Download Free Medical Hypertension PowerPoint Presentation

Hypertension PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on Antihypertensive, which is titled "Hypertension", to know how can we treat hypertension.

Tags : Antihypertensive, Hypertension

Published on : May 25, 2021 | Views : 4528 | Downloads : 28

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Hypertension
Slide 2-

Normal BP: <120/<80 Prehypertension: 120-139/80-89 Hypertension stage1 140-159/90-99 Hypertension stage 2 160/100 Emergency >210/>120 Resistant hypertension Failure of BP control with three drug regimen Isolated systolic >140/<90 hypertension
Slide 3-

How can we treat hypertension Secondary hypertension- treat underlying cause Essential hypertension- cause not known Factors involved- stress, weight, dietary habits, salt retention, increased angiotensin production, , increased sympathetic tone Approaches- Reduce salt/water content of body Reduce sympathetic tone Reduce effects of circulating angiotensin II Reduce cardiac force of contraction Dilate peripheral vessels to reduce cardiac filling & consequent stroke volume
Slide 4-

Drugs used for treatment of hypertension: Diuretics Centrally acting agents- methyl dopa, clonidine -Adrenoceptor blockers -Adrenoceptor blockers Combined  and  blockers ACE inhibitors ARBs CCBs Vasodilators Hydralazine, Minoxidil, Diazoxide, Fenoldopam (arteriolar) Sodium nitroprusside (arteriolar + venular)
Slide 5-

Need for life-style changes: Weight loss/control Restricted sodium intake Increasing aerobic exercise Moderating alcohol consumption These changes in life-style may be sufficient to control hypertension in early stage I They also facilitate pharmacological treatment
Slide 6-

Diuretics: Thiazides, loop diuretics and K+ sparing diuretics They are antihypertensive when given alone Also enhance the efficacy of other antihypertensive agents Exact mechanism not known Initially decrease extracellular volume and enhance Na+ excretion by inhibiting Na+Cl- co-transporter which leads to  in CO
Slide 7-

Long term therapy- CO and extracellular volume returns to pretreatment value due to compensatory mechanisms but antihypertensive effect persists due to decrease in PVR  in PVR may occur due to direct vasodilatory effect of thiazides or due to their effect on kidney
Slide 8-

Thiazides should be avoided in patients with concommitant: Diabetes mellitus Gout Hyperlipidaemia Renal insufficiency
Slide 9-

High efficacy (ceiling) diuretics Severe reduction in blood volume & electrolyte imbalance Strong diuretic Weak antihypertensive than thiazide diuretics Indicated in HT when complicated by Chronic renal failure Coexisting CHF Severe edema due to use of potent vasodilators
Slide 10-

Sympatholytic agents: Centrally acting:  methyldopa, clonidine  Adrenoceptor blockers  Adrenoceptor blockers Combined  and  adrenoceptor blockers- labetalol, carvedilol
Slide 11-

Methyldopa: It is an analog of DOPA (dihydroxyphenylalanine) It is a pro drug- metabolized in brain by L-aromatic amino acid decarboxylase in adrenergic neurons to  methyl dopamine and then converted to  methyl norepinephrine  Methyl norepinephrine is stored in the vesicles in place of NE and released in response to stimulus Acts in the CNS to reduce sympathetic outflow from brain stem
Slide 12-

Also, probably acts an an agonist of central presynaptic 2 receptors to reduce central sympathetic outflow Rapidly absorbed, t½ approximately 2 h Even after i.v. injection effects starts after a delay of about 6-8 h
Slide 13-

Why the delay in action? probably due to time taken for transportation to brain and conversion to methyl NE ADRs: Sedation, transient Dryness of mouth Parkinsonian signs Hyperprolactenemia leading to gynecomastia or galactorrhoea
Slide 14-

Clonidine, Guanbenz and Guanfacine: Stimulate 2A subtype of 2 receptors in the brain stem and reduce the central sympathetic outflow  in plasma concentration of NE correlates with the decrease in BP Decreased sympathetic outflow also reduces cardiac output & HR In supine position, when the sympathetic tone to vasculature is low, the effect is mainly by reducing HR and stroke volume
Slide 15-

In upright position, the vasculature tone is high and effect is mainly by reducing the PVR Since they block peripheral vasoconstriction, postural hypotension may occur
Slide 16-

ADRs: Sedation Xerostomia Dryness of eye, nasal mucosa Parotid swelling Postural hypotension Erectile dysfunction Bradycardia, sinus arrest, AV block Rebound hypertension
Slide 17-

Guanadrel: Exogenous false neurotransmitter Actively transported to adrenergic neuron by NET (NE transporter) Previously NET was known as Uptake 1 Stored in adrenergic neurons where it is concentrated in storage vesicles and replaces NE Released in place of NE and acts as false neurotransmitter It has no activity on adrenergic receptors
Slide 18-

This inhibits the functioning of peripheral adrenergic neurons Antihypertensive effect is achieved by reduction in PVR Postural hypotension
Slide 19-

-Adrenergic blockers: Decrease HR, output and stroke volume (1) Inhibit renin release from JG apparatus (1) Block -receptors of peripheral blood vessels so they constrict (2) PVR increases initially but gradually returns to pretreatment values or less Those crossing the BBB also reduce central sympathetic tone
Slide 20-

Do not cause retention of salt and water Often combined with diuretics- additive effect Highly preferred drugs for hypertensive patients with complications like angina, MI or CHF
Slide 21-

-Adrenoceptor blockers produce: Decreased myocardial contraction & cardiac output (1) Decreased renin secretion (1) Decreased central sympathetic activity (Presynaptic 2 effect)
Slide 22-

All -adrenoceptor blockers produce: Reduced exercise tolerance Mild chronic fatigue Sedation Increased airway resistance Bradycardia Sleep disturbances-  melatonin release
Slide 23-

All -adrenoceptor blockers initially produce vasoconstriction by blocking vascular -receptors that relax vascular smooth muscles This vasoconstriction disappears after some time (adaptability ?)
Slide 24-

-Adrenoceptor blockers with intrinsic sympathomimetic activity: Advantages: Less bradycardia & myocardial suppression- useful in patients having low cardiac reserve Less likely rebound hypertension Less worsening of lipid profile Less effect on exercise tolerance
Slide 25-

β-Adrenoceptor blockers with intrinsic activity: Oxeprenolol Pindolol Penbutolol Acebutolol
Slide 26-

Nebivolol: 1 selective antagonist Promotes vasodilation due to  production of NO in arterial smooth muscle Has antioxidant properties also
Slide 27-

1-Adrenoceptor blockers: Block 1-adrenoceptors on smooth muscles of arterioles Reduce arteriolar resistance and increase venous capacitance Reflex increase in HR and plasma renin activity Return to normal during long term therapy Postural hypotension may occur depending on plasma volume
Slide 28-

Reduce total plasma concentration of triglycerides and LDL Increase plasma levels of HDL- beneficial effect Effect on lipids persists even when combined with diuretics Preferred in hypertensive patients with BPH
Slide 29-

Combined  and  adrenoceptor blockers: Labetalol and carvedilol Labetalol is a mixture of four stereoisomers- one isomer is  blocker like prazosin, another is a non-selective  blocker with partial agonist activity like pindolol Other two isomers are inactive Carvedilol is a  receptor antagonist with 1 receptor blocking activity Pheochromocytoma
Slide 30-

Vasodilators: Hydralazine: Directly relaxes the arteriolar smooth muscle Mechanism uncertain Does not relax venous smooth muscle Compensatory reflex increase in sympathetic outflow Increase in HR, cardiac output, plasma renin activity and fluid retention Selective decrease in vascular resistance in coronary, cerebral and renal vascular beds Postural hypotension- uncommon because it does not dilate veins
Slide 31-

ADRs: Extension of pharmacological effects: headache, flushing, hypotension, palpitation, tachycardia, dizziness, nausea Can precipitate angina or MI due to increased myocardial O2 demand Immunological reactions- drug induced lupus syndrome, serum sickness, hemolytic anemia Pyridoxine responsive polyneuropathy- probably because hydralazine combines with pyridoxine to form hydrazone
Slide 32-

Minoxidil: Converted in liver to active form- minoxidil N-O sulphate Produces arteriolar vasodilation No effect on venous capacitance vessels Causes increase in cardiac output Blood flow to skin, skeletal muscles, GIT and heart is increased Dilates renal artery, nett effect depends on hypotension and extent of dilatation
Slide 33-

Potent stimulator of renin secretion- by increasing sympathetic outflow and effecting renal regulation of renin release Minoxidil sulphate opens ATP-modulated K+ channels K+ efflux occurs, cell is hyperpolarized
Slide 34-

May precipitate severe bradycardia/sinus arrest Hepatotoxicity- Coombs test (antiglobulin) necessary because autoantibodies are produced against Rh antigen Preferred drug for treatment of hypertension during pregnancy
Slide 35-

ADRs: CVS: same as hydralazine Hypertrichosis: (abnormal hair growth in the body) may occur Uses: Severe hypertension- should never be given alone; always with a diuretic to prevent fluid retention and a sympatholytic drug to control reflex CVS changes Baldness- topical
Slide 36-

Diazoxide: Chemically related to thiazide diuretics but has no diuretic activity Instead causes retention of sodium and water Acts by opening K+ channels in arteriolar smooth muscle cells No effect on venules Causes hyperglycemia Used for short term treatment of hypertensive emergencies Often combined with a diuretic and a  blocker
Slide 37-

Fenoldopam: Agonist of dopamine D1 receptors Causes dilatation of arterioles and natriuresis Oral bioavailability is poor t½ approx. 5 min Onset of action is rapid Increases renal output, creatinine clearance and sodium excretion so concomitant use of diuretic or  blocker is not required ADRs: reflex tachycardia, headache, flushing Increases intraocular pressure so should be avoided in glaucoma
Slide 38-

Sodium nitroprusside: Releases NO which dilates the blood vessels Mechanism of NO release not known but mimics endogenous NO release by vascular endothelial cells No development of tolerance (it occurs to nitroglycerine) Dilates both arterioles and venules CO falls due to venous pooling and reduction in PVR Plasma renin activity increases Unlike arteriolar dilators hydralazine, minoxidil and diazoxide, it causes only modest increase in HR and reduces cardiac O2 demand
Slide 39-

Used to treat hypertensive emergencies, aortic dissection, controlled hypotension during anesthesia Effect of light on drug
Slide 40-

Toxicity: Headache, nausea, vomiting-disappear after the drug is discontinued Cyanide or thiocyanate accumulation Thiocyanate toxicity- psychosis, disorientation and convulsions Methemoglobinaemia- due to cyanide
Slide 41-

Administration of sodium thiosulfate and hydroxycobalamine Sodium thiosulfate- acts as a sulfur donor and facilitates metabolism of thiocyanates Hydrocobalamine- combines with cyanide ion to form non-toxic cyanocobalamine
Slide 42-

Pregnancy If taken before pregnancy, most anti-HTN can be continued except ACE inhibitors and angiotensin II receptor blockers. Methyldopa is most widely used for hypertension during pregnancy. Beta-blockers are not recommended early in pregnancy.
Slide 43-

Drugs to be avoided for treatment of hypertension associated with other diseases: