Lecture 6 Flashcards
Dx Hypertension
TWO readings of at least 140/90 at TWO appointments
Primary Hypertension
Most Common
Unknown Etiology
Older People
Secondary Hypertension
Less Common
Has some cause
Younger People
Hypertension Results in
End organ damage- heart, kidneys, brain, eyes
Stage 1 Hypertension Numbers
140-159/90-99
Normal Tension Numbers
Stage 2 Hypertension Numbers
160-179/100-109
Pre-Hypertension
120-139/80-89
Hypertensive Emergency
>180/>110 AND have symptoms: Confusion Chest Pain Renal Failure Visual Changes
Five Types of hypertension drugs
Diuretics (Thiazides, Loop) Adrenergic Agents CCB ARB ACEI
Thiazides: Mechanism
Act on distal Convuluted Tubule
Inhibit Na reabsorption
SE of Thiazides
Hypokalemia
Hyperuricemia
Xerostomia
Anorexia
Loop Diuretics: Mechanism
Act on Ascending Loop of Henle
Inhibit Na reabsorption
SE of Loop Diuretics
Hypokalemia
Hyperuricemia
What type of pts use Loop Diuretics
Hypertensive pts with CHF
Can cause rapid diuresis
Potassium Sparing Diuretics: Mech
Spirinolactone and Eplereone - Block Aldosterone Receptor
Amiloride and Triamterene - Block Na channels
Potassium Sparing D’s
Not as strong as other D’s- used as adjunct
SE of K Sparing D’s
Hyperkalemia
Arrythmia
Adrenergic Meds for Hypertensions: Types
A2 agonist
A1 antagonist
B blocker
B1 selective blocker
Adrenergic System Responses
A1 - Inc BP
A2 - Inhibits NE
B1 - Inc HR and Contraction
B2 - Inc vasoDILATION
A2 Agonist: Action
Inhibit Epi and NE –>
Vessel Dilation
SE of A2 Agonist
Drowsiness
Sedation
A1 Antagonist: Action
Block receptors in arteries and veins–> relax smooth muscle–> Reduce HTN
SE of A1 Antagonist
Postural Hypotension
Disadvantages of Non-selective B blockers and of Selective B1 Blockers
Non selective - reactive airway disease
Selective - hypotension and bradycardia
CCB’s: action
Inhibit movement of Ca into cardiac cells –> vasodilation and reduces afterload
Uses for CCB’s
Hypertension
Arryhthmias
Angina
SE’s of CCBs
Gingival growth
Excessive hypotension
Nausea/vomiting
Bradycardia
ACEI’s: Mech
Blocks ACE and thus blocks conversion of Angiotensin I to II
Angiotensin II produces vasoconstriction and stimulates aldosterone release and water retention
ACEI’s SE’s
Hypotension URI Nausea and vomiting LICHENOID ORAL LESIONS Drug interaction w/ NSAID's
ARB’s: Mech
Bind to Angiotensin II receptor and block action
–> blocks release of aldosterone
When is BP an EMERGENCY
> 180/110