Brainscape's Knowledge GenomeTM

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


See full index

LCRS Pharma > Drugs and the CVS: vasculature > Flashcards

Drugs and the CVS: vasculature Flashcards

1
Q

what is released by the SNS to cause vasoconstriction?

A

noradrenaline

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

name examples of VSM mediators that cause contractions by increasing [ca2+]

A

o AngII –>AT1r
o PGG2, PGH2 –>TP (T-prostanoid receptor).
o ET1 –> ETA/B

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

name examples of endothelial cell agonists that stimulate relaxation by increasing [ca2+]

A

o NO.
o CNP – C-Type Naturietic Peptide.
o PGI2.
o EDHF – Endothelial Hypopolarising Factor.

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

state the BP formula

A

CO x TPR

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

what vessel contributes the greatest to BP regulation?

A

arterioles

these exhibit vascular tone and are in a partial state of constriction

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

what state are arterioles in hypertensive patients in?

A

raised base vascular tone that increases TPR and therefore BP

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

what is hypertension the most important risk factor in?

A

stroke

main risk factor in MI and CKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the overview of hypertension treatment?

A 
o Step 1 – Single Therapy:
Under 55 
– ACEi or ARB (Angiotensin Receptor Blocker).
Over 55, Afro-Caribbean 
– CCB or Thiazide diuretic.

o Step 2 – Dual Therapy:
ACEi and CCB.
ACEi and thiazide diuretic.

o Step 3 – Triple Therapy:
ACEi, CCB and thiazide diuretic.

o Step 4 – Symptomatic Relief:

  • Low-dose spironolactone (diuretic therapy).
  • alpha -blockade or beta-blockade.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how is hypertension defined?

A

a BP consistently higher 140/90 or higher

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what stimulates the production of renin?

A
  • reduced sodium reabsorption
  • reduced renal perfusion pressure
  • increased SNS stimulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how does ANGII contribute to blood pressure?

A
  • increases thirst sensation (so you drink more)
  • activates the SNS
  • vasoconstrictor
  • salt +H20 retention via aldosterone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what drug eliminates ANGII? what also does it do?

A

ACEi e.g. enalapril
decreases ANGII production and increases Bradykinin (stops it breakdown by ACE)

less ANGII–> less vasoconstriction
more bradykinin–> more vasodilation

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

what are the uses of ACEi?

A 
o Hypertension.
o Heart failure.
o Post MI.
o Diabetic nephropathy.
o Progressive renal insufficiency.
o High CVS-disease-risk patients.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the suffix for ACEi?

A

-pril

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the main two effect of ACEi in reducing hypertension?

A

(1) reduction of TPR

(2) reduction of sodium retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how do ACEi reduce TPR in hypertension ?

A

accumulation of bradykinin and reduction in ANGII:

  • less AT1R mediated vasoconstriction
  • more bradykinin mediated vasodilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how does ACEi reduce sodium retention in hypertension?

A

less Na+ retained:

  • via blocked actions of ANGII on AT1R in the kidney
  • therefore less aldosterone secretion due to blocked AT1R in the adrenal medulla
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are the effects of ACEi in heart failure?

A

(1) reduce TPR

(2) reduce preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how do ACEi reduce preload in heart failure?

A

venodilation reduces preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

how do ACEi reduce TPR in heart failure?

A
  • less vasoconstriction via AT1R in peripheral vasculature
  • reduced TPR
  • decreased after load on the heart so inotropic effects decreased
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what drug stops ANGII having its effects?

A

Angiotension Receptor Blockade (ARB) e.g. losartan prevents binding to AT1 receptors on arteries, kidneys and adrenal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are the uses of ARBs?

A
  • hypertension

- heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

why would an ARB be used over an ACEi?

A

ARB does not affect ACE so bradykinin is not spared:

  • Bradykinin induces cough
  • ACEi causes Bradykinin to accumulate causing the cough
24
Q

what are the side effects of ACEi and ARBs?

A 
	Cough – ACEi increased bradykinin
	Urticaria/angioedema – ACEi rarely.
	Hypotension 
	Hyperkalaemia
	Foetal injury 
	Renal failure (in patients with renal artery stenosis)
25
Q

why is hyperkalaemia a side effect of ACEi and ARBs?

A

no exchange of K+ occurs with the little Na+ present

Aldosterone has been reduced so K+ loss is not being stimulated

26
Q

why should ACEi and ARBs not be used in renal failure patients with renal artery stenosis?

A

these patients cannot maintain adequate glomerular pressure, affecting their GFR (maintained by ANGII essentially)

the drug affects the afferent arteriole and exacerbates this problem by affecting glomerular pressure

27
Q

what is the process outline involved with calcium in smooth muscle contraction?

A

o Membrane depolarisation opens VGCC.
o Ca2+ enters and binds calmodulin (CaM).
o Ca2+-CaM complex activates MLCK.
o MLCK mediated phosphorylation –> VSM contraction.

28
Q

where do DHP selective and non-DHP calcium channel blockers bind (CCB) ?

A

DHP–> blood vessels

non-DHP–> heart and vessels

29
Q

example of DHP aka non- rate slowing drug

A

amlodipine:
no effect on heart
prophylactic treatment of angina

30
Q

example of non-DHP aka rate slowing drug?

A

verapamil:

has a negative inotropic effect

31
Q

which CCB is preferably used in hypertension?

what may be an unwanted side effect?

A

amlodipine (DHP CCB) due to absence of inotropic effects on the heart

reflex tachycardia due to powerful vasodilation

32
Q

how do DHPs reduce BP?

A

remember that DHPs are CCBs:
–>inhibit Ca2+ entry into VSMCs so less contraction of the cells

reduced TPR and therefore BP

33
Q

what is the preferable treatment for those under 55?

why is this?

A

ACEi or ARB

  • good patient adherence compared to other drugs
  • this is due to fewer side effects
  • not much difference in their reduction of BP
34
Q

what is the preferable treatment for those over 55 or of Afro- Caribbean origin?

why is this?

A

CCB or thiazide diuretic

  • they have low plasma renin activity so ACEi will be ineffective
35
Q

examples of alpha blockers?

A

prazosin (alpha 1 ant)

phentolamine (non-selective ant)

36
Q

what is the effect of alpha blockers?

A

block alpha 1 mediated vasoconstriction

37
Q

what is the selectivity of prazosin and phentolamine?

A

prazosin- alpha 1 antagonist

phentolamine- Alpha1/ 2 antagonist

38
Q

what is the effect of the non-selective nature of phentolamine?

A

non-selective alpha blocker:
binding to alpha 2 means it blocks NA release negative feedback so enhances NA release and the SNS response, leading to a non-reflex increase in HR.

39
Q

What is the impact of contraction on arterioles in:

  • radius
  • resistance
  • flow
A

radius decreases
resistance increases
flow decreases

vasoconstriction

40
Q

what is the impact of vasodilation on arterioles in:

  • radius
  • resistance
  • flow
A

radius increases
resistance decreases
flow increases

vasodilation

41
Q

in what state do arterioles stay?

A

have a state of partial constriction (vascular tone)

42
Q

what are the effects of Angiotensin 2?

A
  • increased thirst (via SNS activation)
  • vasoconstriction
  • salt and water retention
  • aldosterone secretion
43
Q

what are the 3 reasons for renin release?

A
  • low renal Na+ reabsorption
    NB water moves with salt
  • low renal perfusion pressure
  • sympathetic nervous system
44
Q

define hypertension

what is hypertension the single most important risk factor for?

A

definition: consistently above 140/90 mmHg

strokes (causing 50% of ischaemic stroke)

25% heart failure

45
Q

what is the ultimate aim for hypertension therapy?

A

reduce mortality from cardiovascular or renal events

46
Q

what should be given for hypertension management for under 55?

A

ACEi or ARBs

47
Q

what should be given for hypertension manage for over 55s or afro-carribeans?

A

CCBs or thiazide like diuretic

48
Q

what is step 2 in hypertension management?

A

ACEi+ TLD
ACEi+CCB

ARB for afro-carribean

49
Q

what is the last step in hypertension management in resistant hypertension?

A

consider further diuretics e.g. low dose spironolactone

consider beta or alpha blocker

50
Q

what are the clinical uses of ACEi?

A 
Hypertension
Heart failure
Post-myocardial infarction
Diabetic nephropathy
Progressive renal insufficiency
Patients at high risk of cardiovascular disease
51
Q

what effect does ATR-1 have?

A

angiotensin II receptor 1

  • -> vasoconstriction
  • -> sodium retention in kidney
52
Q

what effect does bradykinin have?

A

vasodilation

53
Q

name an angiotensin receptor blocker and is MoA

A

Losartan, Irbesartan

  • block ATR1 so ANGII effects
  • blocks renal and vascular effects
54
Q

what are the clinical uses of Losartan (ARB)?

A

hypertension and heart failure

55
Q

describe ARB and ACEi side effects

A
  • Hypotension (both)
  • Hyperkalaemia (both): take care with K+ supplements or K+-sparing diuretics; aldosterone promotes K+ loss so aldosterone inhibitors produce a hyperkalaemia.
  • Foetal injury (both)
  • Renal failure (in patients with renal artery stenosis; both) :Glomerular filtration is maintained by AngII so you need to be careful in renal failure patients.
  • Usually very well tolerated (especially ARB)
  • Cough (ACEi) very common
  • Urticaria and angioedema (ACEi)
56
Q

what is the mechanism of action of alpha blockers?

A

blocker alpha 1 mediated vasoconstriction (skin, mucosal membranes)

e.g. prazosin

57
Q

why does alpha blockade lead to increased heart rate?

A
  • a non selective alpha blocker like phentolamine (Alpha 1 and 2)
  • blocks alpha 2 so no -ve FB on NA release
  • enhanced NA effects–> SNS to the heart
  • heart rate increase

NB this is not reflexive

LCRS Pharma (32 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions