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CSIM2 > Vascular 2.53-2.60 > Flashcards

Vascular 2.53-2.60 Flashcards

1
Q

Three vasodilatory substances? (generally antithrombotic too)

A

NO, PGI2, EDHF.

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2
Q

Four vasoconstrictory/prothrombotic substances?

A

ET-1, ATII, oxidants, TXA2

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3
Q

What counts as significant FHx for IHD?

A

Before 55 (M) or 65 (F) in first degree relative.

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4
Q

Troponin T significance?

A

More specific to cardiac muscle, but can be influenced by other things e.g. sepsis/PE (that damage heart).

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5
Q

Rapid-rule out criteria for troponins?

A

Measure on admission; >99th URL; repeat after 3 hours; need >10ng/L change AND at least 20% change for possible ACS

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6
Q

What to do if (in hs-cTnT) TnTA <99th URL?

A

If pain <6 hours, do TnT 3; if 6 hours or more then non ACS.

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7
Q

First investigations in ACS?

A

Serum lipids, glucose, U&E, ECG. (Echo is second line)

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8
Q

ABPI below 0.9?

A

Indicates some PAD

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9
Q

Causes of hyperuricaemia?

A
  1. Increased production (diet, alcohol, TLS, lymphoma etc)

2. Decreased excretion (diuretics [thiazide/loop], CKD, genetics, HTN)

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10
Q

When to treat hyperuricaemia?

A

Only when symptomatic ie gout or have complications; use allopurinol.

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11
Q

Best and worst prognosis re ECG changes?

A

T wave inversion alone is best. ST elevation alone worst initially; ST depression higher at six months; ST elevation AND depression highest

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12
Q

What if ECG non-diagnostic in ACS?

A

Repeat in 30 mins

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13
Q

When does Tn become detectable in ACS?

A

After 3 hours.

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14
Q

ABCDE of post ACS discharge?

A 
A = antiplatelets and ACEI
B = B blockers and BP
C = cholesterol and cigarettes
D = diet and diabetes
E = education and exercise
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15
Q

When not to give fondaparinux in ACS?

A

High bleeding risk or angiography planned in next 24 hours

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16
Q

Angiography timescale?

A

In 90 hours, unless contraindicated, or unstable/high risk/STEMI (STAT)

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17
Q

Drugs that can cause/exacerbate HTN?

A

Cocaine, amphetamines, oral contraceptives, sympathomimetics (e.g. decongestants with phenylephrine), NSAIDs, systemic steroids (mineral/gluco), erythropoeitin, cyclosporin

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18
Q

BP and CO/PVR?

A

Either one or the other must be elevated to raise BP

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19
Q

Five factors that promote vascular hypertrophy and vasoconstriction?

A

Insulin, catecholamines, angiotensin,endothelin, GH (ie explains why acromegaly is a secondary cause of HTN)

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20
Q

Genetics and HTN?

A

Western black more predisposed, higher BP and mortality. Probably polygenic

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21
Q

HTN and sex?

A

HTN less common in premenopausal women than me (therefore hormones likely involved) but oestrogen/COC/HRT increases HTN?

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22
Q

Renin levels in essential HTN?

A

May be high; usually normal/low because of negative feedback

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23
Q

Insulin resistance and HTN?

A

Clear association, particularly in obese. Insulin is a pressor agent and increases levels of cataecholamines and renal sodium reabsorption

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24
Q

Endothelial dysfunction and HTN?

A

Reduced vasodilatory responses to NO?

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25
Q

ANS and HTN?

A

Increases SNS drive (particularly a feature in young HTNsives) will stimulated renin production, constrict arterioles and veins and increease CO.

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26
Q

Effects of angiotensin II?

A
  1. Increased sympathetic activity
  2. Increased tubular Na/Cl reabsorption, H20 retention, K+ excretion
  3. Increased aldosterone secretion
  4. Increased arterial vasoconstriction
  5. ADH release and therefore water retention.
    (Net effect is increased circulating volume and therefore better perfusion so renin production should be reduced)
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27
Q

Renal contributions to BP control?

A

RAAS, medullipin (potent vasodilator; reduced levels in renal disease), renalase (metabolises circulating catecholamines)

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28
Q

Genetic links with phaeochromocytoma?

A

VHL, MEN2 (A and B), RET.

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29
Q

Investigating phaeohromocytoma?

A

Plasma mets and/or urinary mets/catecholamines to screen; need CT/MRI of head/neck/chest/abdomen to locaise. Rule out other causes. Usually do surgical resection.

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30
Q

Suspect Conn’s syndrome?

A

Low K+ and HTN and not on diuretic.

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31
Q

Causes of Conn’s?

A

2/3 is bilateral adrenal hyperplasia; 1/3 adrenal adeoma; rarely get adrenal malignancy or familial hyperaldosteronism.

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32
Q

Renin in primary vs secondary hyperaldosteronism?

A

Low in primary; increased in secondary because cardiac output usually low.

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33
Q

Genetics of adrenal adenoma (1/3 Conn’s)

A

40% have single genetic mutation (KCNJ5)

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34
Q

Screening Conn’s?

A

Screening considered in high BP with low K+, treatment resistant HTN, family members with condition, or adrenal mass. Measure aldosterone and do A:R.

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35
Q

Diagnosing Conn’s?

A

Do saline suppression/ambulatory salt loading test/fludrocortisone suppression test. Then image (CT); may need to have adrenal venous sampling to clarify if unilateral or bilateral (uni = adenoma therefore surgery; bi = medical treatment with spironolactone)

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36
Q

Tests in Cushings?

A

Measure ACTH, check cortisol, MRI brain, dex. suppression

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37
Q

Liddle syndrome?

A

Rare AD condition with amiloride-sensitive ENac hyperacitivity; get HTN, low K+, high HC03-, met alkalosis, low PRA and aldosterone

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38
Q

Difference in bloods between Liddle’s and Conn’s?

A

Liddle’s has low renin and aldosterone; Conn’s just low renin.

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39
Q

3 types of mineralocorticoid HTN?

A
  1. Conn’s = excess MR ligand
  2. Apparent mineralocoricoid excess (11bHSD2 defect)
  3. Liddle syndrome
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40
Q

Apparent mineralocorticoid excess? (RENIN SHOULD ALWAYS BE LOW; IF NORMAL THEN ALTERNATE DIAGNOSIS)

A

HTN due to genetic 11bHSD2 mutation; cannot transform cortisol to cortisone so get MR activation. Get low renin and aldosterone (-ve FB) Hypernanatraemia, hypokalaemia, HTN.

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41
Q

Diagnosis of AME?

A

Low renin, low aldosterone (as with Liddle) and high cortisol:cortisone

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42
Q

Diagnosis of Liddle?

A

Low renin, low aldosterone (or normal), normal cortisol:cortisone, then do genetics

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43
Q

Bloods in Conn’s?

A

High Na+, low K+, high HC032- = HYPERNATRAEMIC, HYPOKALAEMIC MET ALKALOSIS

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44
Q

Why do radiofemoral delay in HTN exam?

A

Coarctation of the aorta can cause HTN?

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45
Q

AD PKD?

A

Potentially lethal monogenic disorder. Large (ballotable) kidneys. High risk of CKD. Diagnosed usually with US/CT/MRI; can go genetic testing in some cases. Get increased SNS activity and HTN

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46
Q

Investigating HTN?

A

Exam, FBC, BP lying/standing/each arm, end organ damage (U+E, protein creatinine ration, ECG [LVH] fundoscopy), cholesterol/DM/BMI

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47
Q

Investigating HTN (2)

A

CXR, echo, plasma/urinary mets, renin-aldosterone ratio, renal US (polycystic/renal artery stenosis), MR angio (suspected renal artery stenosis), cortisol

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48
Q

Best Ix for renal artery stenosis?

A

MR angiography

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49
Q

DD renal artery stenosis?

A

Fibromuscular dysplasia; young women with severe HTN

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50
Q

Renal US in HTN?

A

Excludes polycystic kidneys and single shrunken kidney (could be renal artery stenosis)

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51
Q

Stage 1 HTN?

A

Clinic >140/90 AND ABMP/HBPM mean >135/85. Do not treat; lifestyle; arrange 24 hour monitor.

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52
Q

Stage 2 HTN?

A

Clinic >160/100 AND ABPM/HBPM mean > 150/95. Need speedyish 24 hour monitor, can treat.

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53
Q

Severe HTN?

A

Clinic >180 or diastolic >110; treat/admit urgently.

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54
Q

White coat HTN?

A

BP >/_ 149/90 in clinic, normal daytime mean <135/85. Does not mean normal risk!

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55
Q

Four principle checks of end-organ damage?

A

Urine (protein), blood (glucose, U&E, cholesterol), fundi, 12 lead ECG.

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56
Q

QRISK2?

A

Risk of MI/CVA in next 10 years (not for people with history of these)

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57
Q

“Severe” WCHTN?

A

White coat will never push BP to very high levels

58
Q

Why might stenting not help in renal artery stenosis?

A

Microvasculature of kidney already disrupted

59
Q

Na in Conn’s?

A

Usually normal

60
Q

Compliance in HTN meds?

A

Often poor as most patients symptomatic; can check urine levels of drugs and re-educate/show risk scores etc.

61
Q

Efficacy of CT in ?CVA?

A

Preferably done within 1 hour to exclude ICH; often normal before 12 hours in ischaemic. Beyond 2-3 weeks, cannot differentiate between the two.

62
Q

Delayed presentation CVA imaging?

A

Need MRI; can detect haemosiderin deposits years later

63
Q

When is MRI best in CVA?

A

Delayed presentation, or cerebellar/brainstem/posterior fossa indications? Really, is better for all but time pressure and metalwork

64
Q

Who needs angiography in CVA?

A

Those being assessed for hyperacute treatment (thrombolysis, intra arterial clot retrieval). CTA usually. Would have started on thrombolytics as soon as ICH excluded.

65
Q

Three early signs of cerebral infarct?

A

Loss of grey/white matter differentiation, loss of insular ribbon, loss of definition of lentiform nucleus

66
Q

Use of MRI DWI sequence in CVA?

A

Can show ischaemia as it happens; CT is delayed by hours. Useful to exclude possible non organic weakness before thrombolysis.

67
Q

Salt sensitivity HTN?

A

Some people can effectively excrete high salt diet while maintaining BP; others cannot (ie salt sensitive). Normally, raised MAP means more excretion of salt/water until blood volume reduced. If SS (arteriopathy/ischaemia/renal damage/genetic) then this curve is shifted further “up”.

68
Q

ANS and BP?

A
  1. Some HTN patients show greater vasoconstrictor response to NE than controls. 2. Angiotensin II mediated resetting of baroreceptors.
  2. Repeated stress = more SNS = vascular hypertrophy and increased PVR/BP.
69
Q

How does aberrant RAAS activation cause HTN?

A

Get remodelliing of pressure vessels, damage to renal microvasculature so less water excretion.

70
Q

How does endothelial dysfunction cause HTN?

A

Balance between constrict and dilate disrupted. Also, get activation and damage of e’thelium causing changes in tone/reactivity/clotting. Get increased inactivation of NO (by ROS). Endothelin levels are increased in some HTN patients.

71
Q

Persistently high Tns?

A

Suggests non-ischaemic process

72
Q

Raised Tn unrelated to ACS?

A
  1. Sepsis/SIRS
  2. PE (RV damaged in acute dilatation; indicates poorer outcomes).
  3. AHF/CHF. Rises with severity of HF. Myocyte loss then aggravates HF.
  4. Strenuous exercise
  5. Peri/myocarditis
  6. Cardiotoxic chemotherapy
  7. Defib/DC cardioversion/ablation
  8. Post heart transplant
  9. Myocardial contusion (blunt chest trauma)
  10. End stage renal disease
73
Q

Why do TFTs when starting statin?

A

Hypothyroid linked to raise cholesterol; also more likely to get statin-related myopathy if hypothyroid.

74
Q

At what point is carotid endarterectomy indicated?

A

Advised if stenosis >50% and symptomatic; consider if asymptomatic and 60-99%. 3% risk of stroke in surgery. Can stent (CAS) if unsuitable for CEA (medically/anatomically) but not recommended for asymptomatic patients.

75
Q

T wave inversion?

A

Can indicate ongoing ischaemia (not necessarily with necrosis) or previous cardiac event. If infarct is not full thickness, see T wave inversion but no pathological Q waves (subendocardial infarction).

76
Q

Non-laboratory indications of MI?

A

Chest pain etc. ECG showing ST changes, new LBBB, pathological Q waves, echo evidence of loss of viable myocardium or new RWMA.

77
Q

Cholesterol targets with statin?

A

LDL under 2, non-HDl under 2.5

78
Q

Core drugs post MI?

A

Aspirin, B blockers, statins, ACEI

79
Q

When to consider FHC?

A

TC >7.5, FHx of premature CAD.

80
Q

Weight loss and gout?

A

During RAPID weight loss, at increased risk of gout.

81
Q

NSAIDs and CVD drugs?

A

Antagonise ACEI/antiplatelets etc.

82
Q

What if one troponin is rising and another is not?

A

Indicates probably non cardiac ie ectopic expression of troponins as should parallel each other!

83
Q

When use digoxin for rate control?

A

When other drugs are contraindicated!

84
Q

Most common cause of syncope in HCM?

A

Still vasovagal; more prone to VT/VF but common things remain common!

85
Q

Typical LOC in cardiac syncope?

A

No prodrome whatsoever; just ‘trip’ and come round feeling fine, speedy recovery.

86
Q

Seizure activity in cardiac syncope?

A

May still occur, as with vasovagal

87
Q

Key red flags for cardiac syncope?

A

Personal history of cardiac disease and MALIGNANT SOUNDING FHx

88
Q

Family history of sudden death but autopsies normal?

A

Suggests microscopic disease e.g. channelopathy rather than HCM etc.

89
Q

Sudden death after loud noises?

A

Associated with long QT strongly!

90
Q

Black out with swimming (diving), exercise, or startle reflex?

A

LQTS!

91
Q

Black out with pain, stress, adrenaline?

A

CPVT in children teens (catecholaminergic polymorphic ventricular tachycardia); DD vasovagal!

92
Q

Carotid sinus hypersensitivity?

A

Occurs in elderly; a sign of carotid artery disease (usually men, over 50, HTN and atherosclerosis). Manual pressure on carotid e.g. shaving, tight collar; get asystole/marked bradycardia/hypotension. Can recreate with carotid sinus massage; usually get some bradycardia. Treatable with pacemakers. Can be problematic if old/alcoholic/on warfarin.

93
Q

Diagnosing carotid sinus hypersensitivity syndrome?

A

Carotid sinus massage; symptomatic (pre) syncope or marked bradycardia is diagnostic.

94
Q

Q waves can be?

A

Normal or sign of old MI

95
Q

Pathology of long QT?

A

Genetic defect (‘channelopathy’) leads to confusion/delay/misfiring that predisposes to torsade de pointes. Essentially electrical turbulence causing delayed repolarisation so QTi (interval) prolongs. Many types e.g. LQT1/2/3/. Get syncope (no prodrome), seizures and death.

96
Q

LQTS and drugs?

A

Can be complicated by using anti-arrhythmics which prolong repolarisation e.g. class III action.

97
Q

Torsade de pointes?

A

A type of polymorphic VT. Used to kill people with complete heart block before had pacemakers. 50% of CHB die of HF, 50% of polymorphic VT. Torsade de pointes is a syndrome of bradycardia, long QTi and “twists”. Can also be caused by QT prolonging drugs e.g. antifungals.

98
Q

Hypetrophic cardiomyopathy?

A

Hypertophic alters the ‘grain’ of the myocardium, ‘tangled’ like rocks in a river. Get turbulence (regional differences); all caused by mutations in sarcomeres, leading to myocyte hypertrophy and myocardial disarray. Lose cavity space due to muscle overgrowth; gets worse with exercise. AD. Leading cause of cardiac sudden death in athletes.

99
Q

What is ARVC?

A

Arrhythmogenic right ventricular cardiomyopathy get clusters of fat and fibrous tissue between cells, leading to non-conducting areas. Fat encroaches onto ventrcicle and appears moth eaten. Thin walled RV. Due to weakened connecting proteins in response to STRETCH (mostly in RV) and worsens with exercise! hence athletes. Tends to get mix of monomorphic VT and VF. AD. A type of non-ischaemic myopathy.

100
Q

What is dilated cardiomyopathy?

A

Can be idiopathic (vast majority), haemochromatosis, chemotherapy, alcohol, excess adrenaline, pregnancy. Chamber dilates and forms scars. Can often be due to MI; combination of scar plus neuroendocrine (RAAS) response to chronic heart failure (ACE, adrenaline and aldosterone to blame)

101
Q

Gadolinium MRI of dilated cardiomyopathy?

A

See late gadolinium enhancement; can be picked up very early (scar).

102
Q

What is the aim of ablation in heart muscle?

A

Aim is to convert damaged low-voltage tissue to dead tissue; the dead stuff is relatively safe compared to the damaged stuff.

103
Q

ICD in cardiomyopathy?

A

Scar is bad for heart; if so bad that LVEF <30% get ICD in case of VT/VF (as HF predisposes to these)

104
Q

WPW ECG?

A

Delta waves (slurred upstroke on QRS) along with short PT interval. Usually have long QRS too.

105
Q

Clinical features of WPW?

A

Young, sudden onset/offset of palpitations; eventually were longer and had syncope. Get SVT. Can kill young men.

106
Q

Diagnosing WPW?

A

ECG! Echo can evaluate LV function and exclude cardiomyopathy. Can do stress testing.

107
Q

Where is T wave inversion allowed to?

A

V1-V2 in Caucasian, and to V3 in Afro-Caribbean. If V2 is, V1 must be! And AvR

108
Q

What is an epsilon wave?

A

Upstroke buried in end of QRS; characteristic of ARVC

109
Q

ECG findings in ARVC?

A

RBBB, epsilon waves, T wave inversion to at least V3!

110
Q

ARVC features?

A

Classically sportsmen, Italian. Causes polymorphic VT and VF. AD. Present with syncope and dyspnoea.

111
Q

Drugs that can cause LQT?

A

Amiodarone, TCAs, Abx, antifungals, haloperidol, SSRIs, quinidine

112
Q

Brugada syndrome?

A

Na+ channelopathy. Cove type ST elevation in V1 and V2. Causes sudden death, in young men, in the middle of the night. Fit ICD. High incidence in Southeast Asia.

113
Q

Brugada type II?

A

Heterozygous for gene. Less risk for sudden death, do not need ICD but implications for family. See mild ECG changes; give flecainide/atropine to induce BRUGADA PROPER. These drugs block Na+ channel. High temperature can also cause Brugada to manifest.

114
Q

Catecholaminergic polymorphic VT? (CPVT)

A

Usually presents in childhood; get runs of polymorphic VT with to-and-fro ectopic. Due to calcium channelopathy. Get syncope when exercised or acute emotion. VT can swiftly turn to VF and die. Diagnosed with exercise stress test (usually normal at rest and heart structurally normal).

115
Q

ApoB lipoproteins and CHD?

A

Enter subendothelium; most leave, but if damaged area then are retained and inflame and activate other cells; attracts monocytes which mature to macrophages then soak up lipid to become foam cells to from plaque base. Then get necrosis of plaque, forming cholesterol crystals which are irritant, get bleeding and fissues causing platelet aggregation and occlusion. Process accelerates by elevated circulating lipid, smoking/DM (damages endo)

116
Q

Why must you fast for LDL-C calculation?

A

Don’t directly measure, but calculate levels based on constant ratio of cholesterol:TG in VLDL which means no chylomicrons in blood which means fasting! Much more common to just measure non-HDL (don’t need to fast).

117
Q

Use of LDL-C and non-HDL-C?

A

LDL-C used for diagnosing familial hypercholesterolaemia; non-HDL-C used to measure response to treatment and more convenient. (TC - HDL-C = non-HDL-C). Non-HDL = atherogenic!

118
Q

Measuring apolipoproteins?

A

Are actually the carriers of lipid in the lipoprotei.

  1. A1 is ‘good’ because main component of HDL. ApoA1 levels correlate with HDL.
  2. ApoB is used for all the others; one copy (B100) in LDL, IDL ,VLDL; truncated form (B48) in chylomicrons and their remnants
119
Q

Secondary causes of dyslipidaemias?

A

DM, hypothyroidism, alcohol excess, obesity, CRF, nephrotic syndrome, cholestasis, gout, pregnancy, anorexia nervosa, hypopituitarism. And many drugs. Must rule these out with U&E, LFT, TFT, HbA1c, urinalysis.

120
Q

Why does myeloma cause hypercholesterolaemia?

A

Light chains bind to LDL-R on liver which means they cannot be removed!

121
Q

Familial hypercholesterolaemia?

A

1/250. LDL-R/APOB/PCSK9 mutations means receptor-mediated clearance of LDL impaired. Autosomal co-dominant. Usually no signs; get tendon xanthomas and corneal arcus; homozygotes get cutaneous xanthomas, aortic stenosis. Very high CHD risk (50% men symptomatic by age 50)

122
Q

Polygenic hypercholesterolaemia?

A

Problematic versions of ~12 cholesterol regulating genes; not directly inherited. 1/20.

123
Q

Familial lipoprotein lipase deficiency and familial apolipoprotien CII def?

A

Very rare causes of primary hypertriglyceridaemia; 1/1000,000. Get recurrent pancreatitis from childhood.

124
Q

Two types of combined hyperlipidaemia?

A

Familial combined hyperlipidaemia (1/100) and familial type III remnant hyperlipidaemia (less common).

125
Q

Familial hypercholesterolaemia biochemistry?

A

Raised LDL-C (*2), TC 9-12, low/normal fasting TG. If homozygotes get TC 25-30.

126
Q

Diagnosing FH?

A
  1. Biochem (TC >7.5, LDL-C >5)
  2. Signs e.g. tendon xanthomas personally or in family
  3. DNA evidence of LDL-R/ApoB100/PCSK9 mut
  4. FHx of early CHD
  5. FHx of raised cholesterol
127
Q

LDL-C in FH?

A

Doubles!

128
Q

Familial combined hyperlipidaemia (FCH)?

A

Often mistaken for FH but has high triglycerides (primary). DD FH with secondary triglyceridaemia so exclude. Mechanism is excess (but normal) VLDL and apoB; multigenic. Physical signs non-specific; may see xanthelasma. High CHD risk. Often features of metabolic syndrome.

129
Q

Familial combined hyperlipidaemia (FCH)

A

Raised LDL-C and/or TG (not raised in FH).

130
Q

When to suspect FCH?

A

Moderate-severe mixed hyperlipidaemia, FHx premature CHD.

131
Q

Remnant (III) hyperlipidaemia? aka Familial Dysbetalipoproteinaemia?

A

Reduction in receptor-mediated remnant clearance; homozygous ApoE2 (substrate on chylomicron remnant). Can get extremely high TC (>20) and TG (TC higher). Lower ration of n-HDL-C:ApoB because particles responsible are so big that there are less of them. See striate palmar/palmar xanthomas (streaks on palms), or eruption xanthomata (yellow crops on elbows/knees). MASSIVE RISK OF CAD AND CVA AND PVD

132
Q

Which primary dyslipidaemia is most associated with low HDL-C?

A

FCH

133
Q

Apo B levels in FH/FCH/TIII?

A

B increased in FH and FCH, normal in TIII because have big remnant particules

134
Q

Familial hypertriglyceridaemia?

A

TC may be normal; TG can be up to 100! Not assoc. with CVD really but with DM and pancreatitis! Genes involved with VLDL handling (TG-rich). Multigenic have TG 2-10; monogenic have 10-15.

135
Q

What is secondary hyperlipidaemia?

A

Caused by system disorder other than lipid transport

136
Q

What do FH and type III hyperlipidaemia cause?

A

Severe early onset atherosclerosis. FCH still high but lower risk, and ones with triglycerides less so

137
Q

FCH vs FH?

A

Usually less severe, but much more common and linked to other risk factors such as HTN, obesity and DM.

138
Q

People not to use Q-RISK on?

A

People at very high risk due to FH/FCH etc, or people with existing CVD/ESRD/T1DM/over 85s (as all will have high risk).

139
Q

When might Q-RISK underestimate risk?

A

If on meds that lower BP, if on drugs that alter lipids, if have AI disease, mental health problems etc.

140
Q

Non-ACS causes of raised Tn?

A

Sepsis, PE, AHF/CHF, strenuous exercise, pericarditis or myocarditis, cardiotoxic chemo, defib/DC cardioverson/ablation, infiltrative disease e.g. amyloidosis, post-transplant, myocardial contusions, ESRD

CSIM2 (21 decks)

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