Block I And II Review Flashcards
Where are Nm receptors found
Somatic skeletal muscle
Where does succinylcholine work
Nm receptors on skeletal muscle
Bethanechol
- bowels and bladder
- used for pts with urinary retention and gastric atony
- M agonist
Pyridostigmine
- Tx for MG
- works on No receptor
- doesn’t enter CNS, no convulsions
- Achase inhibitors
Autoimmune disease where Ab to the Na receptors are produced; it causes weakness in skeletal muscles especially in the facial area
MG
Toxicity of Achase inhibitors
DUMBBEELSS: diarrhea, urination, miosis, bronchoconstriction, bradycardia, excitation (of skeletal muscle and CNS), emesis, lacrimation, salivation, and sweating
Toxicity resembles too much parasympathetic stimulation + sweating + nicotinic effects
Treatment for Achase inhibitors
Atropine
-blocks M, doesn’t stop any Nm
Pralidoxime used in extreme cases to keep diaphragm from stoping
Atropine
- M blocker
- belladonna alkaloid
- central and PNS
- used for Achase inhibitor poisoning
Tropicamide
- shorter half life
- dilated eye exam
- M blocker
Succinylcholine
- Nm blocker that persistently stimulates skeletal muscle until it causes paralysis (depolarizing)
- can cause hyperkalemia
- can cause malignant hyperthermia
Epi
- a1,a2,B1,B2 agonist
- low dose: beta, decrease BP
- high doses: alpha, increase BP
- used for anaphylaxis
Phenylephrine
A1 agonist
- increases BP, reflex Brady
- dilated eye exam
- nasal decongestant
Prazosin
- blocks a1a receptors
- used for BPH and HTN
- may cause orthostatic hypotension and reflex tachy
No specific B blockers
N-Zolols
-bad for COPD and vasospatic angina
B1 specific blockers
A-Molols
-atenolol and metoprolol
Alpha 1 and B blockers
Labetolol and carvedolol
Sotalol
B blocker, K channel blocker
Clinical uses of B blockers
Glaucoma HTN (2nd line) CHF (1st line) SVTs Stable angina
Vasospastic angina and B blockers
Never use!
What is the best combo for CHF
ACEI and BBlocker
Adverse effects of B blockers
- bronchoconstriction
- hypotension, bradycardia, fatigue, drowsiness
- increased plasma lipids;TGs and LDLs
What drugs for HTN increase lipids?
B blockers and Thiazieds
Which drugs could cause increased GI motility
Bethanechol
Pyridostigmine
Which drugs could decrease GI motility
Atropine
Tropicamide
Which drugs lower BP
Prazosin
Atenolol,metoprolol
M agonist (bethanechol)
Epi in low doses
What drugs would raise BP
Epi in high doses
Phenylephrine
Competitive antagonism
Right shift
-maximal effect is not decreased
Non competitive antagonism
Maximal effect is shifted down
Potentiation
Curve shifts left
Allosteric agonist
Refers to the concentration required to produce 50% of that drugs maximal response (EC50)
Potency
-the graph most left is the most potent
Reflects the upper limit response relation on the response axis (Emax)
Efficacy
-height, tallest curve
When pH is less than PKA, the protonated forms __________ dominate
HA and BH+
When pH is greater than PJa, the deprtonates form ________ predominate
A- and B
Increased urine pH
Acid is ionized, gets eliminated
Decreased urine pH
Base gets ionized, gets eliminated
Weeks acid overdoes
Bicarbonate
Weak base overdoes
NH4Cl
What do we want to manipulate to correct ph balance
Urine ph
Stomach ph
1
Small intestine ph
6
Blood ph
7.4
Urine ph
5-8
What does a p450 inducer do to active drug
Enhances metabolism
-decreases drug effect
What does a P450 inhibitor do to active drug
Increases drug effects and toxicity, stops metabolism
What does a P450 inducer do to a prodrug
Makes it moire active, increase effect
What does a p450 inhibitor do to prodrug
Decrease effect, stays inactive