Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

YR2 LCRS Pharmacology > 12. Drugs and the vasculature > Flashcards

12. Drugs and the vasculature Flashcards

1
Q

how is vascular smooth muscle directly affected?

A
  • endothelial cells contain angiotensin converting enzyme which produces angiotensin II which acts on the AT1 receptor on vascular smooth muscle
  • sympathetic nerves releases NA, neuropeptide Y and ATP
  • there are drugs that directly interfere with AT1 receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how do arterioles contribute to BP?

A

arterioles are the biggest contributors to BP - the biggest drop in BP takes place from one end of an arteriole to the other showing that arterioles are the major resistance vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what does arteriolar smooth muscle normal display?

A

a state of partial tone (partially constricted) that allows further constriction/dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the pathophysiology of hypertension?

A
  • consistently over 140/90mmHg

- important risk factor for stroke, heart failure, MI and chronic kidney disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how is hypertension treated?

A

lifestyle changes: drinking, smoking, diet

STEP 1: ACE inhibitor
(ACEi) or angiotensin receptor blocker (ARB) for under 55s, calcium channel blocker (CCB) or thiazide-like diuretic for over 55s/afro-caribbeans

STEP 2: CCB or thiazide-like diuretic & ACEi or ARB

STEP 3: combination of ACEi/ARB with CCB and thiazide-like diuretic

STEP 4: consider low-dose spironolactone, b-blocker or a-blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

why are over 55s not offered ACEi or ARB in step 1?

A

they have low renin/low renin sensitivity so will be less responsive to ACEi or ARB - the RAS probably isn’t causing high BP so will have little effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

which drugs involved in the treatment of hypertension directly affect the vasculature?

A
  • ACEi and ARB (trying to inhibit ATII effects on vasculature)
  • CCBs (targeting channels on vascular smooth muscle)
  • a-blockers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the 3 major stimuli for renin production?

A
  • low [Na+] in the DCT detected by macula densa cells (–> low Na+ reabsorption)
  • decreased renal perfusion pressure
  • increased sympathetic activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what does ATII do?

A
  • very powerful vasoconstrictor (increases TPR)
  • directly affects kidney to promote salt and water retention –> increased blood vol.
  • indirectly affects kidney by stimulating aldosterone production
  • sympathetic activation
  • thirst activation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what does ARB do?

A

block the receptors that AT11 targets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the uses of ACEi?

A
  • hypertension and heart failure
  • post-MI
  • diabetic nephropathy
  • progressive renal insufficiency
  • patients at high risk of CVD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how does ACEi treat hypertension?

A

blocking ATII (vasoconstrictor) will reduce TPR and decrease BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how does ACEi treat heart failure?

A

decreased venous return (due to reduced salt and water retention) –> decreased congestion in the system –> stress on heart alleviated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the side effects of ACEi and ARB?

A
  • cough (ACEi)
  • hypotension
  • urticaria(rash) /angioedema(swelling) (ACEi rarely)
  • hyperkalaemia
  • foetal injury
  • renal failure in patients with renal artery stenosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the steps in smooth muscle contraction?

A
  1. Membrane depolarisation opens voltage-gated calcium (Ca2+) channels (VGCCs)
  2. Ca2+ enters and binds to calmodulin (CaM)
  3. Ca2+-CaM complex binds to and activates myosin light chain kinase (MLCK)
  4. MLCK mediated phosphorylation –> smooth muscle contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what do dihydropyridines (DHPs) do?

A
  • affect smooth muscle only (non-rate limiting CCB)
  • more selective for blood vessels
  • used to treat hypertension
  • also used for prophylaxis of angina
17
Q

what do non-DHPs do?

A
  • rate-limiting CCBs
  • affect heart and smooth muscle
  • verapamil causes large negative inotropic effect
18
Q

what is the primary reason why ACEi and ARBs are used?

A

10-15% of patients stay on them

19
Q

what do RAS inhibitors include?

A

ACEi and ARBs

20
Q

compare RAS inhibitors and CCBs

A
  • ACEi are more effective for heart failure patients

- CCBs are more effective if you are likely to develop stroke

21
Q

compare RAS inhibitors and thiazides

A
  • thiazides are more effective for both heart failure and stroke
  • thiazides also have a more profound effect on systolic BP
22
Q

what are a1 blockers and when are they used?

A
  • a1-receptors are the predominant vasoconstricting receptor in the vasculature
  • a1 blockers (a1 adrenoceptor antagonists) are used as a last resort in antihypertensive treatment
  • blocking a1 receptors reduces vasoconstriction –> reduces TPR –> decreased BP

YR2 LCRS Pharmacology (32 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions