Anti-HTN

mechanisms and terms

Hypertension

\-sustained raise in BP

\-myocardial disease

\-can lead to cardiovascular problems, renal diseases, and blindness

true, it is a factor

Genetics is a factor in having higher possibilities for HTN (true/false)

false, they are a factor as well

Psychological stress is a factor of HTN. Environmental and dietary factors do not matter as much. (true/false)

Specific Causes of HTN

Renal Artery Constriction

Coarctation of Aorta

Pheochromocytoma

Cushing’s Disease

Primary Aldosteronism

Essential HTN

Htn w/o a specific cause

Percentage of having an essential HTN

95%

Percentage of inheriting essential HTN

approx. 30%

false, the other way around

High sodium intake: Low BP (true/false)

dietary factors that affect BP

high salt intake

low potassium and calcium intake

Short term control of BP

Baroceptor Reflex

Long term control of Blood Pressure

Kidneys (via reduction of water and salt in the blood)

Cardiac Output Equation

Stroke Volume \* Heart Rate

Blood Pressure Equation

Stroke Volume \* Heart Rate \* Total Peripheral Resistance

true, idk

The exact cause of HTN is unknown (true/false)

Possible Mechanisms for an Essential HTN (HTN w/o specific cause)

Diet

Stress

Cigarette Smoking

Alcohol

Normal BP accdg to AHA

Elevated BP accdg to AHA

120-129/

Stage 1 HTN accdg AHA

130-139/80-89

Stage 2 HTN accdg AHA

≥140/≥90

Sympathetic discharge

Sympathetic effect on HR

Sympathetic effect on TPR

Norepinephrine and Angiotensin

Diuretics MOA

excrete more urine, renal excretes more water with Na

Thiazide

Diuretic that acts on the distal convoluted tubule and **inhibit the sodium reabsorption**

Loop Diuretic

Diuretic that act on ascending limp of the Loop of Henle, **inhibitting the reabsorption of NaCl**

Potassium Sparing

Diuretics that prevent the secretion of Potassium into the distal tubule; Prevent Hypokalemia.

Hypokalemia

low potassium blood levels

Hyponatremia

low sodium blood levels

Adverse Effects of using Diuretics

* Fluid Depletion
* Electrolyte Imbalance

> Hyponatremia
>
> Hypokalemia
* GI disturbance

> Weakness
>
> Orthostatic Hypotension

Othostatic Hypotension

* most common adverse effect
* a drop in BP when moving from supine to standing in an upright position.

Beta Blockers

* Sympatholytic Drugs
* a mainstay in the HTN treatment
* dec. HR and force of myocardial contraction
* general dec in sympathetic tone

NOTE: some are relatively selective to receptors that are focused sa cardio.

Adverse Effects of Beta Blockers

* Bronchoconstriction - kapag di selective sa receptor
* Excessive decrease of HR and myocardial contractility
* Depression, fatigue, GI disturbance, allergic reaction
* Orthostatic hypotension

Alpha Blockers

* Sympatholytic Drugs
* Blocks _____ 1 adrenergic receptor on vascular smooth muscle (ability to improve blood lipid profiles)
* used for mild to moderate HTN.

Adverse Effects of Alpha Blockers

* GI disturbance

> Vomitting and Diarrhea
* Orthostatic hypotension

Presynaptic Adrenergic Inhibitor

* Sympatholytic Drug
* Postganglionic Sympathetic Nerve terminal blocker
* MOA: prevent normal physiologic release of norepinephrine from postganglionic sympathetic neurons

Centrally Acting Agents

* Sympatholytic Drug
* Inhibits sympathetic discharge from the brainstem
* Decrease sympathetic outflow

Adverse Effect of Centrally Acting Agents

* Dry mouth
* Dizziness
* Drowsiness

Ganglionic Blockers

* Sympatholytic Drug
* Most of these are not available anymore d/t intolerable toxicities related to their primary action.
* MOA: block the synaptic transmission at autonomic ganglia, decreasing the sympathetic activity, nicotinic cholinergic antagonists - between pre- and postsynaptic neurons of both divisions
* Used only in hypertensive crisis.

Adverse Effects of Ganglionic Blockers

* Dry mouth
* GI discomfort, constipation
* Urinary retention
* Visual disturbances like precipitation of glaucoma, blurred vision
* Excessive orthostatic hypotension and sexual dysfunction
* Neuromuscular blockade

Vasodilators MOA

vasodilates peripheral vasculature, inhibiting smooth muscle contraction via increase in 2nd messengers (cyclic GMP)

Adverse Effects of Vasodilators

* Reflex tachycardia
* Dizziness
* Postural hypotension
* Weakness
* Nausea
* Fluid retention
* Headache

Angiotensin Converting Enzyme (ACE) Inhibitors

* Renin-Angiotensin System Inhibitor drug
* MOA: inhibit enzyme that converts angiotensin 1 to angiotensin 2 (renin-angiotensin system)
* Advantage:

> -lowers the incidence of cardiovascular adverse effects.
>
> \-no reflex tachycardia and orthostatic hypotension
>
> \-prevents hypertrophy of heart and vasculature
* Used in mild to moderate HTN, with or without another drug.

Adverse Effects of ACE inhibitor

* Allergic reaction; rash
* GI discomfort
* Dizziness, chest pain
* Persistent dry cough

Angiotensin II Receptor Blockers

* Renin-Angiotensin System Inhibitor drug
* MOA: blocks angiotensin II type 1 (AT1) receptors
* Advantages

> -no effect on bradykinin metabolism and are therefore more selective blockers of angiotensin effects
>
> \-have the potential for more complete inhibition of angiotensin action
>
> \-provide benefits similar to those of (other Renin-Angiotensin System inhibitor drug) in pt.’s w/ heart failure and chronic kidney dse

Adverse Effects of Angiotensin II Receptor Blockers

* Similar to other Renin-Angiotensin System Inhibitor type including hazard to pregnancy
* Cough and angioedema can occur but are less common

Calcium Channel Blockers

* MOA: block calcium entry into vascular smooth muscle cell, decreasing vascular resistance. This tends to decrease HR and myocardial contractile force.

Adverse Effects of Calcium Channel Blockers

* Excessive vasodilation
* Orthostatic hypotension
* Reflex tachycardia
* Abnormal HR
* Dizziness, headache, nausea

\