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
CYP inducers
Benzopyrenes
Chronic ethanol
Carbamazepine
Rifampin
CYP inhibitors
Cimetidine
Erythromycin
Grapefruit juice
A patient is taking warfarin and is later Rxed cimetidine fro peptic ulcers, what happens?
Increased warfarin toxicity=bleeding
First order elimination
- most drugs
- constant fraction eliminated
- constant half life
Zero order elimination
- phenytoin
- ethanol
- aspirin
- constant amount elimainted
- half life not constant
Steady state
4-5 half lives
Function of a drugs half life
Half way to steady state
One half life
75% to steady state
2 half lives
Maintainece dose has to do with: clearance or Vd?
Clearance
Loading dose has to do with: clearance or volume of distribution?
Vd
Normally, acetaminophen has a Vd=70L and Cl=350mL/min. If acetaminophen was administered to a patient with 50% normal rental function, what parameter would differ from normal
Md would be lower
A 55 year old women with HTN is to be started on a thiazides diuretic. Thiazides A in a does of 5 Mg produces the same decrease in BP as 500mg of thiazide B, which two statements are accurate about these drugs
- both drugs have equal efficacy
- A is about 100x more potent than B
We start an IV infusion of a drug using a pump that ensures that rate of delivery of drug over time is constant. Which of the following factors determines how long it takes for the drug to reach steady state concentration in the blood
Half life
A patient is admitted for treatment of drug overdoes. It is observed that when the urine pH is acidic the renal clearance of the drug is less than the GFR. When the urine pH is alkaline, the clearance is greater than the GFR. The drug is probably a
Weak acid
Dopamine via D1 receptors, epinephrine via B2 receptors, and histamine via H2 receptors are important transmitters. When these ligand interact with their cellular receptors, how do they mainly elicit their responses
Activating adenlyl cyclase
Initial fluid loss, long term vasodilation via hyperpolarization of smooth muscle
Thiazides
HCTZ
What CCBs are good for the heart
Verapamil
Which CCB is good for both heart and vessels
Diltiazem
Which CCB is good for the vessels
Amlodipine
What does amlodipine do
Vasodilator, reflex tachycardia
Decreases production of ang II, decreased aldosterone, vasodilation
ACEI
Lisinopril
-blocks ACE
ACEI and bradykinin
Causes dry cough
What accumulates when you take lisinopril
ANG I
Block the action of Ang II, decrease aldosteron, vasodilation
ARBs
Losartan
What happens in cardiac failure to compensate?
Increase Blood volume
Increase end diastolic volume (Preload)
Increase HR
Increase arteriolar constriction (AFTERLOAD)
What do we want to do to decrease preload in CHF
HCTZ, furosemide, lisinopril, losartan
Lisinopril and losartan act like diuretics because they stop aldosterone so lose Na+ and water, can also dilate veins
What do we want to do to decrease heart rate in CHF
Metoprolol
B blocker to control HR
What do we want to do to decrease afterload in CHF
Lisinopril, losartan
-dilates arterioles
What drug do we give for CHF that is a positive inotrope that will help improve contractility
Digoxin
Which drug for CHF has a very low TI
Digoxin
Cardiac remodeling in CHF
Fibrosis of the heart, want to stop this
What drugs do we use to stop cardiac remodeling via aldosterone in CHF
Lisinopril, losartan, spironolactone
Which drug stops aldosteron production and can help fight cardiac remodeling in CHF
Lisinopril and losartan
Which drug blocks aldosteron receptors and can help stop cardiac remodeling in CHF
Spironlocatone
When is digoxin used
CHRONIC CHF
MOA of digoxin
Inhibits Na-K ATPas
Blocks pump= Na increase
Increases Na/Ca exchange
Brings more Ca in and goes to SR=stronger cardiac contractions
Fast response AP
Atrial and ventricular muscle, Perkinje fibers
What kind of drugs would you want to treat ventricular tachycardia
Drugs that ablock Na, K channels
-amiodarone
Slow response AP
SA and AV nodes, supraventricular arryhtmias
What kind of drugs to treat SVTs
Drugs that block Ca, beta blockers
What CCB would you use for AVTs
Diltiazem
What beta blockers would you use to treat SVT
Atenolol and metoprolol
-cause Ca channels to stay closed -decreased phase 4
SVTs and digoxin
Has a PNS affect-slow HR down
-decrease phase 4 and 0
Patient taking antiarrhymic drug, monitored for thyroid drug, which drug are they probably on
Amiodarone
- iodine
- thyroid problems
- blue skin
- eyes, liver, lungs
Three classes of drugs effective for angina either alone or in combination for stable angina
Nitrates (nitroglycerin)
BBlockers
CCB (amlodipine or diltiazem)
What kind of drug would you use prophylatcically for angina
BBlocker every day
How do nitrates work on angina
Venodilation thereby decreasing preload
How do BBlockers work on angina
Decrease the oxygen demands of the heart
How do CCB work for angina
Cause vasodilation of smooth muscle or decrease HR
Patients with variant angina, what are they preferred classes of drugs
Nitrates
CCB
What kind of angina should you only use BBlockers in
Stable (not vasospasm)
What is the drug of choice for acute angina attack
Nitroglycerin under the tongue
MOA of statins
HmG CoA reductase inhibitors
-rate limiting step in cholesterol synthesis
Side effect of statins
Mild muscle pain
What is the drug of choice for hyperlipidemia
Atorvastatin
Most common antiplatelt drug
Aspirin
MOA of aspirin
Inhibits COX to stop TXA2
Stops platelets from aggregating
What drug is common to use in mini strokes
Aspirin
Anticoagulant drugs
Warfarin
Rivaroxaban
Synthesis inhibitor of vit K
Warfarin
What coagulation factors are affected by warfarin
Vit K dependent factors
2,7,9,10
What do you give someone who has had too much warfarin
Vit K
MOA of rivaroxaban
Blocks factor Xa, rapid onset
Site of action of acetazolamide
Proximal convuluted tubule
Site of action of furosemide
Ascending loop of Henle
Site of action of thiazides
Distal convoluted tubule
Site of action of sprinolactone
Collecting duct
MOA of CAIs (acetazolamide)
PCT
- block CA, cant get bicarbonate
- H from the bicarbonate cant swap with the Na to get in the cell
- blocks Na from getting in
MOA of thiazides (HCTZ)
DCT
- block Na/CL transporter
- saves Ca
MOA of loops (furosemide)
Block the Na/L/CL pump
-also lose Ca and Mg
MOA of spironolactone
Blocks aldosterone receptors
- not affecting Na
- K sparing
