Capstone - Ex 2 Flashcards
Albuterol
MOA
Summary
MOA: selective B2 agonist
Summary: bronchodilator
Adrenergic receptors
Sympathetic NS
NE, Epi (Catecholamines)
Muscarinic receptors
Parasympathetic NS
ACh
How are catecholamines metabolized?
- reuptake into adrenergic neuron –> repackaged or metabolized by MAO
- uptake into effector cells or the liver via the blood stream –> metabolized by COMT
Bethanechol (choline ester)
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
Mushroom poisoning (Inocybe geophylla)
Contains lots of muscarine!
Summary: Salivation, lacrimation, urination, defecation, bradycardia, bronchospasm, vomiting, abdominal colic, hypotension, shock
Pilocarpine (alkaloid)
MOA: muscarinic stimulation
Summary: Induces meiosis in the eye
AChE inhibitors
MOA: prevent hydrolysis of ACh
Summary: increase ACh (dec breakdown)
- reverse NMJ blockade
- *Myasthenia gravis
Physostigmine
Counter anticholingeric toxicity
Neostigmine
Stimulate visceral sm mm
Atropine
MOA: Cholinergic antagonist
Summary:
- used as adjunct in anesthesia (dec salivation and airway secretions)
Contraindications: tachyarrhythmia, prolonged GI stasis, urine retention
Scopolamine
MOA: Cholinergic antagonists
Use:
- lose dose: slight sedation
- high dose: excitement
Glycopyrrolate
MOA: Cholinergic antagonist
Use:
- adjunct to gen anesthesia (dec salivation and airway secretions)
- prevents bradycardia
Tropicamide
MOA: Cholinergic antagonists
Use:
topically in eye to produce mydriasis and cycloplegia (ophthalmic exam)
Ipratropium
MOA: Cholinergic antagonists
Use: dec bronchoconstriction and airway secretions - promote bronchodilation
- asthma (cats) and chronic bronchitis (dogs)
- horses with recurrent airway inflammation
Propantheline
MOA: Cholinergic antagonists
Use: dec detrusor contraction and inc trigone and sphincter contraction - promotes urine retention
- treats incontinence due to detrusor instability
Pancuronium
MOA: long acting competitive NMJ blocker
Use: promote and enhance skeletal mm relaxation during sx
Atracurium
MOA: intermediate competitive NMJ blocker
Use: promote and enhance skeletal mm relaxation during sx
Mivacurium
MOA: short-acting competitive NMJ blocker
Use: promote and enhance skeletal mm relaxation during sx
Can you reverse competitive or non-competitive NMJ blockers?!
Reverse COMPETITIVE (e.g. physostigmine, neostigmine)
Succinylcholine
MOA: depolarizing NMJ blocker - NOT reversible
Use: rapid and short-lived NMJ blockade (tracheal intubation)
NMJ blocking agents summary:
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
EPI, NE, and Phenylephrine
MOA: a1 adrenergic agonist
Use: vasoconstriction
Dexmedetomidine
MOA: a2 adrenergic agonist
Use: adjunct for sedation, anesthesia, and analgesia
EPI, NE, Dopamine, Dobutamine
MOA: B1 adrenergic agonists
Use: inc HR and contraction
EPI, albuterol, clenbuterol
MOA: B2 adrenergic agonist
Use: bronchodilation
Prazosin
MOA: a1 adrenergic antagonist
Use: Vasodilation
Atipamezole
MOA: a2 adrenergic antagonist
Use: reversal of a2 agonists (dexmedetomidine)
Phenoxybenzamine
MOA: non-selective a antagonist
Non-competitive, irreversible
Phentolamine
MOA: non-selective a antagonists
Competitive, reversible
Propranolol
MOA: non-selective B1 antagonist
Use: dec HR, reduce cardiac O2 demand, dec BP
Atenolol
MOA: selective B1 antagonist
Use: dec HR, reduce cardiac O2 demand, dec BP
Hypovolemic shock
intravascular volume deficit (e.g. hemorrhage)
Distributive shock
Peripheral vasodilation
Septic, anaphylactic, and neurogenic shock
Cardiogenic shock
myocardial pump failure
Procainamide
MOA: Class IA Na channel blocker
Use; Supraventricular tachycardia
Lidocaine
MOA: Class IB Na channel blocker
Use: Ventricular tachycardia
Flecainide
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
Atenolol
MOA: class II B blocker
Use: slow AV nodal conduction
- A fib
Amiodarone
MOA: Class III - prolong AP
Use: arrhythmias
- but prolonging AP generally assoc’d with inducing arrhythmias
Diltiazem, Verapamil
MOA: Class IV Ca Channel Blocker
Use: dec ventricular response to A fib
Digoxin
MOA: Dec AV nodal conduction - antiarrhythmics
Use: dec ventricular response to A fib
Adenosine
MOA: blocks AV nodal conduction
Use: can terminate SVT involving the AV node (e.g. A fib)
Does complete arrhythmia suppression eliminate the risk for subsequent lethal arrhythmia>
ALL antiarrhythmic drugs can induce arrhythmias
Increase cardiac contractility
- functions as a better pump
- inc CO and tissue perfusion
- “positive inotropic” effect
3 basic ways to inc cardiac performance
- inc B1 adrenergic (sympathetic) stimulation
- inc cardiac myocyte intracellular Ca
- enhance the contractile process directly
Enalapril
MOA: ACE inhibitor - dec BP
Use: tx high BP, diabetic kidney dz, and heart failure
Losartan
MOA: angiotensin receptor antagonist
Use: high BP
Prazosin
MOA: competitive a-adrenergic antagonists - alpha blocker
Use: vasodilation
Diltiazem, Verapamil
MOA: Ca Channel antagonists
Use: vasodilation
Amlodipine
MOA: Ca Channel antagonists
Use: vasodilation
Nitric oxide - cGMP - PKG
MOA/Use: profound vasodilation
Nitroglycerin (exogenous NO)
Aka Nitrovasodilators
Use: venous dilation
- acute cariogenic pulmonary edema
- CHF
Sodium nitroprusside
Aka Nitrovasodilators
Use: arterial and venous dilation
- hypertensive emergencies, acute CHF
- given IV
Sildenafil
MOA: Phosphodiesterase type 5 inhibitor
Use: managing pulmonary hypertension
Minoxidil
MOA: K+ channel activators
Use: dec TPR, dec BP, rarely used
What are the major osmolytes (particles) being reabsorbed? (renal)
NaCl, HCO3, Ca++
What are the major osmolytes (particles) secreted from kidneys?
H+ and K+
Mannitol
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
Acetazolamide
MOA: carbonic anhydrase inhibitors - inc loss of HCO3 & may inc urine pH
(weak diuretic effect)
Use: metabolic alkalosis, glaucoma, altitude sickness
Furosemide (Lasix, Salix)
MOA: Loop diuretic (BEST)inhibits NaCL reabsorption in the thick ascending LoH
Use: oliguric renal failure, CHF, acute pulmonary hypertension, and EIPH
Chlorothiazide
MOA: block NaCl reabsorption - not as good as loop diuretics
Use: nephrogenic diabetes insipidus, udder edema in cattle, Ca containing uroliths
Spironolactone
MOA: competitive aldosterone antagonists (K sparing)
Use: often in combo with loop diuretic; mild diuresis with reduced potential for K loss
Amiloride, triamterene
MOA: principal cell Na channel blockers (K sparing)
Use: in combo with loop diuretics, immediate but mild diuretics
Demeclocycline
MOA: collecting duct V2 receptor antagonists
Use: syndrome of inappropriate ADH production; effective in heart failure but not yet approved
What are the 2 major histamine pools?
- Mast cells (CT) & basophils (circulating)
2. Non-mast cell tissues (lungs, skin, gastric mucosa)
Why is histamine released?
- immune-mediated, IgE hypersensitivity
- drug-induced (e.g. NMJ blockers, morphine)
- plant and animal stings
- physical injury
H1 receptors
allergy, inflammation, pain, itching
vasodilation, edema, bronchoconstriction
*classical antihistamine target these
H2 receptors
gastric acid secretion
Diphenhydramine (benadryl)
MOA: 1st gen H1 antagonist
antimuscarinic, sedating
Dimenhydrinate (Dramamine)
MOA: 1st gen H1 antagonist
antimuscarinic, sedating
Chlorpheniramine (Chlor-Trimeton)
MOA: 1st gen H1 antagonist
less sedating
Promethazine (Phenergan)
MOA: 1st gen H1 antagonist
antimuscarinic, sedating
Loratadine (claritin)
Certirizine (Zyrtec)
Fexofenadine (Allegra)
MOA: 2nd gen H1 antagonist
Less entering CNS, less sedation
Famotidine (Pepcid)
Ranitidine (Zantac)
Nizatidine (Acid)
Cimetidine (Tagamet)
MOA: H2 antagonists
Use: reduce gastric acid secretion; gastric, abomasa, and duodenal ulcers; drug-induced gastritis, reflux
Fluoxetine (Prozac)
Paroxetine (Paxil)
Sertraline (Zoloft)
Fluvoxamine (Luvox)
MOA: Selective serotonin reuptake inhibitors
Use in dogs: separation anxiety; compulsive behaviors, aggression
Use in cats: inappropriate urination (spraying); compulsive behaviors, aggression; psychogenic alopecia
How are NSAIDs and NSIMs (Non-steroidal immunomodulators) similar? different?
Both groups are immunosuppressants
NSIM suppress immune fxn via mechanisms distinct from corticosteroids
NSIMs
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)
Cyclosporine, tacolimus
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
Cyclophosphamide, chlorambucil
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)
Azathioprine, Mycophenolate mofetil
MOA: NSIM - Cytotoxic inhibitors of purine synthesis
Use: IBD, IM-skin dz, IMHA, etc.
- can take weeks for effect
Oclacitinib (Apoquel)
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
Cytopoint (Canine Atopic Dermatitis Immunotherapeutic)
MOA: monoclonal Ab against IL-31 (itch)
Use: atopic dermatitis in dogs
- sq inj lasts 4-6 wks
