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NMSKI > Hypertension and Myocardial Infarction > Flashcards

Hypertension and Myocardial Infarction Flashcards

1
Q

how many litres of blood are pumped each day

A

6000L

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2
Q

composition of blood vessel walls

A

tunica intima, tunica media and

adventitia

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3
Q

risk factors for hypertension

A

Stroke
Cardiac disease
Renal disease

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4
Q

BP in systolic and diastolic state that constitutes as hypertension

A

systolic BP > 140mm Hg

diastolic BP > 90mm Hg

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5
Q

classification of hypertension

A

95% essential - idiopathic

5% secondary - underlying identifiable cause

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6
Q

what %age of hypertension is malignant

A

5% rapidly rising BP that leads to death in 1-2 years if untreated

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7
Q

how is malignant hypertension characterised

A 
high BP (200/120mm Hg) with renal failure & retinal haemorrhage +/-
papilloedema
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8
Q

secondary hypertension

A

Renal
Endocrine
CVS
Neurologic

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9
Q

conditions that cause renal hypertension

A

(polycystic disease, renal artery
stenosis, vasculitis, renovascular
disease.)

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10
Q

conditions that cause endocrine hypertension

A

(phaeochromocytoma,
Cushing’s, acromegaly, Conn’s
syndrome)

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11
Q

conditions that cause CVS hypertension

A

(coarctation aorta, increased

intravascular volume etc.)

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12
Q

conditions that cause neurologic hypertension

A

(acute stress, increased

intracranial pressure)

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13
Q

renin-angiotensin aldosterone system

A

angiotensinogen released from liver and combines w/ renin from kidney
converted to angiotensin I
angiotensin converting enzyme from lungs and renal endothelium converts Angiotensin I to Angiotensin II
Inc. SNS activity
Inc. Na+, Cl-, H2O reabsorption and K excretion
Inc. Aldosterone secretion from kidney
arteriolar vasoconstriction inc. BP
Inc. ADH secretion

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14
Q

cardiac output

A

heart rate x stroke volume

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15
Q

blood pressure

A

Cardiac output x Peripheral

resistance

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16
Q

peripheral resistance

A

to resistance to blood flow at the level of the arterioles – this will increase due to vasocontraction

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17
Q

what does kidney responds to and how

A

hypertension by eliminating salt & water

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18
Q

what may initiate essential hypertension

A

reduced renal sodium excretion

leads to increased fluid volume and cardiac output

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19
Q

what triggers renin-angiotensin aldosterone system

A

low blood pressure
low renin
low Na and Cl

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20
Q

causes of secondary hypertension

A

mineralocorticoid excess

corticosteroid excess

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21
Q

mineralocorticoid

A

type of steroid hormone that regulate salt and water retention in blood

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22
Q

example of mineralocorticoid

A

aldosterone

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23
Q

causes of mineralocorticoid excess

A

aldosterone producing adenoma
bilateral adrenal hyperplasia
aldosterone adrenal carcinoma
ectopic aldosterone secretion

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24
Q

cortisol

A

stress hormone
inc. blood sugar levels,
increase use of glucose etc

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25
causes of corticosteroid excess
exogenous or endogenous increase in cortisol cushing disease hypertension
26
cushing disease
``` pituitary tumour leading to excessive production of ACTH (adrenocorticotropic hormone). – Excessive ACTH stimulates the adrenal cortex to produce high levels of cortisol ```
27
cushing syndrome symptoms
weight gain glucose intolerance moon face acne
28
cause of cushing syndrome
adrenal gland tumours, adrenal hyperplasia, ectopic/paraneoplastic
29
acromegaly
growth hormone excess pituitary gland produces too much growth hormone during adulthood expansion of extracellular fluid volume & increased peripheral vascular resistance
30
catecholamines examples
– epinephrine | and norepinephrine
31
what response are catecholamines involved in
fight of flight response
32
epinephrine | and norepinephrine cause
increase heart rate, | vasoconstriction
33
Phaeochromocytoma
Tumors of Chromaffin tissue of adrenal medulla
34
Paraganglioma
Tumors of Chromaffin tissue of extra adrenal medulla
35
symptoms of Paraganglioma and Phaeochromocytoma
can be functioning or non functioning - may or may not release catecholamines symptoms can vary from asymptomatic to hypertension
36
management of excess catecholamines
Initial management relies upon blockade by medications (alpha and beta blockers)
37
symptpms of thyrotoxicosis
Increased contractile activity of heart increased stroke volume • Increased sympathetic activity -> vasocontraction • Increased angiotensinogen levels • Increased systolic BP
38
symptoms of hypothyroidism
* Impaired endothelial function (in the tunica intima) * Increased vascular resistance * Extracellular volume expansion * Increased diastolic blood pressure
39
causes of hypertension
sleep apnoea syndrome | oral contraceptive use
40
vascular effects of hypertension
Accelerates atherosclerosis • hardening of arteries • Cause degenerative effects in vessel wall leading to dissection • Small vessel disease: hyaline arteriolosclerosis and hyperplastic arteriolosclerosis
41
left sided cardiac effects of hypertension
concentric left ventricular hypertrophy (weight ~ 500g, LV > 1.5cm). Response to systemic hypertension.
42
right sided cardiac effects of hypertension
right ventricular hypertrophy caused by disorders of pulmonary vasculature causing pulmonary hypertension.
43
end organ effects of hypertension
``` Due to ↓ blood flow or rupture of artery/arteriole • Stroke • Heart failure • Angina/MI • Retinopathy • Aortic dissection • Renal failure • Peripheral vascular disease ```
44
arteries that supply blood to the heart
left anterior descending artery left circumflex artery right coronary artery
45
ischaemia
• Imbalance between supply (perfusion) and | demand of oxygenated blood to a tissue
46
ischaemia is characterised by
insufficient O2 and nutrients and inadequate removal of metabolites
47
difference between ischaemia and infarction
Ischaemia - reduced oxygenation of tissue. | • Infarction - necrotic tissue due to Ischaemia
48
modifiable risk factors for ischaemic heart disease
``` Hypertension Smoking Diabetes Hyperlipidaemia Obesity ```
49
non-modifiable risk factors for ischaemic heart disease
Family history Genetics Age Sex
50
clinical manifestation of ischaemic heart disease
``` Angina pectoris (stable and unstable) • Myocardial infarction • Non- STEMI • STEMI • Chronic IHD with heart failure • Sudden cardiac death ```
51
what cells respond to atherosclerotic plaque in blood vessels
macrophages macrophage derived foam cells CD4+T cells infiltrate lipid core
52
what cells respond to ruptured lining of blood vessel due to plaque build up
platelets
53
stable angina
fixed luminal narrowing with reduced distal perfusion lack of oxygen and build up of metabolites = chest pain
54
unstable angina
sudden change in atherosclerotic plaque = severe and transient reduction in coronary blood flow
55
acute coronary syndrome
Unstable angina, acute Myocardial Infarction (MI) and sudden death Ischaemia due to abrupt plaque change (rupture, erosion, haemorrhage) with superimposed thrombus
56
Myocardial Infarction - MI
Sudden change in plaque morphology • Platelets aggregate and adhere to plaque • Vasospasm occurs • Coagulation pathway activated • Thrombus develops on atheromatous plaque and evolves to occlude lumen
57
Symptoms of myocardial infarction
* Chest pain +/- arm pain * Short of breath * Sweaty * Dizzy * Rapid, weak pulse * “silent”- elderly, diabetics
58
how is myocardial diagnosed
History • ECG changes • Cardiac enzymes (troponin, CK-MB, LDH)
59
myocardial changes that occur in first 12 hours of MI
some haemorrhage
60
myocardial changes that occur in 12-24 hours of MI
necrosis and acute inflammation
61
myocardial changes that occur in 1-3 days of MI
more necrosis and neutrophils
62
myocardial changes that occur in 3-7 days of MI
disintegration of myocytes and macrophages
63
myocardial changes that occur in 7-10 days of MI
granulation tissue
64
myocardial changes that occur after 10 days of MI
early scar formation
65
complications of myocardial infarction
* Heart failure (acute, chronic) * Arrhythmias * Rupture (wall, septum, papillary muscle) * Pericarditis * Ventricular aneurysm * Mural thrombus
66
prevention of MI
* Stop smoking * Control BP * Reduce cholesterol & weight * Control of diabetes
67
Treatment of MI
* Medication * Thrombolysis * Percutaneous Coronary Angioplasty and stents * CABG

NMSKI (38 decks)

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