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Pharmacology > Treatment of HTN+HF > Flashcards

Treatment of HTN+HF Flashcards

1
Q

MOA of Thiazide diuretics

A

-Block Na/Cl reabsorption in distal convoluted tubule
-incr. Ca reabsroption
-incr. K excretion
-Incr. serum uric acid

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2
Q

How do thiazides incr. serum uric acid

A

by competing with uric acid for secretion in PCT

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3
Q

Which are the Thiazide diuretics

A

Hydro-chlorthiazide
Indapamide

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4
Q

TU of Hydro-chlorothiazide

A

Hypertension-low dose
Mild HF to mobilize oedema, prevent congestion
For diabetes insipidus

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5
Q

In HF, which other drugs are used with Hydro-chlorothiazide

A

Loop diuretics

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6
Q

Effect of Thiazides

A

Drop in TPR- after 2-3wks

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7
Q

What happens during initial start of thiazide therapy

A

small amount of Na/H2O loss but it normalises after 2-3wks

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8
Q

TU of Indapamide

A

Often added with ACEs/ARBs and B-Blockers to augment antihypertensive effect

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9
Q

AEs of Hydrochlorthiazide

A

Hypokalaemia
Hyperuricaemia
Decr. in serum K

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10
Q

AEs of Indapamide

A

Alkalosis due to H+ loss
Hyperglycaemia: release of insulin
Indapamide is a sulphur drug= incr. risk of melanoma

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11
Q

How to overcome Hypokalemia caused by Hydro-chlorthiazode

A

Combined with K+ sparing drugs
–>amiloride
–>triamterene

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12
Q

Are the thiazides potent or weak diuretics

A

they are weak low ceiling diuretics

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13
Q

Which are the Loop diuretics

A

Furosemide

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14
Q

MOA of Furosemide

A

-inhibits Na/K/Cl co-transporter in AL of LH
-incr. Ca+Mg,K+ excretion
-Incr. Na in CD

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15
Q

TUs of Furosemide

A

CHF to mobilise oedema,prevent pulmonary congestion
Acute Pulmonary oedema
HTN
BIventricular HF
Hypercalcaemia (acute): used to reduce high serum Ca levels due to bone diseases and cancers

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16
Q

DIs of Furosemide

A

NSAIDs: inhibit Prostaglandins=block diuretic effects

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17
Q

Drugs that can be used with Furosemide

A

Thiazide diuretics

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18
Q

AEs of Furosemide

A

Hypotension
Hyponatremia
Hypokalemia
Hypovolemia=Hypotension
Dehydration
Hypouricemia
Alkalosis: H+ excretion
Mg+ loss
Hyperglycaemia
Ca loss

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19
Q

Which are the K+ sparing diuretics

A

Amiloride
Triamterene

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20
Q

MOA of K+ sparing diuretics

A

Block Na/K exchange in CD
=retention of K+ and H+
Blocks Na/K exchange in CD which is independent of ALDO

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21
Q

TU of K+ sparing diuretics

A

Used with Hydrochlorothiazide in HTN

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22
Q

AEs of K+ sparing diuretics

A

severe Hyperkalemia
acidosis
severe Hyperkalaemia renal failure

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23
Q

CIs of K+ sparing diuretics

A

ACEs/ARBs= severe Hyperkalemia
B-Bockers

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24
Q

Which are the Aldosterone antagonist drugs

A

Spironolactone

25
Q

MOA of Spironolactone

A

Blocks ALDO activity in CD
Reduces Na/K exchange

26
Q

MOA of Spironolactone in HF

A

blocks action of ALDO in CD, myocardium and arterioles
decr. mortality

27
Q

TU of Spironolactone

A

Used with Hydro-chlorothiazide in HTN
Also in HF as add on therapy with ACEs/ARBs to prevent ALDO escape which has a major impact on mortality in HF

28
Q

Which are the ACE inhibitors

A

Captopril
Enalapril

29
Q

MOA of ACEi

A

blocks conversion of inactive Ang1–> active Ang2
Blocks vasoconstriction
blocks ALDO release

30
Q

Effects of ACEi

A

decr TPR
reduce the amount of Na and H2O reabsorbed in kidney
Incr. Bradykinin release which is a vasodilator and tissue irritant

31
Q

TU of ACEi

A

HTN to reduce TPR
HF by decr. afterload and preload
Improves morbidity and mortality when used in HF

32
Q

AEs of ACEi

A

dry cough- due to bradykinin
angioedema: due to bradykinin
metabolic acidosis: H+ retention & Na excr.
Rash
Hyperkalaemia: esp. with spironolactone

33
Q

Caution in ACEi

A

Spironolactone

34
Q

CI of ACEi

A

Bilateral renal stenosis

35
Q

Which are the ARBs

A

Lorsartan
Valsartan

36
Q

Admin of ARBS

A

are long acting= taken once a day

37
Q

MOA of ARBs

A

Blocks the binding of Ang2 to its AT1 Receptor
ARBs are competitive antagonists

38
Q

Effects of ARBS

A

decr. TPR
Reduced NA and H20 absorbed

39
Q

TUs of ARBS

A

HTN to reduce TPR
HF by decr. afterload and preload
improved morbidity and mortality-HF
Used when patients are intolerant to ACEi

40
Q

AEs of ARBs

A

Metabolic acidosis
Hyeperkalemia: esp with spironolactone
Rash

41
Q

CIs of ARBs

A

Pregnancy
Bilateral renal stenosis

42
Q

Caution with ARBs

A

Spironolactone: incr. risk of metabolic acidosis and hyperkalaemia

43
Q

Why ARBs used over ACEi

A

Block vasoconstriction
No hypertrophy
Block ALDO release
No Bradykinin produced
=no cough

44
Q

Effects of ARBS+ACEi

A

reduced preload
reduced afterload
reduced filling pressure
reduced vasoconstriction
reduced mortality by 35%
symptoms improve

45
Q

MOA of CCBs

A

Block voltage gated Ca channels
Block L-Type Ca channels
Relaxation of vascular SM
reduced TPR

46
Q

What do CCBs not cause

A

no renin release
no Na and H2O retention
no postural hypotension

47
Q

Which are the dihydropyridines

A

Nifedipine
Amlodipine

48
Q

Admin of Dihydropyridines

A

Nidedipine is short acting=slow release formulation
Amlodipine is long acting=once daily, slow onset of action and prolonged DOA

49
Q

MOA of dihydropyridines

A

Block entry of Ca via L-type voltage gated Ca channels in VSM surrounding the arterioles

50
Q

Effect of dihyropyridines

A

relaxation of VSM=Decr TPR
causes reflex increase in HR and SV

51
Q

TUs of dihydropyridines

A

HTN: primarily vascular resistance
Angina pectoris: decr. O2 consumption by decr afterload
NOT FOR ARRYTHMIA TREATMENT

52
Q

AES of dihydropyridines

A

Headache
pedal oedema: vasodilation causes fluid build-up around ankle
Reflex tachycardia
Nifedipine causes gingival overgrowth= gum disease

53
Q

Which are the non-dihydropyridines

A

Verapamil
Diltiazem

54
Q

Admin of non-dihydropyridines

A

short-acting=slow release formulation
metabolised in liver

55
Q

MOA of non-dihydropyridines

A

-Block Ca entry into VSM cells surrounding arterioles.
-Block L-Type volatge gated Ca channels in contractile tissue of myocaridum
-Block slow Ca channels in SA and AV node

56
Q

Effects of the non-dihydropyridines

A

may decr. contractility by inhibiting Ca entry into contractile tissue of heart
-causes bradycardia by blocking Ca channels in SA node
-AV-nodal blocker
-causes intense vasodilation by dropping TPR

57
Q

TUs of non-dihydropyridines

A

HTN: by decr vascular resistance in angina pectoris by decr. afterload= decr O2 demand
Supraventricular arrythmias by slowing AV conduction

58
Q

AEs of the non-dihydropyridines

A

Headache
Pedal oedema
inhibition of Ca channels in SA and AV node=bradycardia and AV nodal conduction problems

Pharmacology (50 decks)

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