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Exam Revision (Overview) > Year One > Flashcards

Year One Flashcards

1
Q

Describe the key aspects of (non-acute) asthma.

A

Presentation: reversible bronchodilation, wheeze, dyspnoea, cough, atopy/allergy
Investigations: spirometry, peak flow
Treatment: SABA initially, then ICSs. Then consider LABA, increased steroids, methylxanthines, IgE monoclonal antibodies

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2
Q

Describe the key aspects of acute asthma.

A

Presentation: if life threatening, A CHEST
Arrhythmia, cyanosis (normal PaCO2), hypoxia/hypotension, exhaustion, silent chest, threatening PEFR (<33%)
Investigations: spirometry, ABG
Treatment: O SHIT MAN
Oxygen, salbutamol, hydrocortisone, ipratropium bromide, magnesium sulfate, anaesthetist, nebulizer

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3
Q

Describe the key aspects of COPD.

A

Presentation: non-reversible dyspnoea, use of accessory muscles, reduced exercise tolerance, cough and sputum
Investigations: spirometry, CXR, ABG, Chest CT
Treatment: domicilliary oxygen, SABA. then consider triple therapy (SABA/LAMA/LABA). rofumilast and carboxysteine. SMOKING CESSATION VITAL

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4
Q

Describe the key aspects of COPD exacerbation.

A

Presentation: more mucus, different colour, worse cough, fever
Treatment: as for COPD, with antibiotics

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5
Q

Describe the key aspects of cystic fibrosis, along with a brief indication of its scientific basis.

A

Science: defect in the CFTR gene on chromosome 7, blocking Cl secretion making secretions thicker.
Presentation: skin prick test, sweat test, karyotyping
Symptoms: male infertility, chronic lung infections, steatorrhoea, poor weight gain, failure to thrive, meconium ileus
Treatment: airway clearance, antibiotics, pancreatic enzyme supplementation, ivacaftor, trikefta

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6
Q

Describe the key aspects of bronchiectasis. Which pathogen are patients more likely to culture?

A

Presentation: copious coughing up mucus in the morning, recurrent chest infections
Investigations: HRCT (showing signet rings and mucus)
Treatment: airway clearance, antibiotics, azithioprine, ciprofloxacin.
Key culture: P aeruginosa

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7
Q

Describe the key aspects of obstructive sleep apnoea.

A

Presentation: excessive sleepiness, personality change, difficulty driving, cognitive impairment, loud snoring
Investigations: overnight pulse oximetry (showing a sawtooth pattern), or overnight sleep studies
Treatment: BiPAP or modafinil (a short term CNS depressant), or if young mandibular advancement

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8
Q

Describe the key aspects of ARDS, including pathology.

A

Pathology: trauma causes diffuse alveolar damage (DAD), leading to myofibroblasts leaking fibrous exudate and attracting neutrophils
Investigations: CXR, ABG
Treatment: oxygen, prone positioning, fluid management

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9
Q

Describe the key aspects of small cell lung cancer. Describe also the paraneoplastic syndromes associated with SCLC.

A

Presentation: weight loss (cachexia), night sweats, haemoptysis, lethargy, anorexia. Most likely smokes
Investigations: CXR, ABG, CT, bronchoscopy
Management: chemotherapy, radiotherapy, palliative, smoking cessation
Paraneoplastic: Cushing’s (increased cortisol, ACTH, blood glucose, BP), SIADH (hypernatremia, increased BP, oedema), and Lambert Eaton syndrome (causing myasthenia gravis).

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10
Q

Name the types of tumour in the lung, describe their location (peripheral or central), and describe their paraneoplastic actions.

A

Small cell: central, Cushings/SIADH/Lambert Eaton
Squamous: central, hypercalcaemia, increased PTHrP and keratin
Adenocarcinoma: peripheral, most common in non-smokers, HPOA and trosseau’s sign
Pancoast: peripheral (lung apex), Horner’s syndrome

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11
Q

Describe the key aspects of interstitial pulmonary fibrosis.

A

Presentation: insidious dyspnoea, crackles, clubbing, cyanosis and hypoxia
Investigations: CXR, bloods (assess for immune cause), spirometry, CT scan, bronchoscopy
Management: antifibrotics, nintendamib, transplant

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12
Q

Describe the key aspects of extrinsic allergic alveolitis.

A

Inflammation of the alveoli. Social history is key to determine what this is. Treatment is with removal of the antigen, or prednisone.

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13
Q

Describe the key aspects of anaphylaxis.

A

Presentation: sudden dyspnoea, stridor, wheeze, respiratory failure
Treatment: COBRA
corticosteroids, oxygen, beta2-agonists, rush of adrenaline, antihistamine

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14
Q

Describe the key aspects of sarcoidosis.

A

Presentation: SARCOID
skin (erythema nodosum), arthritis, respiratory (bilateral hilar lymphadenopathy, raised ACE), cardiac (arrhythmia, heart block), occular (uveitis), intracranial (haemorrhage), derangement of liver and kidney (hypercalcaemia)
Investigations: CXR, ACE levels, calcium levels, HRCT, biopsy
Treatment: watch and wait (particularly for shins), then offer methotrexate, azathioprine, hydrochloroquine, TNF therapy

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15
Q

Describe the key aspects of granulomatosis with polyangiitis. What is the difference between this and Churg-Strauss syndrome?

A

Presentation: haemoptysis, glomerulonephritis, rhinitis, and haematuria. More likely to affect Scandanavians
Investigations: antibody screening (cANCA, PR3)
Treatment: immunosuppression (methotrexate, cyclophosphamide, steroids)
Churg-Strauss: all of the above plus eosinophillia (i.e. late onset asthma)

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16
Q

Describe the key aspects of Goodpasture’s syndrome. (Hint: investigation involves scientific basis)

A

Presentation: glomerulonephritis, fibrosis
Investigation: look for a3 autoantibodies against collagen IV, CXR
Treatment: plasmapheresis to remove antibodies, immunosuppression

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17
Q

Describe the key aspects of bronchiolitis.

A

Presentation: young, cough, crackles, wheeze, cough, apnoea
Cause: RSV or metapneumovirus (secondary)
Cohort nursing and hygiene prevents

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18
Q

Describe the key aspects of pulmonary embolism.

A

Presentation: rapid onset of dyspnoea, haemoptysis, pleuritic pain, collapse, signs of DVT
Scores: consider Well’s score
Investigations: CXR, ECG (normal, or rarely S1Q3T3), ABG (alkalosis). Then depending on probability:
Well’s < 4: D-dimer, Well’s > 4: CT-PA (or V/Q if allergic to iodine contrast or obese)
If positive, commense heparin or LMWH
Long term: consider HERDOO2 for women (hyperpigmentation, edema, redness, D-dimer, obesity, old age > 65) - 2+ means long term anti-coag. Men must remain anti-coag

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19
Q

Describe the key aspects of tension pneumothorax.

A

Presentation: rapid dyspnoea, sharp chest pain, dyspnoea, raised JVP, hyper-resonant, tracheal deviation
Investigations: clinical suspicion MUST overrule
Treatment: thoracocentesis 2nd ICS, mid-clavic, then chest drain 5th ICS anterior axillary line

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20
Q

Describe the key aspects of mesothelioma.

A

Presentation: exposure to asbestos (crocolite), chest pain, dyspnoea
Investigations: CXR, bloods, drain, bronchoscopy
Treatment: cisplatin, premextred, talc slurry

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21
Q

Describe the key aspects of pneumonia. Also complete the ‘pneumonia microbiology’ deck.

A

Presentation: fever, cough, chest pain, dyspnoea, rigor
Investigations: CXR, ABG, sputum culture
Management: consider CURB65 (confusion, urea > 8, resp rate > 30, BP < 90/60, 65+). Empirical treatment for 1-2 is amoxicillin. 3-4 is co-amoxiclav. Resistant cases offered clarithromycin or erythromycin if pregnant.
Other treatment: oxygen, fluid resus, LMWH if likely to stay mobile, physiotherapy. Abx class switch after sputum culture.

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22
Q

Describe the key aspects of pulmonary tuberculosis.

A

Presentation: night sweats, constitutional, haemoptysis, fever, history of travel or previous TB, immunocompromised
Investigations: sputum x3, bronchoscopy if not possible. CXR
Management: negative pressure room, barrier nursing, contact tracing, immediate start on RIPES treatment, direct observation treatment (DOT), HIV test

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23
Q

Describe the drugs and side effects of TB treatment.

A

Rifampicin - hepatitis, raised bilirubin, thrombocytopenia, pink secretion
Isoniazid - rash/Itch, B6 deficiency
Pyramidaine (first Pass metabolism) - hepatitis, gout
Ethambutamol - (Eyes): red-green colour deficiency
Streptomycin - vestibular nerve damage

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24
Q

Describe the key aspects of pertussis.

A

Presentation: paroxysms of whooping coughs, throat swelling, gasping, swelling, cyanosis
Investigation: PCR
Treatment: vaccine, macrolides

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25
Q

Describe the key aspects of hypertension. This includes staging and presentation, investigation, then treatment.

A

Presentation: usually idiopathic
Investigations: ABPI, fundoscopy, bloods, urinalysis, ECG
Staging: 1: 140/90+, 135/85+
2: 160/100+, 150/95+
3: 180/110+
Malignant: > 130 diastolic
Treatment: diet, smoking, alcohol, exercise, weight
Drugs: < 55: ACEi, CCB, Thiazide diuretic
Drugs: > 55: CCB, ACEi, Thiazide diuretic
Black and diabetic: hydralazine

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26
Q

Describe the key aspects of angina pectoris.

A

Presentation: chest pain on exertion, relieved by rest
Investigations: ECG, FBC, U&E, Glucose tests
Treatment: Beta-blockers/CCB, GTN, 4 A’s
(atorvastatin, aspirin, atenolol, ACEi), lifestyle modification. Advise on when to seek emergency medical treatment (2x GTN w/out relief)

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27
Q

Describe the key aspects of acute coronary syndrome.

A

Presentation: central crushing chest pain, radiating to jaw or left arm. Onset at rest/after 2x GTN
Investigations: ECG, cardiac troponin level
Management: MOVE
Monitor, Oxygen, Venous access, ECG
MONA
Morphine (+ anti-emetic), O2, Nitrates, Aspirin (+ prasugrel/ticagrelor/clopidogrel)
Discharge: SABA
Statin, aspirin, B-blocker, ACEi

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28
Q

Describe the key aspects of acute congestive heart failure.

A

Presentation: dyspnoea, orthopnoea, chest pain, wheeze, crackles, elevated JVP, cardio megaly, hepatomegaly, ascites
Investigations: CXR (ABCDE - alveolar bat wings, kerly B lines, cardiomegaly, dilation of vessels, edema), FBC, LFTs, BNP pre echo, ECG, U&Es
Treatment: OMFG (oxygen, morphine, furosemide, GTN). Then: A Bad Surgeon Does Not Intubate Diseased, Hypoxic Patients (ACEi + Bb, Steroids, Diuretics, Neprilysin inhibitor, Ivabradine, Digoxin, Hydralazine + Isosorbide Dinitrate)

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29
Q

Briefly describe bradyarrhythmias and their management.

A

Sinus, sick sinus, ectopics, tachy-brady. Use atropine (antimuscarinic) or adrenaline/dobutamine (B1 agonists)

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30
Q

Briefly describe the classification of AVN block and the management of these. In addition, name the main drugs responsible for AVN block.

A

Presentation - syncope, palpitations. ECG
1st degree - prolonged PR (5 boxes +), every P wave associated with a QRS. N/A
2nd, Mobitz I (Wenkebach) - PR enlongates until beat is dropped. N/A
2nd, Mobitz II - every nth beat is dropped. Consider vagal manoeuvres if stable, or atropine/transvenous pacing if unstable
3rd degree - complete seperation, may result in blackout attacks (Stoke-Adams). Pacing indicated
Drug blockers: adenosine, amiodarone, B-blockers, CCBs, digoxin

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31
Q

Describe the key aspects of bundle branch block.

A

Both L and R have a QRS > 0.12s.
LBBB - WiLLiaM - V1 has a W shape, V6 an M shape
RBBB - MaRRoW - V1 has a M, V6 a W

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32
Q

Describe the key aspects of atrial fibrillation.

A

Presentation: dyspnoea, chest pain, palpatation, syncope, light-headedness, irregularly irregular pulse
Investigations: ECG, FBC, U&E
Management (acute): hemodynamic instability: cardioversion. Relevant heart disease: amiodarone. No relevant disease: ‘pill in the pocket’: flecanide
RHYTHM control: same as above long term (but dronedarone may be considered in place of amiodarone except in CHF due to side effects) or cardiac ablation
RATE control: inactive lifestyle (digoxin), or if active consider B-blocker or CCB.
Use CHA2DS2-VASc and HAS-BLED to consider anticoagulation

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33
Q

Describe the key aspects of arterial aneurysms. Include also the three main risk factors.

A

Dilation in the arteries due to wall weakness, encompassing all three layers. 60% are abdominal, 40% thoracic.
Presentation: 75% asymptomatic, 25% with bruising and pain radiating to lower back.
Risks: infection, infective endocarditis, Marfans
Investigations: USS screening: normal, small, medium, large (< 3cm, 3-4.4cm, 4.5-5.4, > 5.5cm) should be treated as (N/A, yearly USS, 3 monthly USS, 2 week referral). CT may also be used
Treatment: Lifestyle advice and EVAR (endovascular aneurysm repair) for large aneurysms.

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34
Q

Describe the key aspects of arterial dissections.

A

Presentation: ripping chest pain with different BP measurements in each arm.
Classifications: Stanford A (ascending aorta) and B (descending).
Investigations: CXR, CT angiography, transesophageal echo, MRI
Treatment: type A by surgery (emergency which may progress to shock), B by B-blockers and nitroprusside

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35
Q

Describe the key aspects of peripheral arterial disease (PAD).

A

Presentation: intermittent claudication (‘leg angina’) or critical limb ischaemia (pain at rest).
Examination: ARTS (absent pulses/hair, red/round ulcers, toe or ankle ulcers, sharp leg pain).
6 P’s: pain, pallor, parathesis, polar (cold), pulses, paralysis.
Investigations: ABPI ( < 0.4 = CLI, > 0.4 = IC), or angiography (CT/MRI/catheter, where ABPI is falsely elevated)
Treatment: pain management, statins, smoking cessation, anticoagulation, THEN surgery/amputation

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36
Q

Describe the key aspects of peripheral vascular disease (PVD). Don’t confuse this with peripheral vascular disease (also PVD) which encompasses both PAD and PVD.

A

Presentation: VEINY (voluptuous pulses, edema, irregular shapes, no sharp pain, yellow and green toes/ankles). Varicose veins or superficial thrombophlebitis.
Investigations: D-dimer for DVT
Treatment options: compression stockings, endovenous ablation, foam sclerotherapy, or ligation and removal. For DVT, warfarin and heparin, along with elastic stockings and mobilization is recommended.

37
Q

Describe the four main patterns of S2 splitting.

A

Usually, the pulmonary valve closes after the aortic (A > P). On inspiration, thoracic pressure increases, causing a ‘suction’ effect into the right ventricle.
Physiological: A&raquo_space; P in inspiration.
Paradoxical: LBBB or aortic stenosis cause the aortic valve to close later. In inspiration though, the pulmonary closing is ‘pushed back’ so they close simultaneously. So P > A in expiration.
Wide: A&raquo_space;> P, when the pulmonary valve already closes late (i.e. in pulmonary stenosis).
Fixed: A > P in both inspiration and expiration (i.e. ASD)

38
Q

Describe the characteristics and signs of aortic valve disease.

A

Stenosis: s24 (soft s2, S4). Opening click. Radiates to the carotids. Causes include calcification, bicuspid valves, or rheumatic fever. May cause LVH. Treatment is with valve replacement.
Regurg: early diastolic descrescendo murmur. Radiates to right sternal edge. Main causes include endocarditis, rheumatic fever, syphillis, and Marfans. Collapsing pulse and wide pulse pressure seen.
Specific AR signs: Murmurs Don’t Cease Quickly; They Die Hard. Muller’s (uvula), De-Musset (head bobbing), Corrigan’s (collapsing pulse), Quincke (nail bed pulses), Traube (pistol shot femorals), Duroziez (femoral bruits), Hill’s (Popliteal > brachial by 60mmHg).

39
Q

Describe the characteristics and signs of mitral valve disease.

A

Stenosis: rheumatic disease or AF. Malar flush seen. Loud S1. Valvuloplasty or surgery considered. Radiates to axilla
Regurgitation: s1sp23. Caused by ischaemia or heart failure. Controlled with ACEi/diuretics. Radiates to axilla/back

40
Q

Describe the key aspects of ASDs, VSDs, and patent foramen ovale and ductus arteriosus.

A

ASD: usually asymptomatic/acyanotic, but may cause fixed splitting or an ejection systolic murmur.
Patent foramen ovale: may allow paradoxical embolism
VSD: most common defect. May cause Eisenmonger’s syndrome. Pansystolic murmur. Large VSDs cause cyanosis
Patent ductus arteriosus: usually asymptomatic. May cause harsh machine gun like murmur. Vital to maintain in atresia with prostaglandin E2.

41
Q

Describe the key features of tetralogy of Fallot.

A

A large VSD, subpulmonary stenosis, aorta overriding the VSD, and right ventricular hypertrophy. Heart appears boot shaped on CXR. Tet’s spells (hypoxia causing cyanosis) are often fixed by squatting. Treatment involves shunting or other surgery.

42
Q

Describe the key features of transposition of the great arteries (ToGA).

A

The aorta and pulmonary artery swap places. Incompatible with life unless a VSD also exists. CXR shows an ‘egg on side’ appearance. Atrial switch operation is life-saving.

43
Q

Describe the key features of aortic coarctation.

A

Infant form exists with PDA, adult form without.
Presentation: weak lower pulses, claudication, CXR showing an aorta shaped like a 3, lower limb cyanosis.
Treatment: surgery, balloon dilatation

44
Q

Describe the key features of Marfans syndrome.

A

Cause: autosomal dominant mutation to FBN1 (fibrillin 1) causing poor elasticity and poor removal of TGF-beta (resulting in excess growth).
Presentation: CLAVATE (chest (pectus excavatum), lungs (ptx/bullae), arachnodactyly, valve prolapse (mitral), aortic problems (aneurysm, dissection), tall and thin, eyes (retinal detachment)).
Treatment: 6 monthly monitoring, atenolol and losartan

45
Q

Describe the key features of dilated cardiomyopathy.

A 
Most common ( > 90%).
Causes: CATCH DEAD (cocaine, alcohol, thiamine deficiency, Chagas, haemochromatosis, doxorubicin (chemotherapy), endocrine disorder, AFib, Duchenne dystrophy).
Treatment: short term mechanical support, drugs (as in CHF), heart transplant.
46
Q

Describe the key features of arrhythmogenic right ventricular cardiomyopathy.

A

Autosomal dominant condition where the right ventricle is very thin and replaced with fats. Associated with desmosome genes.
Clinical features: usually asymptomatic. May associate with Daxos syndrome (curly hair and thickening of palmar hand and plantar foot).
Investigations: ECG (showing episilon waves and inverted T waves with RBBB), and echo
Treatment: 3 levels. Beta blockers -> amiodarone/sotalol -> ICD. Transplantation is definitive

47
Q

Describe the key features of hypertrophic cardiomyopathy.

A

Autosomal dominant, affecting myosin genes. Can also be caused by Friedreich’s ataxia.
Clinical features: 4th heart sound, systolic or pansystolic ejection murmurs, sudden cardiac death.
Investigations: ECG (showing inverted T waves with convex/straight diagonal ST segment on V5/6) and echo (diagnostic).
Treatment: consider beta-blockers, verapamil, amiodarone, and ICDs.

48
Q

Describe the key features of restrictive cardiomyopathy.

A

Presentation: dyspnoea, signs of PE, hepatosplenomegaly, Friedreich sign
Causes: amyloidosis, radiation fibrosis, sarcoid
Investigations: CXR, ECG (low QRS voltage, ST/T abnormalities), echo
Treatment: Usually transplant

49
Q

Describe the key features of infective endocarditis. This includes pathology, investigation, scoring systems, microbiology, and empirical treatment. There are some non-infective causes; what are these?

A

Pathology: Damage to the heart valves causes turbulent flow, displacing emboli and allowing vegetations of bacteria to settle. These are friable.
Investigation: first line echo. CXR, CT, and culture
Scoring: EndoCarditis FEVER: Endocardial involvement (i.e. echo), Cultures (2x positive). Fever, Evidence of Immunologic involvement (Osler, Roth, glomerulonephritis, rheumatoid), Vascular evidence (emboli, haemorrhage, Janeway), Early culture evidence (i.e. not major), Risk factors (CHF, PWIDs)
Microbiology (three categories - main, gm negative, atypical): Staph aureus (PWIDs or late skin break), Strep viridans (poor dental hygiene), Strep bovis (GI cancer or Crohn’s), Staph epidermidis (early valve replacement/catheter). -ve: HACEK. Atypical: Coxiella burnetii, chlamydia, bartonella.
Empirical treatment: amoxicillin/vancomycin, gentamycin. PWIDs: flucloxacillin
Non-infective: Libman-Sacks (lupus), rheumatic fever

50
Q

Give the key features of myocarditis.

A

Causes: echovirus/coxsackie viruses/cytomegalovirus. Chagas, Lyme’s, diptheria, rheumatic fever.
Presentation: fever, dyspnoea, palpitation, fatigue, arrhythmia
Investigations: CXR, ECG (ST elevation and non-specific T wave changes), biopsy (showing Aschoff bodies if post-rheumatic fever), PCR
Treatment: bed rest, antibiotics, steroids/CHF treatment

51
Q

Give the key features of pericarditis (which also encompasses tamponade).

A

Presentation: fever, dyspnoea, sharp chest pain relieved by sitting up, muffled heart sounds
Causes: Coxsackie viruses, uremia, autoimmune, cancer, radiation, some drugs
Investigations: CXR (‘water bottle heart’), echo (sways side to side, ‘dancing’), ECG (PR depression and ST elevation, electrical alterans)
Treatment: NSAIDs and Colchicine (prevents recurrence), pericardiocentesis, pericardectomy

52
Q

Briefly describe the key features of heart cancer.

A

The main neoplasm is atrial myxoma (left atrium). Clinical features include loud first and third heart sounds, pedunculated mass on echo.
Surgery is completely curative.

53
Q

Describe the different types of oesophagitis. Include investigations and management plans.

A

Three types: lacerations, chemical, and eosinophillic.
Lacerations: Mallory-Weiss tear (repeated retching causing haematemesis), Boerhaave syndrome (subcutaneous emphysema, may cause mediastinitis, ddx includes MI, affects deeper than muscularis mucosa). Endoscopy and CXR (hydropneumothorax in Boerhaave). Clipping, oversewing, surgery.
Chemical: may be caused by pills, bleach, alcohol, heavy smoking.
Eosinophillic: history of atopy/allergy, or may present with GORD like symptoms. Investigations include endoscopy (‘trachealized’), biopsy. Management by steroids. Note PPI’s don’t help.

54
Q

Describe the key features of gastroesophageal reflux disease (GORD).

A

Presentation: heartburn, indigestion, nausea, waterbrash, cough.
Investigations: without red flag symptoms under 45 do not need investigations. Other options include endoscopy, pH studies, and manometry.
Treatments: antacids, PPIs (i.e. omeprazole), and lifestyle advice (weight loss, smoking, raise the bed at night). Further options: H2RA (i.e. ranitidine), then surgery (i.e. endoluminal gastroplication or Nissen fundoplication).
Complications: Barrett’s, aspiration pneumonia, ulcers, haematemesis.

55
Q

Describe the key features of Barrett’s oesophagus and oesophageal cancer.

A

Barrett’s is a lower oesophagus metaplasia from stratified squamous to simple columnar with goblet cells, typically in response to acid from GORD. It is investigated by endoscopy, which shows a velvety red mucosa.
Risk factors: smoking, alcohol, lack of fruit/veg, radiation, Plummer-Vinson, and achalasia.
Adenocarcinoma: distal 1/3rd. Sqaumous cell: middle 1/3rd.
Presentation: lethargy, weight loss, odynophagia, dysphagia, obstruction, pain, haematemesis.
Treatment: palliative (60%), surgery (if the tumour hasn’t invaded the oesophagus wall) with neo-adjuvant and adjuvant therapy (40%).

56
Q

Describe the key features of Plummer-Vinson (also known as Paterson-Brown-Kelly) syndrome.

A

Presentation: older woman with dysphagia, microcytic anaemia, webs, glossitis, chelitis, angular stomatitis, and koilynchia.
Investigations: endoscopy and barium swallow
Treatment: dilate webs with bougies, fix iron deficiency anaemia.

57
Q

Describe the key features of achalasia, which may be caused by Chagas disease.

A

Presentations: dysphagia, nocturnal regurgitation, cough, rarely aspiration pneumonia.
Investigations: CXR, Barium swallow, manometry (exclude GORD), CT/endoscopy (exclude cancer), blood smear (if Chagas is suspected).
Treatment: Heller’s cardiomyotomy.

58
Q

Describe the pathology of gastritis. Describe also the main cause and clinical features, investigations, and treatment of this.

A

Causes: ABCD (autoimmune, bugs, chemicals, distress). Autoimmune: CD4+ cells are directed against the parietal cells, meaning there is atrophy. Lack of intrinsic factor also causes B12 deficiency and macrocytic anaemia.
Bugs: H. pylori is the main cause. This is a gram negative, helical, aerophillic bacteria. Urease positive. NOUS: negative, oxygen, urease, spiral. Tests include urease test, faecal antigen test, endoscopy with culture. Treatment is by triple therapy; amoxicillin, clarithromycin, omeprazole. (TACO)

59
Q

Describe the key features of peptic ulcer disease.

A

Presentation: epigastric burning/pain (patient points), nausea, worse after eating (gastric), better after eating (duodenal), vomiting, bloating, emergency (i.e. haemorrhage).
Causes: NSAIDs, H. pylori, gastrin and pepsin
Investigation: If < 55 without red flags, triple therapy. If > 55 or with red flag, endoscopy with biopsy.
Treatment: Triple therapy/endoscopy with clipping, litigation, TIPSS

60
Q

Describe the key features of the two types of hypertrophic gastropathy.

A

Menetrier syndrome - TNF alpha causes decreased albumin causing weight loss, diarrhoea, and oedema. Treatment with albumin and enteral nutrition.
Zollinger-Ellison syndrome - caused by gastrin secreting tumours. Causes ulcers and diarrhoea. Can be surgically removed if malignant (60-90%) or treated with somatostatin analogues in multiple endocrine neoplasia type 1 (MEN 1).

61
Q

Describe the key features of gastric cancer.

A

Types: adenocarcinoma, lymphoma (MALToma), carcinoid, stromal (GISTs).
Symptoms: dyspepsia, dysphagia, epigastric pain, anaemia (occult blood loss), weight loss, anorexia, fatigue, haematemesis, epigastric mass, Virchow’s node.
Pathology: adenocarcinoma (loss of CDH1 (E-cadherin) and TP53, and gain of APC), lymphoma (H pylori causes proliferation of lymphocytes), carcinoid (arises from G cells, secreting serotonin), GISTs (from interstitial cells of Cajal, gain of function of tyrosine kinase KIT).
Investigations: endoscopy with multiple biopsies, or USS (showing liver deposits) and 5-HIA urine tests for carcinoid tumours.
Treatment: resection, H pylori eradication, drugs, chemotherapy, palliative care.

62
Q

Give the key management of an upper GI bleed.

A

Ddx: PIVOT (peptic ulcers, inflammation (of stomach/duodenum), varices, oesophagitis, tears (i.e. Mallory-Weiss).
Initial management: standard ABC, then resus if needed. Take bloods for Hb and urea, monitor BP and pulse, and note any co-morbidities.
Scoring: NICE recommends Blatchford (pre-endoscopy) then Rockall (post-endoscopy). Blatchford uses the criteria above in initial management. Rockall is ABCDE (age, BP fall (shock), co-morbidities, diagnosis (from endoscopy, i.e. varices), evidence of bleeding).
Treatment: depends on cause. Most likely need for peptic ulcers, inflammation, and varices. AT CUB (adrenaline + thermal clipping/coagulation, urease test, banding).

63
Q

Give the key management of a lower GI bleed.

A

Ddx: diverticulitis, ischaemic colitis, IBD, colorectal cancer, haemorrhoids. Also consider an overt upper bleed, most typically oesophageal varices.
Initial management: standard ABC, then resus if neede. History may reveal most likely source. ‘Top and tail’ endoscopy may be needed. Take biopsies, may be helpful to diagnose Coeliac’s.
CT may be needed in the elderly.

64
Q

Give the key features of Coeliac’s disease.

A

Presentation: diarrhoea, bloating, gallstones, fatigue, anaemia, weight loss
Pathology: Gliadin is transported into the epithelium by tTG, where it activated IEL proliferation. This causes villous atrophy and crypt hyperplasia.
Investigations: all patients with IBS should be suspected for Coeliac’s. Gluten challenge test (6 weeks with gluten in more than one meal) with IgA:tTG bloods can yield positive (-> biopsy), weakly positive (-> IgA EMAs), or deficienct (-> IgG tTG and EMAs). Biopsy (with 4-6 samples) is diagnostic. Also perform haematology, bone densimetry, and biochemistry. HLA-DQ karyotyping should not be conducted in routine clinical practice.
Management: lifelong gluten free diet. Yearly review with BMI, assessment of diet and symptoms, and consideration of whether dietician/GI specialist is required.

65
Q

Give the key features of irritable bowel syndrome (IBS).

A

Presentation: Consider ABC (abdominal pain, bloating, change in bowel habit) for six months along with: mucus, urgency, change in shape/form, pain relief etc.
Investigations: FBC, ESR/CRP, Coeliac serology are key in initial investigation. History may reveal Ddx. Consider CA-125 if ovarian cancer is probable, or faecal calprotectin if IBD is suspected.
Management: IBS-C - fruit, anti-spasmodics, ispagula husk, laxitaves, linaclotide.
IBS-D - reduce fruit, consider FODMAP, loperamide, codeine, tricyclic antidepressants

66
Q

Describe the key features of inflammatory bowel disease (IBD). This includes pathology, histology, presentation, drug treatment, diet treatment, surgical treatment, and complications.

A

Pathology: Association with genes, many T cells, and dysfunctional tight junctions. Crohn’s (HLA-DR1, HLA-DQw5; TH1 cells) and UC (HLA-DR2, NOD-2; TH1, TH2, NKTC cells).
Histology: Crohns (skip lesions, crypt abscesses, granulomas, strictures), UC (rose thorn ulcers, psuedocysts).
Presentation: Periods of abdominal pain, cramping, diarrhoea (may be bloody), and brought on by stress/NSAIDs/smoking etc. UC may also present with tenesmus, urgency, incontinence, and night rising.
Extra-intestinal: uveitis, apthous ulcers, non-rheumatoid arthritis, pyoderma gangrenosum.
Investigations: FBC, CRP, LFTs, MRI, AXR, endoscopy.
Drug Treatment: 6-8 week course of steroids, decreasing dose, then maintainance immunosuppression (methotrexate, azathioprine). Anti-TNF therapy (i.e. infliximab) may be used in severe cases. 5ASA (sulfonamides) may also be used in UC.
Diet treatment: Steroids, then enteral nutrition, in severe cases both are used. Modulin, a protein shake, should be used for kids.
Surgical treatment: Elective, setons, stomas for Crohn’s (not curative). UC with pouches (curative).
Complications: C (anaemia), UC (PSC), both (toxic megacolon, perforation, malabsorption).

67
Q

Give the six main causes of intestinal obstruction with a brief description, followed by the management plan.

A

Colorectal cancer
Hernias
Adhesions
Volvulus - sigmoid colon
Intussuseption - ileocaecal valve
Hirschprung disease - congenital, loss of ENS
Symptoms - distension, nausea, obstipation, fever, tachycardia. AXR confirms. Management with ABC, resus, and drip and suck. Surgery usually needed

68
Q

Describe the key anatomical features of inguinal and femoral hernias.

A

Muscle wall layers: external oblique, internal oblique, transversus abdominus.
Inguinal canal dimensions: anterior (external oblique aponeurosis), posterior (transversalis fascia), superior (internal oblique, transversus abdominus), inferior (pubic tubercle).
Hesselbach triangle: inferior epigastric artery, rectus abdominus, pubic tubercle
Femoral triangle: pubic tubercle, sartorius, adductor longus. NAVEL (nerve, artery, vein, empty space, lymphatics).
Indirect inguinal: through processalis vaginalis, lateral to IGA. Direct: through Hesselbach, medial.

69
Q

Describe the key features of ischaemic bowel disease.

A

Causes: AF, atherosclerosis, aneursym, oral contraceptive, cocaine.
Presentation: Extreme lower left abdominal pain, bloody diarrhoea, guarding and rebound tenderness.
Investigations: AXR, ABG (showing metabolic acidosis), CT scans.
Treatment: resection, emblectomy, or open and close. They may develop short bowel syndrome.

70
Q

Describe the key features of gastroenteritis.

A

Presentation: fever, dehydration, vomiting, diarrhoea or dysentry, incontinence, nausea, urgency, haemorrhage, perianal itch.
Causes (bacterial, viral, giardia intestinalis/Travellers diarrhoea, T whipplei/Whipple’s).
Investigation: history (travel, food, antibiotics, water). Culture and/or PCR may be required.
Treatment: - Bacterial (Antibiotics Can Confer Treatment: Azathioprine, Ciprofloxacin, Co-Trimoxazole)
- Whipple’s (SPST - streptomycin+penicillin 2 wks, sulfonamides+trimethoprim 1 year).

71
Q

Describe the key features of diverticular disease.

A

Diverticulosis - asymptomatic false diverticula (not all three layers). DIverticulitis - inflammation and bloody diarrhoea with symptoms.
Presentation - Tenesmus, bloating, distension, LIF pain,
Investigation - barium enema, endoscopy, CT
Treatment - oral/IV abx, fluids. Complicated - Hertmen’s. Sepsis/abscess - drainage/lavage.

72
Q

Describe the types, genetics, and morphology of colonic benign polyps. Describe also the genetic progression of benign to malignant.

A

Types: hyperplastic, hamartomatous (juvenile polyposis or Peutz-Jeghers), adenomas (FAP and HNPCC).
Genetics: Hamartomous (JP: SMAD4, PJ: STK11), FAP (dominant, APC tumour suppressor), HNPCC (recessive, MSH1/2 DNA mismatch repair causing microsatellite instability).
Morphology: FAP (villous), HNPCC (serrated/villous).
Progression: normal -> adenoma (APC/MCC/bcl-2/c-myc), growth of adenoma (Kras/c-yes), adenoma -> adenocarcinoma (p53), metastasis (nm23).
Mnemonic: Adenomas May Come By / Certain Karyotypes / Peutz-jeghers / or Non-polyposis (i.e. HNPCC)

73
Q

Describe the key aspects of colorectal cancer. This includes presentation, investigations, risk factors, treatment, and sites of metastasis.

A

Presentation: anaemia, abdominal pain, change of bowel habit, cramping, fatigue, nausea.
Discovered otherwise through: bowel screening (50-72), endoscopy, or emergency (ie. perforation or obstruction).
Investigations: CT (if bowel is suspected), MRI (rectal), endoscopy, faecal occult testing, anaemia/CEA blood testing, (barium enemas - apple core shapes).
Risk factors: smoking, low fibre, processed meat, high salt, low exercise, smoking. NSAIDs seem to be protective.
Treatment: surgery (open/endoscopic), resection, HIPC (for peritoneum metastasis), chemotherapy. 20-35% 5 year survival rate.
Common sites of metastasis: liver (from colon), lung (from rectum - does not pass through portal vein).

74
Q

Describe the key aspects of appendicitis.

A

Presentation: RIF pain, nausea, vomiting, fever, tachycardia, elevated WBC count. Clinical signs include McBurneys point, Rosving, obturator and pointing signs.
Causes: faecolith, cancer, worms, gallstones.
Scoring: Alvorado (MANTRELS: migratory pain, anorexia, nausea, tenderness in RIF, rebound pain, elevated temperature, leukocytosis, shift of WBC to left).
Treatment: antibiotics, analgesia, antipyretics, laparascopic appendicetomy.

75
Q

Describe the key aspects of haemorrhoids.

A

Presentation: fullness in the rectum, pain on defecation, passing of mucus, palpable mass.
Predisposing factors: straining (i.e. constipation), pregnancy, portal hypertension.
Staging: I (prominent vessels), II (prolapses upon bearing down but spontaneously reduces), III (prolapses and requires manual reduction), IV (does not reduce).
Treatment: I/II: high fruit/veg, fibre, sitz bath, steroid cream. III/IV: rubber band ligation, sclerotherapy, infrared coagulation, haemorrhoidectomy.

76
Q

Describe the key aspects of liver failure.

A

Causes: ABCDEF (acetominophen/autoimmune, hep B-E, fatty changes).
Presentation: encephalopathy (ammonia buildup), coagulopathy (i.e. easy bruising), ascites, spider naevi/gynaecomastia/testicular atrophy (oestrogen), jaundice (bilirubin), nausea, vomiting, hepatomegaly. Poor clinical indications are INR > 1.5 and hypoglycaemia.
Investigations: HISTORY, LFTs, prothrombin time, ultrasound, rarely biopsy.
Treatment: acetyl-cysteine for paracetamol overdose, fluids/analgesia/rest otherwise. Lactulose for encephalopathy, ursodeoxycholic acid for symptomatic relief

77
Q

Describe the key aspects of hepatitis A-E. This includes HBV serology.

A

A and E are AcutE, Consonants are Chronic.
Hep A: vaccine available (IgM suggests acute disease, IgG suggests vaccination or past disease). Faecal-oral route. RNA picornavirus.
Hep B: vaccine available. Transmission by Blood, Birthing, Bonking. Double layered DNA virus of hepadnaviridae family. Serology (HBsAg indicates acute disease/early stages of vaccine, HBsAb suggests vaccination, HBeAg suggests virus replication/infectivity, HBeAb suggests immune response, HBcAb with IgG/IgM suggests chronic/acute disease, HBV DNA suggests viral load). Fever, nausea, jaundice, RUQ pain present. Treatment with peginterferon or antivirals.
Hep C: no vaccine. Flaviviridae RNA virus. Serology is not helpful, use PCR instead. Treatment by HAART.
Hep D: delta agent. Requires HBV. Self-limiting, typically limited to IV drug abusers and blood transfusions.
Hep E: self-limiting, Endemic in India and Equatorial areas. No vaccine

78
Q

Give a brief overview of autoimmune hepatitis.

A

Presents with autoantibodies (i.e. ANA, ASMA), associated with HLA-DR3/4. Treatment with steroids or azathioprine. Liver transplant may be needed.

79
Q

Describe the key aspects of primary biliary cholangitis.

A

Presentation: usually female, pruritis, jaundice, xanthelasma. Advanced cases with Sjorgen syndrome, rheumatoid arthritis, and/or Coeliac’s.
Investigation: liver workup (IgM, AMA, ALP/GGT), biopsy showing florid duct lesions.
Treatment: ursodeoxycholic acid (alters composition of bile), obeticholic acid (instead of ursodeoxy), transplant in cases of advanced disease.

80
Q

Describe the key aspects of primary sclerosing cholangitis.

A

Presentation: raised ALP (i.e. screening in UC), fatigue, pruritis, jaundice, steatorrhoea. pANCA, aCL and ANA may also be found.
Investigation: MRCP, showing ‘beading’.
Treatment: cholestyramine, stenting by ERCP, liver transplant.

81
Q

Briefly describe the four types of bilrubin disorder.

A

All are autosomal recessive.
Gilbert: immature UGT results in jaundice in stress and exercise. No treatment needed
Criglar-Nijjar syndrome: lack of UGT. Present at birth, treated by phenobarbitol.
Dubin syndrome: bilirubin cannot be excreted, causing a black/dark liver,
Rotor syndrome: more severe version of Dubin.

82
Q

Describe the key aspects of alcoholic liver disease.

A

Pathology: days (fatty and bilirubin deposits), weeks (alcoholic hepatitis - Mallory-Denk bodies), months (fibrosis), years (cirrhosis). Alcohol is degraded to acetaldehyde by ADH, which disrupts cell function and activates P-450 enzymes.
Clinical signs: AST > ALT, signs of high bilirubin, ammonia, and oestrogen. Portal hypertension may cause varices and peptic ulcers.
Treatment: alcohol cessation, short term prednisone or PTX. Transplant end term.

83
Q

Describe the key aspects of the five types of metabolic liver disease.

A

NAFLD: association with diabetes, central obesity, dyslipidemia, hypertension. Treated by managing these underlying conditions.
Haemochromatosis: autosomal recessive disorder on chromosome 6. Haemosiderin (iron) deposits in the liver, pancreas, heart, and joints. Skin pigmentation, diabetes, arthritis, cardiac dysfunction may occur. High ferratin/transferratin should trigger genetic tests. CT/MRI/Perls Stain (biopsy) can be used to confirm. Regular phlebotomy treats.
Wilsons: autosomal recessive disorder on chromosome 13. Copper excretion blocked due to low ceruloplasmin. Neurological and psychiatric conditions, Keiser-Fleischer rings and anaemia. Treatment with penicillinamine/zinc therapy.
a1-antitrypsin deficiency: autosomal recessive disease on chromosome 14. Lack of a1-antitrypsin allows neutrophil elastase in lungs and liver to run unchecked. Smoking cessation, IV a1-AT, COPD drugs, and lactulose recommended.
Budd-Chiari syndrome: thrombosis of the post-hepatic veins.

84
Q

Describe the key aspects of benign and malignant hepatic tumours.

A

Benign: HNF1-alpha (almost no risk), beta-1 catenin (high risk), inflammatory adenoma (associated with NAFLD, medium risk). Men should have these resected, women observed for 6 months.
Malignant (hepatocellular carcinoma, HCC): caused by activation of beta-catenin and inactivation of p53. Malaise, fatigue, weight loss, upper abdominal pain, hepatomegaly, and raised AFP present. USS, CT, MRI may be used. Treatment by transplant, ablation, or resection.

85
Q

Describe the key aspects of cholelithiasis (gallstones).

A

Risks: female, middle aged, obese, high cholesterol, oestrogen, PBC.
Types: cholesterol and pigment (both of which contain calcium salts).
Presentation: biliary colic (particularly following a fatty meal), pain radiating to the back, indigestion, nausea.
Treatment: weight loss and dietary advice, then MRCP/ERCP. Laparoscopic cholecystectomy is used if recurrence is high over 3-6 months, ursodeoxylic acid if surgery is not possible.
Complications: Bouveret syndrome (gallstone ileus), empyema, perforation, pancreatitis

86
Q

Describe the key aspects of cholecystitis. Also describe briefly the difference between this and ascending cholangitis.

A

Presentation: nausea, vomiting, abdominal pain, no jaundice, fever, tachycardia, anorexia. Murphy’s sign is positive.
Types: calculous (caused by gallstones) and acalculous (caused by ischaemia to the cystic artery).
Treatment: nil by mouth, IV antibiotics, USS to confirm. ERCP/MRCP may be used, but cholecystectomy is the priority.
Complications: perforation, fistula, sepsis, peritonitis, empyema.
Cholangitis is seen with fever, RUQ pain, and jaundice (Charcot triad).

87
Q

Briefly describe the associated diseases with cholangiocarcinoma and gallbladder carcinoma. Describe the main sites of metastasis for secondary liver tumours.

A

Cholangiocarcinoma: NAFLD, hep B/C, PSC.
Gallbladder carcinoma: gallstones (95%) with chronic inflammation.
Colon, breast, lung, pancreas

88
Q

Describe the key aspects of acute pancreatitis.

A

Causes: I GET SMASHED (idiopathic, gallstones, ethanol abuse, trauma, steroids, mumps, autoimmune, scorpion bite, hypertriglyceraemia/calcaemia, ERCP, drugs).
Pathology: the most common causes (alcohol and gallstones, 80% of all cases) block the pancreatic duct (alcohol abuse causes overexpression of pancreatic enzymes, gallstones plug the duct). This allows autodigestion as zymogens are activated by trypsin (which is activated by enteropeptidase). Acinar cells are destroyed causing inflammation.
Presentation: crippling epigastric pain radiating to back and left shoulder, Cullen’s sign (bruising around the umbilicus), Grey Turner’s sign (bruising around the flanks), nausea, vomiting.
Investigations: AXR (shows sentinel loop), USS to assess for i.e. gallstones. Amylase and lipase suggest pancreatitis (lipase > amylase).
Treatment: nil by mouth, IV fluids and analgesia. Abx and nutrition may be necessary.
Complications: pseudocysts, perforation, haemorrhage, ARDS, acute renal failure.
Prognosis: PANCREAS (PaO2 low, Age > 55, Neutrophils high, Ca2+ low, Renal function low, Enzymes (ALP/GGT/LDH high), Albumin low, Sugar high).

89
Q

Describe the key aspects of pancreatic cancer.

A

Pathology: PanIN (pancreatic intraepithelial neoplasm) progresses with the following gene mutations: KRAS, CDKN2A, TP53, SMAD4. They most often appear in the head.
Clinical signs: painless jaundice, weight loss, nausea, fatigue, steatorrhoea, Trosseau’s sign (migratory thrombophlebitis).
Investigations: ERCP, CT, laparoscopy.
Management: Whipples for resectable (<20%), ERCP and stents if not.

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