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Cardiovascular Flashcards

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USMLE® Step 1 flashcards
1
Q

How do you assess direction of polarisation and axis deviation on an ECG

A

R wave shows direction of polarisation, should increase V1-4 (S waves increase V1-3 then decrease)

Axis should be directed towards lead II (most positive deflection)
Left axis Leaves II and III (I only positive, aVF negative), Right axis Returns to II and III (I only negative, aVF positive)

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2
Q

Describe the depolarisation of heart cells

A

HEART CELL DEPOLARISATION: SLOW ENTRY OF SODIUM IONS TO CAUSE MEMBRANE POTENTIAL TO RISE FROM -60 TO -40mV, SPONTANEOUS DEPOLARISATION, CALCIUM ENTER CAUSING STRONGER DEPOLARISATION TO +5mV, POTASSIUM CAUSES REPOLARISATION BACK TO -60mV (CALCIUM AND POTASSIUM CHANNELS CLOSE)

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3
Q

What parts of the clotting process do different anticoagulants affect

A

(Platelet aggregation)
Aspirin inhibits COX-1 and therefore thromboxane A2, less activation and aggregation
P2Y12 inhibitors (clopidogrel, prasugrel, ticagrelor), reduce ADP, less activation and aggregation
(Coagulation cascade)
Warfarin inhibits vitamin K - reduces II, VII, IX, X
Heparins increase antithrombin, inactivates thrombin and Xa, thrombin means less conversion of fibrinogen
DOACs: majority direct and reversible inhibitors of Xa, dabigatran inhibits thrombin

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4
Q

Decsribe CHA2DS2VASc

A

CHA2DS2VASc (stroke assessment): =2 anticoagulant (=1 for men consider)
Chronic HF, hypertension, age >75 - 2, diabetes, stroke / TIA - 2, vascular disease, age 65-75, sex category female
2 = 2% stroke risk per year

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5
Q

Describe the presentation of angina / IHD

A

Chest pain - tight, stab/ belt/ heavy, middle of chest
May radiate to one or both arms, neck, jaw, teeth
Breathless, palpitations, presyncope (sensation you are going to faint)
Very exercise related

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6
Q

How is IHD diagnosed and what investigations are used

A

Diagnosis usually entirely from history
Primary care: ECG, haemoglobin, lipid profile, glucose / HbA1c
CT coronary angiogram gold standard, contrast used, assess flow of coronary arteries
Determine if obstructive coronary artery disease. If left main stem or severe 3 vessel disease → coronary angiography
ECG - usually normal, may show ST depression, flat/ inverted T waves
Cardiac stress test (exercise or dobutamine), monitor with ECG, ST depression = late stage. Many patients unsuitable

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7
Q

Describe the ECG changes in acute coronary syndrome

A

STEMI: ST elevation and new left bundle branch block (wide QRS, V1-6), hyperactive T waves, pathological Q waves

NSTEMI: ST depression and T wave inversion

Pathological Q waves present after 6h of symptoms in full thickness infarction

Specific arteries: left coronary - anterolateral (I, aVL, V3-6); LAD - anterior (V1-4); circumflex - lateral (I, aVL, V5-6); right coronary - inferior (II, III, aVF)

Unstable angina usually has normal ECG

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8
Q

Describe the management of angina / IHD

A

Lifestyle advice
All patients aspirin (clopidogrel if contraindicated) and a statin, dual therapy with aspirin + clopidogrel / rivaroxaban in patients ACS or undergoing PCI

If required also antihypertensives (target 120-130) - ACE / BB / ARB; antidiabetic drugs

Symptom relief: GTN spray, beta blocker, calcium channel blocker, long acting nitrate

Surgery when medical not working, PCI and CABG

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9
Q

Why are antiplatelets the main stay of treatment in acute coronary sundrome

A

When a thrombus forms in a fast flowing artery it is mainly formed by platelets

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10
Q

What is the presentation of ACS

A

Acute chest pain lasting longer than 20 mins, at rest, ⅓ in bed at night
Can radiate to left arm, jaw, neck. Does not respond to GTN
Sweating, nausea, vomiting, breathless, palpitations, anxiety, sense of impending doom
Significant hypotension. brady/ tachycardia

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11
Q

Describe the investigations for ACS

A

Immediate ECG, coronary angiography (within 12h)
Bloods: troponin, glucose, FBC, U+Es, (CRP + lipids)

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12
Q

How is a STEMI acutely managed

A

300mg aspirin + prasugrel / clopidogrel, IV morphine, ondansetron (add O2 and IV GTN if required)
Assess if PCI suitable - within 12h of onset / 2h of when fibrinlysis could be given without contraindications (IV unfractioned heparin in surgery)
Otherwise thrombolysis with alteplase / tenecteplase

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13
Q

How is risk of NSTEMI assessed

A

GRACE score: age, HR, systolic, creatinine, cardiac arrest at admission, ST deviation, abnormal cardiac enzymes, killip class (no CHF, rales / JVD, pulmonary oedema, cardiogenic shock)

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14
Q

How are NSTEMIs acutely managed

A

Grace score
High risk: coronary angiography +- revascularisation, 300mg aspirin + prasugrel / clopidogrel. If required: O2, morphine, GTN, ondansetron, heparin (fondaparinux)
Low risk: same as above but surgery not required if 6m mortality below 3%

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15
Q

How are patients managed following an MI

A

Echocardiogram to assess LV function, cardiac rehabilitation (lifestyle)
Secondary prevention - continue dual antiplatelet, ACE inhibitors / ARB, beta blockers / rate limiting CCB, statins. If HF: spironolactone + dapgliflozin

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16
Q

Define heart failure

A

Heart failure is caused by a structural and/or functional abnormality that produces raised intracardiac pressures and/or inadequate cardiac output at rest and/or at exercise

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17
Q

Describe the pathophysiology of heart failure

A

When drop in arterial pressure in aorta/ heart, baroreceptors activate sympathetic nervous system. In heart failure there is chronic activation, effect is diminished, cardiac output stops increasing

Impaired LV function leads to backlog of blood, LA / pulmonary veins have increased volume + pressure, fluid leaks out

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18
Q

How do you investigate heart failure (what do they show)

A

Transthoracic echocardiogram, ECG, CXR, NT BNP blood test; also: troponin, FBC, U+Es, HbA1c, LFTs, TFTs, CRP
Exercise stress testing, (CT) coronary angiogram
NT-proBNP blood test increased, echocardiogram - chamber size, valvular disease, MI
<400pg/mL HF unlikely, 400-2000 transthoracic doppler + specialist within 6 weeks, >2000 within 2 weeks + poor prognosis
X ray (ABCDE): Alveolar oedema (batwing), Kerley B lines (horizontal - peripheral lungs), Cardiomegaly, Dilated upper lobe vessels, pleural Effusion (costophrenic blunting)
ECG - ischaemia, MI, LV hypertrophy

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19
Q

How is heart failure classified

A

NYHA Classification: I - no limitation (asymptomatic), II - slight limitation, III - marked limitation (symptoms on minimal exertion), IV - inability to carry out physical activity

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20
Q

How is heart failure managed

A

Treat cause, lifestyle (avoid large meals (workload, sodium - water retention), vaccination)

Management ABAL: ramipril (ACE) (evidence sacubitril / valsartan better), bisoprolol (BB), spironolactone (aldosterone antagonist), furosemide (loop)
Symptoms persist - specialist: amiodarone, digoxin, sacubitril + valsartan

Avoid ACE if valve pathology
Calcium channel blockers and dihydropyridines (nifedipine) avoided in reduced

Comprehensive therapy (abs vp): aldosterone antagonist + beta blocker + sacubitril-valsartan + dapagliflozin (SGLT2 inhibitor)

Preserved ejection fraction (specialist): dapagliflozin, furosemide if still fluid overload

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21
Q

What are the causes of secondary hypertension

A

ROPED: renal disease, obesity, pregnancy induced / preeclampsia, endocrine, drugs
Most common causes: renal (CKD, renal artery stenosis, nephritis), sleep apnoea, coarctation of aorta

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22
Q

How is hypertension managed including different demographics

A

ACD pathway - ACE inhibitor (or ARB), calcium channel blocker, diuretics (thiazides then loop)
Ramipril (candesartan), nifedipine, bendroflumethiazide (furosemide)
Beta blockers are not first line but consider in young people
If 55+ or Afro-Caribbean likely low renin, calcium channel blocker first and ARB instead of ACE
In diabetics: ACD no matter the age

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23
Q

What causes supraventricular tachycardia and how does it present on ECG

A

Electrical signal reneters the atria from the ventricles, causes another depolarisation and repeats
Presents with narrow complex tachycardia (< 0.12s or 3 small squares) followed immediately by T wave, P waves usually buried by T waves. HR > 150

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24
Q

How do atrial flutter, AV block and L / R BBB present on ECG

A

Atrial flutter - organised sawtooth waves, regular QRS, two P waves for every QRS

AV block - long PR, 1st - PR and QRS associated, 2nd slightly associated (Mobitz I PR progressively prolonged until dropped, II PR constant but not always followed by QRS), 3rd no association between P and QRS

Left bundle branch block (wiLLiam) - ‘w’ shape in V1 + ‘m’ shape in V6, broad QRS, prolonged / broad R wave in V5/6, dominant S wave in V1, absence of Q waves in lateral leads
Right bundle branch block (moRRow) - ‘m’ shape in V1 + ‘w’ shape in V6, broad QRS, slurred S waves in lateral leads

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25
Q

How do you manage tachycardias

A

Tachycardia: beta blockers and calcium channel blockers. AV node reentry tachycardia most common - catheter ablation. If systolic < 90 - DC cardioversion
Supraventricular T: adenosine, verapamil (can’t be given with BB)
Broad complex: IV amiodarone, DC cardioversion (haemodynamically unstable)

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26
Q

How is AF investigated

A

ECG: irregularly irregular, absent P waves, narrow QRS
Echo to see if structural
Bloods: FBC, U+Es, TFTs, LFTs, clotting profile
Also CHADSVasc and ORBIT

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27
Q

How is AF managed

A

Acute: haemodynamically unstable - electrically cardioverted, stable and <48h rate / rhythm, >48h rate control

Rate or rhythm: rate control FL unless: AF reversible, new onset within 48h, HF caused by AF.

Rate (ventricular): beta blocker (atenolol) or rate limiting CCB (verapamil, diltiazem) (avoid in HF), digoxin if unsuitable, dual therapy

Rhythm (sinus): cardioversion + long term rhythm control, beta blocker FL, dronedarone SL (or amiodarone (LV impairment / HF), consider left atrial ablation
Cardioversion is immediate if <48h or haemodynamically unstable; electrical (defib under sedation), pharmacological - flecainide, amiodarone
Both ineffective or not tolerated: LA ablation, AV node ablation + pacemaker

DOAC for clots, warfarin if DOAC contraindicated, both contraindicated - consider left atrial appendage occlusion

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28
Q

Describe the different types of heart block

A

First degree (PR + QRS still associated): PR interval >0.2s. Usually asymptomatic and does not need to be treated, slower conduction time, age, myocarditis, hypothyroidism, medications

Second degree (slightly associated): Mobitz I: progressively prolonged PR until beat dropped; Mobitz II: PR is constant but P wave often not followed by QRS
Intermittent blockage of waves, usually a structural change: IHD, fibrosis, degeneration of AV node. MII has higher risk of progression to complete block

Third: no association between P and QRS. Atria and ventricles beat independently (atria usually quicker), damage to AVn or bundle of His, MI, congenital

29
Q

What are the 3 presentations of peripheral arterial disease

A

Intermittent claudication: cramping in leg, due to exertion, relieves with rest
Acute limb ischaemia (6 Ps): pain, pallor, pulseless, paralysis, paraesthesia, perishing cold
Leriche syndrome: thigh / buttock claudication, absent femoral pulses, male impotence (occlusion of distal aorta / common iliac)

30
Q

What is Virchow’s triad, what is the difference between arterial and venous clot formation, what are the risk factors for VTE

A

Virchow’s triad for clot formation - stasis of blood flow (longer contact), endothelial injury (exposed collagen and stimulates), hypercoagulation
Arterial platelet driven, inflammation/ trauma/ infection. Venous fibrin driven, stasis usually issue

RF: immobility, recent surgery, cancer, long haul travel, pregnancy, oestrogen, polycythaemia, SLE, thrombophilias

31
Q

What are the signs and examination tests for PAD and DVT

A

Signs: skin pallor, cyanosis, dependent rubor, muscle wasting, hair loss, ulcers, poor wound healing, gangrene, reduce skin temp + sensation, prolonged CRT, changes in Buerger’s
Buerger’s: lie supine with legs at 45 degrees, hold for 1-2m looking for pallor. Sit patient up with legs hanging; healthy will go pink, PAD will go blue then dark red (rubor)

leg pain / tenderness, swelling (pitting oedema), dilated veins, warm, erythema, ulcers
Measure calf circumference 10cm below tibial tuberosity, >3cm bigger than other - positive

32
Q

How is PAD investigated and treated

A

PAD: ankle-brachial index only necessary. Duplex US and angiography for flow and surgery
Ratio of systolic in ankle vs arm 0.9-1.3 healthy, 0.6-0.9 mild, 0.3-0.6 moderate, <0.3 severe

Non limiting claudication: aspirin / clopidogrel, exercise therapy, lifestyle changes; lifestyle limiting add: cilostazol (several cardiac contraindications) or naftidrofuryl, surgical revascularisation
Acute limb ischaemia: emergency, endovascular or surgical revascularisation + thrombolysis / amputation, aspirin / clopidogrel + heparin, appropriate analgesia

33
Q

How is DVT investigated and treated

A

DVT: Well’s score, D-dimer blood test (sensitive not specific), duplex ultrasound (CT/MRI venography), bloods (FBC, LFTs, U+Es, clotting profile)
Well’s score: likely - US, unlikely - d-dimer

DVT: apixaban / rivaroxaban FL (start as soon as suspected), enoxaparin / dalteparin SL (FL in pregnancy), exercise, compression stockings
Long term anticoagulants for unprovoked, 3m for reversible cause, 3-6m cancer

34
Q

What are the causes of pericarditis

A

Majority are idiopathic and seen in young adults
Range of pathogens (viruses, bacterial and some fungal)
Noninfectious: Sjorgen’s, rheumatoid arthritis, SLE, secondary metastatic tumours, trauma, iatrogenic, MI, uraemia

35
Q

How does pericarditis affect the function of the heart

A

Effusion commonly occurs with pericarditis, if volume large enough ventricular filling is compromised (tamponade), reduces diastole and therefore systole - requires emergency drainage

36
Q

How does pericarditis present

A

Chest pain - severe, sharp + pleuritic (not crushing), rapid onset, worse lying flat (alleviated by sitting up), left anterior chest (radiates to arm/ trapezius ridge)

Low grade fever and prodrome of myalgia

Pericardial rub on auscultation (rubbing / scratching)

37
Q

How is pericarditis investigated

A

ECG - PR depression, global saddle shaped ST elevation, (STEMI would just be one infarcted area)
X ray (maybe cardiomegaly), echocardiogram
Bloods: troponin, FBC (slight increase in white count), high ESR indicative of autoimmune, U+Es (uraemia cause)

38
Q

How is pericarditis treated

A

Aspirin / ibuprofen high dose (+ PPI), colchicine (for 3m to stop recurrence), exercise restriction
In more extreme cases oral corticosteroids or pericardiectomy might be appropriate
Treat cause; if purulent: IV abx (tailored to blood cultures), steroids for autoimmune
Tamponade - pericardiocentesis, also for purulent or neoplastic

39
Q

Describe constrictive pericarditis

A

Constrictive - becomes inelastic/ fibrous/ calcified and interferes with diastolic filling. Can occur in any types but common in TB and rheumatic heart disease
Ascites, oedema, right heart failure, atrial dilation

40
Q

Describe the murmurs of valve pathologies

A

Mitral stenosis: mid diastolic, low pitched rumbling, loud S1, LUB dub durr
(In diastole, slow velocity, stiff valves snap back with enough force. Palpable apex beat)

Mitral regurgitation - pan systolic, high pitched, S3, radiates to axilla
(Flowing wrong direction during systole, high velocity from ventricle, backlog of blood in LA causes S3)

Aortic stenosis (most common): ejection systolic, high pitched, crescendo-decrescendo, slow rising pulse + narrow pulse pressure, burrr dub
(High velocity through small gap, reduced cardiac output + systolic pressure, prolonged LV ejection)

Aortic regurgitation: early diastolic soft murmur, collapsing pulse + wide pulse pressure, Lub tarrr
(Small amount returning after systole, drop in aortic pressure during diastole as blood flows back. Aortic thrill)

Tricuspid regurgitation (similar to mitral): pan systolic, high pitched, split S2, inspiration
(Blood returns to RA during systole - faster velocity, RV empties quicker than LV, increased venous return on inspiration)

Pulmonary stenosis: ejection systolic, harsh, crescendo-decrescendo, ejection click
(High pressure through small hole during systole, click due to stenotic valve leaflets, heard best on inspiration, pulmonary thrill)

41
Q

How are valve pathologies investigated

A

Echocardiogram gold standard - size, function, valve structure
Serial echos to monitor
Heart sounds, ECG when hypertrophy
Blood pressure - aortic regurgitation: high systolic, low diastolic

42
Q

Describe the pathophysiology of infective endocarditis

A

Infection of endothelium, most commonly the heart valves, bacteria in bloodstream adhere to damaged area, vegetations form (bacteria, platelets, fibrin)

Most common cause: staph aureus; also streptococcus (viridans), enterococcus (faecalis)

Risk factors: IV drug use, structural heart pathology, CKD (dialysis), immunocompromised, past Hx
Structural: valvular / prosthetic disease, congenital, hypertrophic cardiomyopathy, pacemakers

Complications: valve pathology, HF, infective / non infective emboli, glomerulonephritis + renal impairment

43
Q

How does infective endocarditis present

A

Presentation: fever, fatigue, night sweats, muscle aches, anorexia
Signs: new / changing murmur, splinter haemorrhages, petechiae, janeway lesions, osler’s nodes, roth spots, splenomegaly, finger clubbing
JL: red macules on palms + soles, ON: tender red nodules on pads of fingers + toes, RS: haemorrhages on retina

44
Q

How is infective endocarditis investigated, what criteria is used

A

Blood cultures essential, 3 samples 6h apart from different sites (unless septic). Transoesophageal echo, prosthetic valves - SPECT-CT

Modified Duke criteria: major: persistent positive blood cultures, positive imaging; minor: predisposition, T > 38C, vascular phenomena, immunological phenomena, microbiological phenomena
Diagnosis: 2 major, 1 major + 3 minor, 5 minor
(V: splenic infarction, intracranial haemorrhage, Janeway; I: osler’s, roth spots, glomerulonephritis; M: positive cultures not qualifying as major)

45
Q

How is infective endocarditis managed

A

Managed by specialist team, IV broad spectrum Abx, 4w or 6w for prosthetic
Surgery required for HF related to valve pathology, large vegetations / abscesses, not responding to Abx

46
Q

Describe the types of shock

A

Hypovolaemia, cardiogenic (not pumping), distributive (sepsis, anaphylaxis, neurogenic), obstructive

Hypovolaemic - secondary to haemorrhagic shock, acute loss of blood, loss of fluid (burns, pancreatitis), extreme vomiting / diarrhoea

Cardiogenic - tamponade, pulmonary embolism, acute MI, fluid overload, myocarditis
Decreased cardiac contractility, decreased cardiac output and blood pressure

Obstructive: physical obstruction of great vessels (tamponade, PE, tension pneumothorax)

Distributive: neurogenic: loss of sympathetic tone in vessels (slow HR, less venous return, less CO); vasoactive: release of massive vasoactive mediators, massive vasodilation

47
Q

Describe the types of cardiomyopathies

A

Dilated (LV) most common, contracts poorly, like HF: dyspnoea, fatigue, p oedema, arrhythmias
Genetic, infections (coxsackie B), alcohol abuse (toxic, B1 deficiency, inflammation, hypertension), pregnancy (peripartum CM), SLE, RA

Hypertrophic obstructive: LV hypertrophy, deviated septum blocks outflow, autosomal dominant. Risk of HF, arrhythmias, sudden cardiac death. Non specific symptoms, severe present like HF

Restrictive: stiffening of muscle - impaired systolic filling, HF symptoms
Amyloidosis, sarcoidosis, infiltrative - haemochromatosis, radiation therapy

Arrhythmogenic: muscle replaced with fibrofatty tissue - ventricular arrhythmias and sudden death

Takotsubo: LV dysfunction following severe emotional stress, ‘Broken heart syndrome’, resolves

48
Q

What are the causes of the different types of anaemia

A

Micro (synthesis issue): iron deficiency, thalassaemia (globin chains), lead poisoning (haem)
Normo: haemolytic (rhesus / ABO, sickle cell, malaria, transfusion reaction), chronic disease (TB, HIV, CKD, SLE), haemorrhage, cancer
Macrocytic: B12 + folate (DNA), alcohol abuse (liver → B12 + folate), myelodysplastic syndromes

49
Q

Describe the pathophysiology of sickle cell

A

Sickle cell - mutation causes abnormal beta chain, insoluble and polymerised when deoxygenated (causes spiral effect with acute chest syndrome). RBCs are more rigid, repeated sickling becomes irreversible, carries oxygen less efficiently and blocks vessels.
Acute chest syndrome: lung damage (sickling and infection) → hypoxia → HbS polymerisation → reduced flow → more lung damage

50
Q

How do you investigate anaemia

A

Blood count + film (micro/ normo/ macro)
Reticulocyte count - measure of production (how many young cells)
Serum iron/ ferritin. Direct antiglobulin test for autoimmune. LFT / Bilirubin (increased haemolysis). Sickle cell solubility + Hb separation

51
Q

How is sickle cell anaemia managed

A

Sickle cell - hydroxycarbamide (increases foetal haemoglobin), supportive (vaccines, prophylactic penicillin, analgesia), repeat transfusions, stem cell transplant
Acute chest: oxygen, incentive spirometry, analgesia (depending on pain), broad spectrum abx

52
Q

Describe the different types of leukaemia (age, blood film, specificifiers)

A

Acute lymphoblastic: 2-4, blasts on blood film (children = B, adults = T)
Acute myeloid: 60s, may have normal WCC, most deadly, auer rods
Chronic myeloid: 60s, 80% have philadelphia chromosome, very high WCC, give imatinib (tyrosine kinase)
Chronic lymphocytic: elderly, most common, lack of apoptosis, smudge cells, often no symptoms

Order by age (acutes before chronic): lymphoblastic, myeloid, lymphocytic (also most to least aggressive)
Specifiers: BAPS - blasts, auer roads, philadelphia chromosone, smudge cells

53
Q

How are leukaemias treated

A

Treatment: chemotherapy, radiation, stem transplant, targeted. Staging and overall health considered for treatment type.
Chemo: methotrexate, vincristine, daunorubicin, cytarabine

54
Q

How are lymphomas classified

A

Classifications: Hodgkin (Reed-Sternberg cells - characteristic mirror image nuclei) vs Non-Hodgkin (low grade vs high grade, B vs T vs Nk, Burkitt, MALT). Non-H: 80% B cell (diffuse large B most common)

55
Q

What are the risk factors for lymphomas

A

Hodgkin’s: Ages 20-25 or 80+, HIV, Epstein-Barr virus, autoimmune conditions, family history

Non-Hodgkin’s: HIV, EBV, H pylori (MALT), Hep B+C, exposure to pesticides / trichloroethylene, family history

56
Q

How does lymphoma present

A

Lymphadenopathy, fever, weight loss, night sweats

Fatigue, itching, cough, SOB, abdo pain, recurrent infections

57
Q

What is the pathophysiology of multiple myeloma

A

Accumulation of malignant plasma cells leads to progressive bone marrow failure. They produce excess of one type of monoclonal immunoglobulin (M / paraproteins)
Plasma cells stimulate osteoclasts and inhibit osteoblasts - osteoporosis (releases calcium into blood). Immunoglobulins deposit in kidneys and cause dysfunction - proteinuria
Other immunoglobulin levels are decreased resulting in immunoparesis and susceptibility to infections
Plasma viscosity increases due to increased proteins - haemorrhages (stroke, retinal etc)

58
Q

What is the presentation of multiple myeloma

A

old CRAB: average age is 70. Calcium elevated, Renal impairment, Anaemia, Bone disease
Recurrent infections due to neutropenia
Bone disease leads to osteolytic lesions, pathological fracture and spinal compression
Unexplained fatigue / weight loss / fever, bone pain, abdo discomfort

59
Q

How is myeloma investigated

A

Bloods: calcium, FBC (anaemia), U+Es (raised creatinine + urea, reduced creatinine clearance), peripheral smear (Rouleaux - stacked RBCs), plasma viscosity / ESR in primary care
Bone marrow biopsy most important, clonal plasma cells >10%
Immunoglobulins: serum quantitative immunoglobulins, serum/urine protein electrophoresis + immunofixation (urine = Bence-Jones proteins), light chain assay
Whole body MRI / CT - osteolytic lesions, ‘rain drop’ skull

60
Q

What is the pathophysiology of primary and secondary polycycthaemia

A

Primary - polycythaemia vera blood cancer (malignant proliferation of a stem cell leading to excess proliferation of RBCs, white and platelets)
Secondary - hypoxia (altitude, chronic lung disease), inappropriate high erythropoietin secretion (kidney/ liver cancer), congenital heart disease

61
Q

What are the 3 myeloproliferative disorders and what cells are in excess

A

Polycythaemia vera - RBCs (also white cells and platelets)
Primary myelofibrosis - dysplastic megakaryocytes (also immature white cells and teapdrop RBCs, pantocytopenia in advanced)
Essential thrombocythaemia - platelets (also increased megakaryocytes)

62
Q

What gene is linked to myeloproliferative disorders and what treatments are used

A

Hydroxycarbamide is the chemo of choice, aspirin / clopidogrel and venesection for polycythaemia, JAK2 inhibitor ruxoltinib for primary myelofibrosis

63
Q

What is the pathophysiology of Von Willebrand’s

A

Most types dominant, vW factor - promotes platelet adhesion to damaged endothelium and stabilises VIII. Deficiency causes bleeding; majority type 1 (less severe) partial reduction, type 2 abnormal vW, type 3 complete lack (recessive)

64
Q

How is von Willebrand diagnosed and managed

A

Prolonged PT and aPTT, vW factor antigen
Desmopressin stimulates release of vWF, tranexamic acid, factor infusions (+ VIII)

65
Q

What is the pathophsyiology of haemophilia A and B

A

X-linked recessive (females can be carriers, all males); A - deficiency in factor VIII, B - factor IX

66
Q

How is haemophilia diagnosed and managed

A

Prolonged activated partial thromboplastin time (aPTT), factor VIII and IX assay
Give factor concentrates and tranexamic acid (antifibrinolytic)

67
Q

What is the pathophysiology of antiphospholipid syndrome

A

AI - antibodies bind to phospholipid-binding proteins (i.e. prothrombin), causing damage and activation and venous / arterial thrombosis (causes endothelial damage and platelet activation). Can occur in isolation or part of another condition - most commonly SLE

68
Q

How is antiphospholipid syndrome diagnosed and managed

A

Diagnosis from antibodies: lupus anticoagulant, anticardiolipin, anti-beta2 glycoprotein I
Also thrombocytopenia and prolonged aPTT
Primary thromboprophylaxis - aspirin and enoxaparin (or long term warfarin (INR 2-3))
In pregnancy can cause recurrent miscarriage, pre-eclampsia, placental abruption, pre term, VTE LMWH until 34w

Medical school finals (13 decks)

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