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PHAC 3001 > Mid 2-1 > Flashcards

Mid 2-1 Flashcards

1
Q

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

A

Atherosclerosis

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2
Q

Treatments for hyperlipidemia

A 
TLC (therapeutic lifestyle change)
Statins 
Bile Acid Binding Resins 
Cholesterol Absorption Inhibitor 
PCKS9 Inhibitors
Niacin 
Fibrates
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3
Q

This is a primary approach for treating hyperlipidemia

A

TLC (therapeutic lifestyle change)

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4
Q

What are the benefits of TLC?

A

reduces LDL-cholesterol by 10-30%

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5
Q

Drugs of first choice for patients with elevated LDL

A

statins

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6
Q

What is the primary therapeutic action of statins?

A

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

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7
Q

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

A

Bile Acid binding resins

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8
Q

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

A

Cholesterol Absorption Inhibitors

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9
Q

Inhibits cholesterol from absorption from the small intestine

A

Cholesterol Absorption Inhibitors

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10
Q

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

A

PCSK9 Inhibitors

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11
Q

Its primary site of action is adipose tissue

A

Niacin

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12
Q

Reduces plasma triglycerides

A

Fibrates

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13
Q

What is the consequence of hypertension?

A

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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14
Q

What are the 4 ways to treat hypertension?

DSAV

A

Diuretics
Sympathetic Drugs
Angiotensin Inhibitors
Vasodilation

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15
Q

Types of Diuretics?

A

Thiazides
K-sparring diuretics
Loop Diuretics

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16
Q

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

A

Thiazides

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17
Q

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

A

K-sparring diuretics

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18
Q

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

A

Loop Diuretics

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19
Q

This blocks SNS outflow

A

Sympatholytic Drugs

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20
Q

decreases SNS outflow and blood pressure

If gets into the brain it causes sedation

A

Centrally Acting (Sympatholytic drugs)

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21
Q

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

A

B-blockers

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22
Q

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

A

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

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23
Q

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

A

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

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24
Q

This blocks a1 receptor in the vascular smooth muscle

A

Alpha 1 blockers which causes vasodilation and reduces BP

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25
Q

This angiotensin inhibitor inhibits the formation of AII from AI

A

ACE Inhibitor (ACE-I)

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26
Q

What happens if ACE-I is inhibited?

What’s the adverse effect?

A

Decreases AII, vasodilation, decrease BP, decreases NA and H2O

Cough and malformation of the fetus

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27
Q

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

A

AII Antagonist (ARB)

Angiontensin receptor blocker

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28
Q

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

A

Causes vasodilation and reduces BP

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29
Q

What happens if AII receptor of adrenal gland is blocked?

A

reduces aldosterone release, reduces sodium and water retention and BP

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30
Q

Blocks Renins which inhibits the fromation of AI from angiotensin

(angiotensin —-> AI ——> AII)

A

Direct renin inhibitor

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31
Q

What are the types of vasodilators (sympatholytic drugs)

A

Ca2+ channel blockers (CCB)

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32
Q

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

A

Nifedipine**

Diltiazem & verapamill ***

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33
Q

This CCB only acts on blood vessels?

A

Nifedipine

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34
Q

This CCB only acts on blood vessels and the heart

A

Diltiazem & verapamill

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35
Q

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

A

Transient Ischemia

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36
Q

This is a crushing pain chest due to coronary artery disease

A

Chronic Angina Pectoris

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37
Q

has a problem with oxygen supply and demand

A

Angina

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38
Q

What are the 2 types of angina?

A

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

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39
Q

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

A

Myocardial Infaction (MI)

40
Q

What are the prevention of coronary artery disease?

A

Aspirin (ASA) and statins

41
Q

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

A

Aspiring (ASA)

42
Q

This prevents coronary artery disease because it reduces LDL cholesterol

A

Statins

43
Q

Treatments of Angina?

A

Decrease risk factors

Bypass surgery, angioplasty or stent

Drug Therapy (vasodilation, beta blockers)

44
Q

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

A

Improve O2 supply and reduce O2 demand

45
Q

What are the drugs we used to improve O2 supply?

A

Vasodilators (it dilates coronary vessels and prevent vasospasms)

46
Q

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

A

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

47
Q

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
A

Nitroglycin (dynamite)

48
Q

3 reasons that nitrates are effective for treating angina:

A

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

49
Q

This decreases O2 demand

A

Decrease preload (nitrates treating angina)

50
Q

This improve O2 supply to ischemic areas

A

Redistribute flood flow to ischemic area

51
Q

This improve O2 supply to heart

A

Prevent coronary spasm

52
Q

How does Nifedipine blocks Ca2+ influx into VSM cells?

A

It decreases [Ca] and decrease contraction

53
Q

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

A

It block calcium influx into VSM cells and heart

result: decreas contraction and calcium

54
Q

Why are Beta-blockers effect in angina?

A

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

55
Q

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

A

Congestive Heart Failure (CHF)

56
Q

What happens when a person suffers in CHF?

A

Decreases the ability of ventricles to pump blood,

reduces CO,

increase RAS and SNS

57
Q

Where can CHF arises from?

A

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

58
Q

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

A

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

59
Q

What are the signs/ symptoms of CHF?

A

Fatigue/ shortness of breath, increase HR

Pulmonary Congestion

Systemic Congestion

60
Q

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

A

Pulmonary Congestion (pulmonary edema)

61
Q

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

A

Systemic Congestion (ankle edema)

62
Q

What are the drug to treats CHF?

A

Positive Inotoropic Drugs

Inhibit RAS

Inhibit SNS

Aldosterone Antagonist & other diuretics

Vasodilators

63
Q

How is digoxin (positive inotropic drug) effective?

A

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

64
Q

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

A

This mimics SNS, increasing contractility

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

65
Q

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

A

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

66
Q

What is the MOA of digoxin?

A

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

67
Q

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

A

it can arrise for arrythmias

68
Q

How is inhibiting the RAS effective in treating CHF?

A

DECREASES

peripheral resistance (preoload and afterload,

aldosterone secretion (Na + H2O)

remodeling caused by CHF (fibrosis, hypertophy, cell death)

69
Q

How is ACE inhibitor have beneficial factor action in CHF?

A

Decreases bradykinin breakdown

70
Q

Its a vasodilator peptide that is broken down by ACE

A

Bradykinin

71
Q

So if ACE is inhibited?

A

AII (decrease)

Bradykinin (increases)

72
Q

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

A

Carvedilol***

73
Q

Why are diuretics effective in CHF?

A

Increase secretion of Na and H2O

Reduces plasma volume and decreases preload

Reduces Edema

74
Q

How is loop diuretics effective in treating CHF/

A

Reduce fluid volume

75
Q

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

A

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

76
Q

How is nitroglycerin effective in treating CHF?

A

It relaxes veins, reduces preolad and edema

77
Q

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

A

Arrythmias

78
Q

Two types of cardiac arrythmias

A

Bradycardias

Tachycardias

79
Q

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

A

Bradycardias

80
Q

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

A

Tachycardias

81
Q

What are the treatments of cardiac arrythmias?

A

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

82
Q

Which anti-arrythmia drugs can actually cause arrythmias?

A

Class I and III

83
Q

What are the mechanism of arrythmias and drug action

A
  1. Enhanced automacity

2. Abnormal Impulse conduction

84
Q

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

A

Enhanced automacity

85
Q

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

A

abnormal pacemaker

86
Q

What are the two type of afterdepolarization?

A

Delayed afterdepolarization (DAD)

Early afterdepolarization (EAD)

87
Q

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

DAD or EAD?

A

DAD

88
Q

This happens when action potential is long.

DAD or EAD?

A

EAD

89
Q

In abnonrmal impulse conduction, AP collide in each other’s refractory period.

Normal or reentry conduction of impulse?

A

Normal

90
Q

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?

A

reentry conduction of impulse?

91
Q

Anti-arrhythmic drug action

It BINDS and BLOCKS Na channel in heart cells that are ischemic, depolarized & firing rapidly

A

Class I (Na Channel Blocker)

92
Q

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
A

Class II (B-adrenergic receptor blockers)

93
Q

Prolong APD & refractory period by blocking K+ channels responsible for repolarization

Works on reentry

Increase: APD and refractory period

A

Class III - K-channel blockers

94
Q

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

A

Class IV: Ca2+ channel blockers

95
Q

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

A

Digoxin

PHAC 3001 (2 decks)

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