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Phase2a > cardiology and haematology > Flashcards

cardiology and haematology Flashcards

1
Q

what are the risk factors of atherosclerosis

A 
family history
age
tobacco smoking
high serum cholesterol - oxidised LDL 
obesity
hypertension
diabetes - pericardial fat contains lots of GF's and inflammation factors
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2
Q

what are the components of a plaque

A
  • lipid
  • necrotic core
  • connective tissue
  • fibrous cap
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3
Q

what is the pathogenesis of inflammation in a vessel wall

A
  1. LDL accumulation in wall of artery, undergoes oxidation and glycation
  2. endothelial dysfunction in response to injury causes leukocyte accumulation in vessel wall - inflammation
  3. neutrophils produce inflammatory cytokines such as IL1 which causes an inflammation cascade
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4
Q

which medical test is used to measure inflammation levels

A

C reactive protein

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5
Q

what are the stages of atherosclerosis

A
  1. fatty streaks
    -aggregations of foam cells (lipid laden macrophages) and t lymphocytes within the intimal layer of the vessel wall
  2. intermediate lesions
    - foam cells
    -VSM cells
    -T lymphocytes
    -adhesion and aggregation of platelets to vessel wall
  3. fibrous plaques or advanced lesions
    -impedes blood flow
    -prone to rupture
    -covered by dense fibrous cap made from ECM proteins - collagen and elastin
    - Laid down by SM cells that overly lipid core and necrotic debris
  4. plaque rupture
    -fibrous cap resorbed and redeposited in order to be maintained
    - if balance shift in favour of inflammatory conditions (inc enzyme activity) the cap becomes wake and plaque ruptures
    4b. or plaque erosion
    lesion smaller
    -fibrous cap doesn’t disrupt
    -sm cell rich luminal surface under clot
    - non ST elevation MI
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6
Q

what is the treatment of CA disease

A
  • PCI - percutaneous coronary intervention
  • drug elution - using drugs on stents e.g taxol to stop cell proliferation
  • CABG - coronary artery bypass graft - diverts blood around the clot
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7
Q

what are the intrinsic rates of the SAN, AVN and ventricular pacemaker cells

A

SAN - 60-100bpm
AVN - 40 -60bpm
ventricular cells - 20-45bpm

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8
Q

what does the PR interval show and how long should it be

A

atrial depolarisation + AV node delay (allows time for atria to contract completely)
120-200ms

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9
Q

how long should the QRS complex be

A

110ms

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10
Q

what does a large and small ECG box depict horizontally

A

0.2s and 0.04s

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11
Q

what can hyperkalaemia and hypokalaemia do to an ECG

A

hyperkalaemia - tall T, flat p, broad QRS

Hypokalaemia - flat T, QT prolongation

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12
Q

what can hypercalcaemia and hypocalcaemia do to an ECG

A

hyper - short QT

hypo - QT prolongation

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13
Q

which leads form einthovens triangle and where are they placed

A

Lead I - RA–LA
Lead II - RA -LL
Lead III - LL - LA

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14
Q

Which are the unipolar leads and where do they view from

A 
aVR, aVF, aVL - one point on the body and one virtual reference point with zero electrical potential 
60% view from each other
aVR right shoulder
aVL left shoulder
aVF symphysis pubic
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15
Q

what are the 10 rules of a normal ECG ( don’t cry if u can’t remember them all)

A
  1. PR 120-200ms
  2. QRS 110ms or less
  3. QRS upright in I and II
  4. QRS + T same general direction in limb leads
  5. aVR - all waves negative
  6. R waves grow from V1-V4, S grows from V1-v3 (more muscle mass)
  7. ST segment should be isoelectric
  8. p upright in I,II, V2-V6
  9. Q wave not less than 0.04s in I,II,V2-V6
  10. T wave upright in I, II, V2-V6
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16
Q

what will the appearance be of the p wave in RA and LA enlargement

A

RA - tall pointed p

LA - bifid p

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17
Q

what do a long and short p wave show

A

short - WPW wolf parkinson white syndrome - accessory pathway allows early activation of ventricle
long - first degree heart block

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18
Q

what is the j point

A

between QRS + ST

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19
Q

what would left ventricular hypertrophy show on an ECG

A

taller S than 35mm

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20
Q

what is a U wave and what can it show

A

small wave after T - depolarisation after repolarisation

can show bradycardia

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21
Q

how do you determine the HR using an ECG

A

count large squares between QRD complexes

divide into 300

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22
Q

what is a RBBB and what can it be caused by

A

right bundle branch block

  • block in right conduction system
  • caused by atrial septal defect, RVH, PE, IHD, hypertension, corpulmonale
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23
Q

What can cause a LBBB

A
  • IHP
  • hypertension
  • cardiomyopathy
  • idopathic fibrosis
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24
Q

what is WPW syndrome and what does it show on an ECG

A
  • Congenital accessory conduction pathway between atria and ventricles
  • short PR interval
  • wide QRS
  • type of arrhythmia
  • Kent bundle
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25
Q

what are LQT’s

A

long QT syndromes

  • prolonged repolarisation phases
  • patient then predisposed to ventricular arrhythmia
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26
Q

what is the pathophysiology of angina pectoris

A

mismatch between oxygen supply and demand
- impaired blood flow by proximal artery stenosis
- increased distal resistance e.g LVH
- reduced oxygen carrying capacity of blood e.g anaemia
during exercise microvascular resistance decreases to try and increase flow, when resistance can fall no more flow cannot meet metabolic demand - the myocardium becomes ischaemic and pain is typically experienced

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27
Q

what is a reperfusion injury

A

damage to a tissue caused when flow is restored due to reactive oxygen species being released when O2 restored

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28
Q

what are the modifiable and non modifiable risk factors for angina

A 
non 
-gender
-age 
-family history 
-personal history 
modifiable 
- smoking
-hypertension 
-sedentary lifestyle 
-diabetes
-stress
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29
Q

what are the precipitants for angina (decreased supply/increased demand)

A 
dcr supply
-hypoxaemia 
-anaemia
-hypothermia
-hypovolaemia 
-hypervolaemia 
-polycythaemia
inc demand 
- hypertension 
-tachycardia 
-valvular heart disease
-hyperthyroidism
-hypertrophic cardiomyopathy
-cold weather
-heavy meals
-emotional stress
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30
Q

what is the presentation of angina

A

chest pain

  1. heavy, central, tight, radiation to arms, jaw, neck
  2. precipitated by exertion
  3. relieved by rest/GTN
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31
Q

describe the different investigations for angina

A
  1. treadmill test (NI P)
    - look for ST depression
    - late stage ischaemia
    - many patients unsuitable
  2. CT angiogram (NI A)
    - high NPV low PPV
    - ideal for excusing CAD in younger low risk individuals
  3. invasive angiogram (I A)
    - inject dye into CA
    - X-ray taken
    - functional flow reserve - FFR - pressure gradient against stenosis
  4. stress echo
    - Ultrasound
    - regional wall motion abnormalities
  5. SPECT myoview
    - radio labelled tracer
    - taken up by metabolising
    - under stress and not under stress
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32
Q

what is the primary and secondary management of angina

A

primary
-risk factor modification
-10 year risk of CV event calculated with SCORE tool
secondary
1. lifestyle changes
2. pharmacological - to reduce events and symptoms
3. interventional - PCI + sometimes surgery

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33
Q

what are the pharmacological interventions for angina

A
  1. beta blockers
    - B1 specific bisoprolol and atenolol
    - reduce HR and contractility by antagonising sympathetic nervous system
    - increase time spent in diastole, coronaries have more time to supply heart with blood
    - side effects - cold extremities, erectile dysfunction, bradycardia, tiredness
    - contraindications - asthma, bronchospasm, sever heart block
  2. Nitrates
    - 1st line anginal
    - venodilators
    - reduce preload
    - reduce work of heart and O2 demand
  3. Calcium channel antagonists
    - arterodilators
    - dilate systemic arteries, decrease BP
    - reduce after loads
    - decrease energy for same CO
    - Reduce work on heart
  4. antiplatelets
    - reduce events
    - aspirin
    - cyclooxygenase inhibitor
    - reduce events
    - reduce LDL cholesterol
  5. statins
    - HMG-coA reductase inhibitors
    - reduce events
    - reduce LDL cholesterol
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34
Q

what are the pros and cons of PCI and CABG

A 
PCI
pros 
-less invasive
-convienient 
-repeatable
-acceptable 
cons
-risk stent thrombosis 
-risk restenosis
-cant deal with complex disease
-dual anti platelet therapy 
CABG 
pros
-better prognosis
-deals with complex disease
cons 
-invasive
-stroke risk
-cant do if frail, comorbid
-one time treatment 
- increased length of stay
-increased time of recovery
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35
Q

what is the definition of unstable angina

A
  • cardiac chest pain at rest
  • cardiac chest pain with crescendo pattern
  • new onset angina (no ECG changes, no significant troponin rise)
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36
Q

what is the presentation of an acute MI

A

cardiac chest pain

  • unremitting
  • usually severe but may be mild absent
  • occurs at rest
  • sweating, breathlessness, nausea or vomiting
  • give aspirin 300mg asap
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37
Q

what do P2Y12 inhibitors do

A

used in dual anti platelet therapy with aspirin, stop amplification of platelet activation

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38
Q

why are GPIIb/IIIa antagonists used in MI

A

used in combination with aspirin and oral P2Y12 inhibitors in management of patients undergoing PCI for ACS, cover delayed absorption od oral P2Y12 inhibitors (due to opiates delaying gastric emptying)

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39
Q

which pathway does aspirin block

A

cyclooxygenase 1 pathway

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40
Q

what are the signs of a DVT

A

Calf warmness
tenderness
swelling
discolouration

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41
Q

what are the main tests for a DVT

A

d dimer - sensitive for DVT but not specific for DVT

Ultrasound compression test proximal veins

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42
Q

what is the treatment of a DVT

A

-LMWheparin
compression stockings
-oral warfarin for 6 months
-treat underlying cause - malignancy, thrombophilia

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43
Q

what are the risk factors for a DVT

A 
surgery
immobility
leg fracture
HRT
OC pill
pregnancy
long haul flights
inherited thrombophilia
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44
Q

what is the prevention of a DVT

A
  • hydration
  • early mobilisation
  • Tinzaparin (LMWH)
  • compression TED stockings
  • foot pumps
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45
Q

give an example of a genetic cause of DVT

A

-Factor Vleiden
antithrombin -deficiency
-protein c/s defieciency

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46
Q

what are the causes of secondary hypertension

A
  • renal disease - 75% of which is intrinsic renal disease, 25% renovascular disease
  • endocrine disease e.g cushings syndrome
  • pregnancy
  • drugs
  • OC pill
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47
Q

who should be treated for hypertension

A
  1. people aged under 80 with stage 1 hypertension with one or more of the following
    - target organ damage
    - established CV disease
    - renal disease
    - diabetes
    - a 10 year cardiovascular event risk of 20% or more
  2. people of any age with stage 2
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48
Q

what is stage 1 and 2 hypertension

A

1 - 140/90mmhg

2 - 160/100mmhg

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49
Q

what are the three targets for hypertension

A
  1. CO and PVR
  2. RAAS and SNS
  3. local vascular vasoconstrictor and dilator mediators
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50
Q

how do ACE inhibitors work in management of hypertension

A

block production of angiotensin II
angiotensin II causes vascular hyperplasia and hypertrophy
and salt retention by aldosterone release and tubular sodium resorption

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51
Q

what are the adverse effects of ACE inhibitors

A
  1. related to reduced angiotensin II production
    - hypotension
    - acute renal failure
    - hyperkalaemia
    - teratogenic effects in pregnancy
  2. related to increased kinin production
    - cough
    - rash
    - anaphylactoid reaction
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52
Q

what are the adverse effects of ARB’s in hypertension management

A
  • symptomatic hypotension
  • hyperkalaemia
  • renal dysfunction
  • rash
  • angiooedema
  • contraindicated in pregnancy
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53
Q

what can calcium channel blockers be used to manage

A
  • IHD
  • arrhythmia
  • hypertension
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54
Q

what are the three types of CCB’s and how do they work

A
  1. dihydropyridines e.g nifedipine
    - effect VSM
    - peripheral arterial vasodilators
  2. phenylalkylamines e.g verapamil
    - main effects on the heart
    - negatively chronotrophic, negatively inotropic
  3. benzothiazepines - diltaiazem
    - intermediate heart/ peripheral vascular effects
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55
Q

what are the adverse effects of CCB’s

A
  1. due to peripheral vasodilation (dyhydropyridines)
    - flushing
    - headache
    - oedema
    - palpitations
  2. due to negatively chronotrophic effects (verapamil)
    - bradycardia
    - AV block
  3. due to negatively inotropic effects (verapamil)
    - worsening of cardiac failure
  4. constipation - verapamil
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56
Q

give examples of B1 selective, mixed and non selective beta blockers

A

b1 slsective - bisoprolol
atenolol
propranolol

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57
Q

what are the adverse effects of BB’s

A
  • fatigue
  • headache
  • sleep disturbance
  • bradycardia
  • hypotension
  • cold peripheries
    • erectile dysfunction
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58
Q

what are the classes of diuretics, where do they act and give an example

A
  1. thiazides - act on the distal tubule e.g bendroflumethiazine
  2. loop diuretics - act on loop of henle e.g. furosemide
  3. potassium sparing diuretics
    - spironolactone is a aldosterone receptor antagonist
    - amiloride acts on Enac channels
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59
Q

what are the adverse effects of diuretics

A
  • hypovolaemia and hypotension (loop diuretics)
  • erectile dysfunction and impaired glucose tolerance (thiazides)
  • hypokalaemia/natraemia/magnesaemia/calcaemia
  • hyperuricaemia (gout)
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60
Q

what are the pharmacological stages of treatment for hypertension

A
  1. under 55 yrs - ACEI or angiotensinII receptor blocker
    over 55yrs or afro caribbean CCB’s
  2. ACE I/ARB + CCB
  3. ACEI/ARB +CCB + thiazide
  4. addition of spironolactone or BB or AB
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61
Q

what are the pharmacological stages for treatment of HF

A
  1. symptomatic - diuretics
  2. disease influencing therapy - inhibition of RAAS + SNS
    a. ACEI and BB
    b. Aldosterone antagonists
  3. ACE I intolerant -ARB
  4. both intolerant - hydrazine/nitrate combination
  5. consider digoxin or ivabiadine
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62
Q

How can nitrates be used in HF

A
  • Arterial and venous dilators
  • decreased preload and after load
  • decreased BP
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63
Q

what is the treatment of chronic stable angina

A
  1. anti platelet - aspirin/clopidogrel if intolerant
  2. statins
  3. short acting nitrate - GTN
  4. bb or cbb
  5. if intolerant switch
  6. if not controlled combine
  7. then consider long acting nitrate
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64
Q

what is the pharmacological treatment of acute coronary syndromes

A
  1. pain relief - GTN and opiates
  2. dual anti platelet therapy - aspirin + ticagrelor
  3. antithrombin therapy - fondaparinux
  4. consider glycoprotein IIb/IIIa inhibitor
  5. background angina therapy: BB, long acting nitrate, CCB
  6. statins
  7. therapy for LVSD/HF as required - ACEI, BB, aldosterone antagonist
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65
Q

what are the classes of antiarrhymatic drugs depicted in vaughan williams classification system

A

Class I - sodium channel blockers e.g disopyramide
Class II - BB’s e.g propanolol (non selective) and bisoprolol (B1 selective)
Class III - prolong the AP - amiodarone
Class IV - CCB’s - verapamil

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66
Q

how does digoxin act as an anti arrhythmic drug

A
  • inhibits Na/K pump
  • bradycardia and slowing of conduction due to increased vagal tone
  • increased contractility
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67
Q

describe hypertrophic cardiomyopathy

A
  • sarcomeric protein gene mutations
  • otherwise unexplained primary cardiac hypertrophy
  • causes angina, dyspnoea, palpitations, syncope
  • may cause left ventricular outflow tract obstruction
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68
Q

which genes are mutated in dilated cardiomyopathy and what does this cause

A
  • cytoskeletal gene mutations
  • impaired contractility
  • heart failure symptoms
  • dilation of chambers
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69
Q

which genes are mutated in arrthythmogenic cardiomyopathy and what does this cause

A
  • desmosome gene mutation

- RV muscle cells die off and are replaced by fat and scar tissue

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70
Q

which genes are mutated in inherited arrhythmia/channelopathy

A
  • ion channel protein gene mutation
  • structurally normal heart
  • recurrent syncope
  • long QT, short QT, CPVT or brugada
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71
Q

what is tamponade physiology

A
  • small volume of pericardial fluid added or removed from the pericardial sac has drastic effects on filling
    ( inc fluid, inc pressure, heart can’t fill, heart stops)
  • however chronic accumulation allows adaptation of the parietal peritoneum
  • this compliance reduced the effect on diastolic filling of the chambers
    -slowly accumulating effusions rarely cause tamponade
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72
Q

what volume of pericardial fluid is usually found in the pericardial sac

A

50ml

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73
Q

what are the diagnostic criteria of acute pericarditis

A

2 of 4 from

  • ECG changes
  • chest pain
  • friction rub
  • pericardial effusion
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74
Q

what are the infectious and non infectious causes of acute pericarditis

A
  • viral - enteroviruses, herpes virus, adeno virus, parvovirus
    -bacterial - mycobacterium TB
  • fungal (rare)
    non infectious
    -neoplastic - secondary metastatic tumours most common
  • autoimmune
    -metabolic
  • traumatic + iatrogenic
  • drug related
  • other - amyloidosis, aortic dissection, chronic hf, pulmonary arterial hypertension
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75
Q

what is the presentation of acute pericarditis

A

chest pain
-severe
-pleuritic, sharp (not crushing like ischaemic pain)
-rapid onset
- left anterior chest or epigastrium
- radiates to arm specifically trapezium ridge (phrenic nerve co innervation)
- relieved sitting forward, exacerbated lying down
- dyspnoea, cough, hiccups (phrenic)
-fever, rash, joint pain
- history of cancer, cardiac procedure, MI, pneumonia
-

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76
Q

what may be found on a clinical examination for acute pericarditis

A
  • pericardial rub
  • sinus tachycardia
  • fever
  • pulsus paradoxus - abnormally low drop in BP during inspiration
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77
Q

what are the differential diagnoses of acute pericarditis

A
  • MI
  • GORD
  • PE
  • AD
  • pneumonia
  • shingles
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78
Q

what are the tests for pericarditis

A
  • ECG - diffuse ST segment elevation, saddle shaped, PR depression
  • FBC - small increase in WCC, mild lymphocytosis
  • CXR often normal
  • troponin - elevations suggest myopericarditis
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79
Q

what is the management of pericarditis

A
  • sedentary activity
  • NSAID or aspirin
  • colchicine
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80
Q

what are the factors that indicate a worse prognosis of pericarditis

A 
major 
-fever
-subacute onset 
- tamponade
-large effusion 
-lack of response to treatment
minor 
-myopericarditis
-immunosuppression 
-trauma 
-oral anticoagulants
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81
Q

what is the 5 year mortality rate of heart failure

A

80%

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82
Q

define heart failure

A

an inability of the heart to deliver blood and o2 at a rate commensurate with the requirements of the metabolising tissues, despite normal or increased cardiac filling pressures

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83
Q

what is the difference between HFREF and HFPEF

A

HFREF - heart failure with reduced ejection fraction ( ejection fraction less than 40%)
HFPEF - heart failure with preserved ejection fraction (ejection fraction more than 50%)

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84
Q

what are the causes of heart failure

A
  • myocardial dysfunction
  • hypertension
  • alcohol excess
  • cardiomyopathy
  • endocardial
  • pericardial
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85
Q

what are the symptoms and signs of HF

A

symptoms

  • breathlessness - congested lung due to failure to drain (left)
  • tiredness
  • cold peripheries
  • leg swelling - increased lung pressure (right)
  • increased weight

signs

  • tachycardia
  • displaced apex beat - LV dilation
  • added heart sound
  • raised JVP(right)
  • hepatomegaly
  • ascites (right)
  • cyanosis
  • oedema
  • hypotension
  • paroxysmal nocturnal episodic dyspnoea only in heart failure (left)
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86
Q

describe the new york classification of heart failure

A 
class I - no limitation (asymptomatic)
class II - comfortable at rest, dyspnoea during normal activity 
class III - limiting less than ordinary activity causes dyspnoea 
class IV - dyspnoea present at rest, all activity causes discomfort
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87
Q

what are the complications of heart failure

A
  • renal dysfunction
  • arrhythmia
  • DVT, PE
  • LBBB
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88
Q

what is the treatment of heart failure

A
  1. diuretics
    - thiazides or loop diuretics
    - relieve symptoms
  2. ACE - I
    - for LVSD
  3. B blockers
    - decrease mortality in small doses
  4. mineralocorticoid receptor antagonists (aldosterone antagonism)
    - spironolactone decrease mortality by 30%
  5. digoxin
    - symptoms
  6. vasodilators
    - hydralazine and nitrates
    - transplantation
    - ECG main test
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89
Q

define cor pulmonale

A

right heart failure caused by chronic pulmonary arterial hypertension

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90
Q

what are the causes of cor pulmonale

A
  • chronic lung disease
  • PV disorders
  • Neuromuscular and skeletal diseases
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91
Q

what are the symptoms + signs of cor pulmonale

A 
symptoms
- dyspnoea
- fatigue
-syncope
signs 
- cyanosis 
- tachycardia
- CXR enlarged RA and RV, prominent pulmonary arteries
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92
Q

what is the treatment of cor pulmonale

A
  • management of respiratory and cardiac failure

- heart transplant

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93
Q

what are the four features of tetralogy of fallot

A
  1. ventricular septal defect
  2. pulmonary stenosis
  3. right ventricular hypertrophy
  4. aorta overrides the VSD, accepting the right heart blood
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94
Q

what is the presentation of tetralogy of fallot

A
  • cyanotic
  • restless and agitated child
  • boot shaped heart
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95
Q

what is the management of tetralogy of fallot

A
  • surgery to close VSD and correction of pulmonary stenosis
  • without surgery prognosis = mortality in 95% by age 25
  • with surgery 85% survive to 35 years
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96
Q

what are the symptoms/signs of a ventricular septal defect

A
  • breathlessness
    -failure to thrive
  • may lead to eisenmengers syndrome - reversal of left to right shunt due to increased pulmonary pressures = cyanosis
    signs
  • small breathless skinny baby
  • inc RR
  • tachycardia
  • big heart on CXR
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97
Q

what % of all congenital heart diseases are VSD’s

A

20%

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98
Q

what % of ASD’s are defects in the ostium secundum

A

80%

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99
Q

what do ASD’s cause

A
  • slightly higher pressure in LA
  • shunt left to right
  • not cyanosed
  • increased flow through right heart and lungs in childhood
  • right heart dilation
  • SOBOE
  • increased chest infections
    signs
  • big heart and PA on CXR
  • split second heart sound
  • pulmonary flow murmur
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100
Q

what are AVSD’s and when are they likely to occur

A
  • atrioventricular septal defects
  • one big malformed AV valve
  • often in down’s syndrome
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101
Q

what is a patent ductus arteriosus and what does it cause

A

the ductus arteriosus fails to close after birth leading to

  • continuous murmur
  • breathlessness
  • eisenmengers syndrome
  • more common in prem babies
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102
Q

what is coarction of the aorta and what signs does this cause

A
  • narrowing at site of exertion of ductus arteriosus
  • obstruction of aortic flow
  • collapse with heart failure
    signs
    -right arm hypertension
  • bruits (buzzes) over scapulae and back
    -murmur
    treat with balloon dilation and stenting or surgery
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103
Q

what are the causes of aortic stenosis

A
  • senile calcification
  • bicuspid valve
  • rheumatic heart disease
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104
Q

what happens to the afterload in aortic stenosis

A

it increases due to the pressure gradient between LV and aorta

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105
Q

what is the presentation/signs of aortic stenosis

A
  • syncope on exertion
  • angina
  • dyspnoea
    SAD = stenosis
  • sudden death
    signs
    -slow rising carotid pulse (pulsus tardus) and decreased amplitude (pulsus parvus)
  • soft s2
  • s4 gallop due to LVH
  • ejection systolic murmur
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106
Q

what is the prognosis of aortic stenosis

A

angina + AS 50% survive for 5 years
syncope + AS 50% survive for 3 years
HF + AS < 2yrs

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107
Q

what investigations can be carried out for aortic stenosis

A
  • ECG

- LVH, dilation

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108
Q

what is the management of aortic stenosis

A
  • surgical replacement
  • tavi - transcatheter aortic valve implantation in patients too sick for surgery
  • in asymptomatic - medical management and surveillance
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109
Q

what is mitrial regurgitation

A

back flow of blood from LV to LA during systole

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110
Q

what are the causes of mistrial regurgitation

A 
- mitrial valve prolapse - marfans, SLE 
myxomatous degeneration 
ischaemic MR 
rheumatic MD 
infective endocarditis
111
Q

what happens to the size of LV and contractility in MR

A

left atrial enlargement and hypertrophy, increased contractility

112
Q

what are the signs and symptoms of MR

A

signs

  • soft s1
  • pan systolic murmur at the apex radiating to the axilla (s1-s2 murmur)
  • S3 present (LA overload)
  • intensity of murmur = severity

symptoms

  • exertion dyspnoea
  • fatigue
  • palpitations
113
Q

what are the tests for MR

A
  • ECG - AF, LVH, L atrial enlargement
  • CXR - LA enlargement, central PA enlargement
  • ECHO - estimation of LA + LV size and function
114
Q

what is the management of MR

A

a. vasodilator - ACE-I, hydralazine
b. rate control for AF with BB’s, CCB, digoxin
c. anticoagulants in AF
d. diuretics for symptoms
e. IE prophylaxis

115
Q

what is aortic regurgitation

A

leakage of blood into LV during systole due to ineffective coaptation of aortic cusps

116
Q

what are the causes of AR

A
  • bicuspid aortic valve
  • rheumatic
  • IE
117
Q

What are the signs and symptoms of AR

A

signs
- wide pulse pressure
- displaced apical pulse and hyperdyamic
- diastolic blowing murmur at left sternal border - cresendo-descendo
- austin flint murmur - fluttering of valve due to regurgitant jet
- systolic ejection murmur
symptoms
- palpitations
- dyspnoea
-angina

118
Q

what are the tests for AR

A
  • CXR enlarged heart and aortic root

- echo to monitor

119
Q

what is the management of AR

A

IE prophylaxis
vasodilators (ACEI improve SV + decrease regurgitation in symptomatic pt)
-surgery if symptomatic or EF <50 % or LV dilated

120
Q

what is mitrial stenosis

A

obstruction of LV inflow stops proper filling during diastole, mainly caused by rheumatic fever

121
Q

what are the symptoms and signs of mitrial stenosis

A

symptoms
-progressive dyspnoea - LA dilation —> pulmonary congestion
- increased transmitrial pressure - leads to LA enlargement and AF
- RHF symptoms
- haemoptysis - increased pulmonary pressure ruptures bronchial vessels
signs
- malar flush on cheeks (pink/purple), decreased CO, vasoconstriction
- low volume pulse
- rumbling diastolic murmur
- loud opening s1 snap

122
Q

what are the tests for mitrial stenosis

A
  • ECG - AF and p.mitriale (bifid p)
  • CXR - LA enlargement + pulmonary congestion
  • echo is diagnostic - mitrial orifice area decrease
123
Q

what is the management of mitrial stenosis

A
  • rate control AF
  • diuretics
  • surgery
  • IE prophylaxis
  • anticoagulants
124
Q

what is infective endocarditis

A

infection of the heart valves or other endocardial lined structures within the heart, most likely to effect regurgitant or prosthetic valves

125
Q

who is IE most common in

A
  1. the elderly
  2. i.v. drug abusers
  3. congenital heart disease adults
  4. prosthetic valves
126
Q

what is the pathogenesis of IE

A
  • microbial adherence - staph aureus most common
  • bacterial adherence to platelet fibrin nidus
  • vegetation - lumps of infected fibrin hang off heart valves
127
Q

what is the presentation of IE

A
  • signs of systemic infection - fever, rigor, sweats, malaise, weight loss
  • embolisation, stroke, PE, MI
  • splinter haemorrhages under nails
  • oslers nodes (tender pulp on fingers/toes)
  • janeways lesions (non tender)
  • Roth spots in eye (haemorrhages)
  • valve dysfunction, HF, arrhythmia
128
Q

how is IE diagnosed?

A 
using modified duke criteria 
- 2 major, 1 major 3 minor or all 5 minor needed
major 
- positive blood culture
- typical organism in two separate cultures or persistent positive cultures, or single positive for coxiella burnetii
- endocardium involved
- +ve echo
- new valvular regurgitation 
minor
- predisposition
-fever >38
- vascular or immunological phenomena 
- +ve blood culture doesn't meet major
129
Q

what are the typical microorganisms causing IE

A
  • Staph aureus (IVDU or prosthetic valve)
  • viridians strep
    HACEK - Haemophilus, actinobacillus, cardiobacterium, eikenella kingella
130
Q

what are the two types of ECHO

A
  • transthoracic (TTE)

- transoesophageal (TOE/TEE) - invasive and good pictures

131
Q

what is the treatment of IE

A 
antimicrobials 
- strep viridans - 4-6 week IV benpen (benzylpenicillin) +/- 2 weeks gentamicin
- staph aureus - flucloxicillin 
surgery
treat complications
132
Q

what are the cardiac and non cardiac causes of arrhythmias

A 
cardiac
-IHD
-structural changes
-cardiomyopathy
-pericarditis
non cardiac
- caffeine
- smoking
-alcohol 
-pneumonia
-drugs
-metabolic imbalance
133
Q

what is the presentation of arrhythmias

A
  • chest pain
  • palpitations
  • syncope
  • hypotension
  • pulmonary oedema
134
Q

how is arrhythmia managed

A
  • conservative
  • pacemakers
  • tablets
135
Q

describe the 3 main types of tachycardia

A
  1. sinus tachycardia
    - impulses carried at a higher frequency
    - caused by infection, pain, exercise, anxiety, dehydration, bleed. drugs, pregnancy, PE, hyperthyroidism
  2. ventricular tachycardia
    - broad QRS
    - from circuits or from focuses of rapidly firing cells
  3. supraventricular
    - improper electrical activity in upper heart
    4 types
    - AF
    -WPW
    - atrial flutter
    -paraoxysmal SVT
136
Q

What are ventricular extrasystoles

A
  • palpitations
  • thumping
  • heart missing a beat
  • broad QRS
137
Q

what is atrial fibrillation

A
  • chaotic irregular atrial rhythm at 300-600bpm
  • AV node responds intermittently, hence an irregular ventricular rhythm
  • decreased cardiac output by 20% as ventricles not primed ready
138
Q

what are the causes of AF

A
  • HF
  • PE
  • IHD
  • hypertension
  • mitrial valve disease
  • caffeine
  • alcohol
  • cardiomyopathy
  • post op
139
Q

what are the symptoms and signs of AF

A
  • Chest pain
  • palpitations
  • dyspnoea
  • faintness
    signs
  • irregularly irregular pulse
  • apical pulse higher than radial
  • 1st heart sound of variable intensity
140
Q

what are the tests for AF

A
  • ECG - absent p waves, irregular QRS complexes
141
Q

what i the management of AF

A

rate control - BB or rate limiting CCB - digoxin if this fails
anticoagulant - DOAC or warfarin
rhythm control

142
Q

what is atrial flutter

A

atria beat regularly but faster and more often then ventricles

143
Q

what is an aneurysm

A

when a portion of an artery swells to more than 50% of its original diameter

144
Q

what is the difference between a pseudo and true aneurysm

A

pseudo - blood in adventitia only

true - all layers of vessel wall

145
Q

what are the causes of an aortic aneurysm

A
  • atheroma
  • connective tissue disorders e.g marfans
  • trauma
  • infection
146
Q

what are the complications of an aortic aneurysm

A
  • fistulae
  • rupture
  • thrombosis
  • pressure on other structures
  • embolism
147
Q

what is the presentation of a ruptured aortic aneurysm

A

intermittent or continuous abdo pain - radiates to back, iliac fossa, groin

148
Q

what is an aortic dissection

A
  • blood splits the aortic media with sudden tearing chest pain with or without radiation to the back
  • branches of the aorta occlude sequentially leading to hemiplegia (paralysis on one side of the body) if in carotids, unequal arm pulses and BP, acute limb ischaemia, anuria (non passage of urine) in renal arteries and paraplegia (impairment of motor/sensory function)
149
Q

what are the symptoms and signs of peripheral vascular disease

A
  • intermittent claudation
  • cramping in calf, thigh or buttock after walking for a given distance, that is relieved by rest
  • ulceration, gangrene and foot pain at rest (features of critical limb ischaemia)
    signs
    –absent femoral, popliteal or foot pulses, cold white legs
    -atrophic skin
    -punched out ulcers
150
Q

what are the tests for PVD

A
  • ankle brachial pressure index (ABPI)
  • ECG
  • U+E
  • FBC
  • MR/CT for extent and location of stenoses
151
Q

what is the management of PVD

A
  1. Risk factor modification
    - quit smoking
    - treat hypertension
    - antiplatelet - clopidogrel
    - statin
  2. management of claudation
    - supervised exercise programmes improve collateral blood flow and reduce symptoms
    - vasoactive drugs
    - percutaneous transluminal angioplasty - stent
    - surgical reconstruction - bypass
    - amputation
    - gene therapy in future
152
Q

what are the 6P’s of acute limb ischaemia

A
  • pale
  • pulseless
  • painful
  • paralysed
  • paraesthetic
  • perishingly cold
153
Q

what are the causes of acute limb ischaemia

A
  • thrombosis
  • emboli
  • graft occlusion
  • trauma
154
Q

what is meant by shock

A

circulatory failure resulting in inadequate organ perfusion

155
Q

what are the 5 types of shock

A 
anaphylactic
septic
haemorrhagic 
neurogenic 
cardiogenic
156
Q

describe anaphylactic shock and its management

A
  • type IgE mediated hypersensitivity
  • release of histamine and other agents causes: capillary leak, wheeze, cyanosis, oedema, urticaria
  • secure airway, 100% O2, give adrenaline
157
Q

what is sepsis

A

life threatening organ dysfunction caused by a dysregulated host response to infection

infection + systemic inflammatory response (SIRS)

158
Q

what is septic shock

A

sepsis + either: lactate > 2mmol/L or patient requires vasopressors to maintain MAP > 65mmHg

159
Q

what is haemorrhagic shock

A
  • hypovolaemia of more than 20% of bodies blood or fluid supply
  • trauma, GI bleed, ruptured aortic aneurysm
160
Q

what is neurogenic shock

A
  • spinal cord injury, epidural or spinal anaesthetic

- loss of SVR

161
Q

which cell is affected in myeloma

A

plasma cell - terminally differentiated T lymphocytes

162
Q

what is the pathogenesis of myeloma

A

cloned malignant plasma cells all produce same immunoglobulin instead of different ones

163
Q

what are the tests for myeloma

A
  • serum electrophoresis - looks for immunoglobulins
  • marrow biopsy shows increased umber of plasma cells
  • evidence of end organ damage from myeloma - hypercalcemia, renal insufficiency, anaemia (normocytic)
  • bone lesions on X-ray
164
Q

what are the four defining features of myeloma

A

Calcium - increase due to increased osteoclast activation due to signalling from myeloma cells
Renal - light chain deposition (Ig), increased calcium, NSAIDS, deposition
Anaemia - marrow infiltration by plasma cells, symptoms of anaemia
Bone disease

165
Q

what conditions can abnormal plasma cells cause

A

-MGUS - monoclonal gammopathy of unknown significance
not a disease as no end organ damage
1% a year risk of turning into myeloma
-smoldering myeloma - asymptomatic myeloma
-myeloma - clonal plasma cells and end organ damage
- plasmocytomas - plasma cell tumours (in or out of marrow)

166
Q

what is the prevalence of myeloma in the uk

A

20000

167
Q

what is the presentation of myeloma

A
  • high ESR
  • anaemia
  • Rouleux on blood film - stick together due to a high Ig
  • poor renal function
  • monoclonal protein in urine (Bence Jones protein) or blood
  • tiredness/fatigue - secondary to anaemia
  • bone pain + pathological fractures
  • confused, thirsty, constipated- high calcium
168
Q

what are the complications of myeloma

A
  • spinal cord compression
  • hyper viscosity causes decreased cognition, bleeding, disturbed vision - treat with plasmapheresis to remove light chains
  • may develop amyloidosis - extracellular deposits of protein in abnormal fibrillar form, resistant to degradation
169
Q

what is the treatment of myeloma

A
  • aim to reach plateau phase, controlling symptoms and supportive measures
    supportive
  • analgesia for bone pain (avoid NSAIDS due to renal impairment)
  • bisphosphonate
    -anaemia transfusion
  • dialysis?
  • broad spectrum antibiotics for viral infections
  • chemo and radiotherapy
170
Q

what is the pathogenesis of lymphoma

A
  • malignant proliferations of lymphocytes
  • accumulate in lymph nodes causing lymphadenopathy
  • caused by primary or secondary immunodeficiency, infection or autoimmune disorders
  • impaired immunosurveillance of epsein-Barr virus infected cells (EBV)
  • infected B cells proliferate autonomously
  • however most cases unknown
171
Q

what are the tests for lymphoma

A
  • blood film
  • bone marrow biopsy
  • lymph node biopsy
  • immunophenotyping
  • cytogenetics - karyotyping/FISH
  • molecular techniques (PCR)
  • PET scans for staging
172
Q

what are the subtypes of lymphoma

A
  • Hodgkins - Reed sternberg cells with mirror image nuclei are found - painless lymphadenopathy and B symptoms - sweats/weight loss
  • Non hodgkins:
  • -low grade e.g follicular lymphoma - slow growing, incurable, usually advanced at presentation
    • high grade e,g diffuse large B cell lymphoma - usually nodal presentation, short history, short course chemo + monoclonal antibodies
    • very high grade e.g. Burkitt’s
173
Q

which age groups are affected most by Hogkins lymphoma

A
  • teenagers and young adults

- 70+ year olds

174
Q

what are the stages of hogkins lymphoma

A

Ann Arbor staging

  1. 1 lymph area
  2. 2 or more - one side of diaphragm
  3. both sides of diaphragm
  4. widespread extra nodal
175
Q

how do monoclonal antibodies treat lymphoma

A
  • anti CD-20 on surface of B cells
  • stops proliferation of B cells
  • e.g rituximab
176
Q

how does T engaging therapy treat lymphoma

A
  • targets CD19 on B cells
  • and CD3 on T cells
  • directs own immune system
177
Q

what are the 4 types of leukaemia and which cells are affected in each

A
  • Acute myeloid leukaemia - myeloblasts (precursor of neutrophil)
  • Chronic myeloid leukaemia - neutrophil
  • Acute lymphoblastic leukaemia - lymphoblast (precursor of B lymphocyte)
  • chronic lymphoblastic leukaemia - B lymphocyte
178
Q

what are the risk factors for leukaemia

A
  • congenital
  • environmental
    radio, chemotherapy, benzene
179
Q

what is the presentation of leukaemia

A
  • anaemia - SOB, fatigue
  • thrombocytopenia - bruising, mucosal bleeding, rash
  • infection - fevers/rigor
180
Q

what are the tests for leukaemia

A
  • FBC
  • coagulation screen
  • CXR + CT to look for mediastinal lymphadenopathy
  • U + E
  • bone marrow biopsy
  • cytogenic analysis - genetic changes in the leukaemia
    -bone marrow biopsy
    -
181
Q

which leukaemia is commonest in childhood

A

Acute lymphoblastic

182
Q

what can cause ALL

A
  • ionising radiation during pregnancy

- downs syndrome

183
Q

what are the symptoms of ALL

A

marrow failure: anaemia (decreased Hb), infection (decreased WCC) + bleeding (decreased platelets)
organ infiltration - CNS involvement e.g cranial nerve palsy

184
Q

what is the genetic association of CML and ALL

A

philadelphia chromosome - T9,22

185
Q

what is the treatment of ALL

A
  • induction - remission induction
  • consolidation - high-medium dose therapy chemo in blocks
  • delayed intensification
  • maintenance
  • CNS directed therapy - intrathecal
  • stem cell transplant
  • prognosis 70-90% cure in children
186
Q

describe CLL

A
  • most common leukaemia
  • gradual accumulation of b lymphocytes
  • often incidental finding on FBC
  • generally elderly pts
  • progressive lymphadenopathy/hepatosplenomegaly
187
Q

what are the complications of CLL

A
  1. autoimmune haemolysis
  2. infection due to hypogammaglobulinaemia (decreased Ig)
  3. marrow failure due to replacement
188
Q

what is the Binet staging for CLL

A

A - lymphocytosis - 10-15yr
B + nodes 5-7yrs
C + anaemia 2-3yrs

189
Q

what is the treatment of CLL

A
  • nothing
  • chemo
  • monoclonal antibodies
  • targeted therapy
  • transplant
190
Q

what are the two types of stem cell transplant

A 
Autologous 
- own 
- enables escalation of chemo with stem cell rescue
- straightforward
-mortality 2%
Allogeneic 
-other peoples
-more toxic
- mortality 15-30%
- stem cells attack residual tumour and recipient
191
Q

what can increase your risk of getting AML

A
  • preceding haematological disorders
  • exposure to ionising radiation
  • prior chemo
192
Q

what are the symptoms of AML

A
  • marrow failure - anaemia, infection or bleeding

- infiltration

193
Q

what is the treatment of AML

A
  • blood transfusion
  • prompt infection treatment
  • chemo - curative vs palliative
  • transplant
  • prognosis reflects ability to tolerate treatment and leukaemia related factors
194
Q

what gene is associated with acute promyelocytic leukaemia

A

PML/RARA

- t15:17

195
Q

what are the symptoms of CML

A
  • splenomegaly
  • metabolic fractures
  • weight loss
  • fatigue
  • fever
  • sweats
  • increased WBC on FBC
196
Q

what is the treatment of CML

A

targeted molecular therapy

- tyrosine kinase inhibitors e.g imakinib

197
Q

what is anaemia

A
  • low haemoglobin concentration due to either:
  • -low red cell mass - not enough made or too much lost
  • -increased plasma volume
198
Q

what are the consequences of anaemia

A
  • decreased o2 transport
  • tissue hypoxia
  • compensatory changes - increased tissue perfusion, increased O2 transfer to tissues, increased RBC production
  • myocardial + liver fatty change
  • aggravate angina/claudation
  • skin and nail atrophy
  • CNS cell death
199
Q

what are the symptoms and signs of anaemia

A
  • fatigue
  • dyspnoea
  • faintness
  • palpitations
  • headache
  • tinnitus
  • anorexia
    signs
  • pallor of conjunctivae (lacks vasculature)
  • tachycardia
  • flow murmurs
200
Q

what are the causes of a low RBC count due to less being made

A 
hypoplastic
- renal failure
- endocrine
- PRCA
defective Hb synthesis
-iron deficiency (haem group)
- thalassaemia (globin)
- defective DNA synthesis e.g folate
201
Q

what are the causes of a low RBC count due to loss of RBC

A
  • post haemorrhage
    haemolytic
  • intrinsic RBC abnormality - acquired or due to Hb disorders e.g sickle cell
    -extrinsic abnormality - infections e.g malaria, antibody mediated, mechanical trauma
202
Q

what are the causes of microcytic anaemia (Low MCV)

A
  1. iron deficiency - blood loss, poor diet, malabsorption e.g coeliac
  2. chronic disease
  3. Thalassaemia - abnormal haemoglobin
203
Q

what are the causes of normocytic anaemia

A
  1. acute blood loss
  2. chronic disease
  3. bone marrow failure
204
Q

what are the causes of macrocytic anaemia (high MCV)

A
  1. B12/folate deficiency
  2. alcohol excess
  3. hypothyroidism
  4. haemolysis, chemo, congenital
205
Q

what are the two categories of haemoglobinopathies

A
  • disorders of quality - sickle cell

- disorders of quantity - e.g alpha or beta thalassaemia

206
Q

what is the pathogenesis of sickle cell disease

A
  • amino acid substitution in the gene coding for the beta chain
  • Glu —-> Val which leads to production of HbS
  • HbS polymerises when deoxygenated causing RBC’s to deform, producing sickle cell which are fragile and haemolyse
  • sickle cell diseases arise in the homozygous state (SS)
  • heterozygotes are carriers and are protected from falciparum malaria (SC or Sbeta thalassaemia)
207
Q

what are the complications of sickle cell disease

A

acute
- crisis - microvascular occlusion (10/10 pain)
-sickle chest syndrome - hypoxia –> sickles —> lung infarction
-aplastic crisis - caused by parvovirus - B12 suddenly reduces marrow production
- stroke
chronic
- renal impairment
- pulmonary hypertension
- joint damage

208
Q

what is the treatment of sickle cell

A
  • transfusion
  • hydroxycarbamine
  • stem cell transplant
209
Q

what is the pathogenesis of Thalassaemia

A
  • global chain disorders resulting in diminished synthesis of one or more global chains, reducing the Hb
  • deletions - mainly alpha and beta thalassaemia
210
Q

what are the main types of thalassaemia

A
  • minor - carriers
  • intermedia - moderate anaemia and can survive without regular transfusions
  • B major - significant abnormalities - failure to feed, restless, crying, pale, decreased MCV and MCH (mean corpuscular haemoglobin), transfusion dependent, endocrine supplements, psychological support
  • Alpha thalassaemia - mainly gene deletions, found in eastern med and far east
211
Q

what are membranopathies and what do they cause

A
  • autosomal dominant
  • deficiency of red cell membrane proteins caused by a variety to genetic lesions
  • neonatal jaundice
  • mild to moderate haemolytic anaemia
  • gallstones
  • spherocytosis and eliptocytosis most common
212
Q

give an example of an enzymopathy

A
  • glucose 6 phosphate dehydrogenase deficiency
  • x linked
  • haemolysis
  • jaundice
  • precipitated by infections, drugs, broad beans
  • usually self limiting
  • presence of bite and blister cells
213
Q

what is polycythaemia

A
  • increased RBC
214
Q

what are the causes of polycythaemia

A 
primary/proliferative
- polycythaemia rubra vera
--- myeloproliferative disorder 'overactive bone marrow'
--- predominantly red cells but also white and platelets
-- JAK2 mutation in 95%
secondary/reactive
- smoking
-lung disease
-cyanotic heart disease
-altitude
-androgen excess
215
Q

what is the presentation of polycythaemia rubra vera

A
  • plethoric (redness)
  • itching
  • thrombosis
  • splenomegaly
  • abnormal FBC
216
Q

what is the treatment of polycythaemia rubra vera

A
  • aspirin
  • venesection
  • bone marrow suppressive drugs
217
Q

what is neutrophilia

A

increase WBC/increased neutrophils

218
Q

what are the causes of neutrophilia

A 
proliferative
- CML
reactive 
- infection - bacterial  
-inflammation
-malignancy
219
Q

what is lymphocytosis

A

increased lymphocytes

220
Q

what are the causes of lymphocytosis

A 
proliferative 
-CLL
reactive 
-infection - viral
- inflammation 
- malignancy
221
Q

what is thrombocytopenia

A

low platelets e.g immune thrombocytopenia (anti platelet antibodies)

222
Q

what is thrombocytosis

A

increased platelets

223
Q

what are the causes of thrombocytosis

A 
proliferative
- essential thrombocythaemia (overreactive bone marrow)
reactive 
-infection
-inflammation 
-malignancy
224
Q

what is neutropenia

A

decreased neutrophils

225
Q

what are the causes of neutropenia

A 
underproduction
- marrow failure
- marrow infiltration
- marrow toxicity 
increased removal
-autoimmune
-feltys syndrome
-cyclical
226
Q

which molecule produced in the liver regulates platelets

A

thrombopoietin

227
Q

what are the main platelet surface proteins

A
  • ABO
  • HPA
  • glycoproteins
228
Q

how are platelets activated and what does this lead to

A
  • adhesion to collagen via GPIa
  • adhesion to VWF by GPIb+ IIb/IIIa
  • release of alpha granules containing PDGF, fibrinogen, VWF, PF4
  • dense granules - ADP, calcium, serotonin
  • membrane phospholipids activate clotting factors II (prothrombin), V and X
229
Q

what happens to platelets when they encounter exposed collagen in endothelial wall

A
  • adhere to collagen and VWF
  • this stimulates cytoskeleton shape change within the platelets and they spread out
  • increased surface area and results in activation, granules released that facilitate the clotting cascade ending with production of fibrin
  • cross linking by fibrin —. aggregation
  • activated platelets also provide negatively charged phospholipid surface which allows coagulation factors to bind and enhance clotting cascade
230
Q

what tests can be used to see if platelets are working correctly

A
  • FBC
  • blood film
  • PFA i.e response to aggregating agents e.g ADP, collagen (Platelet Function Assay or Platelet Function Analyser)
  • surface proteins flow cytometry
231
Q

what problems cause bleeding

A
  1. low platelets
  2. abnormal platelet function
  3. vascular disorders
  4. defective coagulation
  5. injury
232
Q

what are the clinical features of platelet dysfunction

A
  • mucosal bleeding
    • epistaxis, gum bleeding, menorrhagia
  • easy bleeding
  • traumatic haematomas
233
Q

what are the causes of impaired platelet function

A
  • congenital - platelet disorders, Von willebrand disease

- acquired - uraemia, drugs

234
Q

what are the causes of thrombocytopenia caused by decreased production

A
  • congenital
    absent/reduced/malfunctioing megakaryocytic in BM
  • infiltration of BM
    leukaemia, metastatic malignancy, lymphoma, myeloma, myelofibrosis
  • reduced production by BM
    low B12, reduced TPO, medication, toxins, infections, aplastic anaemia
    -dysfunction production of platelets
235
Q

what are the causes of thrombocytopenia caused by increased destruction

A
  • autoimmune -ITP, primary or secondary
  • hypersplenism - splenomegaly, portal hypertension
  • drugs related immune destruction - heparin induced
  • consumption of platelets - haemorrhage, haemolysis, TTP, DIC
236
Q

what is the pathogenesis of immune thrombocytopenia (ITP) and how is it caused

A
  • anti platelet antibodies attach to platelet and megakaryocyte surface glycoproteins
  • opsonised platelets removed by reticuloendothelial system

primary
-viral infection

secondary

  • malignancies e.g CLL
  • infections e.g HIV/HepC
237
Q

What is the treatment of ITP

A
  • give platelets if bleeding
  • immunosuppression
  • treat underlying cause
  • Tranexamic acid - decreased fibrin breakdown
238
Q

what is the pathogenesis of disseminated intravascular coagulation (DIC)

A
  • cytokine release in response to systemic inflammatory response syndrome (SIRS)
  • causes activation of clotting cascade, microvascular thrombosis and consumption of platelets and clotting factors
  • leading to organ failure and bleeding
239
Q

a reduction in which enzyme causes thrombotic thrombocytopenic purpura

A
  • ADAMTS13 - failure to break down VWF

- causes spontaneous platelet aggregation in microvasculature

240
Q

what is the presentation of neutropenic sepsis

A
  • fever > 38
  • rigors
  • malaise
  • hypotension
  • CV collapse and death
  • often chemo patients
241
Q

what should you do in neutropenic sepsis

A
  1. see the patient
  2. put in a cannula
  3. antibiotics
242
Q

what is the presentation of spinal cord compression

A
  • back pain, leg weakness
  • loss of urinary retention
  • decreased anal tone
  • neuropathic pain
  • decreased reflexes
  • give dexamethasone
  • urgent MRI
243
Q

What is tumour lysis syndrome

A

as cancer cells die - intracellular components released, kidneys are overwhelmed, and crystallisation happens
- prevent with I.V. throughout chemo

244
Q

what are the tests for arrhythmia

A
  • FBC
  • U&E
  • glucose
  • ECG - for signs of IHD, AF, short PR (WPW) long QT (drugs, metallic imbalance, congenital0
  • cardiac monitoring
  • echo to look for structural heart disease
245
Q

what is the difference between 1st, 2nd and third degree heart block

A

1st degree - PR interval prolonged and unchanging
2nd Mobitz I - PR interval becomes longer and longer until a QRS is missed, then resets
2nd Mobitz II - QRS regularly missed
3rd - no impulses passed from atria to ventricles so p and QRS appear independently of each other. As tissue distal to the AVM paces very slowly the patient becomes bradycardic

246
Q

what are the causes of total heart block

A 
IHD
fibrosis 
congenital
trauma 
aortic valve calcification
247
Q

what would be seen on an examination for haemolytic anaemia

A
  • hepatosplenomegaly
  • jaundiced
  • dark urine
248
Q

Which scoring system is used for DVT

A

Wells scoring system

- 2 or above is likely DVT

249
Q

what are the associations of acute promyeloid leukaemia

A
  • DIC

- t15:17

250
Q

which stain is used to differentiate between types of leukaemia

A
  • sudan black stain
251
Q

how is AML diagnosed by blood film

A

Auer rods

252
Q

what are the side effects of chemo

A 
immediate 
-neutropenia
-nausea and vomiting
-anaemia 
-alopecia 
- thrombocytopenia 
late 
- infertility 
-psychological
-cardiac toxicity
- increased malignancy
253
Q

which type of lymphoma causes pain in lymph nodes with alcohol?

A

hodgkins

254
Q

what are the criteria for diagnosis of SIRS

A
  • temperature > 38.3 or < 36
  • heart rate > 90
  • white cell count < 12
  • hypoxia
255
Q

what is the sepsis 6

A
  • Shivering, fever or very cold
  • Extreme pain or general discomfort
  • Pale of discoloured skin
  • Sleepy, difficult to wake up, confused
  • I feel like i might die
  • Short of breath
256
Q

describe BUFALO sepsis intervention tool

A 
Blood cultures + septic screen, U+E 
Urine output - minitor hourly 
- Fluid resuscitation 
- Antibiotics IV 
- Lactate measurement 
- Oxygen to correct hypoxia
257
Q

what is the management of MI

A

Morphine
Oxygen
Nitrates
Aspirin

ST elevation
PCI within 2 hours
Beta blocker
ACE inhibitor 
Clopidogrel

Non ST elevation
BB
antithrombotic - fondaparinux
clopidogrel and aspirin

258
Q

what are the causes of systolic heart failure

A
  • cardiomyopathy
  • ischaemia
  • hypertension
259
Q

what are the causes of diastolic heart failure

A
  • cardiac tamponade
  • pericarditis
  • hypertension
260
Q

what is seen on a CXR for heart failure

A 
Alveolar oedema 
Kerley B-lines - interstitial oedema
Cardiomegaly
Dilated prominent upper lobe vessels 
Effusions
261
Q

what is BNP and how are its results linked to disease

A

BNP - brain natruetic peptide

  • released from the heart when the ventricles are stretched
  • higher levels indicate heart failure
262
Q

what organism is the mean cause of rheumatic fever

A
  • streptococcus pyogenes
263
Q

what is the treatment of an SVT

A
  • vagal maneuveres
  • drug - adenosine
  • surgery
  • carotid massage
264
Q

what can a ventricular tachycardia lead to if not treat

A
  • Ventricular fibrillation
265
Q

what is the treatment of a VT

A
  • Inserted cardioversion
266
Q

what is the bundle affected in WPW

A
  • kent bundle
267
Q

what is the scoring system used to calculate the risk of stroke in AF

A

CHA2DS2-VASc

268
Q

which system assesses risk of bleed on anticoagulants

A

HAS-BLED

269
Q

which scoring system is used to assess risk of cardiac event in net 10 years

A

Qrisk2

  • age
  • sex
  • height
  • weight
  • cholesterol
  • comorbidities
  • family history
  • DM
270
Q

what troponin level is indicative of acute MI

A

> 14ng/l

271
Q

give one sign of coarction of the aorta that can be found on examination

A
  • radiofemoral delay
272
Q

what is the reversal agent of warfarin

A
  • vitamin K
273
Q

what are the tests for Von willebrand disease

A
  • increased APTT
  • increased bleeding time
  • vWF Ag decreased

Phase2a (10 decks)

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