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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
MOA of Spironolactone
Blocks ALDO activity in CD Reduces Na/K exchange
26
MOA of Spironolactone in HF
blocks action of ALDO in CD, myocardium and arterioles decr. mortality
27
TU of Spironolactone
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
Which are the ACE inhibitors
Captopril Enalapril
29
MOA of ACEi
blocks conversion of inactive Ang1--> active Ang2 Blocks vasoconstriction blocks ALDO release
30
Effects of ACEi
decr TPR reduce the amount of Na and H2O reabsorbed in kidney Incr. Bradykinin release which is a vasodilator and tissue irritant
31
TU of ACEi
HTN to reduce TPR HF by decr. afterload and preload Improves morbidity and mortality when used in HF
32
AEs of ACEi
dry cough- due to bradykinin angioedema: due to bradykinin metabolic acidosis: H+ retention & Na excr. Rash Hyperkalaemia: esp. with spironolactone
33
Caution in ACEi
Spironolactone
34
CI of ACEi
Bilateral renal stenosis
35
Which are the ARBs
Lorsartan Valsartan
36
Admin of ARBS
are long acting= taken once a day
37
MOA of ARBs
Blocks the binding of Ang2 to its AT1 Receptor ARBs are competitive antagonists
38
Effects of ARBS
decr. TPR Reduced NA and H20 absorbed
39
TUs of ARBS
HTN to reduce TPR HF by decr. afterload and preload improved morbidity and mortality-HF Used when patients are intolerant to ACEi
40
AEs of ARBs
Metabolic acidosis Hyeperkalemia: esp with spironolactone Rash
41
CIs of ARBs
Pregnancy Bilateral renal stenosis
42
Caution with ARBs
Spironolactone: incr. risk of metabolic acidosis and hyperkalaemia
43
Why ARBs used over ACEi
Block vasoconstriction No hypertrophy Block ALDO release No Bradykinin produced =no cough
44
Effects of ARBS+ACEi
reduced preload reduced afterload reduced filling pressure reduced vasoconstriction reduced mortality by 35% symptoms improve
45
MOA of CCBs
Block voltage gated Ca channels Block L-Type Ca channels Relaxation of vascular SM reduced TPR
46
What do CCBs not cause
no renin release no Na and H2O retention no postural hypotension
47
Which are the dihydropyridines
Nifedipine Amlodipine
48
Admin of Dihydropyridines
Nidedipine is short acting=slow release formulation Amlodipine is long acting=once daily, slow onset of action and prolonged DOA
49
MOA of dihydropyridines
Block entry of Ca via L-type voltage gated Ca channels in VSM surrounding the arterioles
50
Effect of dihyropyridines
relaxation of VSM=Decr TPR causes reflex increase in HR and SV
51
TUs of dihydropyridines
HTN: primarily vascular resistance Angina pectoris: decr. O2 consumption by decr afterload NOT FOR ARRYTHMIA TREATMENT
52
AES of dihydropyridines
Headache pedal oedema: vasodilation causes fluid build-up around ankle Reflex tachycardia Nifedipine causes gingival overgrowth= gum disease
53
Which are the non-dihydropyridines
Verapamil Diltiazem
54
Admin of non-dihydropyridines
short-acting=slow release formulation metabolised in liver
55
MOA of non-dihydropyridines
-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
Effects of the non-dihydropyridines
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
TUs of non-dihydropyridines
HTN: by decr vascular resistance in angina pectoris by decr. afterload= decr O2 demand Supraventricular arrythmias by slowing AV conduction
58
AEs of the non-dihydropyridines
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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