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Pharm Block 11 > Antiganginal And Hyperlipidemia > Flashcards

Antiganginal And Hyperlipidemia Flashcards

1
Q

Ischemic heart disease, also known as coronary heart disease

A

Atherosclerosis

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2
Q

Important aspects of angina

A 
Quality of pain 
Precipitating factors 
Duration
Pain radiation
Response to nitroglycerin or rest
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3
Q

What causes the chest pain (angina)

A

Clots in arteries reducing blood flow causing chest pain

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4
Q

What is angina caused by

A

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
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5
Q

What is the most common cause of angina

A

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”

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6
Q

Spasms in angina

A

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

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7
Q

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

A

Stable angina
Atherosclerosis
Fine when resting

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8
Q

Vasospastic/variant angina

A

Spasm of B.V., not as common

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9
Q

What is unstable angina

A

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
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10
Q

Stable angina drugs

A
  1. Nitrates
  2. B blockers
  3. CCB
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11
Q

Drugs for vasospastic angina

A
  1. Nitrates

2. CCB

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12
Q

What do nitrates do for stable angina

A

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

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13
Q

B blockers for stable angina

A

Decrease the oxygen demands of the heart

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14
Q

CCB for stable angina

A

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

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15
Q

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

A

B blockers

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16
Q

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

A

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)

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17
Q

What are the treatment options for unstable angina

A

Aspirin or heparin

Nitroglycerin

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18
Q

What kind of drugs should be used for unstable angina

A

Need anticoagulant in addition to regular angina drugs

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19
Q

Other therapies commonly used in angina patients

A
  • prior MI=B blockers, slow conduction, good for arryhthmias
  • diabetes: add ACEI
  • HLD: statins
  • anti-patents drugs: aspirin
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20
Q

What is the most common treatment for angina

A

Nitrates (nitroglycerin)

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21
Q

Therapeutic use of nitroglycerin

A

Drug of choice for prompt relief of an ongoing angina attack

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22
Q

How do we treat acute angina

A

Sublingual nitroglycerin

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23
Q

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

A

Acute is sublingual, prophylaxis is oral

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24
Q

What is used for prophylaxis of stable or vasospastic angina

A

Oral nitroglycerin

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25
Q

MOA of nitroglycerin

A

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
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26
Q

What do nitrates do

A 
Increase nitrites 
Increase NO
Increase cGMP
De phosphorylate myosin light chain 
Vascular smooth muscle relaxation
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27
Q

What kind of drugs are nitrates

A

Prodrugs

  • turn into NO to work
  • must be metabolized
  • NO active ingredient
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28
Q

Histamine and NO

A
  • 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
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29
Q

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

A

Histamine

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30
Q

Bethanochol (M agonist) and NO

A
  • 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
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31
Q

Effects on cardiovascular system of nitrates

A
  • 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
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32
Q

Pharmacokinetics of nitrates

A

Very rapid. Sublingually for acute treatment of angina

-transdermal patch for prophylaxis

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33
Q

How do relieve acute angina

A

Sublingual nitrates

34
Q

How do you prevent angina

A

Transdermal patch

35
Q

Adverse effects of nitrates

A

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

36
Q

Tachyphylaxis of nitrates (tolerance)

A

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
Q

What are the two drugs that show tachyphylaxis

A

Nitrates and dobutamine

38
Q

What are the nitrates that are used for prevention for angina

A

Isosorbide mononitrate and isosorbide dinitrate

39
Q

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

A

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
Q

Therapeutic use of isosorbide mononitrate and isosorbide dinitrate

A

Prevention of angina attacks

41
Q

pharmacokinetics of isosorbide mononitrate and isosorbide dinitrate

A

Longer duration of action, given orally

42
Q

Drug interactions of nitrates

A

Nitrate + phosphodiesterase 5 inhibitors (sildenafil)

-extreme hypotension and death

43
Q

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

A

B blockers

44
Q

Therapeutic use of B blockers for angina

A

Prevent stable angina, not vasospastic

-decreases HR so heart not working as much

45
Q

MOA of B blockers in angina

A

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

46
Q

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

A

B blockers
Nitrates
Aspirin

47
Q

Therapeutic use of CCB in angina

A

Stable or vasospastic angina

48
Q

CCB drugs used for stable angina

A

Versapamil and diltiazem

-these work at level of the heart

49
Q

Which CCB used for treating vasospastic a gain

A

Dipines

50
Q

Which CCB is bad for stable angina

A

Dipines

-decrease BP and reflec tachycardia

51
Q

Raynauds and CCBs

A

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

52
Q

How do CCBs work for angina

A

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
Q

Ranolazine

A

Adjust to other drugs for angina

Prolongs the QT interval and may cause torsades

54
Q

Dyslipidemias

A

Disorders of lipid metabolism

55
Q

How are angina and hyperlipidemia connected

A

Hyperlipidemia causes plaques that cause atherosclerosis that causes angina

56
Q

What are the bad cholesterol

A

LDL

57
Q

What are the good cholesterol’s

A

HDL

58
Q

Drugs to treat hyperlipidemia

A 
Statins
-HMG Co-A reductive inhibitors 
Fibrates: fenofibrate 
Niacin 
Bile acid sequestrants 
Ezetemibe 
PCSK9 inhibitors
59
Q

Number one drug for hyperlipidemia

A

Statins (HMG Co-A reductase inhibitors)

60
Q

What are the HMG Co-A reductase inhibitors for hyperlipidemia

A

Atorvastatin
Simvastatin
Rosuvastatin

61
Q

MOA of statins (HMG co-A reductase inhibitors

A

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
Q

Benefits of statins (HMG Co-A reductase inhibitors)

A

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
Q

Cardio outcomes of statins

A

Reduce the risk of coronary events, reduce mortality

64
Q

Side effects of statins

A

Mild muscle pain, myalgia

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

65
Q

Rate limiting step for the synthesis of cholesterol

A

HMG Co-A reductase

66
Q

Someone with a stable angina should be on a

A

Statin

67
Q

What are the categories of hyperlipidemia drugs

A
  • statins

- everything else

68
Q

What is the second choice drug for hyperlipideami

A

Fibrates (fenofibrate)

69
Q

what drug for hyperlipidemia is only for triglycerides

A

Fenofibrate

70
Q

MOA of fenofibrate

A

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

71
Q

Benefits of fenofibrate in hyperlipidemia

A

Good for patients hypertriglyceridemia. Use in combo with statin

72
Q

Niacin MOA

A

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

73
Q

Side effects of niacin

A

Flushing and itching caused by PGs

-pretreat with NSAID

74
Q

What is the flushing and itching from niacin caused bu

A

PGs

NOT HISTMIANE

75
Q

Bile Acid sequetreants (BAS) in hyperlipidemia

A

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
Q

Side effects of bile acid sequestrants (BAS)

A

May increase trigs

GI upset

77
Q

What is the bile acid sequestrant drug we use for hyperlipidemia

A

Cholestyramine

78
Q

Ezetemibe MOA

A

Decreases the GI uptake of cholesterol

79
Q

Side effects of ezetemibe

A

Often combined with a statin and may increase liver toxicity

80
Q

What drug used to treat hyperlipidemia can affect lipid absorption

A

Bile acid sequestrants

-cholestyramine

81
Q

PCSK9 inhibitor drug for hyperlipidemia

A

Alirocumab

82
Q

MOA of PCSK9 inhibitors

A

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

Pharm Block 11 (7 decks)

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