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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
Q

causes of corticosteroid excess

A

exogenous or endogenous increase in cortisol
cushing disease
hypertension

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26
Q

cushing disease

A 
pituitary
tumour leading to excessive
production of ACTH (adrenocorticotropic
hormone).
– Excessive ACTH stimulates the adrenal cortex
to produce high levels of cortisol
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27
Q

cushing syndrome symptoms

A

weight gain
glucose intolerance
moon face
acne

28
Q

cause of cushing syndrome

A

adrenal gland tumours,
adrenal hyperplasia,
ectopic/paraneoplastic

29
Q

acromegaly

A

growth hormone excess
pituitary gland
produces too much growth hormone during adulthood
expansion of extracellular fluid volume & increased
peripheral vascular resistance

30
Q

catecholamines examples

A

– epinephrine

and norepinephrine

31
Q

what response are catecholamines involved in

A

fight of flight response

32
Q

epinephrine

and norepinephrine cause

A

increase heart rate,

vasoconstriction

33
Q

Phaeochromocytoma

A

Tumors of Chromaffin tissue of adrenal medulla

34
Q

Paraganglioma

A

Tumors of Chromaffin tissue of extra adrenal medulla

35
Q

symptoms of Paraganglioma and Phaeochromocytoma

A

can be functioning or non functioning - may or may not release catecholamines
symptoms can vary from asymptomatic to hypertension

36
Q

management of excess catecholamines

A

Initial management relies upon
blockade by medications
(alpha and beta blockers)

37
Q

symptpms of thyrotoxicosis

A

Increased contractile activity of heart increased stroke volume
• Increased sympathetic activity -> vasocontraction
• Increased angiotensinogen levels
• Increased systolic BP

38
Q

symptoms of hypothyroidism

A
  • Impaired endothelial function (in the tunica intima)
  • Increased vascular resistance
  • Extracellular volume expansion
  • Increased diastolic blood pressure
39
Q

causes of hypertension

A

sleep apnoea syndrome

oral contraceptive use

40
Q

vascular effects of hypertension

A

Accelerates atherosclerosis
• hardening of arteries
• Cause degenerative effects in vessel wall
leading to dissection
• Small vessel disease: hyaline arteriolosclerosis
and hyperplastic arteriolosclerosis

41
Q

left sided cardiac effects of hypertension

A

concentric left ventricular
hypertrophy (weight ~ 500g, LV > 1.5cm).
Response to systemic hypertension.

42
Q

right sided cardiac effects of hypertension

A

right ventricular hypertrophy
caused by disorders of pulmonary vasculature
causing pulmonary hypertension.

43
Q

end organ effects of hypertension

A 
Due to ↓ blood flow or rupture of
artery/arteriole
• Stroke
• Heart failure
• Angina/MI
• Retinopathy
• Aortic dissection
• Renal failure
• Peripheral vascular disease
44
Q

arteries that supply blood to the heart

A

left anterior descending artery
left circumflex artery
right coronary artery

45
Q

ischaemia

A

• Imbalance between supply (perfusion) and

demand of oxygenated blood to a tissue

46
Q

ischaemia is characterised by

A

insufficient O2 and nutrients and inadequate removal of metabolites

47
Q

difference between ischaemia and infarction

A

Ischaemia - reduced oxygenation of tissue.

• Infarction - necrotic tissue due to Ischaemia

48
Q

modifiable risk factors for ischaemic heart disease

A 
Hypertension
Smoking
Diabetes
Hyperlipidaemia
Obesity
49
Q

non-modifiable risk factors for ischaemic heart disease

A

Family history
Genetics
Age
Sex

50
Q

clinical manifestation of ischaemic heart disease

A 
Angina pectoris (stable
and unstable)
• Myocardial infarction
• Non- STEMI
• STEMI
• Chronic IHD with heart
failure
• Sudden cardiac death
51
Q

what cells respond to atherosclerotic plaque in blood vessels

A

macrophages
macrophage derived foam cells
CD4+T cells infiltrate lipid core

52
Q

what cells respond to ruptured lining of blood vessel due to plaque build up

A

platelets

53
Q

stable angina

A

fixed luminal narrowing with
reduced distal perfusion
lack of oxygen and build up of metabolites = chest pain

54
Q

unstable angina

A

sudden change in
atherosclerotic plaque = severe and transient
reduction in coronary blood flow

55
Q

acute coronary syndrome

A

Unstable angina, acute Myocardial Infarction (MI) and sudden death
Ischaemia due to abrupt plaque change
(rupture, erosion, haemorrhage) with
superimposed thrombus

56
Q

Myocardial Infarction - MI

A

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
Q

Symptoms of myocardial infarction

A
  • Chest pain +/- arm pain
  • Short of breath
  • Sweaty
  • Dizzy
  • Rapid, weak pulse
  • “silent”- elderly, diabetics
58
Q

how is myocardial diagnosed

A

History
• ECG changes
• Cardiac enzymes (troponin, CK-MB, LDH)

59
Q

myocardial changes that occur in first 12 hours of MI

A

some haemorrhage

60
Q

myocardial changes that occur in 12-24 hours of MI

A

necrosis and acute inflammation

61
Q

myocardial changes that occur in 1-3 days of MI

A

more necrosis and neutrophils

62
Q

myocardial changes that occur in 3-7 days of MI

A

disintegration of myocytes and macrophages

63
Q

myocardial changes that occur in 7-10 days of MI

A

granulation tissue

64
Q

myocardial changes that occur after 10 days of MI

A

early scar formation

65
Q

complications of myocardial infarction

A
  • Heart failure (acute, chronic)
  • Arrhythmias
  • Rupture (wall, septum, papillary muscle)
  • Pericarditis
  • Ventricular aneurysm
  • Mural thrombus
66
Q

prevention of MI

A
  • Stop smoking
  • Control BP
  • Reduce cholesterol & weight
  • Control of diabetes
67
Q

Treatment of MI

A
  • Medication
  • Thrombolysis
  • Percutaneous Coronary Angioplasty and stents
  • CABG

NMSKI (38 decks)

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