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Pharmacology and Therapeutics > 11. Drugs and the vasculature > Flashcards

11. Drugs and the vasculature Flashcards

1
Q

Where is ACE found?

A
  • Mainly in the capillaries of the lungs

* Can also be found in endothelial and kidney epithelial cells

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2
Q

How does sympathetic discharge effect the arterioles and arterial pressure?

A
  • Increased arteriolar constriction
  • Increased peripheral resistance
  • Increased arterial pressure
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3
Q

Which vessels are the ‘major resistance vessels’?

A
  • Arterioles

* Biggest drop in BP takes place from one end of an arteriole to another

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4
Q

The BP of which vessels determines the blood flow everywhere else?

A

Arterial BP

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5
Q

How do you calculate blood pressure?

A

BP = CO * TPR

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6
Q

What is the definition of hypertension?

A

BP consistently over 140/90mmHg

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7
Q

What is the single most important risk factor for stroke?

A

Hypertension

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8
Q

What are the 4 steps of hypertension treatment?

A

(Lifestyle modifications before thinking about pharmacology)

1) ACE inhibitor or angiotensin receptor blocker (for under 55s)
2) CCB or thiazide-like diuretic (for over 55s or afro-Caribbeans of any age)
3) Combination of ACEi/ARB with CCB and thiazide-like diuretic
4) Consider low-dose spironolactone, beta blocker (used to be first line), or alpha blocker

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9
Q

Why are you less likely to prescribe ACE inhibitors or angiotensin receptor blockers (ARBs) to patients over 55?

A
  • Over 55 - tend to have low renin/renin sensitivity
  • Therefore, the RAS is probably not causing the high BP
  • Less responsive to ACEi or ARBs
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10
Q

How are thiazides thought to have an antihypertensive effect?

A
  • via diuresis

* However, evidence suggests it is a vasodilation effect

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11
Q

What is the suffix for ACE inhibitors?

A

-pril

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12
Q

What are the 3 major stimuli for renin production?

A
  • Decreased renal Na reabsorption
  • Decreased renal perfusion pressure
  • Increased sympathetic activity
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13
Q

Describe how the sympathetic NS affect renin production

A
  • Sympathetic nerves innervate the juxtaglomerular cells, beta receptors
  • Renin production stimulated
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14
Q

Which cells respond to renal [Na], and how do they respond when [Na] is low?

A

Macula densa cells
• Decreased resistance in afferent arterioles
• Increased renin release from juxtaglomerular cells

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15
Q

What does angiotensin II do?

A
  • Powerful vasoconstrictor => increased TPR
  • Directly affects kidney to promote salt and water retention => increased blood volume
  • Indirectly affects kidney to promote sodium retention and potassium excretion, by stimulating aldosterone production
  • Sympathetic activation
  • Thirst activation
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16
Q

Which type of nerves release the following:
• noradrenaline
• neuropeptide Y
• ATP

A

Sympathetic nerves

17
Q

What role does renin play in the RAS?

A

Converts angiotensinogen to angiotensin I

18
Q

What are the uses of ACE inhibitors?

A
  • Hypertension and HF
  • Post-MI
  • Diabetic nephropathy
  • Progressive renal insufficiency
  • Patients at high risk of CVD
19
Q

How do ACE inhibitors treat heart failure?

A
  • Angiotensin II increases salt and water retention => increased blood volume
  • Increase in venous return
  • ACEi decrease venous return in HF patients => reduced work, reduced congestion in system, reduced preload
  • Stress on heart alleviated
20
Q

How do ACE inhibitors cause a cough?

A
  • Inhibit bradykinin breakdown
  • More bradykinin
  • Cough reflex hypersensitivity
21
Q

What are angiotensin II blockers used for and given an example?

A

• Prevent renal and vascular actions of ATII
• Used in hypertension and HF
e.g. losartan

22
Q

What are the side effects of both ACEi and ARBs?

A
  • Hypotension
  • Hyperkalaemia (less ATII effects, less aldosterone, less K excretion)
  • Foetal injury
  • Renal failure in patients with renal artery stenosis
23
Q

What supplements/medication do you need to be careful with when taking ACEi or ARBs?

A

K supplements or K sparing diuretics

24
Q

How can ACEi and ARBs cause renal failure in patients with renal artery stenosis?

A
  • Removal of ATII as a major determinant of efferent vasoconstriction
  • GFR can’t be maintained when renal perfusion is low
  • GFR drops
  • Acute renal failure
25
Q

Describe how depolarisation of smooth muscles lead to contraction?

A
  • Opening of VGCCs
  • Ca2+ enters and binds to calmodulin (CaM)
  • Ca2+-CaM complex binds to + activates myosin light chain kinase (MLCK)
  • MLCK phosphorylates the myosin light chain
  • Cross-bridges can form - smooth muscle contraction
26
Q

Outline the selectivity of dihydropyridines (CCB)

A
  • Affects smooth muscle only
  • More selective for blood vessels
  • e.g. amlodipine - doesn’t cause negative inotropy
  • Licensed for prophylaxis of angina
27
Q

Outline the selectivity of non-dihydropyridines

A
  • Rate-limiting
  • Affects the heart and smooth muscle
  • e.g. verapamil - large negative inotropic effect
28
Q

How does decreased VSMC Ca2+ entry lead to decreased BP?

A
  • Less contraction
  • Lower TPR
  • Lower BP
29
Q

Which antihypertensive drugs have better adherence?

A
  • ACEi
  • ARBs

Primary reason why we use them - patients more likely to stay on them

30
Q

What does elderly hypertension tend to be more based on?

A

Atherosclerosis rather than renin

31
Q

Compare the overall effects of RAS inhibitors with CCBs

A
  • CCBs decrease SBP and stroke risk more
  • RASi decrease HF risk more

• No difference for all-cause death

32
Q

Compare the overall effects of RAS inhibitors with thiazides

A
  • Thiazides decrease SBP more
  • Thiazides decrease HF and stroke risk more

• No difference for all-cause death

33
Q

Compare the overall effects of RAS inhibitors with beta-blockers

A
  • No difference in SBP reduction
  • RASi decrease CV events and stroke more

• No difference for all-cause death

34
Q

When are alpha 1 adrenoreceptor antagonists used and how do they work?

A
  • Last resort
  • Alpha 1 is the predominant vasoconstricting receptor in the vasculature
  • Blocking it reduces vasoconstriction => reduced TPR => decreased BP

Pharmacology and Therapeutics (33 decks)

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