Exam 3: Lauth Lectures

Question 1

What is the MOA for depolarizing (nicotinic receptor agonists) and non-depolarizing (competitive antagonists) NMJ blockers?

Answer 1

depolarizing NMJ blockers stimulate NMJ nicotinic receptors to cause prolonged motor end plate depolarization. initial muscle fasiculation followed by relaxation.

non-depolarizing NMJ blockers prevent motor end plate depolarization (it’s in the name!) therefore there is not action potential and you get flaccid paralysis.

Question 2

What are the clinical uses of NMJ drugs? What is the problem when it comes to monitoring anesthesia with NMJ blockers?

Answer 2

anytime skeletal muscle paralysis is desired: tracheal intubation, (oothapedic manipulation) fractures, balanced anethesia.

NMJ blockers block reflexes and muscle tone so it is hard to monitor anesthesia in this way. Look at resp, BP, HR, temp, and ECG

Question 3

What are the three competitive NMJ blockers, their general duration of action, metabolism and elimination, and degrees of toxicity that we discussed in lecture?

Answer 3

pancuronium: long lasting, renal elimination (half-life increases with renal disease), no histamine release but blocks muscarinic receptors therfore casuing tachycardia.

atracurium: intermediate duration. spontaneous elimination (temp and pH dependent - increased half-life during hypothermia and acidosis), hydrolysis by plasma esterases and renal excretion but half life not increased during renal disease. does promote histamine release.

mivacurium: short duration of action. rapid hydrolysis via plasma esterases. half life not increased with renal disease. does promote histamine release.

Question 4

How do you reverse non-depolarizing drugs? depolarizing drugs?

Answer 4

for competitive, AChE inhibitors are given.

Question 5

What is the polarizing drug discussed in lecture and its general duration of action, metabolism and elimination, and degrees of toxicity?

Answer 5

Succynilchline, rapid onset, short duration for short things like tracheal intubation, some histamin release but not generally ganglioninc bloackade. does cause hyperkalemia so avoid in soft tissue damage or burns. it is not reversible.

Question 6

What are the indications for use of diuretics?

Answer 6

reduce ECF volume (pulmonary congestions or ascites), oliguric renal failure, hypertension (exercise induced pulmonary hemorrhage).

Question 7

What is the drug named for all five classes of diuretics and aquaretics mentioned in lecture? What are their MOA, where are they acting, and what are their special properties or contraindications?

Answer 7

Osmotic diuretics: mannitol, increases diuresis by increasing osmotic gradient in lumen. acts on the proximal tubule and thin loop. don’t use in a blocked cat, can cause bladder to burst. don’t use if there in intracranial bleeding. used to treat o prevent oliguric renal failure, cebral edema, and glaucoma.

carbonic anhydrase inhibitors: acetazolamide, increases loss of bicarb and tendency to increase urin pH. works at proximal tubule. dont give to acidotic patients. treat metabolic alkalosis, glaucome and alittude sickness in dogs (?).

Loop diuretics: furosemide, is our mainly used diuretic. inhibits NaCl reabsorption in the thick ascending limb. used to trwat olifuric renal failure, CHF, acute pulmonary hypertension, and EIPH

Thiazide diuretics: distal convoluted tubule. prevent reabsoprtion of Na and Cl by blocking symporter. chlorothiazide. treats nephrogenic diabetes insipidous, udder edema in cattle, Ca2+ containing uroliths.

K+ sparing diuretics: spironolactone (competitive aldosterone antagonist), amiloride, and traimterene (sodium channel bloackers). used in conjunction with loop diuretics to prevent hypokalemia.

aquaretics: antagonizes A2 receptor in kindey, antagonizing ADH/vasopressin. demecocycline.