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Cardiovascular System > Hypertension and Anti-hypertensives > Flashcards

Hypertension and Anti-hypertensives Flashcards

1
Q

What is the definition of hypertension?

A

Sustained BP of 140/90mmHg or above

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2
Q

What are 5 causes of secondary hypertension?

A

R - renal artery stenosis
E - endocrine (hypercortisolism, pheochromocytoma)
N - neurological (↑ intracranial pressure)
A - aorta (coarctation, atherosclerosis)
L - labile (psychogenic, stress)

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2
Q

Primary/essential hypertension is multifactorial and accounts for ______ of hypertension cases.

A

5-10%

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3
Q

What are 5 modifiable risk factors for HTN?

A

1) Stress
2) Obesity
3) Smoking
4) Physical inactivity
5) Heavy salt consumption

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4
Q

What is the definition of accelerated/malignant hypertension?

A

Systolic > 200mmHg
Diastolic > 120 mmHg

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5
Q

How can hypertension lead to heart failure?

A

LV pressure overload → LV concentric hypertrophy
→ impaired LV diastolic filling → back pressure → LA dilatation → LHF

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6
Q

What are 3 pathological effects of hypertension on the CNS?

A

1) Lacunar infarcts
2) Cerebral hemorrhage
3) Cerebral thrombosis
4) Hypertensive encephalopathy

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7
Q

What are 3 pathological effects of hypertension on blood vessels?

A

1) Atherosclerosis
2) Arteriolosclerosis (Hyaline/hyperplastic)
3) Aneurysms

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8
Q

Describe the pathogenesis of hyaline arteriolosclerosis.

A

HTN → endothelial dmg
→ protein exudation into medial layer + smooth muscle proliferation
→ hyaline arteriolosclerosis
→ can occlude → ischemic change and necrosis

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9
Q

Describe the pathogenesis of hyperplastic arteriolosclerosis.

A

HTN → endothelial dmg
→ concentric laminar thickening of wall by smooth muscle cells w thickened and duplicated basement membrane
→ luminal narrowing ± necrosis of wall

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10
Q

What is the difference between hyaline and hyperplastic arteriolosclerosis?

A

In hyperplastic arteriolosclerosis, the inner walls of arterioles become thickened from the growth of abnormal layers of smooth muscle cells.

In hyaline arteriolosclerosis, the inner walls of arterioles become thickened from the accumulation of hyaline protein deposits.

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11
Q

What is an aneurysm?

A

A localized abnormal dilation of a blood vessel or heart

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12
Q

What is the difference between a true and a false aneurysm?

A

False aneurysm:
Inflammation → vessels fuse with adjacent tissues + form artificial wall
→ fill w blood (haematoma) → abnormal dilatation

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13
Q

Abdominal aneurysms occur more frequently in (M/F), usually >___ and ______.

A

Males >50, smokers

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14
Q

Abdominal aneurysm are usually position below the _____ and above the ______.

A

Below renal arteries and above bifurcation of aorta
(where there is most turbulent blood flow)

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15
Q

Aneurysms can be 1 sided (_______) or bilateral (_______).

A

Saccular (1 side)
Fusiform (both sides)

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16
Q

What do abdominal aneurysms normally present as and when do px present?

A

Pulsating abdominal mass (mimicking tumor)

manifest due to:
1) rupture
2) obstruction of branching vessel
3) embolism
4) Impingement on adjacent structures

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17
Q

What are 2 conditions that predispose a px to hypertension?

A

Hypertension and Marfan’s syndrome

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18
Q

How does a thoracic aneurysm clinically manifest?

A

1) Respiratory difficulty (encroachment on airways/lungs)
2) Dysphagia
3) Bone pain
4) Bone pain (due to erosion)
5) Aortic valve dilation ± valvular incompetence/rupture

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19
Q

What is an aortic dissection?

A

When blood separates the laminar planes of the media to form blood-filled channels within aortic wall

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20
Q

What syndrome is suspected when an aortic dissection occurs in young px?

A

Marfan’s syndrome

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21
Q

What is the pathogenesis of aortic dissection?

A

Aorta of HTN px have medial hypertrophy of vasa vasorum associated with degenerative changes (due to ischaemic changes)

22
Q

What is the most common histological finding in an aortic dissection?

A

Cystic medial degeneration

23
Q

How does an aortic dissection clinically manifest?

A

Rupture through adventitia (thoracic/abdominal cavities, pericardial sac) and can extend towards heart or distally

24
Q

Type A aortic dissections involve ________ whereas Type B aortic dissections involve _____.

A

Type A: either ascending or descending
Type B: only descending

25
Q

What are the histological features of cystic medial degeneration?

A

1) Abnormal formation of elastic fibres
2) Proteoglycan accumulation form spaces between elastic fibres

26
Q

What are 4 first line drug classes against hypertension?

A

1) ACEi
2) ARBs
3) ß-blockers
4) DHP Ca channel blockers
5) Diuretics (thiazide/thiazide-like)

27
Q

What are 3 second line drug classes against hypertension?

A

1) Hydralazine
2) Mineralocorticoid receptor antagonists
3) α-blockers

28
Q

What are 3 examples of ACE inhibitors?

A

1) Lisinopril
2) Captopril
3) Enalapril

29
Q

How do ACE inhibitors lower BP?

A

Inhibit ACE → ↓ AT2
1) → ↓ vasoconstriction → ↓peripheral vascular resistance
2) → ↓ aldosterone → ↓Na+/H2O retention

30
Q

What are 4 clinical indications for ACE inhibitors?

A

1) HTN
2) HF
3) Post-MI
4) Renal insufficiency

31
Q

What are 4 AEs of ACEis?

A

1) Hypotension
2) ACute renal failure
3) Hyperkalaemia
4) Angioedema and DRY cough

32
Q

When are ACEis contraindicated?

A

Pregnancy

33
Q

What are 5 examples of ARBs?

A

1) Losartan
2) Valsartan
3) Candesartan
4) Irbesartan
5) Telmisartan

34
Q

What is the moa of ARBs?

A

Bind and block AT1 receptors and prevent binding and action of Angiotensin 2
1) → ↓ vasoconstriction → ↓peripheral vascular resistance
2) → ↓ aldosterone → ↓Na+/H2O retention

35
Q

What is a common AE of ARBs?

A

Less/no dry cough

36
Q

When are ARBs contraindicated?

A

Pregnancy

37
Q

What form of ß-blockers are cardioselective?

A

ß1

38
Q

What are 2 examples of cardioselective ß-blockers?

A

1) Bisoprolol
2) Metoprolol XL (succinate)

39
Q

What is an example of a non-selective ß-blocker approved to treat HF?

A

Carvedilol

40
Q

What is an example of a mixed ß-blocker selective at low doses but non-selective at high doses?

A

Nebivolol

41
Q

What are 5 clinical uses for ß-blockers?

A

1) HTN
2) HF
3) Post-MI
4) Arrhythmias
5) Anxiety disorders

42
Q

What are 6 AEs of ß-blockers?

A

1) Hypotension
2) Bradycardia
3) AV nodal block
4) Reduce exercise capacity
5) Bronchoconstriction
6) CNS: vivid dreams, clinical depression

43
Q

How do ß-blockers lead to bronchoconstriction?

A

Inhibition of ß2 receptors in bronchial smooth muscle → ↓inactivated MLCK → ↓bronchodilation

44
Q

What are 2 thiazides?

A

1) Hydrochlorothiazide
2) Indapamide

45
Q

What is the moa of thiazides?

A

1) Inhibit NaCl cotransporter at DCT → ↓reaborption of Na and Cl
2) Enhance Ca reabsorption at DCT
→ ↓Na/water reabsorption → ↑ diuresis → ↓ blood volume

46
Q

How do NSAIDs interfere with thiazides?

A

Reduce prostaglandin synthesis (thiazides depend on renal PG synthesis)

47
Q

What are 4 clinical uses of thiazides?

A

1) HTN
2) CHF
3) Nephrolithiasis (due to idiopathic hypercalciuria)
4) Nephrogenic diabetes insipidus

48
Q

What are 6 AEs of Thiazides?

A

1) Hypokalemic metabolic alkalosis
2) Hyponatremia
3) Hyperuricemia
4) Hyperglycemia
5) Hyperlipidemia
6) Hypercalcemia

49
Q

What are 2 examples of α-antagonists used for HTN?

A

1) Prazosin
2) Tamulosin

50
Q

What is the moa of α-antagonists used for HTN?

A

Bind and antagonise post-synaptic α1 adrenoceptors on vascular smooth muscles that mediate vasoconstriction
→ ↓vasomotor tone → ↓decrease peripheral vascular resistance → ↓BP

51
Q

α-antagonists used for HTN are (safe/unsafe) for px with renal impairment and (safe/unsafe) for pregnant women.

A

Safe for impaired renal function
Safe for pregnant women (no teratogenicity @ clinically relevant doses)

52
Q

What are 5 common AEs of α-antagonists?

A

1) Reflex tachycardia
2) Palpitations
3) Orthostatic hypotension
4) Depression
5) Urinary frequency
6) Flushing

Cardiovascular System (12 decks)

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