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House Pharmacology > Cardiac glycosides > Flashcards

Cardiac glycosides Flashcards

1
Q

Cardio-tonic drugs

Cardio_________ drugs (also called “cardiotonic drugs”)

A

stimulatory

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2
Q

Cardio-tonic drugs

Enhance cardiac function by
– increasing heart rate (_____tropy)
– myocardial contractility (___tropy),
– May increase electrical conduction (_______tropy) within the heart and
– augment relaxation (_____tropy).

A

chrono

ino

dromo

lusi

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3
Q

Cardio-tonic drugs

The cardiac effects of these drugs make them suitable for
–____ failure
–________ shock
– ______tension.

A

Heart

Cardiogenic

hypo

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4
Q

Classes of Cardiostimulatory Drugs

________
____________
________________
____________

A

Beta-agonists
Digitalis compounds
Phosphodiesterase inhibitors PDEI
Calcium sensitizers

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5
Q

Cardiac glycosides are _____ compounds containing a _______(_____) that act on the ____________ of the cardiac muscle.

A

organic

glycoside (sugar)

contractile force

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6
Q

Cardiac glycosides

Important class of (naturally or artificially ?) occurring drugs whose actions include both ______ and ________ effects on the heart.

A

naturally

beneficial and toxic

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7
Q

Cardiac glycosides

Found as (primary or secondary?) metabolites in several plants , but also in some _____, such as the __________ ————

A

secondary

insects

milkweed butterflies.

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8
Q

Chemistry of cardiac glycosides

All of the glycosides of which digoxin is the prototype combine a

–_____ nucleus linked to an unsaturated ____ membered _______ ring at the ____ position

– and a series of _____ at ______ of the nucleus.

A

steroid; 5 ; lactone; 17

sugars; carbon 3

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9
Q

Chemistry of cardiac glycosides

Because they lack an easily ionizable group, their _____________________________________.

_______ nucleus with ———- ring is essential for myocardial action.

A

solubility is not pH dependent

Steroid; lactone

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10
Q

CVS effect of Cardiac Glycosides in Heart Failure

Mechanical and Electrical effect

(+ve) ____tropic.
(-ve) _____tropic

→Binding to ———- in the plasma membrane of central & peripheral nervous system → (-) of symp.

A

ino; chrono

Na pumps

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11
Q

CVS effect of Cardiac Glycosides

its positive inotropic action results in,

– a. increased _______
– b. decreased _________
– c. decreased ____________
– d. decreased ___________________________
– e. _______ and relief of oedema

A

cardiac output

heart size

venous pressure

circulating blood volume

diuresis

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12
Q

Electrical activity of Cardiac Glycosides

——-eased automaticity of SA node indirectly

_____eased Refractory period of the AV node

____eased Condution Velocity at the AV nodal Tissue

(Stimulate or Depress?) vagal Nerve

A

Decr

Incr

Decr

Stimulate

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13
Q

Therapeutic uses of Digitalis Compounds

During Heart Failure, to cause:
– ____eased inotropy
– ____eased ejection fraction
– ____eased preload
– ____eased pulmonary congestion/edema

A

Incr
Incr
Decr
Decr

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14
Q

Therapeutic uses of Digitalis Compounds

Arrhythmias

– ______ease AV nodal conduction (parasympathomimetic effect)
– ____ease ventricular rate in atrial flutter and fibrillation

A

decr

decr

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15
Q

Contraindications of Digitalis Compounds

•Ventricular Tachycardia - because digitalis _____________ especially at high doses

•——————.

A

increase automaticity

Heart block

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16
Q

Mechanism of action of Digitalis Compounds

Inhibits the ________, which is responsible for —————- across the muscle cell membrane

Leads to ____eased force of myocardial contraction.

A

Na+/K+-ATPase

Na+/K+ exchange

Incr

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17
Q

Digoxin and _____ ions compete for a “receptor” (Na+/K+-ATPase) on the (internal or external?) membrane.

So, the effects of digoxin may be dengerously increaseed by ________, produced, for example, by diuretics.

A

K+

External

hypokalemia

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18
Q

Cardiac glycosides : mechanism of action.

Inhibits _______ pump
Increase intracellular ____ conc.

Inhibits ______ exchangers
Decrease ______ efflux from the cell
Increase intracellular _____

____ease cardiac contractility

A

Na/K atpase; sodium

Na/Ca2+; calcium; calcium

Incr

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19
Q

Pharmacokinetics of Digoxin

absorption of digoxin after ___ administration ranging from ____-___%.
absorption can be retarded by,

– a. the ______ in the GIT
– b. delayed ________
– c. ______ syndromes
– d. antibiotics, such as ____________
– e. steroid binding _____

A

oral; 40-90

presence of food

gastric emptying

neomycin

resins

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20
Q

Digoxin:

Oral availability =
Half life =
Elimination is by??

A

75

40 Hours

Kidneys

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21
Q

Adverse effect of Digoxin

1.Extracardiac

On GIT→ Anorexia, nausea,vomiting Fatigue ,weakness, diarrhoea

Neurological problems ————-,———-

Due to steroid nucleus -_________ in male

A

blurring of vision, confusion

gynaecomastia

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22
Q

Adverse effect of Digoxin

Cardiac effect:

i)All type of arrythmia (increased ________ in high dose)

ii) Slowing A-V nodal Conduction- _________ ________

A

Automaticity

Bradycardia Heart block

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23
Q

Drug interaction Pharmacodynamic interaction

_________ + digoxin= ↓ AV Conduction - Heart Block

_________+ digoxin= ↓ AV Conduction –Heart Block

Digitalis+ ____________________ = cause K+ loss

A

B –blocker

Verapamil

Diuretics(Thiazide/Frusemide)

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24
Q

Drug interaction Pharmacokinetic interaction

Verapamil+ digoxin→_____eased plasma digitalis concentration by ________________________ leading to increased conc. of digoxin →toxicity

A

incr

competing with digoxin for renal excretion

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25
Q

Drug interaction Pharmacokinetic interaction

Digitalis+Quinidine= ______ digitalis from ___________ , leading to \___eased concentration of digitalis →↑toxicity

A

displace

tissue binding site

incr

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26
Q

Digoxin Toxicity

________ is earliest symptom

__________ is earliest sign ( if <—— b/min, digitalis not given)

Low Therapeutic Index of ____nmol/L

A

Anorexia

Bradycardia; 60

1-2.6

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27
Q

Toxicity of digoxin

Treatment: treatment is different in 2 different condition
(i) ________
ii) Monitor ____ level( if ________ administer K+, IV KCL)

A

Stop the drug

K+ ; hypokalemia

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28
Q

Hypokalemia K+ and digitalis, interact in two ways-

First – hypokaelamia causes ______eases the myocardial localization of digoxin.

(Increase or reduction?) in extracellular K+,

Cause increased _________ of _______.

Digoxin has (lower or higher?) affinity for the phosphorylated form of Na pump.

Second – ___________________ is inhibited by hyperkalemia.

A

incr

reduction

phosphorylation of Na pump

Higher

abnormal cardiac automaticity

29
Q

Digoxin Toxicity

Effect of other electrolytes imbalance on digoxin use –
Causing toxicity

– _______calcaemia Ca++,
– _____magnesaemia Mg++

A

Hyper

Hypo

30
Q

Ca++ facilitates the toxic actions of cardiac glycosides by _____________________________ that appears to be responsible for digitalis-induced ______________

A

accelerating the overloading of intracellular Ca++ stores

abnormal automaticity.

31
Q

______calcemia therefore increases the risk of digitalis induced arrhythmia.

A

Hyper

32
Q

Hypomagnesemia

Decreased Mg++ concentration _______________ of cardiac glycosides.

A

enhances toxicities

33
Q

Digitalis Toxicity – Use of Antidote

If patient still refractory to treatment –
Antidotes to digoxin

–_________________ (Fab fraction)

– digoxin binding specific antibody ( _________ ) given to _________________

A

monoclonal antibody

digibind

remove excess digoxin from the body.

34
Q

HEART FAILURE DRUGS

DRUGS FOR _____________

DRUG FOR ——————

DRUG FOR _____________________

A

PREVENTING CARDIAC REMODELLING

TREATING SYMPTOM

IMPROVING CONTRACTILITY

35
Q

Drugs for PREVENTING CARDIAC REMODELLING

LIST !!!!

A

ACE INHIBITORS

ANGIOTENSIN RECEPTOR BLOCKERS

BETA BLOCKERS

VASODILATORS

36
Q

Mechanisms of ACE inhibitors

Inhibits ANGIOTENSIN CONVERTING ENZYME
Alters the __________ and _______

Thus prevents cardiac remodeling

A

Pre-load and Afterload

37
Q

MECHANISM OF ACTION of ANGIOTENSIN RECEPTOR BLOCKERS

Inhibits Angiotensin II receptor

Alters the __________________

Thus prevents cardiac remodeling

A

Pre-load and After load

38
Q

MECHANISM OF ACTION of beta blockers

Inhibits Beta adrenergic receptors

Reduces ________ and ___________

Thus prevents cardiac remodeling

A

Heart rate and Force of Contraction

39
Q

MECHANISM OF ACTION of vasodilators

Lead to vasodilation

Alter the _________________
Thus prevents cardiac remodeling

A

Pre-load and Afterload

40
Q

CARDIOTONICS

Are

____________,_________, and ______

A

CARDIAC GLYCOSIDES

BETA 1 AGONIST

PDE INHIBITORS

41
Q

CARDIAC GLYCOSIDES

_________ type

_______ type

A

CARDENOLIDE

BUFADINOLIDE

42
Q

EXAMPLES of cardiac glycosides
• Cardenolide
–_________
–_________

Bufadenolide
– Drimia maritima – Kalanchoe
daigremontianin – Daigremontianin

A

Digitalis lanata

Digitalis purpura

43
Q

CARDIAC GLYCOSIDES
•
Made up of a combination of

– _______
– _______
– _______

A

– Steroid nucleus
– Lactone ring
– Sugar

44
Q

CARDIAC GLYCOSIDES

Causes _____eased inotropy and ____eased chronotropy

A

incr

decr

45
Q

CARDIAC GLYCOSIDES

PHARMACODYNAMICS : Drug Effect
Usually leads to two types of Drug effect

________ effect
_________ effect

A

Mechanical

Electrical

46
Q

Cardiac glycosides

Electrical effect
Decreased ___________ indirectly
Increased _________ of the AV node
Decreased _________ at the AV nodal Tissue
Stimulate _______ Nerve

A

Automaticity of SA node

Refractory period

Conduction Velocity

vagal

47
Q

CARDIAC GLYCOSIDES are highly toxic

T/F

A

T

48
Q

Factors affecting toxicity of cardiac glycosides

__________mia
__________emia
___________emia

A

Hypercalcemia

Hypomagnesaemia
Hypokalemia

49
Q

CARDIAC GLYCOSIDES

Extracardiac
–_____ like syndrome
– ______tension
– Headache
– Nausea
– Diarrhea
– Flushing
– Tachycardia

A

Lupus

Hypo

50
Q

CARDIAC GLYCOSIDES
ADVERSE EFFECT
Cardiac
– Arrhythmia
•__________ lock
•_______ arrhythmia
• ___________ arrhythmia

A

Conduction

Atrial

Ventricular

51
Q

CARDIAC GLYCOSIDES
Treatment
TOXICITY

– Treat arrhythmia
Atrial arrhythmia –_______
Ventricular arrhythmia – _________
Heart block - ___________

A

Phenytoin

Lignocaine

Atropine

52
Q

BETA AGONIST

EXAMPLES
Dobutamine

Supplied in ______ mixtures
Increases ____tropy without increasing ______tropy

A

racemic

Ino

Chrono

53
Q

BETA AGONIST
EXAMPLES
Dopamine

Given _____
Dose is between 1 to 5 μgm/kg/min
Has a (short or long?) half life of _____________

Metabolized in the _____ by _____

A

IV

Short

2 to 3 mins

Liver

COMT

54
Q

BETA AGONIST

MECHANISM OF ACTION
Stimulate to Beta 1 adrenergic receptors in the Heart
Causes increased ______________________
This leads to improvement in the myocardial contractility

A

INOTROPY

55
Q

PDE INHIBITOR
Give 3 examples

EXAMPLES

A

Amrinone

Milrinone

Enoximone

56
Q

MECHANISM OF ACTION of PDE INHIBITOR

Inhibit Phosphodiesterase enzyme

This causes an
•Increase in _____
•Activation of __________
•Activation of _____________channel
•Increase in _____tropy

A

cAMP

protein kinase

sarcolemma calcium

ino

57
Q

__________ represent the newest class of cardiostimulatory drugs.

A

Calcium sensitizing drugs

58
Q

Calcium sensitizing drugs

These drugs increase the _________________ so that more calcium becomes bound to troponin-C, which enhances contractility.

At present, these drugs are ___________________________, and therefore not yet approved.

A

sensitivity of troponin-C for calcium

under clinical investigation for heart failure

59
Q

With dobutamine, there is increase in cardiac workload

T/F

A

F

Decrease

60
Q

Dobutamine does not activate dopaminergic receptors.

T/F

A

T

61
Q

__________ is the preferred beta agonist for the management of patients with end-stage systolic dysfunction and CHF.

A

Dobutamine

62
Q

Dobutamine is supplied as a racemic mixturethat stimulates ___________ receptor subtypes.

A

both b1 and b2

63
Q

Dobutamine

In addition, the (–) enantiomer is ______ for a adrenergic receptors, whereas the (+) enantiomer is a ___________

A

an agonist

very weak partial agonist.

64
Q

DA has limited utility in the treatment of most patients with cardiogenic circulatory failure.

T/F

A

T

65
Q

Dopamine

At low doses (≤—— μg/kg lean body mass per minute)

DA causes vaso_____ by stimulating _______ receptors on smooth muscle

Also by stimulating presynaptic ____ receptors on sympathetic nerves in the peripheral circulation(___________ and reducing __________ stimulation of vascular smooth muscle); thesereceptors are prominent in ______ and _________ arterial beds

A

2

dilation; dopaminergic

D2

inhibiting NE release ; a adrenergic

splanchnic and renal

66
Q

Dopamine

At intermediate infusion rates (_____ μg/kg/min),

DA directly stimulates _____ receptors on the _____ and vascular sympathetic neurons, enhancing cardiac contractility and neural NE release.

A

2–5

Beta; heart

67
Q

Dopamine

At higher infusion rates (_____ μg/kg/min),

peripheral arterial and venous _______ occur, mediated by _______ receptor stimulation.

A

5–15

constriction

a adrenergic

68
Q

Tachycardia is more pronounced with dobutamine than with dopamine

T/F

A

F

Tachycardia, which is more pronounced with DA than with dobutamine, may provoke ischemia in patients with coronary artery disease.

69
Q

Dopamine

it is a drug of choice.(T/F)

Very (short or long?) half life ( _______)

A

T

Short

2- 3minutes

House Pharmacology (50 decks)

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