Slinisky - Non-Pharm

Front 1

Lecture 155

Back 1

Lecture 155

Front 2

3 Parts of local anesthetic

Back 2

1. Aromatic residue. 2. Intermediate chain (determines degradation. 3. Terminal Amino group

Front 3

Which types of anesthetics are excreted which way

Back 3

Amides - out liver. Esters - Broken in blood.

Front 4

Henderson Hasselbach

Back 4

pKa - pH = log (BH/B)

Front 5

TTX-R vs TTX-S

Back 5

TTX-R contain Na1.8 channel, and conduct pain.

Front 6

Epinephrine and local anesthetic -

Back 6

Epi increases duration of action. - via decreased blood flow.

Front 7

Ca and local anesthetic

Back 7

Ca decreases local anesthetic efficacy.

Front 8

Local anesthetic site of action

Back 8

Na channel - a S6 domain IV

Front 9

Lecture 156

Back 9

Lecture 156

Front 10

ACh synthesis enzyme

Back 10

choline acetyltransferase

Front 11

Components of the 'Fusion Machine'

Back 11

Taxin(binds membrane), Brevin(binds vesicle), S-25(interconnects), Tagmin (senses Ca)

Front 12

Myasthenia Gravis

Back 12

Auto immune disease w/ reduced # of nicotinic ACh receptors

Front 13

Lambert Eaton (myasthenic) syndrome

Back 13

Decrease calcium channels on nerve terminal

Front 14

Aminoglycoside antibiotics & neuropathy

Back 14

Aminoglycoside antibiotics block calcium entry into nerve terminal (Also blocked by Mg2+ & other polyvalent cations

Front 15

3 uses of nondepolarizing blockers

Back 15

1. Orthopedic manip. 2. Abdominal surgery 3. Bronchoscopy

Front 16

4 CI's of SUX

Back 16

1. Burns 2. Cardiac Arrythmia 3. Liver disease/ChE def 4. Long use

Front 17

2 short term drugs for intubation

Back 17

1. SUX 2. Rocuronium

Front 18

3 drugs paralytics pop for duration of surgery

Back 18

1. Vecuronium 2. Atracurium 3. Pancuronium

Front 19

Which drug reverses nondepolarizing block

Back 19

Anticholinesterases (neostigmine) because nondep block is competitive inhib

Front 20

Which 2 non-dep blockers are excreted by liver

Back 20

Vecuronium, Rocuronium

Front 21

159

Back 21

159

Front 22

Explain adrenergic control of the blood vessels.

Back 22

Skin and periphery are innevated by sympathetic alpha receptors. Muscles and liver have b2 receptors so they dilate in response to epinephrine

Front 23

Explain ANS control of sexual function

Back 23

Parasympathetic: Erection and mucus production, Sympathetic: alpha 2 inhibit erection alpha 1 cause detumescence

Front 24

Accomodation is controlled by:

Back 24

Parasympathetic NS

Front 25

3 classes of drugs that cause orthostatic hypertension

Back 25

a1 blockers, Adrenergic neuron blockers, ganglionic blockers

Front 26

160

Back 26

160

Front 27

How do muscarinic and nicotinic receptors differ?

Back 27

Muscarinic have are smaller - bind a diff O on ACh

Front 28

Explain how PS innervation slows heart rate.

Back 28

Inhibitory G protein - opens potassium channels, resulting in hyperpolarization.

Front 29

Explain how PS innervation vasodilates

Back 29

ACh causes release of EDRF --> cGMP

Front 30

Contraindications to muscarinic agonists

Back 30

SOAPT - Shock (cardiogenic), obstruction, asthma, peptic ulcers, hyperthyroid

Front 31

SLUD syndrome

Back 31

Salivations Lacrimation Urinary Defecation in irreversible acetylcholinesterase inhibitors. Also cause twitching in muscles and CNS effects

Front 32

Explain AChesterase

Back 32

Anionic site holds the Ach near to a serine (which partially shares electrons with a nearby histamine) and it's hydrolyzed)

Front 33

How does edrophonium work?

Back 33

Blocks the histamine on ChE

Front 34

How do the nerve gasses work?

Back 34

Phosphate groups binds to serine in ChE

Front 35

Treatment of anti-cholinesterase inhibitors?

Back 35

Atropine + 2-PAM

Front 36

Explain how Atropine can treat parkinsons

Back 36

Parkinsons is a misbalance between Dopamine and Ach. Atropine acts to block the Ach and even out the process (in the nigro striatal pathway)

Front 37

Atropine Toxicity

Back 37

Dry, Hot, Red, Blind, Mad

Front 38

CNS cholinergic muscarinic sites

Back 38

Emesis, Arousal, Memory,

Front 39

Effects of ganglion blockers

Back 39

Mostly similar to Atropine, except vasodilation.

Front 40

162

Back 40

162

Front 41

MAO

Back 41

Monoamine Oxidase - hyrdolyzes adrenergics in nerve & effector

Front 42

COMT

Back 42

Hydrolizes adrenergics in effector only.

Front 43

Uptake 1 vs 2

Back 43

Uptake 1: High affinity low capacity. Uptake 2: low affinity high capacity

Front 44

VMA

Back 44

Product of MAO dehydrogenase in periphery

Front 45

MHPG

Back 45

Product of MAO reducatase in CNS

Front 46

167

Back 46

167

Front 47

Alpha binding

Back 47

EPI > NE (no ISO)

Front 48

Beta binding

Back 48

ISO > EPI >> NE (NE no effect on B2)

Front 49

How do Alpha 1 receptors transduce signal?

Back 49

Phospholipase C --> Inc. Ca. (SOC's & CRAC channel activated too)

Front 50

How do Beta receptors work?

Back 50

G-proteins --> cAMP --> PKA

Front 51

How do Alpha 2 receptors work?

Back 51

Control channels via G protein (G protien --> Block ATP, Block Ca, open K)

Front 52

NE receptors

Back 52

alpha, beta 1

Front 53

EPI receptors

Back 53

alpha, beta 1, beta 2

Front 54

ISO receptors

Back 54

Beta 1, Beta 2

Front 55

Principal effects of alpha 2 agonists

Back 55

Decrease CO, decrease vascular resistance.

Front 56

How is clonidine used to distinguish b/t pheochromocytoma and essential hypertension?

Back 56

It will reduce NE in EH not pheo.

Front 57

Explain the mechanism of tyramine

Back 57

Indirect acting sympathomimetic. Enters nerve terminal via uptake 1, pushes NE out.

Front 58

3 problems w/ indirect sympathomimetics

Back 58

1. Tachyphylaxis. 2. Don't work w/ unptake 1 inhibitors. 3. Hypertensive crisis w/ MAO inhibitor.

Front 59

Tachyphylaxis

Back 59

Depletion of NE w/ indirect sympathomimetics --> reduced response.

Front 60

How do ephedrines work?

Back 60

Work by both indirect actions as well as agonists (esp of B2)

Front 61

Toxicity of ephedrines

Back 61

Very high doses --> a1 peripheral vasoconstriciton.

Front 62

Explain nasal congestions

Back 62

a1 controlled venous capacitance vessels (erectile) fill, & secrete mucous. Prolonged inhibition blocks the arterioles, and reactive hyperemia occurs.

Front 63

Nasal Decong. OD

Back 63

Eventually, dose affects alpha 2 receptors - venoconstriction & damage to nasal mucosa.

Front 64

What are the primary and secondary treatments for cardifenic shock

Back 64

Primary: Dobutamine - specific B1. Secondary : Dopamine - Nonspecific Adrenergic (causes vasoconstriction), may worsen myocardial ischemia.

Front 65

How is yombine an aphrodisiac

Back 65

Blocks a2 - PARASYMPATHETIC alpha 2 receptors inhibit tumescence.

Front 66

Contraindications go phosphidiesterase inhibitors

Back 66

No Nitrates or A1b blockers.

Front 67

Name three adrenerginic neuron blockers

Back 67

Bretylium, Reserpine, Guanethidine. (Sympahtolytics)