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Capstone - Ex 2 Flashcards

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1
Q

Albuterol

MOA
Summary

A

MOA: selective B2 agonist
Summary: bronchodilator

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2
Q

Adrenergic receptors

A

Sympathetic NS

NE, Epi (Catecholamines)

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3
Q

Muscarinic receptors

A

Parasympathetic NS

ACh

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4
Q

How are catecholamines metabolized?

A
  • reuptake into adrenergic neuron –> repackaged or metabolized by MAO
  • uptake into effector cells or the liver via the blood stream –> metabolized by COMT
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5
Q

Bethanechol (choline ester)

A

MOA: muscarinic stimulation - cholinergic agonists

Summary: used to tx urinary retention when no obstruction present
- promotes voiding by contraction of detrusor and relaxation of the trigone and sphincter

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6
Q

Mushroom poisoning (Inocybe geophylla)

A

Contains lots of muscarine!

Summary: Salivation, lacrimation, urination, defecation, bradycardia, bronchospasm, vomiting, abdominal colic, hypotension, shock

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7
Q

Pilocarpine (alkaloid)

A

MOA: muscarinic stimulation

Summary: Induces meiosis in the eye

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8
Q

AChE inhibitors

A

MOA: prevent hydrolysis of ACh

Summary: increase ACh (dec breakdown)
- reverse NMJ blockade

  • *Myasthenia gravis
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9
Q

Physostigmine

A

Counter anticholingeric toxicity

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10
Q

Neostigmine

A

Stimulate visceral sm mm

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11
Q

Atropine

A

MOA: Cholinergic antagonist

Summary:
- used as adjunct in anesthesia (dec salivation and airway secretions)

Contraindications: tachyarrhythmia, prolonged GI stasis, urine retention

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12
Q

Scopolamine

A

MOA: Cholinergic antagonists

Use:

  • lose dose: slight sedation
  • high dose: excitement
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13
Q

Glycopyrrolate

A

MOA: Cholinergic antagonist

Use:

  • adjunct to gen anesthesia (dec salivation and airway secretions)
  • prevents bradycardia
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14
Q

Tropicamide

A

MOA: Cholinergic antagonists

Use:
topically in eye to produce mydriasis and cycloplegia (ophthalmic exam)

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15
Q

Ipratropium

A

MOA: Cholinergic antagonists

Use: dec bronchoconstriction and airway secretions - promote bronchodilation

  • asthma (cats) and chronic bronchitis (dogs)
  • horses with recurrent airway inflammation
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16
Q

Propantheline

A

MOA: Cholinergic antagonists

Use: dec detrusor contraction and inc trigone and sphincter contraction - promotes urine retention
- treats incontinence due to detrusor instability

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17
Q

Pancuronium

A

MOA: long acting competitive NMJ blocker

Use: promote and enhance skeletal mm relaxation during sx

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18
Q

Atracurium

A

MOA: intermediate competitive NMJ blocker

Use: promote and enhance skeletal mm relaxation during sx

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19
Q

Mivacurium

A

MOA: short-acting competitive NMJ blocker

Use: promote and enhance skeletal mm relaxation during sx

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20
Q

Can you reverse competitive or non-competitive NMJ blockers?!

A

Reverse COMPETITIVE (e.g. physostigmine, neostigmine)

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21
Q

Succinylcholine

A

MOA: depolarizing NMJ blocker - NOT reversible

Use: rapid and short-lived NMJ blockade (tracheal intubation)

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22
Q

NMJ blocking agents summary:

A

Given IV: paralyze ALL skeletal mm (Careful for resp failure!)

No effect on sensorium: use with general anesthetic

Helps with balanced anesthesia

Toxicity: histamine release, ganglionic blockade, vagal reflex, malignant hyperthermia

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23
Q

EPI, NE, and Phenylephrine

A

MOA: a1 adrenergic agonist

Use: vasoconstriction

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24
Q

Dexmedetomidine

A

MOA: a2 adrenergic agonist

Use: adjunct for sedation, anesthesia, and analgesia

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25
Q

EPI, NE, Dopamine, Dobutamine

A

MOA: B1 adrenergic agonists

Use: inc HR and contraction

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26
Q

EPI, albuterol, clenbuterol

A

MOA: B2 adrenergic agonist

Use: bronchodilation

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27
Q

Prazosin

A

MOA: a1 adrenergic antagonist

Use: Vasodilation

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28
Q

Atipamezole

A

MOA: a2 adrenergic antagonist

Use: reversal of a2 agonists (dexmedetomidine)

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29
Q

Phenoxybenzamine

A

MOA: non-selective a antagonist

Non-competitive, irreversible

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30
Q

Phentolamine

A

MOA: non-selective a antagonists

Competitive, reversible

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31
Q

Propranolol

A

MOA: non-selective B1 antagonist

Use: dec HR, reduce cardiac O2 demand, dec BP

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32
Q

Atenolol

A

MOA: selective B1 antagonist

Use: dec HR, reduce cardiac O2 demand, dec BP

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33
Q

Hypovolemic shock

A

intravascular volume deficit (e.g. hemorrhage)

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34
Q

Distributive shock

A

Peripheral vasodilation

Septic, anaphylactic, and neurogenic shock

35
Q

Cardiogenic shock

A

myocardial pump failure

36
Q

Procainamide

A

MOA: Class IA Na channel blocker

Use; Supraventricular tachycardia

37
Q

Lidocaine

A

MOA: Class IB Na channel blocker

Use: Ventricular tachycardia

38
Q

Flecainide

A

MOA: Class IC Na channel blocker

Use: life-threatening Vtach or fib and for tx of refractory supra ventricular tachycardia

*Cure is worse than the dz - use in only life-threatening situations

39
Q

Atenolol

A

MOA: class II B blocker

Use: slow AV nodal conduction
- A fib

40
Q

Amiodarone

A

MOA: Class III - prolong AP

Use: arrhythmias
- but prolonging AP generally assoc’d with inducing arrhythmias

41
Q

Diltiazem, Verapamil

A

MOA: Class IV Ca Channel Blocker

Use: dec ventricular response to A fib

42
Q

Digoxin

A

MOA: Dec AV nodal conduction - antiarrhythmics

Use: dec ventricular response to A fib

43
Q

Adenosine

A

MOA: blocks AV nodal conduction

Use: can terminate SVT involving the AV node (e.g. A fib)

44
Q

Does complete arrhythmia suppression eliminate the risk for subsequent lethal arrhythmia>

A

ALL antiarrhythmic drugs can induce arrhythmias

45
Q

Increase cardiac contractility

A
  • functions as a better pump
  • inc CO and tissue perfusion
  • “positive inotropic” effect
46
Q

3 basic ways to inc cardiac performance

A
  1. inc B1 adrenergic (sympathetic) stimulation
  2. inc cardiac myocyte intracellular Ca
  3. enhance the contractile process directly
47
Q

Enalapril

A

MOA: ACE inhibitor - dec BP

Use: tx high BP, diabetic kidney dz, and heart failure

48
Q

Losartan

A

MOA: angiotensin receptor antagonist

Use: high BP

49
Q

Prazosin

A

MOA: competitive a-adrenergic antagonists - alpha blocker

Use: vasodilation

50
Q

Diltiazem, Verapamil

A

MOA: Ca Channel antagonists

Use: vasodilation

51
Q

Amlodipine

A

MOA: Ca Channel antagonists

Use: vasodilation

52
Q

Nitric oxide - cGMP - PKG

A

MOA/Use: profound vasodilation

53
Q

Nitroglycerin (exogenous NO)

A

Aka Nitrovasodilators

Use: venous dilation

  • acute cariogenic pulmonary edema
  • CHF
54
Q

Sodium nitroprusside

A

Aka Nitrovasodilators

Use: arterial and venous dilation

  • hypertensive emergencies, acute CHF
  • given IV
55
Q

Sildenafil

A

MOA: Phosphodiesterase type 5 inhibitor

Use: managing pulmonary hypertension

56
Q

Minoxidil

A

MOA: K+ channel activators

Use: dec TPR, dec BP, rarely used

57
Q

What are the major osmolytes (particles) being reabsorbed? (renal)

A

NaCl, HCO3, Ca++

58
Q

What are the major osmolytes (particles) secreted from kidneys?

A

H+ and K+

59
Q

Mannitol

A

MOA: osmotic diuretic - amount filtered exceeds tubular transport

Use: oliguric renal failure, cerebral edema, acute glaucoma

Don’t use if: can’t establish urine flow or there is intracranial bleeding

60
Q

Acetazolamide

A

MOA: carbonic anhydrase inhibitors - inc loss of HCO3 & may inc urine pH
(weak diuretic effect)

Use: metabolic alkalosis, glaucoma, altitude sickness

61
Q

Furosemide (Lasix, Salix)

A

MOA: Loop diuretic (BEST)inhibits NaCL reabsorption in the thick ascending LoH

Use: oliguric renal failure, CHF, acute pulmonary hypertension, and EIPH

62
Q

Chlorothiazide

A

MOA: block NaCl reabsorption - not as good as loop diuretics

Use: nephrogenic diabetes insipidus, udder edema in cattle, Ca containing uroliths

63
Q

Spironolactone

A

MOA: competitive aldosterone antagonists (K sparing)

Use: often in combo with loop diuretic; mild diuresis with reduced potential for K loss

64
Q

Amiloride, triamterene

A

MOA: principal cell Na channel blockers (K sparing)

Use: in combo with loop diuretics, immediate but mild diuretics

65
Q

Demeclocycline

A

MOA: collecting duct V2 receptor antagonists

Use: syndrome of inappropriate ADH production; effective in heart failure but not yet approved

66
Q

What are the 2 major histamine pools?

A
  1. Mast cells (CT) & basophils (circulating)

2. Non-mast cell tissues (lungs, skin, gastric mucosa)

67
Q

Why is histamine released?

A
  • immune-mediated, IgE hypersensitivity
  • drug-induced (e.g. NMJ blockers, morphine)
  • plant and animal stings
  • physical injury
68
Q

H1 receptors

A

allergy, inflammation, pain, itching

vasodilation, edema, bronchoconstriction

*classical antihistamine target these

69
Q

H2 receptors

A

gastric acid secretion

70
Q

Diphenhydramine (benadryl)

A

MOA: 1st gen H1 antagonist

antimuscarinic, sedating

71
Q

Dimenhydrinate (Dramamine)

A

MOA: 1st gen H1 antagonist

antimuscarinic, sedating

72
Q

Chlorpheniramine (Chlor-Trimeton)

A

MOA: 1st gen H1 antagonist

less sedating

73
Q

Promethazine (Phenergan)

A

MOA: 1st gen H1 antagonist

antimuscarinic, sedating

74
Q

Loratadine (claritin)
Certirizine (Zyrtec)
Fexofenadine (Allegra)

A

MOA: 2nd gen H1 antagonist

Less entering CNS, less sedation

75
Q

Famotidine (Pepcid)
Ranitidine (Zantac)
Nizatidine (Acid)
Cimetidine (Tagamet)

A

MOA: H2 antagonists

Use: reduce gastric acid secretion; gastric, abomasa, and duodenal ulcers; drug-induced gastritis, reflux

76
Q

Fluoxetine (Prozac)
Paroxetine (Paxil)
Sertraline (Zoloft)
Fluvoxamine (Luvox)

A

MOA: Selective serotonin reuptake inhibitors

Use in dogs: separation anxiety; compulsive behaviors, aggression

Use in cats: inappropriate urination (spraying); compulsive behaviors, aggression; psychogenic alopecia

77
Q

How are NSAIDs and NSIMs (Non-steroidal immunomodulators) similar? different?

A

Both groups are immunosuppressants

NSIM suppress immune fxn via mechanisms distinct from corticosteroids

78
Q

NSIMs

A

MOA: weaken or modulate the activity of the immune system

Use: when immunosuppression is desired after NSAIDs (corticosteroid) therapy fails

  • IMHA
  • ITP
  • SLE
    (i. e. autoimmune dz involving multiple organ systems)
79
Q

Cyclosporine, tacolimus

A

MOA: NSIM - Calcineurin inhibitors

Use (Cyclosporine):

  • systemic (IMHA, IBD, IMPA, atopic dermatitis, perianal fistulas, organ transplants)
  • topical ophthalmic (keratoconjunctivitis sicca - dry eyes)

Use (tacolimus): minimal use in vet med

80
Q

Cyclophosphamide, chlorambucil

A

MOA: NSIM - Cytotoxic alkylating agents

Use (cyclophosphamide): IMTP, SLE, RA, pemphigus, IMHA?

Use (chlorambucil): can be used as a substitute for cyclophosphamide
- often used for immune-mediated skin dz in cats (pemphigus)

81
Q

Azathioprine, Mycophenolate mofetil

A

MOA: NSIM - Cytotoxic inhibitors of purine synthesis

Use: IBD, IM-skin dz, IMHA, etc.
- can take weeks for effect

82
Q

Oclacitinib (Apoquel)

A

MOA: NSIM - JAK1 and JAK3 inhibitor; dec effects of inflammatory cytokines (IL2, 4, 6, 13); also dec IL-31 which is directly involved in sensation of itch

Use: manage chronic itching

  • causes bone marrow suppression (must monitor)
  • good alternative for dogs who do not tolerate steroids or cyclosporine
83
Q

Cytopoint (Canine Atopic Dermatitis Immunotherapeutic)

A

MOA: monoclonal Ab against IL-31 (itch)

Use: atopic dermatitis in dogs
- sq inj lasts 4-6 wks

spanish (5 decks)

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