Antiganginal And Hyperlipidemia Flashcards Preview

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Flashcards in Antiganginal And Hyperlipidemia Deck (82):
1

Ischemic heart disease, also known as coronary heart disease

Atherosclerosis

2

Important aspects of angina

Quality of pain
Precipitating factors
Duration
Pain radiation
Response to nitroglycerin or rest

3

What causes the chest pain (angina)

Clots in arteries reducing blood flow causing chest pain

4

What is angina caused by

Accumulation of metabolites in striated muscle
-pain that occurs when coronary blood flow is inadequate to supply the oxygen required by the heart
-spasm of vascular smooth muscle or from obstruction of blood vessels causes by atherosclerotic lesions

5

What is the most common cause of angina

Atheromatous obstruction of the large coronary vessels which is known as atherosclerotic or classic or stabler angina


STABLE ANGINA
AKA “angina of effort or exercise induced”

6

Spasms in angina

Close off B.V. and can cause decreased blood flow

7

If a patient climbs the stairs and gets chest pain, what is it and why?

Stable angina
Atherosclerosis
Fine when resting

8

Vasospastic/variant angina

Spasm of B.V., not as common

9

What is unstable angina

When you had stable angina and but now something has changed
-change in the character, frequency, duration, and precipitating factors
-medical emergency
-probably have clot and about to have a MI

10

Stable angina drugs

1. Nitrates
2. B blockers
3. CCB

11

Drugs for vasospastic angina

1. Nitrates
2. CCB

12

What do nitrates do for stable angina

Venodilation thereby decreasing preload and thus the oxygen demand of the heart; some dilation of coronary vessels to increase oxygen delivery

13

B blockers for stable angina

Decrease the oxygen demands of the heart

14

CCB for stable angina

Cause vasodilation of smooth muscle in peripheral vasculature to decrease oxygen demands of the hearr; dilation of coronary vessels to increase oxygen delivery

15

What drug do we use for stable angina that we never use for vasospastic angina

B blockers

16

What do we want to do to treat vasospastic angina and why do B blockers not work for it

Want to dilate the vessels to relax smooth muscle
-B blockers will decrease relaxation. Block B2 and this will worsen vasospastic by vasoconstriction. Should be avoided (especially nonspecific B blockers)

17

What are the treatment options for unstable angina

Aspirin or heparin
Nitroglycerin

18

What kind of drugs should be used for unstable angina

Need anticoagulant in addition to regular angina drugs

19

Other therapies commonly used in angina patients

-prior MI=B blockers, slow conduction, good for arryhthmias
-diabetes: add ACEI
-HLD: statins
-anti-patents drugs: aspirin

20

What is the most common treatment for angina

Nitrates (nitroglycerin)

21

Therapeutic use of nitroglycerin

Drug of choice for prompt relief of an ongoing angina attack

22

How do we treat acute angina

Sublingual nitroglycerin

23

When do you take nitroglycrin sublingually and when do you take it orally

Acute is sublingual, prophylaxis is oral

24

What is used for prophylaxis of stable or vasospastic angina

Oral nitroglycerin

25

MOA of nitroglycerin

Relaxers vascular smooth muscle by conversion of nitrite ions to NO
-activates guanylyl cyclase which increases cGMP
-cGMP leads to dephosphorlyation of the myosin light chain resulting in vascular smooth muscle relaxation

26

What do nitrates do

Increase nitrites
Increase NO
Increase cGMP
De phosphorylate myosin light chain
Vascular smooth muscle relaxation

27

What kind of drugs are nitrates

Prodrugs
-turn into NO to work
-must be metabolized
-NO active ingredient

28

Histamine and NO

-receptors on endothelial cells (H1)
-coupled to NO synthase (enzyme), takes arginine and turns into citrolline: this process forms NO
-chemical mediators that works on endothelial cells that produces NO to vasodilation and increase permeability

29

What is a chemical mediator that’s works on endothelial cells that produces NO to vasodilate and increase permeability

Histamine

30

Bethanochol (M agonist) and NO

-M3 in B.V.
-produces NO
-relaxes smooth muscle
-Gq: phospholipids C, Ca2+, B.V. is the only place where this doesn’t cause constriction
-not coupled with phospholipid C on blood vessels
-most M receptors on endothelial cells
-this is why action is different

31

Effects on cardiovascular system of nitrates

-Dilation of large veins
-Pooling of blood in the veins; this diminishes preload
-reduces work of heart
-dilation of coronary vasculature providing increased blood supply to the heart muscle

32

Pharmacokinetics of nitrates

Very rapid. Sublingually for acute treatment of angina
-transdermal patch for prophylaxis

33

How do relieve acute angina

Sublingual nitrates

34

How do you prevent angina

Transdermal patch

35

Adverse effects of nitrates

Headache (vasodilation causes HA), reflec tachycardia, orthostatic hypotension (dilation of veins)

36

Tachyphylaxis of nitrates (tolerance)

Need to have a nitrate free interval to restore sensitivity to the drug (usually 6-8 hours at night without patxch)
12 hours on and 12 hours off
-cant wear the patch all the time

37

What are the two drugs that show tachyphylaxis

Nitrates and dobutamine

38

What are the nitrates that are used for prevention for angina

Isosorbide mononitrate and isosorbide dinitrate

39

When taking nitrates for prophylaxis, when do you take them?

Take in the morning (or when you’re the most active) so they wear off at end of day and you can do your nitrate free night

40

Therapeutic use of isosorbide mononitrate and isosorbide dinitrate

Prevention of angina attacks

41

pharmacokinetics of isosorbide mononitrate and isosorbide dinitrate

Longer duration of action, given orally

42

Drug interactions of nitrates

Nitrate + phosphodiesterase 5 inhibitors (sildenafil)
-extreme hypotension and death

43

What is the most common drug to take for prevention of stable angina

B blockers

44

Therapeutic use of B blockers for angina

Prevent stable angina, not vasospastic
-decreases HR so heart not working as much

45

MOA of B blockers in angina

Blockade of B1 receptors; these drugs reduce the frequency and severity of angina attacks

46

What three drugs have shown to reduce mortality in patients with stable angina

B blockers
Nitrates
Aspirin

47

Therapeutic use of CCB in angina

Stable or vasospastic angina

48

CCB drugs used for stable angina

Versapamil and diltiazem
-these work at level of the heart

49

Which CCB used for treating vasospastic a gain

Dipines

50

Which CCB is bad for stable angina

Dipines
-decrease BP and reflec tachycardia

51

Raynauds and CCBs

CCBs are good for raynauds, a condition associated with vasospastic and cold extremities

52

How do CCBs work for angina

Ca2+ + calmodulin=MLCK—phosphorylate myosin light chain—interacts with actin and causes contraction

CCB blocks Ca from getting in
Nitrates dephosphorylate myosin light chain

53

Ranolazine

Adjust to other drugs for angina
Prolongs the QT interval and may cause torsades

54

Dyslipidemias

Disorders of lipid metabolism

55

How are angina and hyperlipidemia connected

Hyperlipidemia causes plaques that cause atherosclerosis that causes angina

56

What are the bad cholesterol

LDL

57

What are the good cholesterol’s

HDL

58

Drugs to treat hyperlipidemia

Statins
-HMG Co-A reductive inhibitors
Fibrates: fenofibrate
Niacin
Bile acid sequestrants
Ezetemibe
PCSK9 inhibitors

59

Number one drug for hyperlipidemia

Statins (HMG Co-A reductase inhibitors)

60

What are the HMG Co-A reductase inhibitors for hyperlipidemia

Atorvastatin
Simvastatin
Rosuvastatin

61

MOA of statins (HMG co-A reductase inhibitors

Competitively block the rate limiting step in the synthesis of cholesterol (conversion of HMG CO-a to mevalonate)
-these drugs are structural analongs of HMG CO-A

62

Benefits of statins (HMG Co-A reductase inhibitors)

Inhibiting hepatic cholesterol synthesis
-causes liver to upregulate LDL receptors which clears LDL and VLDL remnants from the blood, high intensity statins also lower trigs and raise HDLs

63

Cardio outcomes of statins

Reduce the risk of coronary events, reduce mortality

64

Side effects of statins

Mild muscle pain, myalgia

Caution with grapefruit juice (P450 inhibitor), increases risk of toxicity

65

Rate limiting step for the synthesis of cholesterol

HMG Co-A reductase

66

Someone with a stable angina should be on a

Statin

67

What are the categories of hyperlipidemia drugs

-statins
-everything else

68

What is the second choice drug for hyperlipideami

Fibrates (fenofibrate)

69

what drug for hyperlipidemia is only for triglycerides

Fenofibrate

70

MOA of fenofibrate

Activate the peroxide me proliferator activated receptor-alpha (PPAR-a) which increases transcription of lipoprotein lipase by adipocytes
-breaks down triglycerides

71

Benefits of fenofibrate in hyperlipidemia

Good for patients hypertriglyceridemia. Use in combo with statin

72

Niacin MOA

Reduces VLDL synthesis, lowering LDL; inhibits hormone-sensitive lipase in adipose tissue to decrease FA and triglycerides levels; decreases metabolism of HDL

73

Side effects of niacin

Flushing and itching caused by PGs
-pretreat with NSAID

74

What is the flushing and itching from niacin caused bu

PGs
NOT HISTMIANE

75

Bile Acid sequetreants (BAS) in hyperlipidemia

Not good for increased triglycerides
-bind directly to bile salts which are made of cholesterol, to decrease their recycling, this forces the liver to make more bile salts via upregulation of LDL receptors on the liver

76

Side effects of bile acid sequestrants (BAS)

May increase trigs
GI upset

77

What is the bile acid sequestrant drug we use for hyperlipidemia

Cholestyramine

78

Ezetemibe MOA

Decreases the GI uptake of cholesterol

79

Side effects of ezetemibe

Often combined with a statin and may increase liver toxicity

80

What drug used to treat hyperlipidemia can affect lipid absorption

Bile acid sequestrants
-cholestyramine

81

PCSK9 inhibitor drug for hyperlipidemia

Alirocumab

82

MOA of PCSK9 inhibitors

Protein convertase subtilisin kexin type 9 is a serine protease that degrades LDL receptors
-drug prevents the actions of this enzyme thereby increasing liver LDL

Powerful, stops body from making LDL
VERY EXPENSIVE