Treatment Of Hypertension

Front 1

Determinants of BP

Back 1

Diameter of Arterioles
Heart Rate (B1 Adrenergic Receptors)
Force of Ventricular Contraction (B1 Adrenergic Receptors)
Blood Volume (Renin-Angiotensin System)

Front 2

Baroreceptors

Back 2

Detect stretch in carotid sinus-->relay info to vasomotor center

Front 3

Renin-Angiotensin System

Back 3

Drop in BP detected by baroreceptors, renin is released from juxtaglomerular cells-->convert Agtensin to Agtensin I. Agtensin I converted to Agtensin II in lungs. Agtensin II directs vasoconstriction & aldosterone synthesis in adrenal cortex

Front 4

Antihypertensive Agents

Back 4

Diuretics
Direct Vasodilators
Sympatholytic Agents
Angiotensin Related Agents
Combo Therapy (Most Common)

Front 5

Diuretics

Back 5

Increase in the volume of the urine
Increase in renal sodium excretion

Front 6

Mechanism of action: Thiazides

Back 6

Inhibit sodium reabsorption at distal tubule

Front 7

Mechanism of action: High Efficacy Loop Diuretics

Back 7

Work at Loop of Henle
Inhibit sodium reabsorption from Loop of Henle
Increased Na+ in collecting duct results in increased K+ eliminated -->hypokalemia

Front 8

Mechanism of action: Potassium Sparing Agents

Back 8

Work at Collecting Duct
Promotes increase in K+ reabsorption -->potassium sparing

Front 9

Spironolactone

Back 9

Potassium Sparing Drug
Reduced expression of the basolateral Na+/K+ ATPase

Front 10

Triamterine

Back 10

Potassium Sparing Drug
Blockers of Na+ channels on the apical membrane-->prevents reabsorption of Na+ and excretion of K+

Front 11

Determinants of BP

Back 11

Diameter of Arterioles
Heart Rate (B1 Adrenergic Receptors)
Force of Ventricular Contraction (B1 Adrenergic Receptors)
Blood Volume (Renin-Angiotensin System)

Front 12

Baroreceptors

Back 12

Detect stretch in carotid sinus-->relay info to vasomotor center

Front 13

Renin-Angiotensin System

Back 13

Drop in BP detected by baroreceptors, renin is released from juxtaglomerular cells-->convert Agtensin to Agtensin I. Agtensin I converted to Agtensin II in lungs. Agtensin II directs vasoconstriction & aldosterone synthesis in adrenal cortex

Front 14

Antihypertensive Agents

Back 14

Diuretics
Direct Vasodilators
Sympatholytic Agents
Angiotensin Related Agents
Combo Therapy (Most Common)

Front 15

Diuretics

Back 15

Increase in the volume of the urine
Increase in renal sodium excretion

Front 16

Mechanism of action: Thiazides

Back 16

Inhibit sodium reabsorption at distal tubule

Front 17

Mechanism of action: High Efficacy Loop Diuretics

Back 17

Work at Loop of Henle
Inhibit sodium reabsorption from Loop of Henle
Increased Na+ in collecting duct results in increased K+ eliminated -->hypokalemia

Front 18

Mechanism of action: Potassium Sparing Agents

Back 18

Work at Collecting Duct
Promotes increase in K+ reabsorption -->potassium sparing

Front 19

Spironolactone

Back 19

Potassium Sparing Drug
Reduced expression of the basolateral Na+/K+ ATPase

Front 20

Triamterine

Back 20

Potassium Sparing Drug
Blockers of Na+ channels on the apical membrane-->prevents reabsorption of Na+ and excretion of K+

Front 21

Direct Acting Sympatholytic Agents

Back 21

Receptor Antagonists
Beta-Blockers
A1 Adrenergic Recepor Antagonists

Front 22

Indirect Acting Sympatholytic Agents

Back 22

Interfere with sympathetic neurotransmission
CNS-Acting (Clonidine)
Catecholamine Release Inhibitors (Reserpine)

Front 23

A1 Adrenergic Receptor Antagonist

Back 23

Direct Acting Sympatholytic Agent
Vasodilation-->decrease in BP

Front 24

B1 Adrenergic Receptor Antagonist

Back 24

Direct Acting Sympatholytic Agent
Descrease contractility in heart-->decrease in BP

Front 25

Indirect Sympatholytic Agent

Back 25

Reserpine - Inhibits release of catecholamines from sympathetic nerves

Front 26

CNS Acting Sympatholytic Agents

Back 26

Clonidine
Tricks A2 receptors into thinking there are high enough levels of catecholamines around-->inhibits production of more

Front 27

Sympatholytic Vasodilators

Back 27

Block sympathetic NS induced constriction of arterial smooth muscle
-A1 adrenergic receptor antagonists

Front 28

Direct Vasodilators

Back 28

Directly dilate arterial smooth muscle without inhibiting sympathetic NS

Front 29

Oral Hypertension Drug

Back 29

Hydralazine - Opens potassium channels
Calcium Channel Blockers - Block voltage dependent Ca+ channels on vascular smooth muscle
Minoxidil - Reserved for severe hypertension

Front 30

Parenteral Drug Vasodilators

Back 30

Used for emergency hypertensive situations
-Too efficacious for outpatient use & too many side effects

Front 31

Side Effects of Vasodilators

Back 31

Postural Hypotension
Flushing, Sweating
Headache
-Reflex Responses
Reflex Tachycardia (rational for co-administration with beta blockers)
Reflex Fluid Retention( rational for co-administration with diuretic)
VASODILATORS ARE GENERALLY GIVEN WITH A BETA BLOCKER/DIURETIC TO PREVENT REFLEX RESPONSES

Front 32

Indirect effects of vasodilators

Back 32

Reflex increase in HR, Reflex increase in Na+ reabsorption-->increased blood volume/edema

Front 33

ACE Inhibitors

Back 33

Angiotensin Converting Enzyme Inhibitors
-Inhibits conversion of Agtensin to Agtensin II-->results in reduced BP
CAPTOPRIL
*all ACE inhibitors end in '-pril'

Front 34

Mechanism of action for Angiontensin Receptor Antagonists

Back 34

Inhibits binding of Agtensin II to its receptor-->results in reduced BP

Front 35

Side Effects of ACE Inhibitors

Back 35

Dry cough (accumulation of bradykinin)
Change in taste
Edema
Hyperkalemia

Front 36

Angiotensin Receptor Blockers (ARBs)

Back 36

Comeptitive Antagonists at AT1 angiotensin receptors
Selective: no effects on bradykinin metabolism (no dry cough)
Complete: blockade of all angiotensin II effects
LOSARTAN
*all ARBs end in '-artan'

Front 37

First Choice Drugs

Back 37

Most people: Thiazide Diuretics
Diabetics: ACE Inhibitors
CHD: Beta Blockers