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cardiovascular diseases 1 Flashcards

1
Q

what factors reduce blood supply to the myocardium resulting in ischameia

A

reduced coronary flow
myocardial hypertrophy
vasculitis, amyloid deposition, coronary artery dissection.

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2
Q

pathogenesis if acute and chronic ischameia.

A

auto-regulation of coronary blood flow which breakdown in occlusion.
low diastolic flow- especially subendocardial.
Active aerobic metabolism of cardiac muscle- reduced
Myocytes dysfunction and eventually will lead to cell death.

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3
Q

what is the time frame for recovery via repercussion of a oxygen starved heart

A

15-20 mins

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4
Q

4 common ischaemic heart disease syndromes

A

angina pectoris
acute coronary syndrome
sudden cardiac death
chronic ischaemic heart disease

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5
Q

3 types of angina pectoris

A

typical/stable- luminal narrowing and manifestation upon stress.

Crescendo/unstable plaque- disrupted so thrombus or emboli form, resulting in pain in an uncontrollable fashion.

Variant/prinmetal- fixed obstruction but effects are not predictable.

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6
Q

what is shown on an ECG in acute coronary syndrome

A

ST elevation

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7
Q

what are the main factors resulting in acute ischaemia

A 
atheroma and thrombosis.
lipid rich plaques.
Transmural MI
Thrombolysis
Myocardial stunning- contractility of the heart is abnormal
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8
Q

how is acute iscahemia diagnosed

A

ECG, cardiac proteins

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9
Q

what are the 3 categories of MI

A

transmural
subendocardial
regional

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10
Q

pathogenesis of a subendocardial MI

A

At the surface the epicardial has a direct supply of blood and the endocardial has a supply of blood from smaller infiltrating arteries and diffusion, however the space in-between is poorly perfused (subendocardial region)

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11
Q

what 2 factors cause the subendocardial to infarct

A

Stable athermanous occlusion of the coronary circulation

An acute hypotensive episode

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12
Q

what are the main blood markers of myocytes damage and which ones are used rottenly in clinic

A

Raised Troponin-most common measure- detectable from 3 hrs and peaks at 12hrs- present for unto 7 days.

Creatine Kinase
detectable from 2-3hrs and parks between 10-24hrs- present for 3 days, 3 subtypes

Myoglobin peak at 2hrs

LDH peaks at 3 days and is detectable for 14 days

Aspartate transminase

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13
Q

what conditions is troponin raised in excluding MI

A

pulmonary embolism, heart failure, & myocarditis.

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14
Q

what damage does creatinine kinase show excluding MI

A

skeletal muscle damage

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15
Q

what damage does myoglobin show excluding MI

A

skeletal muscle damage

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16
Q

what damage does aspartate transaminase show excluding MI

A

liver damage

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17
Q

what is the mechanism of action of troponin.

A

binds to actin to prevent contraction,

Ca2+ ions allow troponin to release tropomyosin and therefore bind to actin.

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18
Q

most common prognosis post MI

A

cardiac death within 1-2 hrs.

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19
Q

complications of MI

A

Arrhythmias, ventricular fibrillation, Ischaemic pain, Left ventricular failure, shock, pericarditis, cardiac mural thrombus or emboli, DVT, PE, myocardial rupture, ventricular aneurysm, autoimmune pericarditis (dressler’s syndrome), pleurisy, ventricular wall rupture, infarct extension, haemopericardium, mural thrombus.

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20
Q

define mural thrombus

A

layers of organised fibrin in the wall of the myocardium, which are unstable and can dislodge into circulation.

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21
Q

what cause chronic ischaemic heart disease

A

Coronary artery atheroma produces relative myocardial ischemia & angina pectoris on exertion

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22
Q

what type of genetic defect is familial hypercholesterolemia

A

autosomal dominant.

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23
Q

commonest gene mutations familial hypercholesterolemia

A

Low density lipoprotein receptor gene

Apolipoprotein B

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24
Q

what is the difference between homozygous and heterozygous familial hypercholesterolaemia
and which has a better prognosis

A
  • Homozygous- no functioning liver LDL receptors.
  • Heterozygotes – Still have some functioning liver LDL receptors

heterozygous has a better prognosis.

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25
symptoms of familial hypercholesterolaemia
xanthomas- tendons, perioccular, corneal arcus | atheroslerosis
26
treatment of familial hypercholesterolaemia
statins | Treatment of homozygotes is more complex and less effective
27
what is classed as abnormally high blood pressure
140/90
28
what are the 2 types of hypertension and which is more common
primary and secondary hypertension.
29
what are the main causes of primary hypertension (congenital)
``` cardiac baroreceptors don't function. RAS breakdown kinin-kallikrekin system breakdown Naturetic peptides adrenergic receptor system autocrine factor produced by blood vessels autonomic nervous system. ```
30
pathogenesis of all primary hypotension involves a increased net balance of what chemical/food
salt.
31
pathogenesis of primary hypertension
increased intravascular volume due to renal salt absorption, increased cardiac output. tissue perfusion exceeds metabolic demands, leading to auto-regulation of bloodflow in tissues. this results in steady state haemodynamic pattern of elevated blood pressure with increased systemic vascular resistance and normal cardiac output.
32
Renal causes of secondary hypertension.
``` – Acute glomerulonephritis – Chronic renal disease – Polycystic kidneys – Renal artery stenosis – Renal artery fibromuscular dysplasia – Renal vasculitis – Renin – producing tumour ```
33
Endocrine causes of secondary hypertension
– Adrenocortical hormones (Cushing syndrome, primary aldosteronism, congenital adrenal hyperplasia, liquorice ingestion) – Exogenous chemicals (glucocorticoids, oestrogen including pregnancy and oral contraceptives, monoamine oxidase inhibitors, amphetamines, cocaine) – Phaeochromocytoma – Acromegaly – Hypothyroidism – Hyperthyroidism – Pregnancy – preeclampsia if severe
34
cardiovascular causes of secondary hypertension
– Coarctation of the aorta – Polyarteritis nodosa – Increased intravascular volume – Increased cardiac output
35
when is the renin angiotensin system activated, when BP is low or high.
BP is low
36
where is renin synthesised
juxtaglomerular apparatus in the wall of the afferent arterioles of the kidney
37
what is the function of renin
cleaves angitensinogen to angiotensin 1.
38
in which organ is angiotensin I converted to angiotensin II
lungs
39
what is a major side effect of ACE inhibitors
chronic cough
40
main function of angiotensin II
Potent natural vasoconstrictor | stimulate aldosterone production.
41
main function of aldosterone
renal action cause sodium and water retention | circulating blood volume therefore increases
42
what are the consequences of renal artery stenosis
reduced blood pressure in the kidney Juxtaglomerular apparatus stimulated to produce renin Renin-angiotensin system stimulates adrenal cortex zona glomerulosa cells to produce aldosterone
43
define co-arctation of the aorta
Congenital narrowing of the aorta, usually distal to the origin of the left subclavian artery
44
how is coarctation of the aorta detected.
* Detected by difference in BP between the arms and legs- low BP in legs but normal in arms. * Characteristic chest X-ray
45
how is coarctation of the aorta treated
surgically correctable
46
what is conn's syndrome
excessive aldosterone secretion
47
what is the most common cause of conn's syndrome
adrenocortical adenoma
48
how is conn's syndrome diagnosed
CT scan of adrenals in presence of these metabolic abnormalities
49
what chemicals are retained and which chemicals are lost in Conn's syndrome
Renal sodium and water retention. | Potassium loss
50
what are the side effects of excessive potassium loss
Muscular weakness, cardiac arrhythmias, parasthaesesia, metabolic alkalosis
51
define phaechromocytoma
tumour of the adrenal medulla
52
common symptoms of phaechromocytoma
pallor, headaches, sweating, nervousness, hypertension
53
how is phaechromocytoma diagnosed
24hr urine collection for adrenaline metabolites
54
treatment for phaechromocytoma
remove adrenal medulla.
55
Cushing's disease.
Overproduction of cortisol by the adrenal cortex.
56
effects of cortisol overproduction
– Potentiating sympathetic nervous system activity. | – Mineralocorticoid action on the kidneys, thus causing hypertension.
57
Cause of Cushing's disease.
– Adrenocortical neoplasm usually an adenoma. – A pituitary adenoma --paraneoplastic effect of other neoplasms (particularly small cell lung carcinoma) producing adrenocorticotrophic hormone that stimulates the zona fasciculata cells of the adrenal cortex to produce cortisol
58
what 3 organs does hypertension severely effect
heart, renal and brain.
59
pathogenesis of hypertensive heart disease
– Systemic hypertension leads to increased left ventricular blood pressure – Initially left ventricular hypertrophy- recognized cause of cell death. – When the pressure is too great the left ventricle fails to pump blood at a normal rate and dilates.
60
what renal changes occur due to systemic hypertension
– Vascular changes- arterial intimal fibroelastosis, and hyaline arteriosclerosis. – Slow deterioration in renal function leading to chronic renal failure- due to damage and scarring in the intima.
61
what are the common conditions which occur in the brain due to hypertension
* Athermanous plaque can rupture.(intracerebral haemorrhage) * Berry aneurysm (inherited) of the Circle of Willis (subarachnoid haemorrhage) * Massive basal ganglia haemorrhage * Lacunar infarct.
62
define hypertensive crisis
rapid rise in BP (increased risk of stroke).
63
what blood pressure reading shows hypertensive crisis
BP 180/120mmHg
64
clinical signs of hypertensive crisis
* Renal failure * Retinal haemorrhages * acute hypertensive encephalopathy
65
what are the clinical symptoms of acute hypertensive encephlopathy
confusion, vomitting, convulsions, coma and death
66
what are the causes of pulmonary hypertension
loss of pulmonary vasculature- Chronic obstructive lung disease, pulmonary interstitial fibrosis, pulmonary emboli and thrombosis, under ventilated alveoli secondary to left ventricular failure Systemic to pulmonary artery shunting Primary or idiopathic
67
risk factors for cardiovascular disease
* Gender * Hypertension * Smoking * High blood cholesterol * Low blood high density lipoproteins * Diabetes * Sedentary lifestyle * Obesity – especially central obesity * High alcohol use * Ethnicity – south Asian
68
what study calculates an individual’s risk of cardiovascular disease based on assessment of multiple risk factors.
The Framingham Heart Study
69
risk assessment methods for cardiovascular disease include
* SCORE * QRISK2 * Joint British societies risk prediction charts.

Clinical Pathology (45 decks)

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