Pharmacology Unit 3

anaglesics

pain management medicine

chemical, nociceptor, spinal cord

Pain recognition: stimulus causes a — release that is detected by — neurons that send signals to the — — that are then sent to the brain

A-delta, myelinated

—  nerve fibers are — neurons in the spinal cord that typically identify sharp pain 

C nociceptor, unmyelinated

— nerve fibers are — neurons in the spinal cord that typically identify dull aching pain

Mu, kappa, delta

Opioids act on —, — and — receptors (GCPRs), the first two are the most targeted

periphery, pain relief

Mu1 receptors are more prominent in the — and where most — — effects are

brain

Mu2 receptors primarily in the —, and is responsible for other effects of opioids

excitability

Nociception signals from reaching spinal cord and decrease nerve —

Ca2+, GLU, substance P, open, K+, excitability, respiratory, convulsive, pregnancy, CNS

Opioids are analgesics

there are 2 general MOA for opioids:

in the periphery, opioids acting on Mu receptors block — inflow to neurons → decrease — and - — release

in the spinal cord, opioids acts on Mu receptors to — K+ channels causing — to leave the neuron and decrease nerve —

Contraindications: — depression, — disorders, biliary obstruction, — (can be used during labor though)

Drug interactions: — depressants and MAOI

opiate

Codeine is an —

opiate

hydrocodone is an —

opiate

oxycodone is an —

opioid

fentanyl is an —

dextromethorphan

is a combination opioid product that is used in cold medicines

ADH, bile/GI/bronchiole, respiratory

non-analgesic effects of opioids: nausea and vomiting, increased release of —, increased — duct/—/— spasms, — depression

OD

Opioid antagonists are good to use in case of opioid —

pure

Naloxone is a — opioid antagonist

antagonist, partial agonist

buprenorphine is an opioid — that is a — —, it can be used to decrease pain and when given with opioids it competes for binding

cough suppressant

an antitussive is a — —

antitussive

dextromethorphan is an opioid —that is available over the counter, there is still the potential for abuse

consciousness, antipyresis, analgesics, anti-inflammatory

Non-opioid analgesics and NSAIDs do not affect —, they primarily act as one of the 3As: —, —, and/or —

vasodilation, permeability, phagocytes

Process of inflammation: chemical messengers increase — and — allowing for swelling, recruitment of — occurs, causes redness, swelling, warmth, pain, reduced/loss of function

arachidonic acid, phospholipase A2

some mediators of inflammation include — — that is produced from — -

prostaglandins, thromboxanes

arachidonic acid produces — and — via cyclooxygenase (COX 1 and COX2)

most, macrophages

COX-1 is expressed by — cells, COX2 is expressed by inactivated —

steroidal, salicylates, synthetic NSAIDs, non-NSAIDS

what are the 4 classes of anti-inflammatories and analgesics?

opium, structurally, sharp, addictive

anti-inflammatories and analgesics have 3 major differences from opioids: none are related to — → — different, not effective for — visceral pain, non- —

non-NSAID, toothache, muscle, backaches, hepatoxicity, NAPQI, glutathione, NAC

Acetaminophen is a —, it is not specifically anti-inflammatory

MOA is unknown

Clinical indications: headaches, —, — aches, menstrual cramps, —

OD: has significant risk for — because it produces — which is a toxic metabolite that — detoxifies, OD decreases (prev) levels

Antidote for OD: —

salicylates, acetylation, inactivates, switches, inflammation, toothaches, menstrual cramps, preeclampsia, GI, anticoagulant (blood thinner), Reyer’s Syndrome

Aspirin is a — anti-inflammatory drug

MOA: — of COX1&2, with COX1 it — the enzyme and with COX2 it — the catalytic activity

Clinical indications: —, headaches, —, muscle aches, — —, backaches, fever, in pregnancy it can be prescribed to women who are at risk for —

Adverse effects: — effects, —/cardiovascular benefits, in children can cause — —

synthetic NSAID, mediators, COX 1+2, inflammation, muscle, fever, GI

ibuprofen is a — —

MOA: makes anti-inflammatory — that are reversable inhibitors that interact with — -

Clinical indications: —, headaches, toothaches, — aches, menstrual cramps, backache, —

Adverse effect: — effects

synthetic NSAID

naproxen is a — —

selective Cox2

Celecoxib is a — — inhibitor

allergic, megoblastic

Adverse side effects from NSAIDs/non-opiods: — reactions/skin rashes, — anemia

chronic heart failure, hypertrophy, edema

— — —: when the heart experiences an inability to sufficiently pump blood, this can be caused by heart dilation/— (causes blood to pool in the heart, increases the size of heart chambers) or by pulmonary and peripheral —

cardiac output

how much blood the heart is able to get out

stroke output

how much blood leaves the heart at any given beat

preload

the volume of blood returning to the heart periphery

afterload

resistance that the heart has to overcome to push blood out

compensatory

— responses are the body’s attempt to return to homeostasis in CHF, but don’t actually serve as a long term fix to the problem

sympathetic, NE, juxtaglomerular, renin, Aldosterone, ADH

some compensatory responses include — response (— increases to cause vasoconstriction), — cells in the kidneys release — which triggers vasoconstriction, — (hormone) is released that causes Na+ retention in the kidneys (this increases blood volume and thus blood pressure), — is also released

vasodilators, diuretics, cardiac glycosides, B-blockers

what are the 4 still drug classes generally used to treat CHF?

urination, afterload

diuretics increase —, using them for therapeutic use causes a decrease in BP and therefore decreasing the — on the heart

diuretic, CHF, hypotension, hyperglycemia

Hydrochlorothiazide is a thiazide — used to treat —

MOA: it inhibits the Na+/Cl- transporter in the — — of the kidneys

Adverse effects: nausea, —, hypokalemia, —

loop, CHF, loop, Henle, nausea, hypokalemia

Furosemide is a — diuretic used to treat —

MOA: inhibits the Na+/K+/Cl- transporter in the — of —

Adverse effects: —, hypotension, —, hyperglycemia

potassium-sparing, CHF, aldosterone, hypotension, hyperglycemia

Spironolactone is a — — diuretic that is used to treat —

MOA: antagonizes — receptors

Adverse effects: nausea, —, hypokalemia, —

arterial, CHF, direct, NO, postural hypotension, reflex tachycardia

hydralazine is a — vasodilator used to treat —, it is a — acting smooth muscle relaxant in the arteries → reduces afterload

MOA: increases endothelial release of — to produce relaxation of arteriolar smooth muscle

Adverse effects: nausea, — —, headaches, — —

venodilator, formation, relaxation, postural hypotension, reflex tachycardia

isosorbide dinitrate is a — of larger veins/vena cava → reduces venous return and preload, used to treat CHF

MOA: leads to — of NO which causes — of venous smooth muscles

Adverse effects: nausea, — —, headaches, — —

relaxes, veins

Nitrous Oxide (NO) is a fairly potent vasodilator because it — smooth muscle, — seem to be more responsive to it

ACEI, CHF, angiotensin 2, bradykinins, dry cough, allergic

Lisinopril is a — that is used to treat —

MOA: it inhibits the ACE enzyme which produces — —, thus decreasing (prev) levels and increasing —. the combined effect causes vasodilation

Adverse effects: headache, — —, — reaction

ARB, antagonist, headache, hypotension

Losartan is an — that is used to treat CHF

MOA: is an angiotensin 2 receptor —, does not increase bradykinins

Adverse effects: —, dizziness, —, hyperkalemia

cardiac, glycoside, ATPase, Ca2+, force, efficiency, headache, ventricular tachycardia, digibind

Digoxin is a — — used to treat CHF

MOA: inhibits Na+/K+ — that causes an increase of Na+ in the muscle cell and a decease of — exchange thus increasing the — of myocardial contraction and improving heart — and blood flow

Adverse effects: nausea, —, visual disturbances, — — → ventricular fibrillation → cardiac arrest

— is a digoxin antibody used to treat an OD

SA node, atrial, AV node, AV bundle, Purkinje, ventricular

How the heart contracts: the — — fires/depolarizes causing excitation to spread through the — myocardium → the — — fires and excitation spreads down the — — → — fibers distribute excitation through — myocardium

automaticity

the heart can start the contraction process with out external signaling, the SA node mediates this

NE

the sympathetic system influences heart contraction by releasing — by binding to beta-1 receptors

ACH

the parasympathetic system influences heart contraction by releasing — that binds to cholinergic receptors

5

during cardiac action potentials there are # phases for non-pacemaker cells

Phase 0

the depolarization phase (Na+ channels open)

Phase 1

phase where Na+ channels are inactivated → K+ channels open → K+ leaves the cells

Phase 2

Ca2+ channels open -. influx of Ca2+ as K+ is still exiting the cell, the plateau phase

Phase 3

phase where Ca2+ channels close, K+ channels are open still leaving cell

Phase 4

phase where membrane potential at rest, ion channels are reset

P wave

on the ECG this shows the depolarization of atrium

QRS wave

on the ECG this shows the ventricular depolarization, atrial repolarization occurs as well

T wave

on the ECG this shows the ventricular repolarization

PR interval

on the ECG this shows the time it takes for conduction to go from the SA node to the AV node

QT interval

on the ECG this shows the time from ventricle depolarization to repolarization

abnormal

arrythmias are some — heart conduction system

supraventricular

— arrythmias take place at the AV node or above, indicates an issue in the atria

ventricular

— arrythmia where there is an issue in the ventricles

atrial flutter

in atria, ECG looks like sawtooth P waves, has pattern and more P waves, depolarization occurs before AV node, supraventricular arrythmia

atrial fibrillation

no effective atrial contractions, ECG shows random chaotic tracings, “shaking” atrium, supraventricular arrythmias

Premature atria contraction (PAC)

has an ectopic foci, ECG shows abnormal P wave, QRS may not be seen, “skipped beats”

ectopic foci

group of cells depolarizing more quickly than atria or ventricle depending on location

ventricular fibrillation

no effective contractions, ECG shows no defined waves, blood pooling occurs

Premature Ventricular Contractions (PVC)

ectopic foci, ECG shows inverted QRS without a P wave, “skipped beats”

1A, Na+, QT, ventricular, lupus, premature, proarrythmia, torsades

Procainamide is a — antiarrhythmic drug

MOA: — channel blocker, prolongs the PR, QRS, and — intervals

Used for outpatient treatment of — arrhythmias (can be used for both though)

Adverse effects: nausea, — -like symptoms, — contractions, —, — de pointes

2, beta, PR, bradycardia, cardiac arrest, asthma

propranolol is a class # antiarrhythmic drug

MOA: — blocker by blocking Ca2+ channels, increases — interval

Adverse effects: —, hypotension, heart failure, — —

Contraindicated in —/ causes bronchoconstriction

3, K+, depolarize, QT, PR, QRS, both, thyroid, pulmonary fibrosis

Amiodarone is a class # antiarrhythmic drug

MOA: blocks — movement/outflow of (prev) making it take longer to —, also blocks Na+, Ca2+, and beta/alpha receptors, prolongs —, —, and —

Used for — arrhythmias

Adverse effects: — disturbances, bradycardia, — —, heart failure

4, Ca2+, decrease, postural hypotension, cardiac depression, CHF

Verapamil is a class # antiarrhythmic drug

MOA: — channel blocker

Goal is to — SA and AV node depolarization

Adverse effects: headaches, — —, GI issues, — —

Contraindications: pre-existing node problems, —