Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ACVIM.Pharm > Other drugs > Flashcards

Other drugs Flashcards

1
Q

Examples of Direct Sympathomimetics

A

epinephrine
norepinephrine
dopamine
dobutamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Adrenergic agonists examples

A

phenylephrine
isoproterenol
albuterol
terbutaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

adreneric antagonists examples

A

phenoxybenzamine
propanolol
metoprolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Alpha 1 receptors:
MOA
location
action
preferred substrate

A

MOA: PLC activated–> INC IP3–> and DAG –> INC intracellular Ca
Location: vascular smooth mm (prostrate, heart, pupillary dilator mm)
Action: promotes vasoconstriction
substrate: EPI > NE> Isoproterenol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Alpha 2 receptors
MOA
Location
Action
Preferred Substrate

A

MOA: AC inhibited–> decreased cAMP
Location: Nerv terminals of adrenergic and cholinergic neurons
Action: inhibit release of neurotransmitters
substrate: EPI> NE> Isoproterenol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Beta 1
MOA
Location
Action
Preferred Substrate

A

MOA: AC activated–> inc cAMP
Location: Heart
Action: INC rate and contractility
Preferred substrate: Isoproterenol> Epi> NE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Beta 2
MOA
Location
Action
Preferred Substrate

A

MOA: AC activated–> inc CAMP
Location: SMooth mm of respiraotry, vascular and uterine tissue
Action: bronchodilation, vasodilation, promotes relaxation
Preferred substrate: Isoproterenol> Epi> NE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Beta 3
MOA
Location
Action
Preferred substrate

A

MOA: AC activated–> inc CAMP
Location: Adipose tissue
Action: enhances lipolysis & suppresses leptin
preferred substrate: Preferred substrate: Isoproterenol> Epi> NE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

D1
MOA
Location
Action
Preferred Substrate

A

MOA: AC activated–> INC cAMP
Location: smooth mm of splanchnic and renal vessels
Action: vasodilation of renal blood vessels
Preferred substrate: Dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

D2
MOA
Location
Action
Preferred Substrate

A

MOA: AC inhibited–> decreased cAMP
Location: nerve terminals of CNS neurons
Action: regulates neurotransmitter release
Preferred substrate: dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

epinephrine MOA

A

alpha agonist at high doses
beta agonist at low doses

**vasoconstriction, inc heart rate and contractility
**bronchodilation (beta 2 agonist)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

norepinephrine MOA

A

alpha 1, alpha 2 and beta 1 receptor agonists

**vasoconstriction, inc contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Dopamine MOA

A

high doses: alpha 1 receptors
lower doses: beta and D1 receptors

**vasoconstriction, inc heart rate and contractility, promotes renal perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Dobutamine MOA

A

B1 receptor agonists: INC heart rate and contractility
weak alpha 1 and beta 2 effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

ephedrine MOA

A

stimulates release of norepinephrine: alpha and beta receptors
inc systolic and diastolic blood pressure: alpha 1 and beta 1
bronchodilation: beta 2 stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

phenylephrine moa

A

alpha 1 agonist: systemic vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

albuterol moa

A

beta 2 receptor agonist: bronchodilation (& transcellular shifts of potassium into the cell)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Propanolol MOA

A

beta 1 and beta 2 receptor antagonist: dec HR and contractility, dec blood pressure, bronchoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

anti-fungal agents that act on ergosterol

A

amphotericin B
fluconazole
ketoconazaole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is ergosterol?

A

only found in fungal cell membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

MOA of amphotericin B

A

binds ergosterol and causes formation of holes in fungal cell membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

MOA of azoles (ie: fluconazole)

A

reduce ergosterol synthesis by inhibiting fungal cytochrome P-450 enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Mechanism of Ivermectin

A

activates GABA receptors, thereby leading to worm paralysis and death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

MOA of albendazole

A

inhibits microtubule syntehsis and function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

MOA of pyrantel pamoate

A

activates parasitic nicotinic receptors, thereby causing worm paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

MOA of praziquantel

A

increases cell Ca uptake, thereby causing parasite contraction and paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

MOA of the acetaminophen

A

preferentially inhibits COX02 in the CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the antidote for the acetaminophen overdose?

A

N-acetylcysteine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

MOA of cyclopsorine

A

inhibits calcineurin, therefore IL-2 production is decreased, results in reduced proliferation, differentiation and activation of T cells
**metabolized by cytochrome P-450 enzyme sys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

site of action of 5-fluorouracil

A

interferes with nucleotide synthesis or degradation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

site of action of Vincristine

A

interferes with mitosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

site of action of cisplatn/cyclophosphamide

A

damages DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

MOA of cylcophosphamide

A

alkylating agent and cross-links DNA; supression fo B and T cell function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

MOA of Cisplatin

A

alkylating agent, inhibits DNA and RNA synthesis by binding DNA strands. leads to formation of cross-links between strands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

MOA of 5-Fluorouracil

A

inhibits thymidylate synthasese; leads to disruption of nucleotide synthesis
cell cycle specific– during S phase of the cell cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

MOA of vincristine and vinblastine

A

bind to tubulin; depolymerization of the mitotic spindle;
cell cycle specific: acts during the M phase of the cell cycle

37
Q

Examples of Angiotensin-converting enzyme inhibitors

A

enalapril, benazepril, quinzpril, ramipril

38
Q

MOA of ace-inhibitors

A

decrease levels of angiotensin II and increase levels of activated bradykinin, the ACE inhibitors act to decrease peripheral vascular resistance adn dec effective circulating volume of fluid in the body
**used to tx hypertension and CHF

39
Q

MOA of acetazolamide

A

inhibits carbonic anhydrase in the cell sof the proximal convoluted tubules of the nephron
**diuresis in patients with metabolic alkalosis

40
Q

Examples of loop diuretics

A

furosemide and torsemide

41
Q

MOA of furosemide/ torsemide

A

loop diuretics: inhibits coupled Na/K/2Cl transport system in the thick ascending portion of the loop of Henle

42
Q

Example of thiazide diuretics

A

Hydrochlorothiazide

43
Q

MOA of hydrochlorothiazide

A

inhibits the Na/Cl cotransporter in the early distal convoluted tubule

44
Q

MOA of Spironolactone

A

competitive aldosterone receptor antagonist works at cortical collecting tubule and late distal tubule of the nephron
**decreased urinary potassium excretion
**tx primary hyperaldosteronism/heart failure

45
Q

MOA of sildenifil

A

selectively inhibits cGMP-specific phosphodiesterase type 5– smooth mm relaxation in the pulmonary vascular bed results in vasodilation

46
Q

MOA of digoxin

A

inhibits Na/K ATPase pump on the cell membrane of the cardiac myocyte; inc parasympathetic outflow of the SA and AV node leading to dec HR and dec AV node automaticity

47
Q

Benzodiazepines MOA

A

enhanced GABA receptor activation; dec activity of neurons of limbic, thalamic and hypothalamic regions of CNS

48
Q

Benzodaizepine overdose characterized by cardiac and respiratory dperession and is treated supportively and by:

A

flumazenil, competitive antagonist of benzodiazepines at the GABA receptor

49
Q

MOA of barbiturates (phenobarbital, pentobarbital)

A

potentiate GABA receptor activity in the brain, inc flow of CL ions through adjacent chloride ions, which leads to cell membrane hyperpolarization and dec activity of CNS neurons

50
Q

MOA of local anesthetic agents: lidocaine, mepivicaine, bupivacaine

A

blocking sodium channels on neuronal cell membranes, decreasing activation of these neurons

51
Q

MOA of inhaled anesthetic agents: isoflurane, sevoflurane

A

not completely understood
activate GABA receptors throughout the brain, leading to decreased neuronal activity

52
Q

MOA of ketamine

A

PCP analog that acts as an NMDA receptor antagonist, thereby decreasing neuronal conduction

53
Q

MOA of Propofol

A

unknown, may act to prolong activity of GABA receptor, thereby potentiating effects of GABA at the postsynaptic membrane

54
Q

MOA of butorphanol

A

partial agonist activity at Mu receptors and agonist activity at opioid Kappa receptors
**hyperpolarization and decreased activity of neural cells

55
Q

Tx of malignant hyperthermia and MOA

A

Dantrolene: inhibits calcium release form the sarcoplasmic reticulum of myocytes by binding to the ryanodine receptor–> mm relaxation

56
Q

Gabapentin MOA

A

GABA analogue, exact MOA unknown

57
Q

M1 receptor type MOA, location, action, substrate

A

PLC activated–> inc IP3–> and DAG–> INC intracellular Ca
location: CNS (brain & sympathetic ganglia)
action: CNS stimulation
substrate: AcH

58
Q

M2 receptor type MOA, location, action, substrate

A

MOA: AC inhibited–> dec cAMP, also increase K conductance
location: heart
Action: decreases heart rate and contractility
substrate: Ach

59
Q

M3 receptor type, MOA, location, action, substrate

A

MOA: PLC activated–> INC IP3–> and DAG increased intracellular Ca
Location/ACtion:
smooth mm GI tract/GU tract, bronchi and eye: inc gut peristalsis, increases bladder contraction, inc bronchoconstriction, contracts spinchter mm
substrate: Ach

60
Q

Nm receptor type, MOA, location, action, substrate

A

MOA: activaiton of Na/K channel
location: neuromuscular junction
action: promotes mm contraction
substrate: nicotine

61
Q

Nn receptor type, MOA, location, action, substrate

A

MOA: ACtivation of Na/K channel
location: Autonomic ganglia & CNS, adrenal medulla
action: vasodilation of renal blood vessels, stimulates epinephrine release
substrate: nicotine

62
Q

Bethanechol MOA

A

muscarinic (M2 and M3) agonist; promotes relaxation fo the bladder sphincter promoting urination
M3- inc gut motility

63
Q

Atropine MOA

A

competitive muscarinic (M1, M2, M3) receptor antagonist: M2- tachycardia; M3: dec GIT motility, cycloplegia

64
Q

Ipratropium MOA

A

muscarinic receptor antagonist: M3 receptors in lung, relaxs the smooth mm around the bronchi: bronchodilation

65
Q

Neostigmine MOA

A

reversible inhibition of acetylcholinesterase in the synaptic junction; inc stimulation of both nicotinic and muscarinic receptors
**tx of myasthenia gravis

66
Q

MOA of metformin

A

inhibits hepatic gluconeogenesis, dec absorption of glucose form GIT, and inc peripheral utilization of glucose by adipose and skeletal mm

67
Q

GLP-1 analogues MOA

A

agonists of GLP-1 receptor; insulin secretion is upregulated and glucagon secretion is down regulated

68
Q

sodium glucose cotransporter 2inhibtors

A

SGLT-2 found in proximal tubule of the nephronand responsible for promoting glucose reabsorption
**drugs inhibit SGLT-2, leading to decreased renal glucose reabsorption

69
Q

Bisphosphonates MOA

A

decrease osteoclastic bone reabsorption

70
Q

MOA of levothyroxine

A

synthetic form of T4, normally secreted by follicular cells of thyroid gland

71
Q

MOA of vasopressin

A

V1 receptors: vascular smooth mm: vasoconstriction
V2 receptors: found on renal tubule cells in collecting ducts of kidney: inc permeability to water in the collecting ducts and inc water reabsoprtion
V2-l

72
Q

MOA of metoclopramide

A

antagonist of D2 dopamine receptors; stim gasric and small intestinal motility

73
Q

MOA of lactulose

A

lactoluse in gut degraded by bacteria in gut, which acidify the gut PH and promote nitrogen excretion

74
Q

Ursodiol MOA

A
  1. dec cholesterole synthesis
  2. decreases intestinal reabsorption of choelsterol
  3. inhibits the secretion of choelsterol into bile
75
Q

define zero-order kinetics

A

drugs eliminated at a constant rate over time,
(plasma concentration decreases in a linear manner over time)

76
Q

define first-order kinetics

A

Drugs eliminated at a rate that is proportional to the serum concentration of the drug
(plasma concentration decreases exponentially over time)

77
Q

MOA of mannitol

A

osmotic diuretic, acts at proximal tubule and descending limb of the loop of Henle of nephron to increase tubular osmolarity, drawing water into the tubular lumen
**dec intracranial pressure

78
Q

Platelet plug: step 1 Adhesion

A

von Willebrand factor binds to the subendothelial matrix. When the endothelium is damage, glycoprotein Ib/IX on the plt surface binds to vWF thereby causing plts to adhere to the damaged endothelium

79
Q

Platelet plug: step 2 Aggregation

A

after plt is stimulated, the GP!!B/IIIa complex on the plt surface binds one end of a molecule of fibrinogen, while the other end of the molecule of fibrinogen binds to GPIIb/IIIa complex on another platelet. this results in the cross-linking of plts together

80
Q

Platelet plug: step 3 secretion

A

stimulated plts release multiple factors that promote platete aggregation and stimulation

81
Q

Platelet plug: step 4 procoagulation

A

when activated, platelets produce factor V on their surface, thereby assuring coagulating cascade will take place at the site of the platelet plug

82
Q

MOA of Anti-thrombin III

A

inhibits thrombin and factor Xa

83
Q

Fibrinolysis occurs through which factor?

A

Tissue plaminogen activator: released from damaged endothelial cells and converts plasminogen to plasmin, which degrades firin

84
Q

Nitric oxide MOA

A

inhibits plt adhesion and aggregation

85
Q

(unfractionated) Heparin MOA

A

binds ATIII in order to accelerate the action of anti-thrombin III, responsible for degrading several activated clotting factors, including thrombin and factor Xa

86
Q

low molecular weight heparin MOA

A

action on ATIII, promotes inhibition of thrombin and factor Xa. activity of LMWH on thrombin is lower than that of unfractionated heparin

87
Q

Clopidogrel MOA

A

irreversibly inhibits the binding of ADP to the platelet P2Y receptor, thereby blocking ADP mediated plt aggregation

88
Q

Aminocaproic acid MOA

A

inhibits plasminogen activation, resulting in inhibition of fibrinolysis

89
Q

MOA of synthetic erythropoietin (ie darbopoetin)

A

stimulates bone marrow to enhance erythroid proliferation and differentiation

ACVIM.Pharm (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions