Mid 2-1 Flashcards by Kathleen Cabillan

This is a cardiovascular disease where there’s a reduce in blood flow - due to aging and elevated blood lipids

Atherosclerosis

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Treatments for hyperlipidemia

TLC (therapeutic lifestyle change)
Statins 
Bile Acid Binding Resins 
Cholesterol Absorption Inhibitor 
PCKS9 Inhibitors
Niacin 
Fibrates

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This is a primary approach for treating hyperlipidemia

TLC (therapeutic lifestyle change)

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What are the benefits of TLC?

reduces LDL-cholesterol by 10-30%

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Drugs of first choice for patients with elevated LDL

statins

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What is the primary therapeutic action of statins?

To increase hepatocyte LDL receptor levels (cholesterol from the blood into liver) - through an indirect effect of cholesterol depletion

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This increase the expression of LDL receptors and increase hepatic LDL-cholesterol uptake to lower blood LDL-cholesterol levels

Bile Acid binding resins

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This drug blocks the reabsorption of that cholesterol that endogenous cholesterol that was originally secreted in the bile

Cholesterol Absorption Inhibitors

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Inhibits cholesterol from absorption from the small intestine

Cholesterol Absorption Inhibitors

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This increase STEADY-STATE levels of LDL receptor on hepatocyte surface

PCSK9 Inhibitors

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Its primary site of action is adipose tissue

Niacin

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Reduces plasma triglycerides

Fibrates

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What is the consequence of hypertension?

It affects the profusion or the ability of blood to flow at any type of organ.

Increase size of ventricles, low blood flow bc of decrease of oxygen (ischemic)

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What are the 4 ways to treat hypertension?

DSAV

Diuretics
Sympathetic Drugs
Angiotensin Inhibitors
Vasodilation

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Types of Diuretics?

Thiazides
K-sparring diuretics
Loop Diuretics

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This targets distal convoluted tubules that causes hypokalemia (loss of K+) and increase [Na] + H2O, and moderates diuresis

Thiazides

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This targets collecting ducts causing a block on K+ resulting hyperkalemia and increases [Na]

K-sparring diuretics

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This targets loop of henle that increases [Na], H2O in urine

Loop Diuretics

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This blocks SNS outflow

Sympatholytic Drugs

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decreases SNS outflow and blood pressure

If gets into the brain it causes sedation

Centrally Acting (Sympatholytic drugs)

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Uses these drugs to treat hypertension because it might be associated with other illnesses.

B-blockers

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What happens if the b1 receptor in the heart is blocked?

It reduces HR, the force of contraction of heart, cardiac output

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What happens if the b1 receptor in the kidney is blocked?

It reduces the renin release and causes vasodilation. Reduces aldosterone, and Na with H2O retention

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This blocks a1 receptor in the vascular smooth muscle

Alpha 1 blockers which causes vasodilation and reduces BP

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This angiotensin inhibitor inhibits the formation of AII from AI

ACE Inhibitor (ACE-I)

What happens if ACE-I is inhibited? What’s the adverse effect?

Decreases AII, vasodilation, decrease BP, decreases NA and H2O Cough and malformation of the fetus

This blocks AII receptors of the vascular smooth muscle and adrenal gland

AII Antagonist (ARB) Angiontensin receptor blocker

What happens if AII receptor of vascular smooth muscle is blocked?

Causes vasodilation and reduces BP

What happens if AII receptor of adrenal gland is blocked?

reduces aldosterone release, reduces sodium and water retention and BP

Blocks Renins which inhibits the fromation of AI from angiotensin (angiotensin —-> AI ——> AII)

Direct renin inhibitor

What are the types of vasodilators (sympatholytic drugs)

Ca2+ channel blockers (CCB)

What are the types of Ca2+ channel blockers (CCB)?

Nifedipine**** | Diltiazem & verapamill ***

This CCB only acts on blood vessels?

Nifedipine

This CCB only acts on blood vessels and the heart

Diltiazem & verapamill

This describes the low blood flow that decreases O2 delivery to heart mucle

Transient Ischemia

This is a crushing pain chest due to coronary artery disease

Chronic Angina Pectoris

has a problem with oxygen supply and demand

Angina

What are the 2 types of angina?

Stable Agina (consistent each time) and Unstable Angina (attacks more frequently)

This happens when a plaque ruptures, causing blod clots, blocks the coronary arteries, all of the tissues that is being fed with blood

Myocardial Infaction (MI)

What are the prevention of coronary artery disease?

Aspirin (ASA) and statins

This prevents coronary artery disease because it inhibits platelet aggregation (1st step in blood clot)

Aspiring (ASA)

This prevents coronary artery disease because it reduces LDL cholesterol

Statins

Treatments of Angina?

Decrease risk factors Bypass surgery, angioplasty or stent Drug Therapy (vasodilation, beta blockers)

What are the goals of drug therapy in treating coronary artery disease?

Improve O2 supply and reduce O2 demand

What are the drugs we used to improve O2 supply?

Vasodilators (it dilates coronary vessels and prevent vasospasms)

When treating coronary artery disese, in which the drug therepy goal is to reduce O2 demands, what is the result?

Reduce: contractility, HR, afterload (dilate arteries) and preload (dilate veins)

It is an organic nitrates (a vasodilator) used for angina treatment in late 1800’s - slightly volatile, odourless, oily liquid that explodes on heating or percussion

Nitroglycin (dynamite)

3 reasons that nitrates are effective for treating angina:

Decrease preload, redistribute blood flow to ischemic area, and prevent coronary spasms.

This decreases O2 demand

Decrease preload (nitrates treating angina)

This improve O2 supply to ischemic areas

Redistribute flood flow to ischemic area

This improve O2 supply to heart

Prevent coronary spasm

How does Nifedipine blocks Ca2+ influx into VSM cells?

It decreases [Ca] and decrease contraction

Why are verapimil, diltiazem (CCB) effective in agina?

It block calcium influx into VSM cells and heart result: decreas contraction and calcium

Why are Beta-blockers effect in angina?

They block beta receptors and reduce O2 supply which results do decrease HR, force of contraction, and RAS

A disease where heart is so weak it cannot pump enough blood

Congestive Heart Failure (CHF)

What happens when a person suffers in CHF?

Decreases the ability of ventricles to pump blood, reduces CO, increase RAS and SNS

Where can CHF arises from?

Ischemic heart diseasem hypertension, diebetic & other cardiomyopathy, valve disease, arrythmias

What happens when there’s a damage in the heart (brain, kidney, blood vessels involve)?

At the heart, there’s decreas of CO that is sense by the brain the brain sends info to heart, increaseing SNS through beta-1 receptor. the brain also sends info to the kidney increasing the release of renin, and to the alpha receptor of blood vessel causing and increase in vasoconstriction (due to activation of AII. the increase of RAS eventually result to increase in aldosterone

What are the signs/ symptoms of CHF?

Fatigue/ shortness of breath, increase HR Pulmonary Congestion Systemic Congestion

When the left side of heart fails, which forces fluid to the lungs

Pulmonary Congestion (pulmonary edema)

When the right side of heart fails, which forces fluid into vessels

Systemic Congestion (ankle edema)

What are the drug to treats CHF?

Positive Inotoropic Drugs Inhibit RAS Inhibit SNS Aldosterone Antagonist & other diuretics Vasodilators

How is digoxin (positive inotropic drug) effective?

It increase CO, contractility of failing heart, and increase Ca2+

How is B-adrenergic agonist (positive inotorpic drug) effective?

This mimics SNS, increasing contractility For ex: when someone develop heart failure amd has damage valves, B-andregenics agonist is used to pump blood

How is phosphodiesterase type 3 inhibitor (positive inotorpic drug) effective?

This inhibits the breakdown of cAMP and increases it levels, causing an increase with Calcium levels

What is the MOA of digoxin?

It inhibits the Na-pump (makes it move out of the cell) and make Ca2+ to come into the cell

With too much levels of calcium in the heart, what could happen?

it can arrise for arrythmias

How is inhibiting the RAS effective in treating CHF?

DECREASES peripheral resistance (preoload and afterload, aldosterone secretion (Na + H2O) remodeling caused by CHF (fibrosis, hypertophy, cell death)

How is ACE inhibitor have beneficial factor action in CHF?

Decreases bradykinin breakdown

Its a vasodilator peptide that is broken down by ACE

Bradykinin

So if ACE is inhibited?

AII (decrease) Bradykinin (increases)

This highly non-selective drug inhibits SNS activity and slow progression of CHF, blocks Beta-1 and Beta-2 and Alpha-1

Carvedilol***

Why are diuretics effective in CHF?

Increase secretion of Na and H2O Reduces plasma volume and decreases preload Reduces Edema

How is loop diuretics effective in treating CHF/

Reduce fluid volume

How is Aldosterone congestive anatgonist (k-sparring diuretics) effective in treating CHF?

Blocks aldosterone receptors (bc this one is involve in fibrosis and remodeling)

How is nitroglycerin effective in treating CHF?

It relaxes veins, reduces preolad and edema

It’s a disruption in rate, rythm, origin or conduction of the heartbeat, reduces the ability of the heart to pump blood Decrease CO and BP

Arrythmias

Two types of cardiac arrythmias

Bradycardias | Tachycardias

Too few beats per minute (slow heart rate), has damage to pacemaker, due to aginf and low CO

Bradycardias

Too many beats per minute (fast heart rate), impairs the ability of heart to fill properly

Tachycardias

What are the treatments of cardiac arrythmias?

Artificial pacemaker, removal abnormal tissue, implantable cardioverter-defibrilator (ICD)

Which anti-arrythmia drugs can actually cause arrythmias?

Class I and III

What are the mechanism of arrythmias and drug action

1. Enhanced automacity | 2. Abnormal Impulse conduction

This can occur in cells that normall show spontaneous depolarization such as SA and AV nodal cells

Enhanced automacity

Can occur in atrial ventricular cells that do not show spontaneous depolarization

abnormal pacemaker

What are the two type of afterdepolarization?

Delayed afterdepolarization (DAD) Early afterdepolarization (EAD)

Theres a series of beats happening, you get sponatanous flunctuation . If fuse gets big enough, they can trigger extra beats. DAD or EAD?

DAD

This happens when action potential is long. DAD or EAD?

EAD

In abnonrmal impulse conduction, AP collide in each other’s refractory period. Normal or reentry conduction of impulse?

Normal

The activity encounters dead cells and cant get enough one direction. So it makes a continual activation and dysfunctional vetricles Normal or reentry conduction of impulse?

reentry conduction of impulse?

Anti-arrhythmic drug action It BINDS and BLOCKS Na channel in heart cells that are ischemic, depolarized & firing rapidly

Class I (Na Channel Blocker)

Anti-arrhythmic drug action Inhibits SNS activation in the heart Result: - slow HR and speed of impulse - increase AV node refractory period - Uses for supraventricular tachycardias

Class II (B-adrenergic receptor blockers)

Prolong APD & refractory period by blocking K+ channels responsible for repolarization Works on reentry Increase: APD and refractory period

Class III - K-channel blockers

Blocks Ca2+ influx in the heart Slows conduction velocity through the AV node Increase AV node refractory period Have moderate slowing effect on HR Used fro supraventricular tachycardias Same as Class III

Class IV: Ca2+ channel blockers

Mimics effect on PNS in the heart, esp at AV node Slows AV node conduction allows ventricles time to fill like Class II and IV

Digoxin

Mid 2-1 Flashcards

(95 cards)