Treatment of HTN+HF Flashcards
MOA of Thiazide diuretics
-Block Na/Cl reabsorption in distal convoluted tubule
-incr. Ca reabsroption
-incr. K excretion
-Incr. serum uric acid
How do thiazides incr. serum uric acid
by competing with uric acid for secretion in PCT
Which are the Thiazide diuretics
Hydro-chlorthiazide
Indapamide
TU of Hydro-chlorothiazide
Hypertension-low dose
Mild HF to mobilize oedema, prevent congestion
For diabetes insipidus
In HF, which other drugs are used with Hydro-chlorothiazide
Loop diuretics
Effect of Thiazides
Drop in TPR- after 2-3wks
What happens during initial start of thiazide therapy
small amount of Na/H2O loss but it normalises after 2-3wks
TU of Indapamide
Often added with ACEs/ARBs and B-Blockers to augment antihypertensive effect
AEs of Hydrochlorthiazide
Hypokalaemia
Hyperuricaemia
Decr. in serum K
AEs of Indapamide
Alkalosis due to H+ loss
Hyperglycaemia: release of insulin
Indapamide is a sulphur drug= incr. risk of melanoma
How to overcome Hypokalemia caused by Hydro-chlorthiazode
Combined with K+ sparing drugs
–>amiloride
–>triamterene
Are the thiazides potent or weak diuretics
they are weak low ceiling diuretics
Which are the Loop diuretics
Furosemide
MOA of Furosemide
-inhibits Na/K/Cl co-transporter in AL of LH
-incr. Ca+Mg,K+ excretion
-Incr. Na in CD
TUs of Furosemide
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
DIs of Furosemide
NSAIDs: inhibit Prostaglandins=block diuretic effects
Drugs that can be used with Furosemide
Thiazide diuretics
AEs of Furosemide
Hypotension
Hyponatremia
Hypokalemia
Hypovolemia=Hypotension
Dehydration
Hypouricemia
Alkalosis: H+ excretion
Mg+ loss
Hyperglycaemia
Ca loss
Which are the K+ sparing diuretics
Amiloride
Triamterene
MOA of K+ sparing diuretics
Block Na/K exchange in CD
=retention of K+ and H+
Blocks Na/K exchange in CD which is independent of ALDO
TU of K+ sparing diuretics
Used with Hydrochlorothiazide in HTN
AEs of K+ sparing diuretics
severe Hyperkalemia
acidosis
severe Hyperkalaemia renal failure
CIs of K+ sparing diuretics
ACEs/ARBs= severe Hyperkalemia
B-Bockers
Which are the Aldosterone antagonist drugs
Spironolactone
MOA of Spironolactone
Blocks ALDO activity in CD
Reduces Na/K exchange
MOA of Spironolactone in HF
blocks action of ALDO in CD, myocardium and arterioles
decr. mortality
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
Which are the ACE inhibitors
Captopril
Enalapril
MOA of ACEi
blocks conversion of inactive Ang1–> active Ang2
Blocks vasoconstriction
blocks ALDO release
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
TU of ACEi
HTN to reduce TPR
HF by decr. afterload and preload
Improves morbidity and mortality when used in HF
AEs of ACEi
dry cough- due to bradykinin
angioedema: due to bradykinin
metabolic acidosis: H+ retention & Na excr.
Rash
Hyperkalaemia: esp. with spironolactone
Caution in ACEi
Spironolactone
CI of ACEi
Bilateral renal stenosis
Which are the ARBs
Lorsartan
Valsartan
Admin of ARBS
are long acting= taken once a day
MOA of ARBs
Blocks the binding of Ang2 to its AT1 Receptor
ARBs are competitive antagonists
Effects of ARBS
decr. TPR
Reduced NA and H20 absorbed
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
AEs of ARBs
Metabolic acidosis
Hyeperkalemia: esp with spironolactone
Rash
CIs of ARBs
Pregnancy
Bilateral renal stenosis
Caution with ARBs
Spironolactone: incr. risk of metabolic acidosis and hyperkalaemia
Why ARBs used over ACEi
Block vasoconstriction
No hypertrophy
Block ALDO release
No Bradykinin produced
=no cough
Effects of ARBS+ACEi
reduced preload
reduced afterload
reduced filling pressure
reduced vasoconstriction
reduced mortality by 35%
symptoms improve
MOA of CCBs
Block voltage gated Ca channels
Block L-Type Ca channels
Relaxation of vascular SM
reduced TPR
What do CCBs not cause
no renin release
no Na and H2O retention
no postural hypotension
Which are the dihydropyridines
Nifedipine
Amlodipine
Admin of Dihydropyridines
Nidedipine is short acting=slow release formulation
Amlodipine is long acting=once daily, slow onset of action and prolonged DOA
MOA of dihydropyridines
Block entry of Ca via L-type voltage gated Ca channels in VSM surrounding the arterioles
Effect of dihyropyridines
relaxation of VSM=Decr TPR
causes reflex increase in HR and SV
TUs of dihydropyridines
HTN: primarily vascular resistance
Angina pectoris: decr. O2 consumption by decr afterload
NOT FOR ARRYTHMIA TREATMENT
AES of dihydropyridines
Headache
pedal oedema: vasodilation causes fluid build-up around ankle
Reflex tachycardia
Nifedipine causes gingival overgrowth= gum disease
Which are the non-dihydropyridines
Verapamil
Diltiazem
Admin of non-dihydropyridines
short-acting=slow release formulation
metabolised in liver
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
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
TUs of non-dihydropyridines
HTN: by decr vascular resistance in angina pectoris by decr. afterload= decr O2 demand
Supraventricular arrythmias by slowing AV conduction
AEs of the non-dihydropyridines
Headache
Pedal oedema
inhibition of Ca channels in SA and AV node=bradycardia and AV nodal conduction problems
