Cardiovascular Drugs Part 1 Pharm Test 4

Front 1

The functioning unit of the kidney is

Back 1

The nephron

Front 2

The door in

Back 2

Afferent Arteriole

Front 3

The Rotary

Back 3

The Glomerulus (a capillary plexus) where filtration takes place

Front 4

The door out

Back 4

The efferent arteriole.

Clean blood

Front 5

What does the kidney sens?

Back 5

At any given moment, the kidney is "sensing" the pressure and volume of blood flow throughout the body.

Front 6

Low Volume or low BP

Back 6

The kidney releases renin from a small area (the JGA) just inside the afferent arteriole

Front 7

The cyle

Back 7

Renin (the messenger) goes to the liver where angiotensisn 1 goes to angiotensin 2 via Angiotensin Converting Enzyme (ACE).

Front 8

Angiotensin 2

Back 8

Triggers the release of aldosterone from the adrenal cortex causing sodium and water retention.

Vasoconstriction and acts directly on vascular smooth muscle to cause contraction (Acts directly on blood vessels).

Causes BP to rise.

Promotes synthesis and secretion of aldosterone.

Blood vessels are constricted which means that there is decreased blood flow coming to the kidneys.

Front 9

Aldosterone Levels

Back 9

secretion is enhanced when sodium levels are low and when potassium levels are high.

Front 10

Angiotensin II Affects on heart

Back 10

May cause hypertrophy (increased cardiac mass) and remodeling (redistribution of mass within the heart). In hypertension, angiotensin II may be responsible for increasing the thickness of blood vessel walls. In heart failure and MI, it may be responsible for causing cardiac hypertrophy and fibrosis.

Front 11

What does angiotensisn 2 do?

Back 11

Tenses your angios- vasoconstricts.

Triggers the release of Aldosterone (from the adrenal cortex to save Na+ and H20.

Increases inflammation in the arteries.

Prothrombotic

Increases tissue resistance to insulin

Potent growth factor.

Front 12

Actions of Aldosterone

Back 12

After being released from the adrenal cortex, aldosterone acts on distal tubules of the kidney to cause retention of sodium and excretion of potassium and hydrogen. Because retention of sodium causes water to be retained as well, aldosterone increases blood volume, which causes blood pressure to rise.

Can also promote cardiac remodeling and fibrosis.

Front 13

Direct Renin Inhibitor (DRI)

Back 13

Drugs that act on renin to inhibit the conversion of angiotensionogen into angiotensin I.

Example: Aliskiren

Front 14

Aliskiren (Tekturna)

Back 14

Used for hypertension.

Blood pressure redution equals that seen with ACE inhibitors. Aliskiren causes less cough and angioedema than the ACE inhibitors but poses risk to developing fetus.

MOA: Binds with renin and inhibits the cleavage of angiotensionogen into angiotensin I.

Front 15

ACE inhibitors

Back 15

Treat hypertension, heart failure, diabetic nephropathy, and myocardial infarction. Used to prevent adverse cardiovascular events in patients at risk.

Example: CaptoPRIL (Capoten)

Dilates bolld vessels, reducrs blood volume, and prevent or reverse pathologic changes in the heart and blood vessels mediated by angiotensin II and aldosterone.

Front 16

ACE inhibitors Function

Back 16

As Anti-hypertensive agents via vasodilation and inhibition of aldosteron (Na+ and H20 diuresis)

To treat CHF- CHF is a hyperreninemic state (low volume/low pressure as the heart is not pumping effectively)- increased renin-angiotensin-aldosterone-the PRILS stop the cycle.

To act as an Anti-inflammatory agent

To act as an Anti-thrombotic agent

To provide a Hypoglycemic effect (be careful when starting ACE inhibitors in diabetics on anti-glycemic drugs)

To decrease growth of tissues or remodeling

Front 17

Hyperreninemic State

Back 17

A lot of renin in the blood. You are vasoconstricting and hanging on to sodium and water. That is what CHF is.

Front 18

Hypoglycemic effect

Back 18

Makes tissues resistant to insulin and insulin tries to bring the sugar in- ACE inhibitor makes cell less resistant to insulin. If you give an ACE inhibitor to a diabetic, you could have really low blood sugar. You give diabetic insulin to lower blood sugar and ACE will lower blood sugar.

Front 19

Remodeling in the heart

Back 19

After a MI, angiotension 2 remodels and enlarges the myocardium and disrupts the conduction system. In your heart with chronic heart failure- remodeling increases the risk of ventricular dysrhthmias. It disrupts the conduction system.

Front 20

Remodeling and Angiotensin

Back 20

Angiotensin increases vascular fibrosis resulting in hypertension. Angiotensin Vasoconstricts and increases inflammation in arteries. Angiotensin increases intraglomerular blood pressure resulting in intraglomerular hypertension leading to CKD (chronic kidney disease).

Front 21

Summary of why ACE Inhibitors are used

Back 21

To decrease the risk of first and second myocardial infarctions in high-risk patients due to anti-inflammatory effects.

For stroke prevention

For prevention of diabetic nephropathy

To decrease insulin resistance and reduce the risk of progression to type 2 diabetes

For prevention of diabetic retinopathy

Front 22

Side Effects of ACE inhibitors

Back 22

Hypotension

Hyperkalemia (excreting sodium and water and retaining potassium) (When getting rid of sodium, you hang on to K

Hypoglycemia (especially when the patient is already on hypoglycemic drugs)

Cough- hacking, dry

Angioedema (Does my voice sound funny to you?)- increased swelling of the lips and toungue.

Front 23

S/S of hyperkalemia

Back 23

dsryhthmias, muscle weakness, nasuea, vomitting, the T wave (time of repolarization) is tall and tented like a teepee. Potassium has everything to do with electrical conduction through the heart. ACE inhibitors will cause hyperkalemia.

Front 24

What is the mechanism of the ACE inhibitor-induced angioedema?

Back 24

Angiotensin Converting Enzyme normally breaks down bradykinin, a potent vasodilator.

ACE inhibitors inhibit the breakdown of brdaykinin resulting in the accumulation of bradykinin with 2 effects: vasodilation and increased permeability.

High-risk patients- patients with a C1 esterase inhibitor deficiency, smokers (3.1%) and African Americans (5.54%)

Front 25

Hyperkalemia

Back 25

Add a thiazide diuretic to the PRIL:

Capozide (captopril + thiazide)

Vaseretic (enalapril + thiazide)

Zestorectic (as above)

Lotensin HCT (benazepril + hydrochlorothiazide)

Decrease foods containing postassium expecially when the ACE inhibitors are combined with potassium-sparing agents spironolactone (Aldactone) or eplerenone (Inspra)

Front 26

Thiazide diuretic (HCTZ)

Back 26

Mild diuretic

Gets rid of potassium

ACE inhibitors combined with Thiazide

Front 27

Aldactone is

Back 27

a potassium sparing diuretic. It hangs on to K. Makes K go up.

Front 28

Foods high in potassium

Back 28

Banana (1 med) 422 mg

Potato (with skin) 540 mg- potato skins are high in potassium

French Fries (1 med) 924 mg

Halibut (3 oz) 490 mg

Spinach (1c) 839 mg

Pasta Sauce (1c) 839 mg

Oranges (1 m) 237 mg

Prunes (10) 615 mg

Any dried fuit