numbness around mouth and fingers,
shortness of breath, low blood pressure, cardiac arrhythmias
o Oral or IV calcium
 Hypermagnesemia – nausea, flushing, tiredness, paralysis, respiratory failure, decreased
deep tendon reflexes
o Stop source of mg if kidney function is normal, dialysis to remove magnesium
 Hypomagnesemia – electrolyte abnormalities, arrhythmias, seizures, tetany
o Oral magnesium
Condition: Hip fracture

Definition: Most common fracture in the UK; Intrascapular or extrascapular → intrascapular


fractures run a high risk of avascular necrosis due to retrograde blood supply (medial circumflex
femoral artery)
Presentation:
Risk factors: elderly, frequent fallers, osteoporosis, high impact trauma, post-menopausal women
Symptoms:
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative: AP pelvis and lateral xray → intrascapular fracture → displaced? →
Yes → mobilises with a stick or better? → Yes? → total hip replacement; No? → hemiarthroplasty
No → head sparing surgery (cannulated screws, Dynamic hip screw)
Extrascapular fracture → intertrochanter → extramedullary nail (DHS); Subtrochanter →
intramedullary nail

Garden classification
Garden classification Risk of AVN Description Most common
surgery
1 Low Non complete, Non Head sparring (1,2 fix
displaced with a screw)
2 Complete, non-
displaced
3 High Complete, partially Head replacement
displaced (3,4 use an Austin
4 Completely displaced moore)

Medical: Pre-operatively → analgesia including a fascia iliaca block, stop anticoagulants and anti-
platelets
Post-operatively → thromboprophylaxis, early mobilisation, beware of delirium
Surgical:
Miscellaneous:
Complications:

Condition: Pain management


Definition: 1 – mild pain → non opioid +/- adjuvant (paracetamol, NSAIDs, aspirin)
2 – moderate pain → weak opioid +/- adjuvant (codeine, tramadol, low-dose morphine)
3 – severe pain → strong opioid +/- adjuvant (morphine, oxycodone, fentanyl)
Adjuvants – antidepressants, anticonvulsants
Entonox – 50:50 mixture of O2 and NO; good for short tern relief; avoid in head injuries, chest
injuries and suspected bowel obstruction
Ketamine – NMDA receptor antagonist used as an adjunct or alternative to opiates; avoid risk of
cardio-respiratory depression; side effects: hallucinations and dissociative mental state
Presentation:
Risk factors:
Symptoms:
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative
Medical:
Surgical:
Miscellaneous:
Related: Neuropathic pain
Sx: burning, shooting or stinging pain; pins and needles; allodynia
Causes: diabetic neuropathy, multiple sclerosis, stroke, entrapment neuropathy
Tx: amitriptyline/ duloxetine/ pregabalin/ gabapentin → stop 1st line drugs and trial one of the
other 3 → refer for specialist input (+/- tramadol as short-term rescue medication +/- topical
capsaicin cream for localised pain in patients who cannot tolerate, or wish to avoid oral treatment

Condition: Anaphylaxis

Definition: severe, potentially life-threatening allergic reaction


Presentation:
Risk factors:
Symptoms:
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative: ABCDE and skin changes -> call for help (resuscitation team or ambulance) ->
remove trigger if possible and lie the patient flat or in a sitting position for easier breathing, if
patient is pregnant, lie them on their left side -> establish airway, give high flow oxygen, apply
pulse oximetry, ECG, blood pressure -> repeat IM adrenaline after 5 minutes and IV fluid bolus if
no response -> if still no response, confirm resuscitation team or ambulance has been called and
follow refractory anaphylaxis algorithm
Medical: IM adrenaline at anterolateral aspect and middle third of thigh 1mg/ml (1:1000)
concentration
 Adult and child > 12 years: 500 micrograms IM
 Child 6-12 years: 300 micrograms IM
 Child 6 months to 6 years: 150 micrograms IM
 Child <6 months: 100-150 micrograms IM
Surgical:
Miscellaneous:
Complications:

Condition: Acute epistaxis

Definition: bleeding from the nose caused by damage to the blood vessels in the nasal mucosa.
Most common site = anterior part of nose (kiesselbach’s plexus) because it is where the anterior
ethmoid artery, posterior ethmoid artery, posterior nasal artery and nasolabial artery
anastomose; inferior turbinate
Localised causes: trauma (nose picking and foreign bodies), inflammation (sinusitis, recent URTI),
vascular (telangiectasia), tumours (angiofibroma, SCC), dry membranes (air conditioning, nasal
cannulae), post-operative bleeding, topical drugs (e.g. decongestants, cocaine)
Generalised causes: atherosclerosis, raised venous pressure, haematological disorders (VWD,
haemophilia, leukemia), systemic drugs (anticoagulants, antiplatelets), alcohol excess, NOT
arterial hypertension
Presentation:
Risk factors:
Symptoms: signs of posterior bleed: profuse bleeding, bleeding from both nostrils, no bleeding
points can be found, suspected anterior bleed has not been resolved
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative: if person is haemodynamically compromised, transfer immediately to A&E, use first
aid measures to control bleeding, lean forward to decrease blood flow through the nasopharynx,
allow spitting out of blood, pinch the cartilaginous part of nose firmly and hold for 10-15 minutes
while breathing through the mouth + tranexamic acid
 Anterior: silver nitrate cautery
o Bleeding stops -> discharge with topical naseptin
o Bleeding persists -> rapid rhino unilateral anterior packing -> discharge with
packing for ENT review the following day
 Posterior: admit to hospital -> bilateral posterior packing, antibiotics, surgery if indicated,
replace blood and reverse coagulation if needed
Medical:
Surgical:
Miscellaneous:
Complications:

Condition: Poisoning

Definition:
Presentation:
Risk factors:
Symptoms: hypotension (systolic BP of less than 70 mmHg may lead to irreversible brain damage
or renal tubular necrosis), hypertension (less frequent and associated with sympathomimetic
drugs like amphetamines, phencyclidine and cocaine), cardiac conduction defects and arrhythmias
(TCAs, antipsychotics, antihistamines), hypothermia
 Alcohol intoxication: ataxia, drowsiness, nystagmus, hypotension, acidosis, vomiting
 Aspirin poisoning: hyperventilation, deafness, vasodilation, sweating, tinnitus
 Opioid poisoning: coma, respiratory depression, pinpoint pupils
 Paracetamol poisoning: renal tubular necrosis, nausea and vomiting, onset of right
subcostal pain and tenderness which develops into hepatic necrosis
 Lithium poisoning: vomiting, diarrhoea, ataxia, weakness, muscle twitching, tremor,
convulsions, coma, renal failure, electrolyte imbalance, dehydration, hypotension
 Carbon monoxide poisoning: headache, dizziness, weakness, upset stomach, chest pain,
confusion
Examination findings/Signs:
Investigations:
Bedside:
Bloods: blood test – CO poisoning: more than 30% indicates severe exposure
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative:
 Hypotension: raise foot of bed and administer infusion of sodium chloride or colloid
Medical:
 Alcohol intoxication: manage supportively and maintain clear airway
 Aspirin poisoning: measure plasma salicylate, ph and electrolytes; activated charcoal given
within 1 hour of ingesting more than 125mg/kg of aspirin; IV sodium bicarbonate to
enhance urinary salicylate excretion; replenish fluids (potassium chloride) and dialysis
 Opioid poisoning: naloxone hydrochloride in repeated injections according to respiratory
rate and depth of coma
 Paracetamol poisoning: IV acetylcysteine within 24 hours of ingesting paracetamol, most
effective given within 8 hours of ingestion (divided between 3 doses)
o Avoid underestimating toxic paracetamol dose in obese patients who weigh more
than 110kg, use a body weight of 110kg
o If within 1 hour or less, give activated charcoal, more than 75mg/kg or more of
paracetamol can lead to serious toxicity
 Lithium poisoning: supportive tx for electrolyte balance, renal function and control of
convulsions
 CO poisoning – 100% oxygen until carboxyhaemoglobin levels decrease to less than 10%
Surgical:
Miscellaneous:
Complications:

Condition: Sepsis

Definition: life-threatening organ dysfunction due to dysregulated host response to infection.


Septic shock = persistent hypotension or lactate >2 despite adequate fluid resuscitation
Presentation:
Risk factors:
Symptoms:
Examination findings/Signs: Qsofa = bedside assessment tool to predict poor outcomes
H = hypotensive (SBP < 90 mmHg)
A = altered mental status
T = tachypnoea (RR>22)
Investigations:
Bedside:
Bloods: bloods including lactate, blood cultures, urine output
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Immediate management: Sepsis Six (within <60 mins from presentation)
 Give O2 to keep sats above 94%
 Take blood cultures
 Give IV antibiotics
 Give a fluid challenge (crystalloid fluids 20ml/kg)
 Measure lactate
 Measure urine output
*Remember using mnemonic BUFALO
BLOOD CULTURES
URINE OUTPUT
FLUID MONITORING
ANTIBIOTICS
LACTATE LEVELS
OXYGEN LEVEL MAINTENANCE ABOVE 94%
Miscellaneous:
Complications:

Neurology
Management of psychosis

 Psychosis is when people lose some contact with reality – might hear or see things that
other people cannot see or hear
 Causes: Schizophrenia, bipolar disorder, severe depression (can be triggered by trauma,
stress, drug misuse, side effects of prescribed medicine, brain tumour)
 Treatment: antipsychotic medicine, CBT, social support

Diagnosis of facial pain

 History
o Site: unilateral or bilateral? – unilateral = dental conditions, trigeminal neuralgia,
salivary gland conditions; either = sinus infection, temporomandibular disorders,
headaches, giant cell arteritis; pain in region of ear = skin, teeth, tonsils, pharynx,
larynx or neck; tenderness over maxilla = sinusitis, dental abscess or carcinoma
o Character: continuous or episodic? – trigeminal neuralgia = intermittent sharp,
severe pain in the distribution of the trigeminal nerve; infections of teeth mastoid
and ear = dull, aching
o Precipitating factors? – food or chewing: dental abscess, salivary gland disorder,
temporomandibular joint disorder, jaw claudication due to temporal arteritis;
trigeminal neuralgia = eating, talking, toughing the face
o Others? Herpes zoster infection = unilateral erythema and vesicles in the distribution
of the trigeminal nerve
 Investigation
o FBC, ESR, CRP, Xray, ultrasound (suspected salivary gland pathology), MRI, CT
 Treatment
o First line for atypical facial pain = TCA such as amitriptyline; fluoxetine and
venlafaxine
o CBT

Diagnosis of vertigo

 Cause can be peripheral or central vertigo


 Features of central = prolonged, severe vertigo; new onset headache or recent trauma; CVD
risk factors
 Features of peripheral = normal neurological exam, severe nausea and vomiting, hearing
loss e.g. benign paroxysmal positional vertigo, meniere’s disease
 Tx
o Central: Admit and refer to balance specialist -> buccal or IM prochlorperazine for
immediate tx for nausea and vomiting (less severe = give short oral course of
prochlorperazine)
o Peripheral: admit and refer to specialist -> same as central

Motion sickness

 Tx: hyoscine > cyclizine > promethazine

Diagnosis of intracerebral vascular anomaly

Peripheral nerve compression

 Can be caused by repetitive injury and trauma to a nerve and can result in microvascular
changes, edema, injury to outside layers of the nerve

Causes of confusion

Causes of headaches

 Cluster headaches
o More common in men and smokers, alcohol may trigger an attack
o Fx: pain typically occurs once or twice a day, each episode lasting 15 mins – 2 hours,
clusters can last to 4-12 weeks, intense sharp pain around one eye, restlessness and
agitation, red, lacrimating eye, nasal stuffiness, ptosis and miosis
o Mx: 100% oxygen, subcut triptan, verapamil for prophylactic mx
 Tension headahces
o Fx: tight band around head and pressure sensation, bilateral symptoms unlike
migranes, lower intensity than migraines, may be related to stress, not associated
with nausea and vomiting
o Tx: aspirin, paracetamol, NSAID, up to 10 sessions of acupuncture over 5-8 weeks or
low-dose amitriptyline for prophylactic tx.

Anatomy of referred pain


Management of first seizures

 Epilepsy most commonly occurs in isolation but some are associated with cerebral palsy,
tuberous sclerosis, mitochondrial disease
o Febrile convulsions: usually occur early in a viral infection as the temperature rises
rapidly, typically occur in children between ages 6 months and 5 years
o Alcohol withdrawal seizures: occur in patients with a history of alcohol excess who
suddenly stops drinking -> long term alcohol consumption enhances GABA mediated
inhibition in the CNS (Similar to benzodiazepines) and inhibits NMDA-type glutamate
receptors, withdrawing causes decreased inhibitory GABA and increased NMDA
glutamate transmission. Peak incidence of seizures is at around 36 hours following
cessation of drinking – patients often given benzodiazepines following cessation of
drinking to reduce the risk
o Psychogenic non-epileptic seizures – describes patients who present with epileptic-
like seizures but do not have characteristic electrical discharges
 Mx: start antiepileptics following second epileptic seizure
o Sodium valproate for patients with generalised seizures
 MOA: increases GABA activity
 ADR: increased appetite and weight gain, alopecia, P450 enzyme inhibitor,
ataxia, tremor, hepatitis, pancreatitis, teratogenic
o Carbamazepine for patients with focal seizures
 Moa: Binds to sodium channels increasing their refractory period
 ADR: P450 enzyme inducer, dizziness and ataxia, drowsiness, visual
disturbances, leucopenia and agranulocytosis
o Lamotrigine (second line)
 MOA: sodium channel blocker
 ADR: stevens Johnson syndrome
o Phenytoin
 Binds to sodium channel increasing their refractory period
 ADR: P450 enzyme inducer, dizziness and ataxia, drowsiness, megaloblastic
anaemia, peripheral neuropathy, osteomalacia
 Benzodiazepines such as diazepam are typically used and administered rectally or under the
tongue for acute seizures that don’t terminate after 5-10 minutes. If patient continues to fit,
it is termed status epilepticus and is a medical emergency requiring hospital treatment ->
treat with benzodiazepines eg. Diazepam, lorazepam, midazolam

Causes of delirium

 UTI – most common in elderly or people with dementia


 Stroke or TIA
 Low blood sugar
 Head injury
 Alcohol poisoning or alcohol withdrawal
 Carbon monoxide poisoning
 Asthma attack
 Management = haloperidol or olanzapine. If patient has Parkinson’s, give lorazepam

Management of brainstem death

 Tests for brain death: a torch is shone into both eyes to see if they react to light, eye is
stroked with a tissue
 High corticosteroids may reduce brain death-induced inflammation and help to modulate
immune function

Differential diagnosis of foot drop

 Sport injuries, slipped disc, crossing your legs for long periods of time, peripheral
neuropathy, hip or knee replacement surgery

Investigation of tremor

Anatomy of brain lesions

 Classification: meningioma, glioma, neuroma, pituitary adenoma, craniopharyngioma (most


common is glioma)

Peripheral nerve lesions of the upper limb

Recognition of causes of weakness in shoulders

Condition: Meningitis

Definition: Inflammation of the meningitis (viral and bacterial) – more common=viral


Presentation:
Risk factors:
Symptoms: fever, headache, photophobia, neck stiffness (less in viral), muscle pain, blotchy skin,
confusion, vomiting, convulsions, non-branching rash (meningococcal)
Examination findings/Signs:
Investigations:
Bedside: lumbar puncture (performed once stable)
 Step. Pneumonia = gram positive diplococci (most common)
 Neisseria meningitides = gram neg diplococci (encapsulated yeast on india ink staining)
 Listeria monocytogenes = gram positive bacilli (pregnant women, older adults and
immunocompromised are at risk groups -> treat with ampicillin/ amoxicillin
 E.colli and klebsiella = gram neg bacilli
 Haemophilus influenza
CSF Normal Bacterial Viral TB
Appearance Clear Cloudy/ purulent Clear Turbid
Opening 10-20cm CSF Increased Increased Increased
pressure
WCC <5 >100 10-1000 50-500 cells/
cells/microlitres cells/microliters cells/microliters microliters
(neutrophils) (lymphocytes) (lymphocytes)
Glucose >50% of serum decreased increased decreased
Protein <45 mg/dl increased increased Super increased

Bloods:
Imaging: CT head, reduced GCS, raised ICP, immunocompromised
Management:
Patient Education/ Counselling/ Resources:
Conservative: >3months = start IV ceftriaxone without delay for suspected bacterial meningitis;
<3months = start IV ceftriaxone and amoxicillin/ampicillin; add vancomycin if patient has travelled
outside the UK or have had prolonged exposure to antibiotics
*if calcium-containing infusions are being administered, used cefotaxime
 s. pneumoniae (gram positive diplococci) = ceftriaxone
 Hib (gram negative) = ceftriaxone
 group B strep (gram negative) = cefotaxime
 Listeria monocytogenes = IV amoxicillin or ampicillin
 Meningococcal disease = IM benzylpenicillin
Medical: do not give corticosteroids in children <3months with bacterial meningitis. Give
dexamethasone for suspected or confirmed bacterial meningitis ASAP if lumbar puncture reveals
(1) purulent CSF, CSF with high WBC, raised CSF WBC with protein conc. greater than 1g/litre,
bacteria on gram stain
Start dexamethasone and antibiotics before lumbar puncture in al patients with suspected
meningitis who must undergo cranial CT first
Meningococcal septicaemia (Neisseria meningitides) = ceftriaxone, do not used corticosteroids
Surgical:
Miscellaneous:
Complications:

Condition: Cauda Equina Syndrome

Definition: acute loss of neurological function of nerve roots below the conus medullaris (L4-L5)
Presentation:
Risk factors:
Symptoms: numbness in perianal region, episodes of urinary incontinence, loss of anal tone
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative:
Medical:
Surgical: urgent MRI → refer to neurosurgeon or orthopaedic spinal surgeon → lumbar
decompression and discectomy
Miscellaneous:
Complications:

Condition: Multiple sclerosis

Definition: most common immune-mediated demyelinating disease of the CNS


Presentation:
Risk factors:
Symptoms: spasticity, cerebellar ataxia, UMN signs only, optic neuritis, bilateral internuclear
opthalmoplegia, urinary urgency/incontinence, neropathic pain, cognitive decline, Lhermitte’s
syndrome, weakness, numbness, tingling in arms and legs
Examination findings/Signs: weakness in specific muscle groups
Investigations:
Bedside:
Bloods:
Imaging: white matter lesions in corpus callosum, infrafrontal region, periventricular; hyperdense
lesions in T2 MRI and hypodense lesions in T1 MRI
Management:
Patient Education/ Counselling/ Resources:
Conservative:
Medical: spasticity sx → baclofen or gabapentin → symptoms not resolved? → trial other first line
agent → symptoms not resolved? → trial of combination of first line options or second line
(dantrolene or tizanidine) → symptoms not resolved → benzodiazepines
Surgical:
Miscellaneous:
Related: Gullian Barre syndrome – destroys the myelin of the peripheral nerves
Sx: ascending paralysis often secondary to infection, usually just presents with weakness that may
last years
Chronic inflammatory demyelinating polyneuropathy (CIDP) – same sx as GBS but lasts longer and
can cause lasting damage if not caught early

Condition: Wernicke’s Encephalopathy

Definition: acute neurological condition characterized by a triad of ophthalmoparesis: nystagmus,


ataxia and confusion
Presentation:
Risk factors:
Symptoms:
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative: hypoglycaemia → treat hypoglycaemia → IV pabrinex immediately after glucose →
continue for 5 days
Normoglycaemia → IV pabrinenx → continue for 5 days → prophylactic thiamine
Medical:
Surgical:
Miscellaneous:
Complications: Dry beri-beri – bilateral motor and sensory peripheral neuropathy; wet beri-beri –
dilated cardiomyopathy, pulmonary oedema, high cardiac output state; korsakoff syndrome –
retrograde and anterograde amnesia, confabulation, preserved long-term memory
Hypoglycaemia → awake + alert → glucogel → check BM → long-acting carb e.g. toast; reduced
conscious level → no IV access → glucagon IM; has IV access → dextrose 20% → check BM → give
long acting carb

Condition: Stroke and TIA

Definition: serious life-threatening condition that happens when the blood supply to part of the
brain is cut off
Presentation:
Risk factors: high blood pressure, diabetes, smoking, oral contraceptives, history of TIAs, high
cholesterol and lipids
Symptoms: neurological symptoms, limb/ face weakness, slurred speech, hemianopia, LOC/
syncope very uncommon
Examination findings/Signs: cranial nerves exam, upper and lower limb neuro exam
Investigations:
Bedside: FAST screening tool, blood glucose as hypoglycaemia can present with dizziness and
weakness. Swallowing screened by trained healthcare professional before any oral food, fluid,
medication
Bloods: FBC, U&E, TFT and lumbar puncture 12 hours later or if suspected meningitis
Imaging: non-contrast CT head, MR head
 Ischaemic stroke: hypodense (area of dead cells)
 Haemorrhagic stroke: hyperdense (acute so blood clot is brighter on scan)
Management: TIA
Medical: offer aspirin 300mg daily unless contraindicated -> refer immediately for specialist
assessment and investigation
 Use FAST (face arm speech test) if outside hospital to screen people
 If in the A&E, use ROSIER (recognition of stroke in the emergency room)
 If they are a candidate for carotid endarterectomy, offer urgent carotid imaging
 Do not offer CT brain unless there is alternative diagnosis
 Consider MRI to determine territory of ischaemia or haemorrhage
Management: Ischaemic stroke
Patient Education/ Counselling/ Resources:
Conservative: maintain glucose, hydration, oxygen sats and temp within normal limits
Medical: thrombolysis if patient presents within 4.5 hours of onset, unless they have uncontrolled
hypertension, are pregnant or have had a previous intracranial haemorrhage. Alteplase is the drug
of choice for thrombolysis.
 If raised ICP, give mannitol immediately or EVD (external ventricular drain) or VP shunt
(ventriculoperioneal shunt) if hydrocephalus is causing a mass effect -> parietal-temporal
craniotomy if needed
 Aspirin 300mg (orally or rectally) should be given ASAP as you rule out a haemorrhagic
stroke and continue aspirin for 2 weeks
 Patient is discharged with anticoagulant – clopidogrel is recommended by NICE
Surgical: Thrombectomy -> criteria: if there is occlusion of the proximal anterior circulation
confirmed by a CT scan, thrombectomy is to be done within 6 hours of symptom onset and
patient should also be thrombolysed -> perform imaging with CT contrast angiography following
non-enhanced CT
Management: Haemorrhagic stroke
Conservative: consult neurosurgeon, risk factors such as significant co-morbidities, a GCS < 8 due
to hydrocephalus makes surgery a less likely option. Location and size of haemorrhage also are
factors
 Supportive management – consciousness, blood glucose, BP, O2 hydration, temperature,
cardiac rate, ICP if patient has signs of raised ICP
Medical: stop anti-coagulant and try to reverse the effect – i.e. if the patient was on warfarin,
administer vitamin k and prothrombin complex concentrate
Surgical:
Miscellaneous:
Complications:

Psychiatry
Management of depression

Diagnosis of psychiatric disorder

Treatment of ADHD

 Methylphenidate
o Most commonly used medicine for ADHD – increases activity in the brain,
particularly in areas that play a part in controlling attention and behaviour
o Common side effects: small increase in BP and HR, loss of appetite, trouble sleeping,
headaches, stomach aches, feeling aggressive
 Lisdexamfetamine
o Offered if treatment with methylphenidate has not helped
o Adults may be offered this as first choice
o Common side effects: decreased appetite, aggression, drowsiness, dizziness,
headaches, diarrhoea, nausea and vomiting
 Atomoxetine
o SNRI
 Guanfacine
o Can reduce blood pressure

Diagnosis of psychiatric disorder

Acute psychiatric conditions

Management of psychiatric illness

Condition: Anxiety

Definition: panic disorders, agoraphobia, specific phobias, GAD, OCD (low levels of GABA and
glutamate)
Presentation:
Risk factors:
Symptoms:
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative:
Medical: SSRIs and SNRIs → pregabalin → benzodiazepines (lorazepam and diazepam)
Surgical:
Miscellaneous:
Complications:

Definition:
Presentation:
Risk factors:
Symptoms:
Examination findings/Signs:
Investigations:
Bedside:
Bloods:
Imaging:
Management:
Patient Education/ Counselling/ Resources:
Conservative:
Medical:
Surgical:
Miscellaneous:
Complications:

Cancer
Condition: Breast cancer

Definition: Differentials for breast lumps: fibrocytic breast condition – noncancerous changes in
the breast, cysts: small fluid-filled sacs
Presentation:
Risk factors: increasing age (BC in young women up to 5-10 years postpartum are associated with
increased risk for metastasis and death), female, obesity, family history, past history, inherited
genes that increases cancer risk, radiation exposure
Symptoms: new lump in breast or underarm, thickening or swelling of part of breast, irritation or
dimpling of breast skin, redness or flaky skin in the nipple area, pulling in the nipple or pain in the
nipple area, nipple discharge, change in size or shape of breast, pain in any area of the chest
Examination findings/Signs: Annual mammography until they enter the Breast Test Wales
Screening Programme (BTWSP) – x-rays of breast for women aged 50 and over
Investigations:
Bedside: oestrogen receptor, progesterone receptor and human epidermal growth receptor 2
(HER2) status of all invasive breast cancers
Bloods:
Imaging:
 Preoperative assessment of the breast and axilla – offer ultrasound of axilla for early
invasive breast cancer screening
 Do not routinely offer MRI if patient has invasive breast cancer or ductal carcinoma unless
there is a discrepancy regarding the extent of the disease from clinical examination,
mammography and ultrasound assessment for planning treatment
 Offer genetic testing for BRCA1 and BRCA2 mutations to women under 50 years old with
triple-negative breast cancer (do not have hormone receptors so they do not respond to
hormonal therapy medicines), including those with no family history of breast or ovarian
cancer
Surgical: offer sentinel lymph node biopsy to determine whether the cancer has spread beyond a
primary tumour into the lymphatic system – unless they have ductal carcinoma -> offer axillary
node clearance or radiotherapy if there is a proven lymph node macrometastasis (do not offer if it
is micrometastases)
Management:
Patient Education/ Counselling/ Resources: offer specialist psychological support and clinical
nurse specialist support; consider adjuvant therapy after surgery for people with invasive breast
cancer by using the PREDICT tool
Conservative:
Medical: Endocrine therapy - offer tamoxifen, or an aromatase inhibitor for ER-positive BC of
post-menopausal women. Consider ovarian function suppression in addition to endocrine therapy
for premenopausal women with invasive breast cancer. Offer bisphosphonates as adjuvant
therapy to postmenopausal women with node-positive invasive cancer and DEXA scans for those
not receiving bisphosphonates. Offer neoadjuvant chemotherapy or endocrine therapy to people
with ER-negative invasive breast cancer or triple-negative invasive breast cancer
*Neoadjuvant = before surgery
Surgical: breast-conserving surgery -> offer further re-excision or mastectomy if needed but
discuss benefits and risks
Miscellaneous:
Complications: Lymphoedema; menopausal symptoms – stop systemic hormone replacement
therapy

Condition: Mastitis

Definition: Inflammation of breast tissue that involves an infection


Causes: blocked milk ducts, bacteria entering the breast
Presentation:
Risk factors: previous bout of mastitis while breast feeding, sore nipples, improper nursing
technique, becoming overly tired or stressed, poor nutrition, smoking
Symptoms: breast pain, swelling, warmth and redness, fever and chills, malaise, thickening of
breast tissue or lump
Examination findings/Signs:
Investigations:
Bedside: breast examination, culture breast milk
Bloods:
Imaging: mammogram or ultrasound, biopsy if antibiotics don’t work
Management:
Patient Education/ Counselling/ Resources: advice patient to avoid prolonged overfilling of the
breasts. Massage breast while feeding and making sure the breast is completely drained
Conservative:
Medical: antibiotics 10-day course (flucloxacillin, co-amoxiclav, erythromycin and clarithromycin,
metronidazole), pain relievers (acetaminophen and ibuprofen)
Surgical:
Miscellaneous:
Complications:
Social population, health and research

Screening test statistics

TP = true positive; FP = false positive; TN = true negative; FN = false


negative

Disease present Disease absent


Test positive TP FP
Test negative FN TN

The table below lists the main statistical terms used in relation to
screening tests:

Measure Formula Plain english


Sensitivity TP / (TP + FN) Proportion of patients with the
condition who have a positive test
result
Specificity TN / (TN + FP) Proportion of patients without the
condition who have a negative test
result
Positive predictive TP / (TP + FP) The chance that the patient has the
value condition if the diagnostic test is
positive
Negative predictive TN / (TN + FN) The chance that the patient does not
value have the condition if the diagnostic
test is negative
Likelihood ratio for a sensitivity / (1 - How much the odds of the disease
positive test result specificity) increase when a test is positive
Likelihood ratio for a (1 - sensitivity) / How much the odds of the disease
negative test result specificity decrease when a test is negative

Medical ethics

Mental Health Act 1983

 A person can be compulsorily admitted to hospital or another mental health facility


(sectioned) if they:
o Have a mental disorder of a nature or degree that makes admission appropriate
o Should be detained in the interests of their own safety, for the protection of others,
or both
 Length of time a person can be sectioned is: 72 hours, 28 days and 6 months
 Person can appeal against the decision to a mental health tribunal
 In situations where there is serious doubt or dispute about what’s in someone’s best
interests, healthcare professionals can refer the case to the court of protection for a ruling
(mental capacity act 2005)
o Sterilisation for contraceptive purposes
o Donation of organs or regenerative tissue such as bone marrow
o Withdrawal of nutrition and hydration from a person who’s in a permanent
vegetative state or minimally conscious state

Driving after a provoked seizure

 Epilepsy – 2 or more unprovoked seizures over a period which exceeds 24 hours


 MUST not drive and must notify DVLA
o Epilepsy or multiple unprovoked seizures – (car and motorcycle) cease for 12
months from date of most recent seizure; (bus and lorry) cease for 10 years
o First unprovoked epileptic seizure – (car and motorcycle) cease for 6 months or 12
months if there is an underlying causative factor that may increase risk; (bus and
lorry) cease for 5 years and neurologist has to make an assessment
o Provoked seizure – (car and motorcycle) cease for 6 months; (bus and lorry) cease
for 5 years
o Withdrawal of epilepsy medication – must not drive for 6 months after last dose; if
driver has epilepsy had a seizure within 6 months, they must not drive for 12
months; (bus and lorry) must be free of epileptic seizures for past 10 years

Safeguarding of vulnerable adults

Medical aspects of fitness to drive

Recognition of non-accidental injury

You might also like