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Pharmacology > Anti-Anginal Drugs > Flashcards

Anti-Anginal Drugs Flashcards

1
Q

The most COMMON cause of death in the world————

A

I.H.D

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2
Q

Transient reversible cardiac

ischemia—————

A

Angina=

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3
Q

Presentation: of Angina

3 things

A

1- Centralized pain (retrosternal pain)
2- Sense of tightness
3- Should not last ˃ 15-20 min

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4
Q

———– is the first priority and the most important tool for the diagnosis of MI
and can confirm the diagnosis in 80% of cases.

A

ECG

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5
Q

Coronary artery contain beta——— adrenoreceptor

A

2

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6
Q 
Parienzmetal angina
People with angina have alpha in
coronary artery more than beta,
so once you give beta blocker
the --------- will take the hand and
lead to severe vasospasm
“NEVER EVER GIVE B
BLOCKER”
A

Alpha

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7
Q

If u don’t treat stable angina within ——min

Unstable&raquo_space;

A

15-20

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8
Q

Angina of effort or
exercise (Chest pain)
Fixed subintimal
Atheroma deposition

A

Classic Angina
/typical/exertional
or chronic stable
Angina

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9
Q

subendcardial

myocardial ischemia in

A

Classic Angina

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10
Q 
Acute coronary syndrome
- Unstable Angina
Rupture ; Partial
coronary obstruction
(-------------)
A

Sudden chest pain)

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11
Q

————-: Complete Coronary

obstruction (irreversible)

A

MI

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12
Q 
Vasospastic or
Variant
(Prinzmetal)
(-----------------angina)
Chest pain
during the ------------------
= Coronary ---------------
A

Tansmural -rest-VC

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13
Q

in ————— angina we can use

beta blocker - CCBs - other drugs work on BV

A

Stable

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14
Q

In ————–angina we can use Thrombolytics and antiplatelet , coronary vasodilator

A

Unstable

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15
Q

in —————- angina we try to make coronary vasodilation and use CCBs and we never never never use Beta blocker

A

Prinzmetal

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16
Q 
Cardiac work (O2 ------------) α Coronary blood flow (O2---------)
 Contractility x HR α O2 supply
A

demand-supply

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17
Q

CAD=I.H.D

  • ——-Cardiac work
  • ——–O2 supply
A

inc

dec

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18
Q

Your goal is to restore this balance

  • ———O2 demands (cardiac work)
  • ———-O2 supply (coronary blood flow)
A

dec

inc

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19
Q

↓HR & myocardial contractility: 2drugs

Both——–Ve chronotropics and ———Ve inotropics

A
  • β-blockers
  • C.C.Bs
  • negative
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20
Q

-↓ Preload (EDV) ( strong venodilatation)

1 drug

A
  • Nitrates: venular VD
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21
Q

-↓Afterload

3 drugs

A
  • CCBs: arteriolar VD
  • βBlockers: ↓BP
  • Nitrates: arteriolar VD (in higher doses)
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22
Q

increase O2 supply (coronary blood flow)

3 drugs

A 
A. Nitrates: VD of epicardial
coronary arteries-redistribution
of blood to ischemic areas- VD
of collaterals.
B. CCBs: coronary VD
C. βBs: ↓BP -↑diastolic period
→↑coronary filling (not good).
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23
Q

First strategy to reduce heart work

• ↓ Preload (EDV) ( strong venodilatation)

A 
A.
ƒ Decrease venous return
ƒ Decrease preload
ƒ Decrease EDV (EDP)
ƒ Blood pooled to periphery
ƒ Decrease the stretch of myocardium
ƒ Decrease contraction
ƒ Decrease O2 demand
ƒ Reduced coronary blood flow (O2 supply)
B.
ƒ Less preload less pressure on deeper myocardial circulation
 better flow to the deeper myocardium
 Less radius less tension less O2 need
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24
Q

↓ Afterload ( arteriolodilation)

A 
Ca++ channel blockers
ƒ Decrease T.P. resistance
ƒ Decrease PRESSURE
ƒ Decrease TENSION to maintain C.O
ƒ Decrease cardiac work
ƒ Decrease O2 demands
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25
Q

What is the main arteriolodilator in angina?

A

Calcium channel blocker

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26
Q

———- H.R
A.————————
ƒ SA node (Ca++ dependent depolarization)
ƒ If you block Ca++ channel; Decrease A.P ( - Ve chronotropic)
ƒ β- blockers
ƒ SA node ( ———– receptors)
ƒ If you block β1- receptors ; Decrease H.R ( - Ve chronotropic)
ƒ Cardiac cells loaded by Ca++ depend on Voltage gated Ca++ channels
(———–type) + β1- receptors
ƒ If you block both ; decrease Ca++ loaded ; decrease contractility;
decrease O2 demand (- Ve inotropics)

A

↓
Ca++ channel blockers
β1
L

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27
Q

1- decrease the preload by Venodilator (——— )
2- decrease the after load by arteriolodilation ( ———– )
3- decrease HR which decrease sympathetic activity ( —————- )

A

nitrateCa+ -chanel blocker-Beta 1 blocker

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28
Q 
Between Attack
1- -------------- blockers
2- ----------- channel blockers
(except Nifedipine) ( c. work )
3- Nitrate (intermediate or long
acting) ( c. work )
( c. work )
4- Ranolazine
5- Preventive FFA oxidation
inhibitors (Trimetazidine)
6- Plaque stabilizers (Statins)
7- Antiplatelete (Aspirin)
8- Thrombolytic drugs
A

β
Ca++
Nifedipine

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29
Q 
Acute
attack
also
(Prophylactic)
Short acting
A

Amyl nitrate
Nitroglycerin
=Glyceryl
Trinitrate

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30
Q

Inbetween
attack
Intermediate
acting drug

A

Isosorbide

dinitrate

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31
Q

What is the dose of Amayl nitrate that patient will have ?and root? onset? duration ?

A 
Ampoule
 0.3 ml
Inhalation
1 min
5 min
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32
Q

Prototype is ——-

A

Nitroglycerin (Glyceryl

Trinitrate) ( NTG )

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33
Q

Dose of NTG ?

A 
S.L 0.5 mg
(Sublingual
Plexus)
Spray (Buccal
Mucosa)
I.V µg/ml
(Monitoring)
Oral SR
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34
Q

can we give Beta blockers to a patient with Prinzmetal’s angina?

A

No if we block beta receptors we are decreasing vasodilation, and the
vasoconstriction caused by Alpha receptors will worsen .NEVER EVER GIVE
B BLOCKER

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35
Q

What is the main arteriolodilator in angina?

A

Calcium channel blocker

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36
Q

How to Avoid Nitrate Tolerance ?

A

Due to prolonged administration
‡ Stop give nitrate A.M and P.M ; Give nitrate for 12 h only and
substitute other 12 h with another medication in case of
angina attack very frequently 12 h with another medication in case of
angina attack very frequently

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37
Q

How to avoid the side effect of beta blocker or nitrate?

A

Nitrate and vise versa

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38
Q

Drug strategies in stable angina?

A

dec cardiac work
1- decrease the preload by Venodilator ( nitrate)
2- decrease the after load by arteriolodilation ( Ca+ chanel blocker )
3- decrease HR which decrease sympathetic activity ( Beta 1 blocker )

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39
Q

A 60-year-old man presents to his primary care physician with a complaint of severe
chest pain when he walks uphill to his home in cold weather. The pain disappears when he
rests. After evaluation and discussion of treatment options, a decision is made to treat him
with nitroglycerin.
1. Which of the following is a common direct or reflex effect of nitroglycerin?

A

(D) Increased cardiac force

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40
Q

In advising the patient about the adverse effects he may notice, you point out that
nitroglycerin in moderate doses often produces certain symptoms. Which of the following
effects might occur due to the mechanism listed?

A

(D) Headache due to meningeal vasodilation

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41
Q

One year later, the patient returns complaining that his nitroglycerin works well when he
takes it for an acute attack but that he is now having more frequent attacks and would like
something to prevent them. Useful drugs for the prophylaxis of angina of effort include

A

(E) Verapamil - betablocker

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42
Q
  1. If a β blocker were to be used for prophylaxis in this patient, what is the most probable
    mechanism of action in angina?
A

(A) Block of exercise-induced tachycardia

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43
Q

A 60-year-old man experiencing sudden onset of chest pain
radiating to his left shoulder while climbing upstairs. He
has past history of angina and his family physician had
instructed him to take nitrates sublingually in case of acute
pressure or squeezing chest pain. Which of the following
nitrate preparation is NOT prescribed for sublingual
administration?

A

B. Isosorbide mononitrate

D. Amyl trinitrate

44
Q

Nitroglycerin administered sublingually may contribute to
the relief of myocardial pain by each of the following
mechanisms, except:

A

Decreased venous pooling resulting in increased cardiac

preload

45
Q

in Asthma patient has angina can use ——- and ——–
because they will decrease HR
m.work - Relaxation of coronary s.m
and can not use ——— bacause of ———–

A 
Nitrate + C.C.B (Verapamil)
dec. HR &dec. Contractility
m.work
Relaxation of coronary s.m
Relaxation of Bronchial s.m
Beta Blocker - Bronchospasm
46
Q

CHF with angina can use ———–and———– not ————-or————-because ————-give them —————for long acting

A 
Nitrate + C.C.B
Verapamil (-ve inotropes)
= Myocardial depression
NoT Nifedipine:
-R. Tachycardia
Give Amlodipine (long.A.)
47
Q

HTN can use ——————-and—————-and——————and——————and least preferred to use Nitrate

A

beta-blockers
C.C.Bs (long.A.)
-VD dec preload+dec afterload
-Coronary VD

48
Q

D.M
can use ————- not ————and can use ————— for long action and least preferred to use—————–

A 
Nitrate + C.C.Bs
Verapamil (dec insuline release , however not
clinically important)
Not Nifedipine
Give Amlodipine (long.A.)
49
Q 
3- Ca++ channel blockers
‡ Competitive blocking of--------------- channel.(Ltype)
ƒ Ca++ dependent cardiac activity:
1- ----+------ nodal
depolarization 
2- Atrial + ventricular contraction
A

voltage-gated Ca++

SA +AV

50
Q 
drug of CCBs do :
dec HR
dec Conduction
dec Contraction
dec velocity
decCa++ med. C. myocyte necrosis
decC. work
A

Verapamil

51
Q 
drug of CCBs do :
Vasodilatation
------------ (Short acting; R.
Tachycardia; increase the incidence of
MI)
A

Nifidipine

52
Q

Give ———— (Long acting; does
not cause R.tachycardai; DOES NOT
affect HR and CO)

A

Amlodipine

53
Q

——— cause Arteriolar smooth m.s (Ca++ channels) dec T.PR (
afterload)dec c.work (D.O.C. in preinzmetal’s
angina); ———— is the best
To prevent R.T: + *—————— (Asthma-D.M)
Or give Cardioselective

A

Nifedipine
Amlodipine
Beta blockers

54
Q

S.E of C.C.B:

A

1- Constipation ( Inhibit Ca++ channels on GIT s.m)

2- ankle edema ( Decrease B.P; R.T; Activate RAAS)

55
Q

To avoid side effects of Beta blocker give ————-and vise versa

A

Nitrate

56
Q

Propranolol, bisoprolol, metoprolol, atenolol, Carvedilol

are all ———————

A

Beta blockers

57
Q

Beta Blockers
—–Cardiac work ——–O2 demands ———-infarct size (post MI mortality)
——— HR & contractility ———-CO and———— BP———– SV———-EDV
Bradycardia cause ———–diastolic filling time ; ——————–coronary blood
flow——————–coronary filling
THIS IS NOT GOOD for angina pts therefore nitrate will
cause VD which will reduce EDV.

A

all dec. except the last one is inc

inc - inc - inc

58
Q

Block B-2 receptor on coronary artery( ———–of the

blood)

A

redistribution

59
Q

Do metabolic switch : switch of the metabolism in infarct size
from oxidation of ———which need more O2 to glucose

A

FFA

60
Q

Beta blockers in angina:
————–HR X decrease SV= decrease C.O= decrease cardiac work= decrease need of O2
-B-blockers protect the heart not even at rest but even
if person under——————- .
*NB:
B1 selective blockers are ———–.
- Pindolol (with intrinsic sympathetic activity; ISA) should be————- .

A

ƒ Decrease -exertional stersses-preferred-avoided

61
Q

Stable angina (1st choice —————–; 2nd choice——— )
‡ Beta-blockers C/I with ——– angina (unopposed alpha effect)
‡ Never ever stop Beta-blockers suddenly?
ƒ Beta in heart upregulation: Precipitate ——

A

Beta-blockers-C.C.Bs-variant-MI

62
Q

PKs of NTG
1. Can be given by——,——–,——- (both avoid first pass metabolism).
2. —————- have long half lives and are used TO prevent nocturnal angina.
3. Oral bioavailability of nitroglycerine and isosorbide dinitrate is very —————-(extensive
first pass metabolism).
4. Because of its ——action, long established safety and low cost Nitroglycerin is the most useful drug of the organic nitrate given
—————
5. Isosorbide mononitrate by pass hepatic metabolism and has ————– bioavailability after
oral Admin, delayed onset and long duration (elimination t1/2~ ———–). Therefore has been
formulated as Tablet and as a sustained release preparation

A 
IV, sublingual & transdermal patches
Transdermal patches
low 
rapid 
sublingually.
100%
4-5 h
63
Q

Why you give NTG S.L in acute attack (stable angina)
- To avoid ————–
- If frequent attack; daily
- If not frequent attack?
- As required (prophylaxis) SR or Transdermal patch or
ointment

A

first pass effect-

64
Q
  • Which one of oral antinational medication does not
    undergo under first pass effect and therefore has excellent
    bioavailability after oral administration ?
A

Isosorbide mononitrate

65
Q

Organic nitrates: M.O.A
‡ They are all have the same M.O.A , the difference only in———————– .
‡ Nitrate is prodrug of ——————

A

PK-nitric oxide

66
Q

Nitrate - NO (EDRF) - increase —————in vein(present in _________and__________) lead to ————
——-PGE2/I2 lead to VD

A

cGMP -vascular B.V and smooth muscle -VD

increase

67
Q

Organic nitrates: Phramacological effects
A. Effect of nitrate on blood vessels:
1. ———— (generalized ) Vein —– than artery
2. Venular VD —–preload ——-cardiac work —–O2 demands
3. Coronary VD Redistribution of the blood (——- infarct size)
reduce post MI mortality
4. ——-Afterload—— T.PR ——-cardiac work —–O2 demands
5.——— in head and neck blood vessels (Flushing)
6.———- in meningeal artery in brain (Throbbing headache)
B. Effect of nitrate on Heart:
1. ————- on the heart only on the blood vessels
2. Due to the their VD lead to R. Tachycardia (Not good for
angina patients) (—————-)

A 
VD
more
dec
dec
dec
dec
dec
dec
dec
dec
vd
vd
does not work
high dose
68
Q

Organic nitrates: Phramacological effects
A. R.Tachycardia ————-Tachypnia
‡ Therefore, You have to monitor the dose which does not cause hypotension.
B. Nitrate——————- NO (Nitric Oxide)
- Oxide is a free radical with high dose of nitrate; Oxide
oxidation_________ Hemoglobin (F3+) _______MetHb
(Cyanosis;———————- )

A

methemoglobinemia

69
Q

Organic nitrates: Indications
‡ 99% in ————–
‡ Not contraindicated in any type of I.H.D, however; more used in ————— angina with B- blockers.
‡ MI : To limit the—————— and post MI mortality
‡ Acute Heart Failure: Nitrate I.V Both (Arteriolodilator + Venular ————–)
‡ —————- edema : NTG S.L Both (Arteriolodilator + Venular VD)
‡ A —————- (CN - bind with Hb Hb cannot carry O2 tissue
hypoxia ; cyanosis. (Give high dose of 300 mg nitrate; NO; ————)
CNMetHb , then you give Na+ ————- injection
CN- Thiocynate (Kidney)

A 
I.H.D-classic
 infarction size
VD
Pulmonary
cyanide Toxicity
MetHb
thiosulfate
70
Q

Organic nitrates: S.E
1. B.P : Reflex. T (Not good for ————)(at high doses)
2. Flushing of the face (VD of the facial blood vessels)
3. ———– Headache (Good)( Give simple analgesics)
4. Nitrate Tolerance
Nitrate show very high tendency to produce tolerance with ————-hr
A- NO (oxidizing agent) Oxidation Mitochondrial aldehyde dehydrogense________ Inhibit NO production
B. Prolonged VD________ Kidney activate RAAS (Salt,H2O retention)
C. Brain; reflex tachycardia —————–

A

angina patients
Throbbing
12-16 hr
VC

71
Q

How To Avoid Nitrate Tolerance
‡ Due to prolonged administration
‡ Stop give nitrate A.M and P.M ; Give nitrate for 12 h only and
substitute other 12 h like —–with another medication in case of
angina attack very frequently

A

beta blocker

72
Q
  • In exertional angina: Nitrate-free interval (Should be at ———–)
  • In prinzmetal’s angina: Nitrate-free interval (———-)
A

night-at noon

73
Q

Organic nitrates: Precaution

7 things

A
  1. Do not exceed the recommended dose
  2. Keep some nitrate at home (nocturnal chest pain)
  3. Patients must consult the doctors if the pain does not
    disappear with 15 min.
  4. Given I.V infusion
  5. Check expiry date
  6. Photosensitization (Foil)
  7. Sildenafil ——inc NO——-inc cGMP—– VD in Corpus cavernosum in
    penis
74
Q

Recurrent Attack
(Prophylaxis) drugs
5 things

A 
1- B- blockers
2- Ca++ channel blockers( dec c. work)
3- Nitrate (intermediate or long
acting) (dec  c. work )
4 - Antiplatelete (Aspirin)
5- Thrombolytic drugs
75
Q

we can us isoprenoid in —————-attak

A

acute

76
Q

What is the dose of Isosorbide

mononitrate that patient will have ?and root? onset? duration ?

A 
Oral
Ext. R
30 min
30 min
~8 h
~12 h
77
Q

What is the dose of Isosorbide

dinitrate that patient will have ?and root? onset? duration ?

A 
S.L
Oral
SR
5 min
15 min
30 min
~1 h
~5 h
~ 8 h
78
Q

What is the dose of Nitrate that patient will have ?and root? onset? duration ?

A

~ 2 min
30 min
~15 min
~ 7 h

79
Q

What is the dose of Amyl nitrate that patient will have ?and root? onset? duration ?

A

1 min

~ 5 min

80
Q

oral Isosorbide dinitrate is—————–only———- will reach circulation

A

oral metabolized by liver

23%

81
Q

Angina pectoris is characterized by
• Sever, pressing chest pain that occurs when coronary
blood flow is ———- to supply O2 required by the
heart.

A

inadequate

82
Q

Angina Pectoris
- It is the primary symptom of ——————
caused by accumulation of ———— in cardiac muscle.
• -These transient episodes result from imbalance
between myocardial O2 supply and demand.

A

ischemic heart disease

metabolites

83
Q 
Angina Pectoris
•----- Demand may be due to:
• - ----HR.
• - ---- Ventricle wall tension (as in hypertension).
• --- ventricular contractility
A

inc
inc
inc
inc

84
Q

Decreased O2 supply:
• Decreased blood coronary flow due to:
• -Fixed atherosclerotic narrowing in ———–angina
• -Coronary spasm in ———–angina
• -Non occlusive thrombus in ————angina

A

Stable
Paienzemtal
Non-Stable

85
Q

Management of angina pectoris:
• I-Reduce ————–: smoking, obesity,
treat hypertension, diabetes& dyslipidemia.
• II- Decrease incidence of ———– and increase survival rate

A

risk factors
myocardial
infarction

86
Q

III-Antianginal agents:
• 1-Angina of effort:
A-acute attack: ——————–
(nitroglycerine) - ————————
(sublingual).
B- Prophylaxis: ——-,————,——–

A

glyceryl trinitrate-isosorbide dinitrate-

long acting nitrates- βBs – CCBs

87
Q

type of Angina ?————–
• -coronary flow is decreased due to fixed
atherosclerotic narrowing of coronary arteries
(occurs on exertion &relieved by rest or nitroglycerin).

A

Typical - angina of effort

88
Q

type of Angina ?————–
• - Due to reversible coronary spasm (occurs at rest
&unrelated to exercise).
• -Relieved by VDs and CCBs not by βBs.

A

Parinzmetal - Varient -Vasospastic - Alpha mediated syndorme Angina

89
Q

type of Angina ?————–
• -Due to episodes of ↑epicardial coronary artery spasm
&formation of non-occlusive thrombi resulting from
rupture of atherosclerotic plaque (not related to
exercise and not relieved by rest or nitroglycerine)

A

Unstable Angina

90
Q

type of Angina ?————–
in patients with advaned
coronary artery disease .

A

Mixed form of Angina

91
Q
  • ↓O2 demand: work done by heart &O2 consumption through
    dec. HR+ Myocardial contractility ——————–
    dec. Preload (venodilation) ————-because it is ——–
    dec. afterload ——— -because it is ——–and———because it is————and ————–because at high doses
A 
βBs and CCBs
Nitrates: mainly venular VD
CCBs: arteriolar VD
- βBs: ↓BP
-nitrates: arteriolar VD (in higher doses)
92
Q

-↑O2 supply: ↑——————–
(direct)—————- VD of epicardial coronary arteries-redistribution of
blood to ischemic areas- VD of collaterals.
coronary VD
-:(direct)———– coronary VD
•(indirect) ————- : ↓BP -↑diastolic period →↑coronary filling

A

coronary blood flow
Nitaite
CCBs-βBs

93
Q

-ORGANIC NITRATES:

• Mechanism of action ?

A

Nitrates bind to nitrate receptors in vascular
endothelial cells and vascular smooth muscle cells →
nitrite ions are released then converted to nitric oxide
→ ↑c-GMP→ dephosphorylation of myosin light chain
kinase→ vascular smooth muscle relaxation.

94
Q

• Pharmacological actions of Organic Nitrate ?

A

• Relax all segments of vascular system especially
veins; it is a potent venodilator( veins responds at
the lowest concentrations, arteries at higher ones) →
decreasing preload → decreasing work done by the
heart and myocardial O2 consumption.
• - Vasodilatation of epicardial coronaries → increasing
blood supply

95
Q

Pharmacokinetics:
• Can be given by ———–, ——-&————
patches (both avoid first pass metabolism).
• Transdermal patches have ———– half lives and are
used TO prevent —————angina.
• - Oral bioavailability of nitroglycerine and
isosorbide dinitrate (metabolized into two
mononitrates) is very———— (extensive first pass
metabolism).
• - Sublingual→ rapid onset (——to—minutes).
• -Isosorbide mononitrate by pass hepatic
metabolism and has ——– bioavailability, delayed
onset and long duration(more than one hour).
• - all Excreted by the ———–

A 
oral-sublingual-transdermal
long-nocturnal 
 low
1-3
100%
kidney
96
Q

Adverse effects of Organic Nitrate :

A

• -Flushing, throbbing headache, temporal
& meningeal pulsations.
• - Postural hypotension even syncope and
tachycardia.
• -Sildenafil (Viagra) potentiates its action
(increases c-GMP) → sever hypotension
and myocardial infarction have been
reported.
• Thus an interval of six hours is needed
between the ingestion of the two drugs.

97
Q

using Nitrate with Sildenafil will cause ———– then————–then ————

A

Reflex Tachy - Ischemia - Death

98
Q

Organic nitrate -Tolerance:
• Nitrate ———– (–to—- hours) is necessary
for drugs with —— t1/2 and sustained release
formulations (24 hours) → overnight or remove
the transdermal patch for few hours if tolerance
is suspected (for ———- angina, nitrate free
interval should be late in the afternoon as this
type of angina worsens early in the morning).
• -Dependence so nitrates should not be
abruptly withdrawn→ withdrawal symptoms.
-Can cause —————– at high blood concentration

A 
free period
10-12
long
few
variant
methemoglobinemia
99
Q

Beta blockers:
• ————-, ————, ————,————
atenolol.
• ——O2 demand&↓work done by heart:
• - ——- HR& contraction → ↓ CO and BP.
• ———–O2 supply: ↑coronary blood flow by
↓HR→———-ED period→ ↑coronary filling
• NB:
• ———- selective blockers are preferred.
• ——– (with intrinsic sympathetic
activity; ISA) should be avoided.

A

Propranolol(Non selective)-bisoprolol-metoprolol-atenolol
↓ - ↓- ↑-↑
β1
Pindolol

100
Q

Beta blocker
• Best indicated in patients with
—————–→ decrease size
of infarction, incidence of attacks &
prolong survival.
• -Useful in stable & unstable angina but
contraindicated in ————- →↑ spasm

A

myocardial infarction
variant or
vasospastic angina

101
Q

Beta Blocker
Contraindicated in ?
4 things

A 
asthmatic,
diabetics,sever bradycardia& peripheral
vascular disease (selectivity is lost
within higher doses).
• -Should be gradually stopped over 2-3
weeks to avoid infarction or sudden
death (up regulation of the receptors)
102
Q 
Calcium influx is increased in -----------
which depletes energy stores and
worsening ischemia. These drugs bind
more effectively to channels in
------------ membrane → ↓ the
frequency of opening in response to
depolarization → marked decrease in
transmembrane Ca²+ current in smooth
muscle, cardiac muscle→
vasodilatation and reduction in
contractility &in SAN pacemaker and
AVN conduction velocity
A

hypoxia

depolarized

103
Q

CCBs Classes
1-Dihydropyridines:
• A-Short acting preparations: e.g. ————–
(mainly affects —————– than
myocardium) → reflex tachycardia, hypotension,
flushing, headache and peripheral edema.
• Short preparations should be avoided in
patients with ——————– as it
increases incidence of infarction. Slow-release and
———— vasoselective calcium channel blockers
are usually well tolerated
B- Long acting as amlodipine which does not
affect ———– or —————-, amlodipine cause ————–

A 
nifidepine
vascular smooth muscles
coronary artery disease
long-acting
heart rate or cardiac output
ankle edema(Swelling) ( lower limb edema)
104
Q
  • Non dihydropyridines:
    • A- Verapamil:
    • -Mainly affects the —————- (directly
    affects ——- conduction) than smooth muscle
    (weak VD) → slows HR and 02 demand.
    • - Extensively metabolized by the liver (dose
    must be adjusted in ——————).
    • -Contraindicated in ———- conduction
    abnormalities or depressed cardiac function.
    • -Verapamil with digoxin →——- level of digoxin
    as a result of decreased tissue binding and↓
    excretion.
    • - Main adverse effect is ——————-
A 
myocardium-AV
liver dysfunction
AV
↑
constipation
105
Q

Dihydropyridines have NO

effect on ——- conduction

A

AV

106
Q

Diltiazem:
- ———–in its actions between nifedipine and
verapamil.
- ———— AV conduction & decrease the rate of firing of
SAN pacemaker →decrease HR and BP.
- Extensively metabolized by————.
-Contraindicated in ———— conduction abnormalities→
heart block
-Useful in ———– angina while βBs are contraindicated.
• If response to a single antianginal group is
inadequate, a combination of 2-3 drug groups may
be used to increase beneficial effects and decrease
adverse effects:
• -Decrease HR by ————— can prevent undesirable
increase in HR by —————–

A 
Intermediate
Slows
liver
AV
variant
βBs
nitrates

Pharmacology (6 decks)

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