Pharm Flashcards

1
Q

First order kinetics

A

Constant fraction

1/2 life’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Weak acids

A

Cations Na, K

Propofol and barbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Weak bases

A

Anions Cl-

Locals, opioids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Blood gas partition coefficients

A

Halothane- 2.5 This is saying 2.5:1 or 250:100 parts in
ISO- 1.46 Blood over gas.
Sevo- 0.65 He is doing nothing, most to least soluble
Des- 0.42
Nitrous- 0.46

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Vapor pressures

A

Sevo- 170
Enflurane- 175

ISO- 240
Halo- 243

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

A1 agonist

A

Increases CA+ causes muscle contraction

Phenylephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

A2 agonist

A

Inhibits adenylate cyclase which limits exocytosis of norepinephrine, in the CNS produces sedation and reduced sympathetic outflow leading to peripheral dilation and decrease BP.
Clonadine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Beta 1 agonist

A

Activate adenylate cyclase➡️ATP to cAMP➡️positive chrono, ino, dromotrophic effects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Beta 2 agonist

A

Activates adenylate cyclase and promotes smooth muscle relaxation, gluconeogenesis, and insulin release
Promotes:
Hyperglycemia, hypokalemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Alpha 1 Antagonist

A

Prazosin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Alpha 2 antagonist

A

Yohimbine, used to treat impotence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Beta antagonist

A

“OLOL”
A-M= beta 1
N-z= beta 2. ( with beta 2 blockade K+ levels increase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What drug class inactivate acetylcholinesterase and plasma cholinesterase? Examples?

A

Cholinesterase inhibitors

Reversal agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Cholinesterase inhibitor used to diagnose myasthenia gravis

A

Edrophonium, short acting, electrostatic bonds.

Give up to 10mg, if increased weakness it cholinergic crisis, if symptoms improve implies its myasthenia gravis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Neostigmine and pyridiostigmine

A

Covalent bond, also direct agonist effect on nicotinic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Antilirium?

A

Physostigmine, tertiary amine, crosses BBB, used to treat anticholinergic toxicity caused by antimuscarinic overdose.

17
Q

Echothiopate

A

Cholinesterase inhibitor
Irreversible bond, used to treat glaucoma

Can cause prolong SUCCS and mivacurium blockade bc pseudo cholinesterase inhibition.

18
Q

Cholinergic syndrome/crisis

A

Physostigmine or organic insecticide can produce symptoms of excessive acetylcholine
Miosis, salivation, Brady, bronchoconstriction, confusion, seizure

Tx with atropine

Cholinergic crisis cause by ANTICHOLINEesterase drug.

19
Q

Class of drugs that combine with muscarinic receptors and prevent acetylcholine from attaching to receptors. Examples

A

Antimuscarinic- atropine, glyco, scopolamine.

Most Tachy- atropine
Least sedation- glyco

20
Q

Anticholinergic syndrome

A

Response to high dose atropine or scopolamine.
Tachy, excitation, agitation, dry and flush skin

Tx with physostigmine

Anticholinergic syndrome caused by an ANTIMUSCARINIC.

21
Q

Myasthenia gravis

A

Autoimmune Destruction of post synaptic acetylcholine receptors
Causing weakness, fatigue of skeletal muscle

Tx with Anticholinesterases, unknown response to succs, but very SENSITIVE to NDMB

22
Q

Myasthenic crisis

A

Acute exacerbation of myasthenia gravis

23
Q

Characteristics of muscle relaxants

A
100% ionized at PH
Highly protein bound
Do not cross BBB or Placenta
Trapped in renal tubule bc of ionization
All can be excreted in kidney if other routes unavailable
24
Q

Muscle relaxation and disease

A

Disease that cause increase in ACH RECEPTORS such as muscle denervation injury make the patient sensitive to SUCCS but bc more receptors require increase dose of NDMB.

Dsease like myasthenia decrease receptors so the opposite is true.

25
Q

Long acting NDMR

A

PGP- MD
Pancuronium,gallamine, pipecuronium
Metocurrarine, d-tubocurarine

26
Q

Intermediate acting NMB

A

Vec and roc

27
Q

Short acting

A

Miv
Atra
And cistatracurium

28
Q

Renal excretion primary route

A

All long acting

PGP-MD

29
Q

Biliary Excretion primary route

A

Vec and roc

30
Q

METAbolism primary route of elimination

A

Succs- pseudocholinesterase
Mivacurium- plasma cholinesterase
Atracurium- ester hydrolysis and hoffman
Cistatracurium- Hoffman

31
Q

Relaxants with histamine release

A
DAMMS
d-tubo 
Atra 
Mivacurium 
Metocurarine 
Succs
32
Q

Relaxants with Autonomic blockade

A

MD

Metocurarine
D-tubo

33
Q

Relaxants with bradycardia

A

Succs

34
Q

Relaxants with tachycardia

A

Reflex- MAD
Metocurarine, atra, d-tubo

Antimuscarinic-
Pancuronium
Gallamine

35
Q

Hypotension from NMB

A

Succs, d-tubocurarine, metocurarine

36
Q

Hypertension from NMB

A

Pancuronium and Gallamine

37
Q

Opioid receptors

A

Mu1- euphoria, pruitus, low abuse, supraspinal
Mu2- resp depression, dependence, constipation, spinal analges
Kappa- dysphoria, sedation, low abuse potential
Delta- resp depression, dependance, constipation

38
Q

Opioid agonist/antagonist

A

Nubaine, stadol

Work on kappa and delta

39
Q

Zero order kinetics

A

Constant amount (2mg per min)

Alcohol, Asa, phenytoin