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Pharm Block 11 > Antiganginal And Hyperlipidemia > Flashcards

Antiganginal And Hyperlipidemia Flashcards

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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
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

Pharm Block 11 (7 decks)

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