Exam Flashcards
clonidine
SYMPATHOLYTIC
a2 agonist - hypertension
low NE in CNS –> low SNS –> low CO & PVR
Tox: bradycardia, constipation, sedation, impaired conc.
Metroprolol
SYMPATHOLYTIC
B1 antagonist - hypertension, CHF, angina, antiarrhythmias
Class II antiarrhythmic agent
block B1 in heart –> low CO
block in juxta-glom reg –> less renin –> low PVR
-Low myocardial O2 requirement in angina
-Inhib SNS effect, slow HR
Tox: bradycardia (B1)
Propranolol
SYMPATHOLYTIC
B1, B2 antagonist - hypertension, CHF, arrhythmias, angina
Class II antiarrhythmic agent
block B1 in heart –> low CO
block in juxta-glom reg –> less renin –> low PVR
-Low myocardial O2 requirement in angina
-Inhib SNS effect, slow HR
Tox: bradycardia (B1) & B2 block side effects (asthma)
prazosin
SYMPATHOLYTIC
a1 antagonist - hypertension
-block vasoconstriction = dilation
Tox: rare & mild: dizziness, palpitations, headache
Sodium nitroprusside
VASODILATOR-Nitric Oxide Donor
NO–> cGMP - hypertension
-emergencies, short acting
-dilate arterial & venous vessels (relax sm muscle)
Tox: hypotension, cyanide accumulation
Verapamil
VASODILATOR/CA2+ BLOCK
Low Ca2+ conductance - hypertension, angina, arrhythmias
-long term & emergency
-inhib Ca2+ influx into bl vessel sm muscle → dilation
-inhib Ca2+ influx into cardiac sm muscle → low cardiac contractility
-lower O2 requirement in sm muscle + heart
Class IV antiarrhythmia agent
Tox: bradycardiia, heart failure
Enalapril
ACE INHIBITOR
Ace inhib - hypertension, CHF
Stops angiotensin I –> II conversion
(Angiotensin II - renin Na2+ & water retention & vasoconstriction = increase BP) (block = water excretion & vasodil = decrease BP)
Tox: cough, hypotension, hyperkalemia, dizziness, headache
Losartan
AT1-ANTAGONIST - hypertension, CHF
(BLOCK AT1)
AT1 = increase DAG & IP3
-PRESYNAPTIC: Increase NA+ release
-SMOOTH MUSCLE: IP3 → increase Ca2+ release (contract)
-high aldosterone and ADH secretion
-potent vasoconstrictor (ANTAGONIST = vasodilate)
blocking=opposite of all this
Tox: hypotension, hyperkalemia, dizziness, headache
Hydrochlorothiazide
DIURETIC - THIAZIDE
Increase Na+ & H2O excretion - hypertension, CHF
-mild-moderate hypertension
-inhib NaCl transport in distal convoluted tubule
Tox: hyperkalemia (HARZARDOUS W ARRHYTHMIAS), actue myocardial infarction, taking digitalis; gout (cuz uric acid reabs), hyponatremia (dehydration)
Furosemide
DIURETIC - LOOP
Inhibit co transport of Na+,K+, Cl- in LofH - hypertension, CHF
-more powerful diuretic for severe hypertension & pulmonary edema
-rapid and short acting
Tox: same as hydrochlorothiazide ( hyperkalemia, acute myocardial infarction, gout, hyponatremia) plus dose depdnant ototoxicity (hearing loss)
Nitroglycerin
VASODILATOR - CHF, angina
-patients w edema
NO → cGMP → relax of sm muscle cell = vasodil
Acts on smooth muscle in other tissues (ie bronchioles)
-low venous return
-low PVR
-dilation of coronary arteries
-Low O2 requirement and increase O2 delivery
Tox: hypotension, tachycardia (reflx high in SNS), headache, myocardial infarction
-tolerance CAN occur (theory: less NO released, lower guanylyl cyclase sensitivity, increased metabolism of cGMP, systemic compensation (increase SNS, salt & water retention))
Viagra
Nitroglycerin + sildenafil
Inhibit phosphodiesterase → prevent breakdown of gGMP → relax sm muscle
Can alter vision (discrim. between green and blue)
Types of angina pectoris
Atherosclerotic:
Most common, irreversible atherosclerotic obstruction in coronary arteries
Precipitated by exertion
Vasospastic:
Spasm of part of coronary vessel (often at atherosclerotic plaque site)
Can occur at anytime
Unstable:
Atherosclerotic plaque + platelet aggregation + vasospasm (precursor of myocardial infarction)
Quinidine
NA+ CHANNEL BLOCKER
- antiarrhythmic
-MODERATE Na+ chan blockers (Class IA)
- lower Na+ conductance
- less frequently used b/c side-effects
Tox:nausea, vomiting, headache, dizziness, anticholinergic effects, enhance digoxin tox)
-increase effective refractory period (ERP)
Lidocaine
NA+ CHANNEL BLOCKER- antiarrhythmia
- lower Na+ conductance (Class IB)
- most common for IV antiarrhythmic (vent tachycardia/fibrillation)
-reduce Na+ channel recovery - low conduction and excitation
-shorten ERP
Amiodarone
K+ CHANNEL BLOCKERS
- lower K+ conductance (also affects other ion channels)
-prolong AP duration
-also affects B receptors & Na+/Ca2+ channels
Cardiac muscles contract by ___________ and name process steps
Excitation-contracting coupling
1. AP → high Ca2+ - enter during plateau, Ca2+ induced release from SR
2. High Ca2+ binds troponin C - uncovers myosin bind site on actin
3. Actin & myosin cross-linkages form → contraction
Edema
excess fluid in venous system can leak into tissues (eg. extremities, lungs)
CVS compensation methods for low CO & symptoms
-Increase SNS
-Increase renin-angiotensin system
Low CO → low blood flow to kidney → SNS activation of B1 → increase renin
-Increase force of contraction of heart
-Ventricular hypertrophy - cardiac muscle cells increase in size to compensate for damage/stress
Symptoms; tachycardia, shortness of breath, sweating, edema, low exercise tolerance, enlargement of heart, hypertension/hypotension, urine retention
Digoxin
CARDIAC GLYCOSIDE - CHF & atrial fibrillation or enlarged/dysfunction left vent
Na+/K= ATPase inhibitor
Direct effects (cardiac muscle cell)
Increase NA+ in → low CA2+ efflux out → increase intracell Ca2+ → increase interaction between actin & myosin → increase cardigan contractility
Indirect effects (barorec)
Improve circulation → barorec → increase PSNS, low SNS
OVERALL: increase force (direct) and lower rate of contraction (indirect)
-narrow therepeutic index, give large initial dose first and daily maintenance doses
Tox:
Cardiac: arrhythmias (brady & tachycardia) - common in patients w low K+ (from diuretic or diarrhea)
Quinidine (anti-arrhythmic): low digoxin clearance → increase plasma levels
Gi/CNS: anorexia, nausea, vomiting, diarrhea, dizziness, headache, visit disturb.
Alzheimer’s loss of ______ neurons
cholinergic
Parkinson’s loss of ________ neurons
dopaminergic
Haloperidol
Blocks D2 > 5-HT2A
Olanzapine
Blocks 5-HT2A > D2
monoamine theory - bipolar
Monoamine (NE, 5-HT, dopamine)
Low monoamine transmission → depression
High monoamine transmission → increase mood - over activation = mania
Lithium
Mood stabilizer: low in precursors for IP3 & DAG synthesis
Low IP3 & DAG when rec linked to 2d messengers activated (ie muscarinic, a1 & 5-HT2A rec)
May increase serotonin and GABA, decrease NE, DA & glutamate
Tricyclic antidepressant (TCA)
Anti-Depressant: prevent NE and serotonin reuptake
-not as first line of treatment
Tox:
-block cardiac sodium channels (like quinidine)
-Antagonist at muscarinic: dry mouth, constipation, etc
-Antagonist at H1 and a1: sleepiness/sedation
Fluoxetine
SSRI
Anti-depressant: Inhibits CYP2D6 (metabolizes serotonin)
Also used for panic disorder, anxiety, OCD, bulimia
Tox: insomnia, sexual dysfunction
-dangeous when combined w other antidepressants –> seratonin syndrome
Buproprion (atypical)
Anti-depressant: Inhibit DA & Ne reuptake
Inhibits CYP2D6 - alters metabolism of TCA’s, B-blockers & haloperidol
Tox: anti-muscarinic and nicotinic effects
Benzodiazepine: diazepam (valium)
Sedative hypnotic: Enhance GABA neurotransmission → enhance Cl- conduct
→ inhibit many neurons in many brain regions
-Bind to subset of GABAA receptors at site distinct from GABA
-Increases frequency of GABA-mediated opening of Cl- channel
-GABA required for affect - (binding of drug to benzodiazepine site does not activate GABAA rec)
Can be used to treat ethanol withdrawal
Phenelzine
MAO inhibitor
Anti-depressant: Inhibits metabolism of NE, serotonin, dopamine, & tyramine)
Only used if TCAs not effective
Tox: Hypertensive crisis - if tyramine-containing food ingested or if taking CNS stim (cocaine,amphetamine)
Can cause serotonin syndrome if taken w SSIs, SNRIs, TCAs
Barbiturates: phenobaribital
Sedative hypnotic: Enhance GABA neurotransmission → enhance Cl- conduct
→ inhibit many neurons in many brain regions
-Bind to all GABAA receptors at site distinct from GABA and benzodiazepine bind sites
-Increases duration of GABA-mediated opening of Cl- channel
-At high dose: barbiturates can directly activate GABAA rec & inhib glutamate rec & some Na+ & Ca2+ channels
Methadone
Opioid detox
oral, longer acting opioid receptor agonist
Clonidine can be used for
autonomic symptoms of withdrawal
amphetamine
higher release of NE, dopamine and serotonin
cocaine
lower reuptake of NE, dopamine and serotonin
Overdose: intercranial hemorrage,stroke, seizure, arrhythmias, hyperthermia, heart attack, coma, death
LSD
agonists at several 5-HT rec –> most agonist or partial agonists of 5-HT2A rec
particularly harmful in pregnancy
PCP
NDMA rec antagonist
overdose can be fatal
marajuana mechanism
cannabinoid receptor (CB1- CNS; CB2-PNS) – linked
to G-protein → inhibit GABA or glutamate release
Endocannibinoid
increase Ca++ (postsynaptic neuron)
→ increase endocannabinoid →
binds presynaptic CB1
receptor → lower glutamate (or GABA) release
THC
activates the CB1 receptor → lower glutamate (or GABA) release
Therapeutic uses of cannabinoids
Cancer : less pain, nausea & vomiting
AIDS: appetite stimulation
Glaucoma*: lower intraocular pressure
opioids pre and post synaptic affects
pre: low Ca2+ –> low release of NT
post: increase K+ efflux –> inhibit postsynaptic neurons
Haloperidol and olanzapine adverse effects
CNS
-Parkinson-like symptoms (D2 antagonism in striatum)
-Hormonal/metabolic dysregulation, weight gain (D2 antagonism in diencephalon)
-Sedation (H1 & a1 antagonism)
Autonomic;
-Hypotension (a1 rec-blockade)
-Also muscarinic rec antagonists → atropine like side-effects (dry mouth, blurred vision, constipation)
Sedative inhibits
irritability and excitement
Anxiolytic inhibits
apprehension and fear
-does not induce sleepiness/hypnosis - used for anxiety
“minor tranquilizers”
Neuroleptic
suppresses spontaneous movements and complex behaviour
Phenothiazine (ex. chlorpromazine) effect and mechanism
neuroleptic and sedative
Effect:
-Profound reduction of fear & anxiety
-Reduction of activity & response to stim
-Muscle relax
Mechanism:
-Block D2 rec in brain → sedation, reduced anxiety
=Also blocks peripheral a1 rec = side effects: vasodilation
Alpha-2 agonist effect and mechanism
ex, dexmedetomidine
a2a & 2c receptors located on
pre-synaptic CNS neuron and postganglionic SNS fiber on peripheral organs
a1 & a2b receptors located on:
Target organs
Selective a2 rec agonist if injected slowly at low to moderate dose
A1 and a2b rec stim on bl vessel sm muscle when injected rapidly or at high dosages → transient hypertension
In pre-synaptic CNS neurons a2 stim K+ chan open → inhibit depol & NT release in wakefulness, pain, SNS outflow and motor activity = sedation, analgesia, hypotension, relax
anti-diarrheal opioids
-loperamide
-diphenoxylate
benzodiazepine is a
sedative and anxiolytic
full mu agonist
fentanyl, morphine
full kappa agonist
pentazocine
Local anesthetics
-lidocaine
-bupivacaine
-levobupivacaine
Physiological effects of full Mu agonist → morphine
CNS - 2-6 hours of analgesia + sedation
Sedation in dogs and primates, excitation in cats, horses, ruminants, pigs, etc (“sham rage”)
Cardiovascular - little effect
Histamine release → vasodil → hypotension
Respiratory - dose-dependant depression
More intense when combined w anesthetic
Death from overdose b/c of respiratory arrest (Mu)
Reverse w naloxone
Suppress cough
Gastrointestinal
Increase segmentation, reduce propulsion in large bowel → dehydrated stool → constipation
Bile duct sphincter contract → biliary colic
Nausea and vom
Urinary
Bladder sphincter tone increase, bladder wall muscle tone increased → urgency to urinate but difficult
opioids that restrain wildlife
Carfentanyl
Etorphine
drug that can help w alzheimers
donepezil
Benzodiazepine (ex. diazepam) reversal agent
flumazenil
lidocaine
most widley used anesthetic
bupivacaine
-used almost as much as lidocaine
-slower onset, longer duration
-greater CVS tox –> IV bolus (severe vent arrhhythmias)
local anesthesia
loss of sensation, not unconsciousness
-safer than general anesthesia
