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CSIM > Vascular > Flashcards

Vascular Flashcards

1
Q

Pathogenesis of Atherosclerosis plaque

A

Mechanical sheer streets lead to damage to endothelium from HTN, increased LDL’s, toxins from smoking leads to inflammation of the tunica intima and LDL deposition. The deposition of LDL leads to an inflammatory response and recruitment of macrophages due to cytokine production. Macrophages in turn phagocytose the LDL transforming into lipid laden foam cells. Further irritation leads to TGFb and other cytokines production which promote SM proliferation to form a fibrous cap over the lipid core

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2
Q

PC of atherosclerosis

A

Stenosis - claudication, angina, mesenteric ischemia, renal artery stenosis - HTN/CKD

Plaque rupture - Stroke/TIA, MI, acute limb schema

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3
Q

Plaque thrombus formation

A

1 - Endothelial injury exposes the connective tissue matrix beneath, platelets adhere to the collagen fibres forming a thrombus

2 - Deep endothelial fissuring allows blood to enter the plaque, the mix of macrophages, LDL’s and tissue factor is highly thrombogenic and leads to an expansive thrombus in the plaque

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4
Q

Peripheral arterial disease

A

Most asymptomatic only 7% require intervention. Due to atherosclerosis of the aorta-iliac vessels. If a pt has PVD they have CAD!

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5
Q

Limb ischemia PC

A

Stage I - asymptomatic
II - intermittent claudication (relieved by rest)
III - rest/night pain a sign of critical ischemia
IV - gangrene

Can present with cold extremities, hair loss, eczema,
arterial ulcers - deep punched out, over pressure points
Burgers test +ve

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6
Q

Acute limb ischemia

A

Embolic event leading to occlusion. 6 P’s

Pain pulseless, parathesia, paralysis, perishling cold and pallour

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7
Q

ABPI

A

Ankles brachial pressure index.
>1.30 = calcification of vessels
0.71-0.90 = mild PAD
<0.4 = severe PAD

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8
Q

Coronary Artery disease risk factor

A

Modifiable - smoking, HTN, cholesterol levels - HDL and triglycerides, DM, obesity and exercise, hyper coagulability, COCP

Non modifable - age, male sex, afro-carribean, FHx

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9
Q

Myocardial ischemia

A

Reduced blood flow - atheroma, thrombus, embolus, arteritis,

Reduced oxygenation of the blood - anaemia, hypotension, hypoventilation

Increased demand - hypertrophy of cardiac muscles, increased cardiac output (hyperthyroid)

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10
Q

Metabolic syndrome

A

3/5 of the following: insulin resistance (DM), HTN, central obesity, hyperlipidemia - high TG, low HDL

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11
Q

Angina PC

A

PC crushing centra/retrosternal chest pain brought on by exertion, stress or cold relieved by GTN or rest. May radiates to the jaw or left arm

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12
Q

Cardiac Chest Pain

A

MI central crushing, high troponin, ST changes ECG, PMHx or risk factors!

Angina relieved by rest or GTN

Pericarditis pleuritic pain better on sitting forward, saddles shaped ST changes globally on ECG

Dissection tearing retrosternal pain often accompanied by hypotension, unequal BP in arms, neurological sequale

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13
Q

Respiratory Chest Pain

A

PE sudden onset SOB, sinus tachy, +/-haemoptysis, risk factors/DVT

Pneumothorax sudden onset SOB, hyperresonant to percussion, absent breathe sounds

Pneumonia fever, SOB, green/purulent sputum, crackles on auscultation, CXR - shadowing

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14
Q

Gastro Chest Pain

A

GORD/PUD retrosternal pain, worse on large meals or lying down

Gallstones - PMHx, fat, female, forty, fertile, classic bilary colic pain worse after eating

Pancreatitis - severe epigastric pain, vomiting, nausea, diarrhoea, jaundice, high amylase

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15
Q

Other Chest pain

A

Anxiety - hyperventilation, stressed, tight chest

Boerhaave taer - rupture oesophagus

MSK - costochondritis/fracture specifically localised pain, worse on inspiration, ?trauma

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16
Q

Definition of MI

A

Universal definition of myocardial infarction =

troponin >99 centile and symptoms/ECG evidence of ischemia or necrosis

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17
Q

Risks of Obesity

A

1x GORD,PCOS, infertility, Cancer
2x CHD, HTN, OA, gout
3x T2DM, OSA, dyslipiemia

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18
Q

Type I MI

A

Related to atherosclerotic plaque rupture from ulceration, fissuring leading to intraluminal thrombus

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19
Q

Type II MI

A

Imbalance in o2 delivery to myocardium may be seen in tachyarrythmias, anaemia, respiratory failure

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20
Q

Type III MI

A

Post mortem diagnosis of sudden cardiac death

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21
Q

Type IV and V MI

A

IV - due to PCI (trop 5x) or stent thrombosis

V - due to CABG (trop 10x URL)

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22
Q

Stable angina Mx

A

Lifestyle advice, treat HTN, DM and give statins
Short acting GTN spray for symptomatic relief
- Used Blocker or CCB
- If continue to be symptomatic/significatn stenosis offer revascularisation
PCI - single vessel + suitable anatomy
CABG - multi vessel, DM

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23
Q

ACS

A

i) STEMI
ii) NSTEMI
iii) Unstable angina - crucially = ischemia not infacrtion so no increase in trop

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24
Q

PC ACS

A

Severe sudden onset retrosternal chest pain radiating to jaw/ left arm. No relief by GTN or rest. N/V, sweating and palpatiatons

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25
Q

O/E ACS

A

tachycardia (bradycardia if RCA occlusion due to SAN/AVN supply
apex displacement, S4 gallop
hypotension, new pan systolic murmur - VSD rupture
mitral regurg = papillary muscle rupture

Signs of other pathology - aortic dissection unequal BP

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26
Q

Atypical MI

A

DM or elderly can present with SOB, abdo pain completely asymptomatic

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27
Q

Leads on the ECG

A

Inferior leads - II,III and avF = RCA
Anterior leads - V1-V4 = LAD
Lateral - V5,V6, I and avL = L circumflex

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28
Q

ECG signs in ACS

A

ST elevation or depression - T wave inversion - Pathological Q waves (1mm wide, 2mm deep)

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29
Q

Troponin T

A

Expressed in cardiac and skeletal muscle responsible for coupling sarcomeres when high intracellular Ca2+, binds to tropomyosin to position actin

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30
Q

Causes of raise trop

A

sepsis, PE, rhabdomyolysis, LVF, AF, post op, pericarditis, myocarditis, cardiomyopathy

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31
Q

ACS diagnostic troponin

A

> 99URL = diagnostic. 2nd troponin post 3hrs

- different in 10mg/l or 20% rise

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32
Q

GRACE Score

A

Predictor of death/MI 6months post discharge.
Uses age, HR @ presentation
Findings during stay = SBP, Hx of CCf or MI,cardiac enzymes, ST depression, PCI and creatinine level

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33
Q

NSTEMI Mx

A

Loading dose of aspirin 300mg and ADP receptor antagonist i.e. clopidogrel or ticagrelor
- These acts anti platelets

LMWH/fondaparinaux to anticoagulate

Morphine for pain

GRACE score or clinical picture dictates PCI intervention if deemed need PCI should occur within 72hrs

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34
Q

STEMI Mx

A

Morphine, aspirin 300mg, clopidogrel/ ticagrelor, LMWH o2 high flow
PCI within 2hrs

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35
Q

Fibrinolysis

A

Only if unable to reach PCI centre.

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36
Q

PCI to fibrinolysis

A

Recent surgery, GI bleed, aortic dissection, Hx bleeding disorders, haemorraghic stroke, ischemic within 3months,

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37
Q

Post hospital discharge MI

A

Lifestyle - cardiac rehab, dietician input, stop smoking, reduce alcohol, BMI <25, physically active

Medical - antihypertensives, control DM, aspirin 75mg od, clopidogrel, statins, ACEi

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38
Q

Complications of MI

A

Heart failure

Myocardial rupture of LV free wall often fatal event leads to haemodynamic collapse and cardiac arrest

VSD gives a pansystolic murmur

MR due to severe LV dysfunction leading to annular dilation, MI of inferior wall leading to papillary dysfunction, Infarction of the papillary muscle = sudden onset HF and cardiogenic shock

Dresslers 6-8wks post MI self limiting pericarditis

Arrthymias are v common

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39
Q

Hypertension diagnosis

A

Anyone with SBP >140/90 is offered ABPM to confirm the diagnosis

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40
Q

Complications of HTN

A

Heart - MI, LV hypertrophy due to increased afterload from high PR. Can lead to hypertensive cardiomyopathy and HF

Brain - Stroke/TIA, vascular dementia, hypertensive encephalopathy

Renal - hypertensive nephropathy. Thickening of arteriole walls leads to reduced blood flow, tubular atrophy and interstitial fibrosis and glomerular ischemia = ESRF

Hypertensive retinopathy, PVD

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41
Q

Hypertensive encephalopathy

A

Rare due to cerebral blood pressure >200/130 spasm of cerebral vessels leads to ischemia

PC occurs approx 36hrs post BP increase, severe headache, reduced GCS, impaired cognition and neurological signs

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42
Q

Hypertensive retinopathy

A 
I = vasospasm, increased arteriolar tone narrowing retinal arteries - silver wiring (tortuous and increased reflective)
II = sclerosis and intimal thickening  AV nipping
III = disruption of blood-retinal barrier SM and endothelial dysfunction. Cotton wool spot (ischemia), hard exudates(lipids) and dot/blot haemorrhages
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43
Q

1 HTN

A

Essential HTN (90%) due to increasing age, males, obesity, high salt, FHx, lack of exercise

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44
Q

2 HTN

A

Always think if treatment resistant, young
Endo - Conns, acromegaly, cushings, phaechromocytoma

Renal - Anything that leads to ESRF, renal artery stenosis, ADPKD,

Vascular - coarctication

Drugs - cocaine, epo, steroids, caffeine, nicotine, NSAIDs
OSA and white coat HTN

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45
Q

RAS

A

Angiotensinogen produced by liver in response to low BP, activated by renin (produced by juxtaglomerularappartus hypoperfusion)

This produces angiotensin I which is cleaved by ACE to angiotensin II.

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46
Q

Actions of angiotensin II

A

Vasoconstrictor - binds to At1 receptors on endothelium to inhibit bradykinin synthesis, therefore NO
Aldosterone secretion from adrenal = Na+ retention and K+ excretion
ADH production from post pituitary = aquaporin insertion @ collecting duct therefore h20 reabsorbed

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47
Q

Phaechromocytoma

A

PC headaches, severe HTN, sweating and palpitations

linked to MEN2 and von hippel lindau. Inv = high plasma/urine metaepinephrines

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48
Q

Cushings syndrome

A

PC wt gain, central obesity, proximal myopathy, high glucose, facial plethora, striae, hirsutism

Inv - 24hr urinary cortisol, morning cortisol, low dose dexamethasone, plasma ACTH

HTN due to cortisol having affinity for aldosterone receptors

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49
Q

Hyperaldosteronism

A 
1 = Conn's or adrenal hyperplasia
2 = LVF, cirrhosis, cor pulmonale all lead to high renin

Aldosterone:renin need to identify which

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50
Q

Conn’s

A

PC HTN, muscle weakness, fatigue, headache, low K+, high Na+, high serum aldosterone:renin

May need adrenal vein sampling

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51
Q

Renal artery stenosis

A

May be linked to fibromuscular dysplasia esp young females, may = gradual decline in renal function or abrupt flash pulmonary oedema. Abdo bruit
Inv - MR angiography

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52
Q

Liddle syndrome

A

Hyperactivity of ENaC. AD leads to high levels of ENaC channels present and activated in the collecting duct hence hypernatremia and HTN

hypokalemia, metabolic alkalosis due to increase bicarb retention

Mx = K+ sparing diuretic

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53
Q

AME - apparent mineralocorticoid excess

A

AR condition due to deficiency in 11B dehyrdoxysteriod dehydrogenase preventing cortisone to cortisol. This leads to cross reaction and simulation of aldosterone receptor

Inv = urinary cortisol:cortisone

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54
Q

Classification of HTN

A 
I = >140/90 in clinic or 135/85 on ABPM
II = >160/110 in clinic or 150/95 on ABPM
III = >180 EMERGENCY
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55
Q

Acute stroke imagine

A

CT. Haemorrhage = white, Ischemia = grey

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56
Q

Early signs of ischemic stroke on CT

A

loss of grey white matter differentiation, lack of definition of lentiform nucleus

57
Q

Carotid imaging

A

Carotid duplex USS used to screen for carotid stenosis

58
Q

Pericarditis PC and Mx

A

Inflammation of the pericardium. sharp chest pain made better on leaning forward, radiates to trapezius, may have fever, dry cough, AKI

Mx = self limiting NSAID’s if large pericardial effusion pericardiocentesis

59
Q

O/E Pericarditis

A

ECG - globally saddled shaped ST elevation, flattened t waves,
Huge troponin often 1000’s
Pericardial rub
CXR = globular “water bottle” heart

60
Q

Complication of pericarditis

A

Pericardial effusion which can lead to tamponade

61
Q

Causes of pericarditis

A 
Viral - coxsackie, influenza, mumps
TB, Bacterial (strep, staph, Hib)
Post MI - dresslers
Ureic pericarditis
AI - SLE, RA, systemic sclerosis
62
Q

Consider familial hypercholestrolemia

A

total cholesterol > 7.5mmol or FHx premature coronary disease

63
Q

Aortic dissection

A

Tear in the tunica intima allows blood to enter inbetween the intima and media forming a false lumen which can compress vessels coming off the aorta as it expands.

64
Q

PC aortic dissection

A

PC = sudden onset severe chest pain, radiating to the back. hypotension, vomiting and sweating

O/E = hypotension - difference in-between arms

Complications

  • Ascending = AR,MI, tamponade, neurological defect
  • Descending = AKI, acute mesenteric ischemia, acute limb ischemia
65
Q

Causes of aortic dissection

A

HTN, coarctation, Marfans and Ehlers damlos. Turners and Noonans

66
Q

Pathogenesis of dissection

A

Normally @ aortic arch or 2cm above aortic root
I = ascending and descending
II = only ascending aorta
III = descending aorta only

67
Q

Invx dissection

A

CXR = widened mediastinum. TOE = gold standard, ECG and troponin to rule out MI

68
Q

Number needed to treat

A

NNT = 1/ARR

69
Q

Q RISK 2

A

Predicts a persons 10yd cardiovascular risk. Anyone with risk >10% needs statins, HTN contract and advice about exercise, diet, smoking and BMI

70
Q

Measuring the JVP

A

Used as no valves between the internal jugular vein and the RA. Hence is an indicator of RA pressure

71
Q

S3 and S4

A

S3 - due to rapid ventricular filling present in HF
S4 - associated with atrial contraction

If heard together = gallop rhythm

72
Q

Cardiac tamponade

A

Build up of fluid in the pericardium leading to compression of the heart. Causes = trauma, pericardial effusion,retrograde aortic dissection.

73
Q

PC and O/E of tamponade

A

Cardiogenic shock - SOB, hypotension, cold peripheries

O/E = Beck’s triad - muffled heart sounds, low BP and JVP distention, rapid weak thready pulse, cool clammy mottled skin due to vasoconstriction and hypoperfusion

pulsus paradoxus - drop in BP >10mmHg on inspiration

74
Q

Inv and Mx tamponade

A

ECG may show electric alternans - alternation of QRS complex amplitude between beats
Echo = diagnostic

Mx = pericardiocentesis via 5th ICS or xipisternal

75
Q

Signs of hyperlipidemia

A

Xanthelasma - cholesterol deposits on eyelids/ under the eyes

Corneal arcus - cholesterol deposit around cornea

Tuberous xanthoma - orange streaks of cholesterol on palms

Tendon xanthomas- nodules @ achilles tendon or digital extensors

In hypertriglyceridemia = pancreatitis and eruptive xanthoma

76
Q

Lipid physiology

A

Lipids are insoluble in water and so are transported in the bloodstream as macromolecular complexes. The central lipid core is surrounded by a coat of phospholipids. These apoproteins transform the lipid into a lipoprotein. There are 5 main types of lipoprotein separated by their relative size and density

77
Q

Chylomicrons

A

Triglyceride rich allowing transport of lipids from the intestine to the adipose, cardiac and skeletal tissue. Lipoprotein lipase present in these tissues hydrolyses the triglycerides to fatty acids. The rememant chylomicron is taken up by the liver. ApoB48

78
Q

VLDL

A

Synthesised by the liver contain endogenous triglycerides. Main energy source when fasting. Triglycerides are removed via apoprotein CII binding to the capillary endothelium. When depleted of TG = IDL
ApoB100

79
Q

LDL’s

A

Main carrier of cholesterol delivering it to the liver and peripheral cells. Contains a single apolipoprotein B100 which allows it to bind to receptors on the surface of the hepatocytes. It is then internalised and degraded by liposomes

80
Q

HDL’s

A

Nascent HDL produced by intestine and liver travel to peripheral tissues they transmutate into mature particles with the acquisition of phospholipids and A and C apoproteins they can then removed cholesterol from the periphery. ApoA1

81
Q

Terminology of lipids

A

Cholesterol - structural component of cell membranes used to produce bile acids, steroid hormones and transport fat soluble vitamins (ADEK)

Triglycerides = glycerol and 3x fatty acids

82
Q

Secondary hyperlipdemia

A

High triglycerides and VLDL = DM, CKD, alcohol and hypopituitarism, drugs - steroids, b-blockers, diuretics, HIV meds

High cholesterol = nephrotic syndrome, hypothyroidism, Cushings, choleostasis

83
Q

Total cholesterol

A

Total cholesterol = LDL,VLDL, HDL and IDL approx 5.0 mol/l

84
Q

Triglyceride levels

A

Not considered directly atherogenic but important to consider due to role in metabolic syndrome.

Can = pancreatitis or eruptive xanthoma in high levels

12hr fasting TG <1.7 mol/l

85
Q

HDL levels

A

HDL - antiatherogenic molecule shown to be protective against CVD and atherosclerosis

86
Q

LDL level

A

Calculated using Freidewald equation. Prolonged fasting state is needed so rarely used!

High levels linked to CVD and atherosclerosis

87
Q

Non HDL cholestrol

A

Frequently used as fasting isn’t required

88
Q

Familial hypercholesterolemia

A

1/500 people AD mutation in LDR receptor. This leads to reduced removal of LDL from the blood.

PC often asymptomatic, tendon xanthomas or corneal arcus. High LDL and total cholesterol

89
Q

Codominance in familial hypercholestrolemia

A

Homozygous = 50% of 60y/o pt will die if untreated

Heterozygous = rare no LDL receptors leads to hugely elevated LDL leading to mass deposition in arterial walls. Death from IHD in childhood or adolescents

90
Q

Diagnosis of familial hypercholesterolemia

A

1) Total cholesterol > 7.5mmol/l or LDL > 4.9mmol/l

+ 2)Tendon xanthomas or 1st degree relative
3)DNA evidence LDL mutation

91
Q

Familial combined hyperlipidemia

A

High LDL and TG levels, Low HDL approx 1/200

92
Q

Remnant (type III) hyperlipidemia

A

AR 1/5000 due to a mutation in apoplipoprotein E which prevents the normal metabolism of IDL, VLDL and chylomicrons. Hence accumulation of chylomicron remnants

PC = eruptive xanthoma, xanthum striatum palmare

Inv = v high TG, high total cholestrol

93
Q

Familial hypertriglyceridemia

A

AD can be due to excessive VLDL production or defects in LPL and apoCII leading to vv high triglyceride levels >10mmol, with normal cholesterol

PC = eruptive xanthoma, pancreatitis, lipideamia retinals
very high CVD risk

94
Q

When not to use Q risk 2

A

Pt with 1 lipid disorders, high risk CVD conditions such as DM, CKD - eGFR <60, 85+y/o

95
Q

Amaurosis fungax

A

Sudden onset transient loss of vision usually lasts mins-hrs described as black curtain descending +/- fogging of vision

96
Q

Causes of amaurosis fungax

A

Embolic/hameodynamic - atherosclerotic carotids, cardiac emboli (AF, myxoma), vasospasm, GCA, SLE, antiphospholipid syndrome, malignant HTN, post endoarchtectomy. bypass

Ocular - closed angle glaucoma, iritis/keratitis

Neurological - optic neuritis, papilloedema, migraine

97
Q

Ocular ischemic syndrome

A

Chronic hypoperfusion to the eye due to severe carotid artery stenosis (90%)

PC - males 65+y/o dull pain over eyebrow, visual loss, often PMHx of DM, HTN

Mx - rule out vasculitis, stroke prevention and increase blood flow to retina

98
Q

Causes of carotid bruit

A

Carotid artery stenosis, AS, hyperthyroidism

99
Q

Carotid endoarchectomy

A

Diagnosed via duplex USS 1st line for pt with 50-99% stenosis

100
Q

Reversible causes of a cardiac arrest

A

6H’s and 6T’s

101
Q

6H’s

A

Hypoglycaemia,
Hypothermia - body temp <35 rewarming via bypass or irrigation of cavities
Hyper/hypokalemia - If K+ calcium gluconate, Neb salbutamol, IV insulin/glucose
Hypoxia - O2, tracheostomy if needed
Hypovolemia - IV fluids, tranfusion, find and stop the cause of bleeding. Surgical tamponade for varies/PPH
H+ acidosis often from prolonged hypoxia - glycolysis produces lactate. Sodium bicarb buffer

102
Q

6T’s

A

Thrombosis = PCI
Tamponade = Pericardiocentesis stat. PC muffled heart sounds, distended neck veins, narrow pulse pressure, rapidly falling BP
Tension pneumothorax = needle thoracotomy 2nd ICS mid clavicular
Toxins = TCA’s, B-blockers, cocaine, aspirin
Trauma - Commotion cordis
Thromboembolism = Massive PE

103
Q

Cardiac channelopathies

A

Congenital disorder caused by genetic mutations that affect the cardiac ion channels and electrical activity of the heart. Eg Brugada, long QT, CPVT

104
Q

Ventricular fibrillation

A

Broad complex tachycardia QRS >0.12 ECG shows shapeless rapid oscillations with no organised complexes

Disorganised contraction of the heart leads to low CO and can = ischemia of heart muscle

Pulseless pt becomes rapidly unconscious leading to cardiac arrest

Mx = defibrillation stat

105
Q

Long QT syndrome

A

Rare inherited cardia syndrome usually AD but can be AR. Channelopathy involving abnormal repolarisation of the heart giving different refractory periods in myocytes. These can propagate to neighbouring myocytes = re-entrant ventricular arrhythmia

Due to reopening of L-type Ca2+ channels @ plateau phase early after depolarisation.

106
Q

Causes of long QT

A

Inherited = Romano ward (AD), Jervell-Lange-Neilsen (AR)

Acquired = hypokalemia, hypocalcemia, acute MI, bradycardia, DM, drug induced, hypothermia

107
Q

Drug induced long QT

A 
Fluoroquinolones: cipro
 Neuroleptics: phenothiazines, haldol
 Macrolides
 Anti-arrhythmics 1a/III: quinidine, amiodarone, sotalol
 TCAs
 Histamine antagonists
108
Q

Types of inherited long QT

A

Type I = Provoked by exercise esp swimming
Type II = Provoked by emotion or acoustic stimuli
Type III = @ rest or asleep

109
Q

PC long QT

A

Asymptomatic. Can present as syncopal episodes or incidentally

QTc >480mms. Worked out using Bazzetts formula

110
Q

Inv for cardiac syncope

A

ECG crucial
Echo to identify structural abnormalities i.e. cardiomyopathy
Heart monitors

111
Q

Heart monitors

A

ILR - implantable loop recorder small chip implanted under the skin that can record ECG for up to 3 years. It picks up event and notifies hospital switchboard

Halter monitor = pt wears a ECG recorder for 1-7 days

112
Q

Torsades de pointes

A

QRS twisting at isoelectric line. QT prolongation required. This can degenerate to VF

113
Q

Wolff-parkinson white syndrome (WPW)

A

Presence of an accessory pathway connecting atria and ventricles allowing electrical impulses to bypass the AVN leading to premature ventricular contraction

114
Q

WPW ECG

A

slurred delta wave at base of QRS, shortened PR interval <120ms, wide QRS. Can lead to SVT

Mx = ablation of bundle of lent

115
Q

Arrythmogenic RV cardiomyopathy

A

Usually presents in adolescent 80% with syncope and dyspnea. AD with variable expression. Increased incidence in italian males

Fatty infiltration confined to RV leading to atrophy of cardiomyocytes

116
Q

Brugada syndrome

A

20% of cases due to mutation in gene encoding Na+ channels in cardiac myocytes. AD increase prevalence in males and south asian populations

Risk of sudden cardiac death and VF

Mx = ICD

117
Q

ECG brugada

A

Provoked by flecanide administration
type I = coved ST elevation v1-v3 + RBBB
type II = saddle back ST change and biphasic T waves

118
Q

Catecholaminergic polymorphic VT (CPVT)

A

Mutations in Ca2+ channels on sarcoplasmic reticulum. Seen in young people often syncopal episode or MI before 20y/o triggered by exercise or stress

Mx ICD

119
Q

ECG arrythromgenic RV cardiomyopathy

A

T wave inversion v1-v3, RBBB,

Epsilon wave = terminal notch in QS due to slow intraventricular contraction

120
Q

Commotio cordis

A

Blow to pericardial region @ critical time in cardiac cycle. Ascending T wave ventricular repolarisation

121
Q

HOCM

A

Most common cause of cardiac death in young people. 1/500. AD condition mutations in B myosin heavy chain protein. Causes variable myocardial hypertrophy frequently involving the AV septum = LV outflow obstruction

122
Q

PC HOCM

A

Asymptomatic - incidental ECG finding.
Chest pain, SOB and palpitations on exertion

O/E = double apex beat = s4, jerky carotid pulse due to rapid ejection and sudden LV outflow obstruction, ejection systolic murmur @ LL sternal edge

123
Q

Inv and Mx HOCM

A

ECG - LVH, abnormal Q waves in inferolateral leads
Echo = diagnostic of asymmetric LV hypertrophy with septal involvement

Mx = ICD or amiodarone

124
Q

Causes of sudden cardiac death

A

Coronary artery disease - Acute MI, IHD

Non coronary artery disease - HOCM, Brugada, Long QT, dilated cardiomyopathy, Valve disease and congenital heart disease

125
Q

Dilated cardiomyopathy

A

Dilatation of the ventricular chambers and systolic dysfunction with preserved wall thickness

126
Q

Causes of dilated cardiomyopathy

A 
Familial = AD
Acquired = SLE, pregnancy, myocarditis (cox-sackie, HIV, fungi, adenovirus) , alcohol, pregnancy
127
Q

A Wave in JVP

A

Atrial systole

Large a wave - pulmonary hypertension and stenosis
Absent a wave - AF due to dysfunctional syncope
Cannon a wave - complete HB

128
Q

Large v wave

A

Atrial filling against closed tricuspid valve

129
Q

Raised JVP normal waveform

A

HF and fluid overload

130
Q

Prinzmetal’s angina:

A

Refers to an angina that occurs without provocation, usually at rest, as a result of coronary artery spasm
• Occurs more frequently in women
• Arrhythmias (both VT and heart block) can occur during the ischaemic episode

131
Q

Aortic stenosis

A

Syncope, SOB. Ejection systolic murmur radiating to the carotids

132
Q

Causes of cardiogenic shock

A

MI, cardiac tamponade, arrhythmias, tension pneumothorax, aortic dissection

133
Q

Signs and symptoms of RHF

A

PC = peripheral oedema, ascites, fatigue, wt loss, SOB

Signs = transudative pleural effusion, raised JVP, 3rd heart sound

Causes = 2ndardy to LHF, pulmonary hypertension, tricuspid or pulmonary stenosis, cor pulmonale

134
Q

Signs and symptoms of LHF

A

PC = orthopnea, PND, fatigue and SOB

135
Q

Simon Broom criteria

A

Total Cholesterol >7.5mmol/L or LDL >4.9mmol/L
+
Tendon xanthomas in the patient, first or second degree relatives
OR
DNA Evidence of LDLR mutation, ApoB100 or PCSK9 mutation

136
Q

Causes of familial hypertriglyceridemia

A

Familial hypertriglyceridemia

Lipoprotein Lipase Deficiency and Apoprotein C-II deficiency Rare, presents in childhood. Severe hypertriglyceridaemia
Pancreatitis, retinal vein thrombosis, eruptive xanthomas

137
Q

Mx dyslipidemias

A

high triglycerides = fibrates
high cholesterol = statins

combined = fibrates

138
Q

Diagnosing HF

A

Previous myocardial infarction
arrange echocardiogram within 2 weeks

No previous myocardial infarction
measure serum natriuretic peptides (BNP)
if levels are ‘high’ arrange echocardiogram within 2 weeks
if levels are ‘raised’ arrange echocardiogram within 6 weeks

CSIM (12 decks)

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