Pharm Flashcards
Aspirin mechanism of action
Decreased production of prostaglandins and thromboxane A2
What is digitalis and what can it cause in the heart after an overdose is given?
It’s a cardiac glycoside used to treat congestive heart failure and arrhythmias. Also comes from plants such as foxgloves (Digitalis purpurea). It has sympatholytic and positive inotropic effects on the heart. Overdoses can have effects on T wave, Bradycardia, increase in the heart’s output, and a decrease in the size of the heart. Digitoxin and digoxin are commonly used digitalis.
How do α2-adrenergics work?
α2-Adrenergic activate α2-adrenergic receptors inhibiting the positive feedback mechanism for the release of norepinephrine from the presynaptic nerve endings by reducing Ca conductance. Attenuation of norepinephrine release causes dose-dependent sedation and inhibits the afferent pain pathway. It also decreases cardiac output, a centrally mediated reduction in respiratory rate, muscle relaxation, and depression of GI motility.
How do NSAIDs work?
They produce analgesia and antiinflammatory effects by reducing prostaglandin (PG) synthesis through inhibition of the enzyme cyclooxygenase (COX) in the peripheral tissues and CNS.
What are the two ISO form of the cyclooxygenase enzyme and how are they different?
COX-1 and COX-2.
Cox-1 is constitutively expressed in both the peripheral nervous system and CNS, although expression is enhanced by pain and inflammatory mediators.
COX-2 is ubiquitous in the CNS but only becomes a major enzyme for after induction by factors released during cell damage and death.
Because it takes 2 - 8 hrs for maximal COX-2 expression in the peripheral tissues, initial release of PG is primarily due to COX-1.
How does analgesia work with opioids?
Analgesic effects of opioids are associated with binding to spinal and supraspinal mu ( µ ), kappa ( κ ), and sigma ( σ ) receptors. Drug binding decreases propagation of the nociceptive signal by activating receptor-linked potassium channels and inhibiting voltage-gated calcium channels.
What are the common clinical signs of malignant hyperthermia?
What medications is it usually a response to?
Classical signs of MH include marked hyperthermia, tachycardia, tachypnea, increased end-expired carbon dioxide production, increased oxygen consumption, acidosis, hyperkalemia, and muscle rigidity.
Typically a pharmacogenetic disorder that reacts to volatile anesthetic gases like halothane, sevoflurane, desflurane, and the depolarizing muscle relaxant succinylcholine.
What is clenbuterol and how does it work?
It is a β 2 -adrenergic agonists such as albuterol, fenoterol, pirbuterol, and salmeterol.
It produces relaxation of smooth muscle (brinchial, vascular and uterine) by increasing the intracellular levels of cyclic adenosine monophosphate (cAMP).
*Adverse side effects include anxiety, shivering, sweating, and tachycardia. It can occur at higher dosages but appear to be minimized when clenbuterol is increased in a stepwise manner.
What is the difference between low-molecular heparin and regular heparin for the use in laminitis prevention?
Unfractionated heparin causes intravascular agglutination of equine RBCs, arguing that its use might actually exacerbate intravascular cellular plugging. Low-molecular-weight heparin (LMWH), is nonagglutinating but retains anticoagulant activity by inhibition of factor Xa.
What is allopurinol (Zyloprim) and what would it be its recommended use in horses?
It is a hydroxyl radical scavenger and inhibitor of xanthine oxidase activity, that has positive clinical effect
during sublethal endotoxin infusion in horses.
A recommended dose for allopurinol is 5 mg/kg IV.
