Test Review Flashcards
Describe hypokalemia on cardiac conduction
Decreased extracellular potassium concentration (hypokalemia) results in decreased potassium conductance, which reduces potassium current. Hypokalemia is also shown by the appearance of U waves. Hypokalemia would also account for the woman’s muscle weakness (flaccid paralysis) as it decreases the voltage-gated sodium current in nerve, skeletal muscle, and cardiac muscle. In hypokalemia, decreased sodium current in atrial myocytes would increase the duration and decrease the amplitude of the P wave. Hypokalemia would decrease delayed rectifier potassium current in the SA node, which would make the slope of phase 4 steeper and increase heart rate. Excitability of cardiac myocytes would be decreased in hypokalemia due to decreased sodium current (threshold would be shifted more positive than normal). Increased plasma potassium concentration (hyperkalemia) would increase potassium current, which would increase the rate of phase 3 repolarization. The duration of the ventricular action potential would be decreased and a spiked T wave would be seen on the ECG.
Describe the effects of hyperkalemia on cardiac conduction
In hyperkalemia, gK would be increased and EK would be less negative (more positive). The increased gK in hyperkalemia would increase potassium current, resulting in a faster phase 3 repolarization (spiked T wave). Hyperkalemia causes a resting depolarization of atrial and ventricular myocytes, which decreases the number of resting sodium channels. This would decrease the conduction velocity of the action potential through the atria and widen the P wave, and prolong the P-R interval. Hyperkalemia would increase potassium current, decreasing the duration of the ventricular action potential. This would decrease the QT interval. Hyperkalemia decreases sodium current in ventricular myocytes, which would decrease conduction velocity of the action potential. The time to fully depolarize the ventricles would be increased and seen as a wide QRS complex (with a lower amplitude and slower rate of rise than normal).
How do pre and post ganglionic lengths compare in sympathetic vs para sympathetic?
Parasympathetic - Long Pre and short post
Sympathetic - short pre and long post
Why does sympathetic discharge lead to increased blood flow to muscle and decreased to skin?
Muscle contains predominantly Beta receptors and skin has alpha
Miosis
Excessive contraction of the pupil of eye
Mydriasis
Excess dilation of the pupil
What is the area of integration for the autonomic nervous system?
Hypothalamus
Describe norepinephrine metabolism by MAO and COMT in respect to metabolites and location
MAO - Dihydroxymandelic acid and occurs within mitochondria
COMT - Normetanephrine and occurs within extra neuronal spaces
Pilocarpine is a muscarinic _____?
Alkaloid
Carbachol has what type of action on nicotine receptors?
Direct
How do trimethaphan and hexamethonium block ganglions?
Both competitively block nicotinic Ach receptor without causing depolarization
How do neostigmine/physostigmine inhibit AchE?
Act as substrates (competitive inhibition) and are slowly hydrolyzed
How will administering edrophonium affect symptoms of cholinergic crisis?
Make symptoms worse
How do sympathomimetic agents affect metabolism?
Excitation of metabolism mediated by B2 increased glycogenolysis
Norepinephrine can stimulate what Beta receptors?
B1 - increase HR and contractility
Eye effect: alpha 1
Radial muscle leading to mydriasis
Eye effect: M3
Affecting circular and ciliary muscles leading to miosis and accomidation
Eye effect: B2
ciliary body leading to aqueous humor secretion
Mechanism: Tyramine
Acts by releasing NE from cytoplasmic neuronal pool to produce tachyphylaxis
Pindolol/Timolol are used in the treatment of?
HTN and arrythmias
Metryosine forms a compound with what inhibiting what?
Tyrosine hydroxylase leading to inhibition of rate limiting step
Tachyphylaxis
Rapidly diminished effect of a drug after successive administration
Sweat glands are innervated by
Sympathetic CHOLINERGIC nervous system
Patients on MAO inhibitors are at increased risk for what?
Developing HTN crisis following ingestion of meals rich in tyramine
General sympathetic discharge can lead to?
Hyperglycemia - Beta 2
Ephedrine, Amphetamines and Tyramine all produce?
Tachyphylaxis
Toxic activation of nicotinic effects
Stimulation followed by paralysis of ganglia of skeletal muscle
Tubocurarine
Competitive antagonist at ganglia and adrenal medulla leadin to decreased BP, tachycardia, and histamine
Also blocks nicotinic receptor at NMJ producing paralysis
Skeletal muscles have what type of receptors?
Post synaptic NICOTINIC receptors
Epinephrine metabolis
Uptake
Phentolamine before isoproteranol would?
Create greater drop in BP than isoproteranol alone due to decreased sympathetic reflex following Beta receptor stimulation
Butoxamine
B2 selective antagonist
Why is pilocarpine resistant to AchE?
It is not a choline ester
What is the primary control of autoregulation
CO2 which diffuses through the BBB to decrease the pH of the CSF. This will in turn lead to increased respirations
Thiazide diuretics can lead to?
Increased blood calcium and cause kidney stones
GnRH is released in what type of fashion?
Pulsatile fashion to increased FSH/LH
Neuropeptide Y
PNS vasoconstrictor and role in appetite
Estrogen, tamoxifen and methadone effects on TBG?
Increase TBG leading to decreased free T
Sign of primary hyperaldosteronism
Increased urine aldosterone even in presence of high salt diet
Octreotide/somatostatin decrease
PORTAL and splanchnic blood flow
Sucralfate
Protects GI by binding to ulcerated tissue can lead to constipation, requires acid pH for activation
Toxicity: Ergot alk
Drowsiness and Hallucinations
PROLONGED VASOSPASM LEADING TO GANGRENE
Uterine contraction
Uses of Vitamin D
Nutritional rickets
Osteoporosis
Osteomalacia
Older individuals have what to clotting factors
Decreased levels of vitamin K dependent clotting factors
Cyprohepatidine
Used for treatment of serotonin syndrome
Toxicity - H1 antagonist
Sedation, urinary retention and blurred vision
lipophilic drugs are easier to travel?
Pass placental barrier and concentrate in milk
FDA pharmacogenetic tests
Warfarin, Isoniazid, mercaptopurine, Ironotecan, Codeine
Inducers of CYP450
ACIRS
Inhibitors of CYP450
VAIG
Lipophilic teritary amines are able to go where easier?
Cross blood brain barrier
Compare locations of acetylcholinesterase vs butyrylcholinesterases
AchE - found in neurons and RBCs
BchE - found in plasma, glia, and liver
Ipratropium
Antimuscarinic that inhibits vagal stimulation and decreases bronchoconstriction
Mepolizumab/Reslizumab
Anti-IL 5 inhibit IL-5 binding to mast cells and decrease action of eosinophils
Cromolym/Nedocromil
Reduce mast cell degranulation and release of histamine
Theophylline
Methylxanthine adenosine receptor antagonist
Diazoxide
Hyperpolarizing cell and activation of K+ channels
Indapamide
NaCl inhibitor at DCT
Metolazone
NaCl inhibitor at DCT
Bumetanide
Loop diuretic