2008 team: Retesh Bajaj, Maresa Brake, Raekha Kumar 2009 team

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  AD
  
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  Sudden cardiac death (questions often refer to young athletes).
  
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  Prominent apex beat, jerky carotid pulse, harsh ejection systolic murmur
  

—Epidemiology:

—Leading cause of sudden cardiac death in young (Arr, TO).

— 0.2% prevalence.

—Presentation: Angina, SOB, palpitations, syncope, CHF.

—Ex: Double apical beat, jerky pulse, harsh ejection systolic murmur (increases in intensity during valsalva cf. aortic stenosis).

—Pathophysiology:

AD inheritance, but 50% sporadic. Mutations myosin, tropomyosin, troponin.

—Hypertrophy of ventricles, esp interventricular septum > LV outflow tract obstruction

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  Presentation: asymptomatic, chest pain, palpitations, SOB, dizziness, stroke/TIA (5x increased risk).
  
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    Signs: Irregularly irregular pulse
    
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    Ix: ECG (Absent P wave, irregular QRS complexes) to diagnose. Further Assess with ECHO: Assess LA and LV plus valve disease.
    
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  Aetiology: Remember MITRAL:
  
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    M: Mitral valve disease
    
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    I: Ischaemic heart disease
    
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    T: Thyrotoxicosis
    
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    R: Raised BP (HTn)
    
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    A: Alcoholism
    
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    L: Lone AF, unknown. Very common with ageing, 10% >65s.
    

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  Pathology: Chaotic, irregular (fibrillation) atrial rhythm 300-600 bpm, AV node intermittently conducts -> irregular ventricular rate. http://watchlearnlive.heart.org
  
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  Classification
  
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    By Time course:
    
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      Acute: <48h, sudden
      
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      Persistent AF: >1 week, not self terminating, requires tx, often 2* to a reversible cause
      
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      Paroxysmal/intermittent: Self terminating episodes <7d
      
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      Chronic/Permanent AF: Duration >1 year. Consider DC CV – often fails due to enlarged LA
      
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    By Rate:
    
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      Fast: Where HR >100 (tachycardia)
      
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      Slow: Where HR <50 (bradycardia)
      

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  Natural history: Results in LVH, failure and embolic phenomena (Brain, legs and Gut!)
  

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  Management = Rate vs rhythm control vs life threatening
  
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    Acute AF + haemodynamic instability: Emergency electrical cardioversion, irrespective of duration of AF.
    

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  Rate = AVN conducts the impulses so B Blocker
  
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  Rhythm = chemical (amiodarone) or electric (DC CV)
  
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  Anticoagulate (Aspirin vs Warfarin)… CHADS score + pt risk e.g. falls – CHADS₂ (Congestive heart failure, hypertension, age, diabetes, previous stroke/TIA) if >1 then anticoagulate with wafarin. Aspirin should only be used if warfarin contraindicated. Move towards treating patients with a CHADS₂ score =1, they are risk stratified into low and high risk by CHADS₂VASC and high risk should also be anticoagulated. Watchman Left Atrial appendage device being trialled clinically as a surgical alternative to anticoagulation in those who warfarin is inappropriate or INR difficult to control and patient at risk – non-inferiority to warfarin has been demonstrated.
  
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  Find and treat cause!
  
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  Less common Mx = AF ablation – technique is becoming more successful with improved technologies, generally considered for younger patients or those with uncontrollable AF at high risk. Success rates vary ~60-70%, however higher in paroxysmal AF.
  

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  Early:
  
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    Pericarditis: sudden onset of pain + fever, 2-3 days post MI, pericardial friction rub, saddle shaped ST segment elevation on ECG. NSAIDs.
    
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    Mural thrombus: stasis of blood in the akinetic region leads to thrombi formation which may embolise.
    
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    Left ventricular wall rupture: 5-10 days post-op, haemopericardium, cardiac tamponade, death.
    
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    Heart Failure
    
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    Mitral Incompetence/Regurgitation
    
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    Arrythmias
    
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  Late:
  
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    Dressler’s Syndrome: wks-mths post MI, chest pain, pyrexia, pericardial effusion, ↑ ESR
    
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    Ventricular aneurysm: 4-6wks post MI, LVF, angina, recurrent VT, persistent ST elevation. Rupture is rare.
    

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  STABLE ANGINA – STRESS ECG
  
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  A positive test is indicated by;
  
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    Ischaemic symptoms
    
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    ST elevation/depression
    
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    Arrhythmia
    
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    Failure of BP to rise – serious – stop protocol.
    

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  SERUM TROPONIN
  

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  It peaks at 12 hours and can remain elevated for up to 10 days post MI.
  
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  When measured 12 hours post symptoms the sensitivity is almost 100%
  

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  DVT – DOPPLER ULTRASOUND
  

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  You first do a screening questionnaire which looks at the likelihood of having a DVT.
  
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  Following from this, if it is unlikely then do D-dimers
  
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  If it is likely then straight away to Doppler USS.
  

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  Why not thromphophilia screen?
  
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    As clotting factors can be affected by inflammation and so levels won’t be accurate necessarily.
    
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    Won’t really affect initial management
    
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    Can do after patient has recovered IF the patient has a family history.
    

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  Do a trans-oesophageal echocardiography (TOE)
  
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  Patient has signs that point toward infective endocarditis
  
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  TOE is the most accurate way to image the heart valves and view any vegetations that may be present
  
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  Other uses:
  
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    Cardiac sources of emboli
    
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    Review prosthetic valves
    
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    Also has a role in investigation of aortic dissection
    
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    Sometimes used to aid cardiac dissection
    

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  Bradycardia. Management.
  
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    If asymptomatic and rate >40bpm: No tx
    
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    If symptomatic or rate <40bpm:
    
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      Atropine IV (anti-muscarinic)
      
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      Temporary pacing wire if no response
      
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  Heart Block:
  
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    First degree: PR interval prolonged, > 0.2 s, one P wave per QRS complex, delay along conduction pathway
    
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      Management: Usually asymptomatic, needs no Tx.
      
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    Second degree:
    
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      Mobitz type 2: PR interval of the conducted beats constant, one P wave not followed by the QRS. Ratio of AV conduction varies 2:1-3:1. More dangerous of second degree heart blocks, as more commonly progresses to third degree. If symptomatic, treat with pacemaker.
      
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      Mobitz type 1 (Wenckebach): progressive lengthening of PR interval, one non-conducted P wave, next conducted beat has a shorter PR interval than preceding conducted beat. May notice ‘skipped beat’s.
      
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    Third degree: complete dissociation of P wave and QRS complexes which are broad (atrioventiricular dissociation). Heart rate ~40bpm due to ventricular escape rythm (in EMQs at least). Mostly asymptomatic, unless experience a Stokes-Adams attacks. O/E JVP ‘canon a waves’ are diagnostic; where atrium is contracting against a closed tricuspid valve. Treat with pacemaker.
    
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  Wolff-Parkinson-white: accessory conducting bundle – no AV node to delay conduction, a depolarization wave reaches the ventricles early – preexcitation occurs.
  
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    Short PR interval and delta wave
    
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    Can cause paroxysmal tachycardia
    

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  Digoxin effect:
  
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    ‘reversed tick’ sloping depression of the ST segment, which can resemble changes seen in myocardial ischaemia
    
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  Myocardial Infarction:
  
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    Anterior: ST segment elevation leads V1-V4 (left anterior descending artery)
    
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    Inferior: ST segment elevation leads II, III, aVF (right coronary artery)
    
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    Posterior: Tall R wave in V1-2, ST depression V1-V3
    
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  Pericarditis:
  
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    Saddle shaped ST segment elevation (widespread)
    

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  Jervell-Lange Nielson – long QT syndrome, autosomal recessive, also causes congential deafness
  
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  Romano-Ward syndrome – long QT syndrome, can be AR or AD, no deafness
  
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  Catecholaminergic polymorphic VT – stress situations result in syncope and potentially death as heart goes into polymorphic VT (torsade de pointes).
  
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  These are all treated with beta-blocker to prevent arrhythmias occuring and ICD for high risk patients
  

1. 
   A (<50) or (C) (esp if Black)
   
2. 
   A+C
   
3. 
   A+C+D
   
4. 
   Resistant hypertension – consider further diuretic, alpha blocker or beta blocker and consider seeking expert advice
   

myocardium expresses B1 adrenoreceptors. Cardioselective B-blockers, which have a

greater effect at B1 than B2 receptors, thus cause less bronchoconstriction than nonselective agents such as propranolol. Risk of precipitating bronchospasm is still high and all B-Blockers CI in asthma.

Nifedipine: Gum hyperplasia. Uncommon. Calcium channel blocker

Enalapril: Dry cough. ACE-I - cough due to elevated bradykinin levels

Medical Education Society

women – causes hypertrichosis, used in male pattern baldness

phenomenon

hypotension, dizzines, headache, fatigue

arthralgi

Disturbances

- Leriche syndrome: Aortoiliac occlusive disease, also known as Leriche's syndrome, is atherosclerotic occlusive disease involving the abdominal aorta and/or both of the iliac arteries.

—Classically, described in males as a triad of symptoms:

—1. Claudication of the buttocks and thighs

—2. Absent or decreased femoral pulses

—3. Impotence

- Limb Ischaemia. In order of increasing severity

1. Intermittent claudication

-Presentation: Muscle pain during exercise, worse uphill, relieved by rest, largely legs affected. Have a claudication distance.

-Associations: cold feet, sores, loss of hair, ED.

2. Critical limb ischaemia

- Presentation: Inability of vascular tree to meet metabolic demands at rest, so have rest pain requiring analgesia > 2w. Starts in extremities e.g. toes. Often burning pain at night requiring dependency to relieve.

3. Acute limb ischaemia

- Presentation: 5 Ps: Pain (severe), pallor, perishingly cold, pulseless, paraesthisiae.

-- Surgical emergency; have 4-6h to save limb.

—Nerve damage: 30 mins (paraesthesia)

—Muscle damage: 6 h

—Skin damage: 48h (skin mottling)

—Management:

—Dead: Amputation

—Viable: embolectomy or thrombyolysis/revascularisation as appropriate.

—Pathophysiology: Blockage of an artery, more severe if not had time for collaterals to develop.

—Embolic: 38%. Sudden, no PVD, 80% AF, post-MI, post aneurysm.

—Thrombotic in situ: 40%. Less acute, known claudicant, abnormalities in the other limb.

- Doppler and ABPI:

—ABPI: P(leg)/P(arm)

—Cut offs:

—>1.3 may indicate calcification

—1-1.3 is normal

—0.6-0.9 moderate claudication

—<0.6 indicates critical limb ischaemia: severe/rest pain

—<0.3 impending gangrene

—Superficial: Varicose veins

—Deep: venous insufficiency

—Presentation:

—Hx: asymptomatic, aching, heaviness, cramps, itching

—Ex: varicose veins, ulcers (medial malleolus, haemosiderin causes brown edges, eczema), lipodermatosclerosis

(Gastric ulcer=pain when eating)

epigastric pain relieved by antacids and food, episodes of vomitting coffee grounds,
H pylori can be underlying cause
Intestinal Obstruction – vomiting, distension, colicky pain, constipation

Diverticulitis – ‘ Left sided appendicitis’. LIF pain. Lack of dietary fibre.

Fever, vomiting, guarding -acute.

Alternating bowel habits, obstruction. Blood PR -chronic

Don’t forget MI !!!
Scabies

papular rash (abdomen/ medial thigh; itchy at nigh)

burrows (in digital web spaces and flexor wrist surfaces)
Dermatitis herpetiformis

All have a gluten sensitive enteropathy symmetrical clusters of urticarial lesions on the occiput, interscapular and gluteal

regions, and extensor surfaces of the elbows and knees.
! Tropheryma whippelii bacteria get stuck in the lymphatic drainage systems causing backflow and malabsorption. ExtraGI manifestations (arthritis, fever, lymphadonpathy and organ disease) can be present for years before malabsorption.
Giardia Lamblia. A flagellated protozoa which colonises the small bowel causing partial villous atrophy and malabsorption then moves onto the large bowel causing watery diarrhoea and horrific flatus and bad breath. Very common in Eastern Europe and Russia. Treated with metronidazole.
Entamoeba histolytica. A protozoan infection causing chronic diarrhoea which can be bloody, and liver abscess (RUQ tenderness, swinging pyrexia). Stool microscopy demonstrates trophozoites. Also treated with metronidazole.
Lichen planus

shiny, flat topped mauve spots – inside of wrists, shins lower back. May form a white pattern in the mouth.

Commonest presenting symptom is fatigue. Pruritus is common and may be intense. Jaundice appears later. Xanthelasma

Anti-mitochondrial antibodies

associated with RA, thyroid disease

Treatment is with ursodeoxycholic acid. Pruritus treated with colestyramine
Primary sclerosing cholangitis

usually middle aged man pruritus, jaundice, abdo pain

ALP, AMA –ve, may be pANCA +ve

assoc with IBD (UC), beaded appearance on ERCP (due to multiple strictures)

strictures perforation, fistulae. With skip lesions, non-continuous (cobbestone mucosa). Think bombing and destruction! But more in non-smokers.

UC: continuous, much calmer presentation – main symptoms: weight loss and BLOODY DIARRHOEA, but may get a greater Ca risk. Less in smokers.
Pathological comparison of UC/Crohn’s


Remember extraarticular manifestations e.g. clubbing, cutaneous (erythema nodosum), ocular (uveitis, episcleritis, iritis), PSC (more with UC)

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  Cholecystitis
  
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    Inflammation of the Gall Bladder
    
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    Localised Peritonitis
    
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    RUQ tender
    
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    Fever
    
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  Biliary colic
  
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    Pain from an obstructed Cystic duct or CBD
    
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    Severe pain that stays for hours
    
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    Radiates to the right shoulder and right sub scapular region
    
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    No fever, peritonitis
    
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  Ascending cholangitis
  
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    Infection of the biliary tree (from biliary obstruction)
    
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    Charcot’s triad; Fever, Jaundice, and right upper quadrant pain
    
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    RIGORS
    
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    More severe then cholecystitis, SHOCK and JAUNDICE
    

peristalsis

swallowing, dysarthria (articulation)

early satiety

Gastric erosions
Stress ulceration leading to erosions of the stomach is a complication of significant burns (Curling’s ulcer) as well as other traumatic injuries, systemic sepsis, intracranial lesions (Cushing’s ulcer) and organ failure
Oesophageal varices

•raised MCV (due to alcohol induced bone marrow toxicity) and INR (due to severe hepatic dysfunction) – make it likely diagnoses

at the gastrooesophageal junction as a results of repeated retching/ vomitting

(almost always due to alcohol excess usually self limiting
Zollinger-Ellison syndrome
•rare disorder caused by gastrin-secreting tumour, either in the islet cells of the pancreas or in the duodenal wall

•release of gastrin stimulates the production of large quantities of HCl in the gastric antrum leading to predominantly distal ulceration, measure gastrin levels

and tumour imaging
Oeasophageal Carcinoma

– rapidly progressive dysphagia elderly weight loss and

associated hypoproteinaemi, looking wasted