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Hypertension Drugs Cheat Sheet by

pharmocology

Intr­odu­cti­on:

> most common CVS disease
> elevated arterial BP damages vessels in renal, heart and brain
Comp­lic­ati­ons:
Renal failure, Coronary disease, Heart failure, Stroke, Diamentia

Clas­sif­ica­tion:

Clas­sif­ica­tion:
Systolic BP
Dias­tolic BP:
Norm­al:
<120
<80
Pre-­hyp­ert­ens­ion:
120-139
80-89
Stage 1 HTN:
140-159
90-99
Stage 2 HTN:
>= 160
>=100

Types of Hypert­ens­ion:

Esse­ntial Hypert­ension (85-90­%):
Primary hypert­ension, no identi­fiable cause (genetic), can't be cured, can be controlled
Secondary Hypert­ension (10-15­%):
Specific identified cause (comorbid disease or drug), can be cured when cause is eliminated

Seco­ndary Causes of HTN:

> Genetic factors
> Psycho­logical stress
> Enviro­nmental and Dietary Factors:
high salt diet, decreased calcium and phosphate intake, sedentary lifestyle
> Diseases:
renal, endocrine, vascular, renal diseases
> Drugs:
sympat­hom­imetic amines, amphet­amines, oral decong­estants (eg. pseudo­ehe­drine), cortic­ost­eroids, osteogens (C0Cs), NSAIDs, COX-2 inhibitors

Clinical presen­tat­ion:

- Often incidental finding
- Adults should get BP checks once a year
- Severe cases:
Head­ach­es, visual distur­bances, target organ damage (stroke, ischemic heart disease, renal failure)

Normal regulation of BP:

Factors Influe­ncing BP:

Pote­ntial Mechanisms of Partho­gen­esis:

BP= CO x PVR
Incr­eased Cardiac output:
Increased fluid volume from excessive sodium intake or renal sodium retention Venous constr­iction: due to excess stimul­ation of RAAS
Incr­eased Peripheral resist­ance:
Excess stimul­ation of RAAS Sympat­hetic nervous system over-a­ctivity

Anti­hyp­ert­ensive Drugs:

 

Classes of Antihy­per­tensive Agents:

> Diuretics:
Reduce blood volume­=De­pletes the body of sodium, Venodi­lation
> Sympat­hop­legic agents:
Reduce peripheral vascular resist­ance, Inhibit cardiac function, Increase venous pooling capaci­tance vessels
> Direct vasodi­lators:
Reduce peripheral vascular resist­ance, Increase venous pooling capaci­tance vessels
> Angiot­ensin antago­nists:
Reduce peripheral vascular resist­ance, Reduce blood volume

Diur­eti­cs:

- Reduce blood volume and cardiac output
- Cardiac output returns to normal
But peripheral vascular resistance declines
- Sodium
Contri­butes to vascular resistance = Increase vessel stiffness
- Venodi­lation
Altered sodium­-sodium calcium exchange

Vaso­dil­ation mechanism by Diuret­ics:

Thiazide Diuret­ics:

Use of Diuret­ics:

> Lower BP by 10-15 mmHg in most patients
> Thiazide diuretics –mild to moderate HTN
> Loop diuretics – severe HTN and hypert­ensive emerge­ncies
Adverse Effects (Thiazide Diuret­ics):
Potassium depletion – hypoka­lemia

Magnesium depletion

Hyperu­ric­emia- gouty attacks

Glucose intole­rance

Increase serum lipid concen­tra­tions

Sympat­hop­legic Drugs:

Centra­lly­-acting Drugs:
Methyl­dopa, clonidine
Adre­noc­eptor antago­nists
Beta-b­loc­kers, alpha-1 blockers
Gangli­oni­c-b­locking Agents:
No longer used clinically ; hexame­thonium
Adre­nergic neuron blocking agents:
Block the release of noradr­ena­line, Reserpine, guanet­hidine, debris­oquin, Not/rarely used clinically

Cent­ral­ly-­Acting Drugs:

- Methyl­dopa, clonidine
rarely used except clondine
- Reduces sympat­hetic outflow
- Compen­satory response mechanism:
salt retention
- Clon­idi­ne, guanabenz, guanfacine
Stimulate central alpha-2 adreno­ceptors
- Methyldopa – anologue of L-dopa
Results in the synthesis of a false neurot­ran­smitter
 
Alpha-­met­hyl­nor­adr­enaline = Stimulates central alpha-2 adreno­ceptors
Clon­idi­ne:
Reduces cardiac output, PVR, relaxation of capaci­tance vessels
Rarely causes postural hypote­nsion
Adverse effects:
- Dry mouth
- Sedation
Contra­ind­ica­tion: Patients with depression
Caution: Abrupt discon­tin­uation can lead to hypert­ensive crisis
 

Adre­noc­eptor antago­nists: Beta-b­loc­kers

Non-se­lec­tive: Propra­nolol
Beta-1 selective: “BBEAM”
Betaxolol, bisopr­olol, esoprolol, aten­olol, metopr­olol, Cardio­sel­ective
Vasodi­lator beta-b­lockers
Also block alpha-1 recept­ors­,La­bet­olol, carvid­elol, nebivolol
Decrease cardiac output

Decrease peripheral vascular resistance

Inhibit stimul­ation of renin production by catech­ola­mines

Adverse effects= Heart block, bronch­oco­nst­ric­tion, diabetes, vivid dreams

Alpha-1 blocke­rs:

Praz­osin, terazosin, doxazosin
Block alpha-1 receptors in arterioles and veins
Vasodi­lation
Reduce peripheral resistance
Compen­satory mechanism:
salt and water retention
More effective when used with other drugs

Calcium Channel Blocke­rs:

> Dihydr­opy­ridines
amlodi­pine, isradi­pine, nicard­ipine, nimodi­pine, felodi­pine, nisold­ipine, lacidipine
> Non-di­hyd­rop­yri­dines
Verapamil, diltiazem, hydral­azine
 
Benzot­hia­zepine (dilti­azem)
Mech­anism of action:
- Inhibit calcium influx through voltag­e-d­epe­ndent L-type calcium channels
- Relax arteriolar smooth muscle, reduce peripheral vascular resistance
- Cause coronary and peripheral vasodi­lation

CCB: Mechanisms of Action:

Dihydr­opy­ridine CCBs
Primary vasodi­lators (reduce PVR), All decrease cardiac contra­ctility except amlodipine and felodipine
Non-di­hyd­rop­yri­dines (dilti­azem, verapamil)
directly block the AV node, decrease heart rate,d­ecrease cardiac contra­ction
Adverse effects:
1. Flus­hing, peripheral oedema, tachyc­ardia, bradyc­ardia, heartb­lock
2. Head­ache, flushing, dizziness, palpit­ations, hypote­nsion
occur within a few hours of dosing, Associated w high initial doses or rapid increase in dose, Common with short-­acting prepar­ations
3. Ankle oedema: Due to a rise in intrac­api­llary pressure as a result of selective dilatation of precap­illary arteri­oles, NOT due to sodium retention, Relieved by bed rest
4. Gum Hypert­rop­hy: dihydr­opy­ridines
5. GIT: consti­pation (verap­amil), nausea, and vomiting

Inhi­bitors of Angiot­ens­in:

Angiot­ensin converting enzyme inhibitors (ACEIs)
Captopril, enalapril, Ramipril, fosino­pril, trandopril
Angiot­ensin receptor blockers (ARBs)
Losartan, valsartan, telmis­artan, irbesa­rtan, candes­artan
Renin-­inh­ibitors
Aliskiren

Inhi­bitors of Angiot­ens­in:

Adverse Effects
ACEIs =
Dry cough
Can cause hyperk­alemia – potassium monitoring essential
Angioedema (substance P?)

ARBs =
No dry cough
Hype­rka­lemia
Angiodema is less common than ACEIs

Contra­ind­icated in pregnancy

Comb­ination Treatment: Vasodi­lat­ors:

 

Mana­gement Approa­ch:

Firs­t-line agents: “ACD” drugs:
- A: ACEIs and ARBs
- C: Calcium channel antago­nists
- D: Diuretics (Thiaz­ides)

Seco­nd-line agents:
- Beta­-ad­ren­oceptor blockers
- Aldost­erone antago­nists (spiro­nol­actone, eplere­none)
- Alpha-­blo­ckers (doxaz­osin, prazosin, terazosin)
- Loop diuretics (fruse­mide, torsemide)
- Direct vasodi­lators (hydra­lazine, minoxidil) [last-line of therapy]
- Central α-2 agonists (cloni­dine)
- Adrenergic antago­nists (reser­pine)

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