Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm 2 > Final > Flashcards

Final Flashcards

1
Q

Tertiary amine that crosses BBB that has been linked with postop delirium?

A

atropine and scopolamine

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

What are CV side effects of succs?

A

bradycardia (especailly peds)

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

What electrolyte imbalance can succs cause?

A

transient hyperkalemia (0.5 mEq/L) in normal physiology

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

Which populations are at increased risk for hyperkalemia with succs?

A

burns, trauma, paralysis, CVA, GBS, prolonged immobilization, polyneuropathy, head injury, myopathies, Duchenne’s MD

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

When does the risk of hyperK peak for succs?

A

7-10 days

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

What is a common side effect of succs in women and outpatient procedures?

A

myalgia- can use defasciculating dose and NSAIDs to decrease

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

What is a transient effect of succs that lasts 5-10 minutes?

A

increased IOP (increases by 5-15 mmHg for 2-4 min after admin)

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

Besides increased IOP, what can succs also increase?

A

intragastric pressure and ICP

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

How is succs metabolized?

A

rapidly metabolized by pseudocholinesterase to succinylmonocholine and succinic acid

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

How is the action of succs terminated naturally?

A

diffusion away from NMJ

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

Which NMB is associated with a vagolytic effect?

A

pancuronium

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

What is a byproduct of Hoffman elimination with atracurium and what can it cause?

A

laudanosine- seizures

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

The indirect actions of NMBs on cardiac are due to ? and are associated with which two NMBs the most?

A

histamine release; atracurium and mivacurium

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

The aminosteroids are all affected by ? due to liver metabolism and biliary excretion. In liver failure, ? is preferred.

A

liver function; cisatracurium

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

Which aminosteroid is affected most by renal function?

A

pancuronium

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

How do nondepolarizing NMBs affect the elderly?

A

onset is slower due to slower circulation times, and aminosteroids have an increased DoA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do nondepolarizing NMBs affect the obese?

A

require quick onset, DoA is increased with aminos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do nondepolarizing NMBs affect pediatric pts?

A

NMJ is immature and sensitivity changes through life (need dose change)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which NMBs are the most common causes of allergic reactions?

A

roc and succs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

anticholinergic drugs interfere with normal inhibition on the release of ?, which is why their effects are called ? or ?

A

norepinephrine; parasympatholytic or sympathomimetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Anticholinergic drugs are selective for which receptors?

A

muscarinic cholinergic- competes against ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Where are M1 receptors?

A

CNS and stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Where are M2 receptors?

A

heart and lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Where are M3 receptors?

A

CNS, smooth muscles of airway, glandular tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where are M4 and M5 receptors?

A

CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the symptoms of organophosphate poisoning/overdose?

A

narrowed pupils, agitation, excessive secretions, arrhythmias, cardiovascular/respiratory collapse, coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the desired effects of dexmedetomidine?

A

sedative, analgesic, sympatholytic properties; reduces anesthetic requirements- does NOT cause significant resp depression, may reduce postop shivering

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are some SE of dexmedetomidine?

A

bradycardia, systemic hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is considered small doses of dopamine and what are its effects?

A

<2 mcg/kg/min- minimal adrenergic effects- open dopaminergic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is considered moderate doses of dopamine and what are its effects?

A

2-10 mcg/kg/min- beta 1 stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is considered higher doses of dopamine and what are its effects?

A

10-20 mcg/kg/min- alpha 1 stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is malignant hyperthermia?

A

RYR1 gene mutation- allows massive release of Ca from SR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the signs and symptoms of MH?

A

tachycardia, hypercarbia, hyperthermia, masseter spasm, tachypnea, arrhythmias, metabolic acidosis, muscle rigity, myoglobinemia, hyperkalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are some triggers for MH?

A

succs, volatile anesthetics (isoflurane, desflurane, sevoflurane, halothane, enflurane)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

How is esmolol metabolized?

A

rapid redistribution and hydrolysis by RBC esterases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Hoffman elimination is dependent on?

A

temp and pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What do you use when there is no response to TOF? Describe what it is and what it’s used to assess.

A

post-tetanic facilitation; 50 Hz stimulus for 5 seconds, then apply 1 Hz stimulus and count responses- assesses for deep blockade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Dopamine is an endogenous catecholamine that is an immediate precursor to?

A

norepinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is a direct precursor of dopamine?

A

L-dopa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Beta 1 selective blockers should have less inhibitory effect on beta 2 receptors and are preferred for? What is an example of a beta 1 selective antagonist?

A

those with COPD and PVD; metoprolol

41
Q

List some opioid agonists

A

morphine, meperidine, fentanyl (and others in fentanil family), codeine, dilaudid, oxy, hydrocodone, methadone, heroin

42
Q

List some opioid agonist-antagonists

A

pentazocine, butorphanol, nalbuphine, buprenorphine, nalorphine, bremazocine, dezocine, meptazinol

43
Q

List the opioid antagonists

A

naloxone, naltrexone, nalmefene

44
Q

What is metoprolol?

A

cardioselective (B1) antagonist

45
Q

What is milrinone and how does it work?

A

phosphodiesterase inhibitor; positive inotrope with vasodilation by blocking cAMP breakdown

46
Q

What are some adverse effects of beta blockers?

A

heart block, heart failure, AV block, sinus arrest, hypotension, bronchospasm in asthma patients

47
Q

What is the MoA of propofol?

A

GABA agonist (potentiates inhibitory transmission)

48
Q

Who should you avoid propofol in?

A

allergy to egg yolk (soy lecithin)

49
Q

When should you discard propofol?

A

6 hours if in syringe, 12 hours if in tubing

50
Q

How quickly does propofol work and when do pt start to wake up due to redistribution?

A

30 seconds; 2-8 minutes

51
Q

How is propofol metabolized?

A

extrahepatic clearance (pulmonary uptake and first pass elimination), conjugation in liver to inactive metabolites

52
Q

What are s/s of propofol infusion syndrome?

A

metabolic lactic acidosis, hypertriglyeridemia, hypotension, arrhythmia, rhabdo, acute renal failure, hepatomegaly

53
Q

What are the desired effects of propofol?

A

antiemetic, antipruritic, anticonvulsant, amnesia, sedation

54
Q

What are the CV effects of propofol?

A

tachycardia on induction, decreased contractility and preload, hypotension

55
Q

What are the respiratory effects of propofol?

A

apnea on induction

56
Q

What are the cerebral effects of propofol?

A

decreased CBF and ICP- sometimes can have excitatory phenomena like m. twitching, opisthotonus

57
Q

What is the MoA of etomidate?

A

depresses RAS and mimics inhibitory effects of GABA

58
Q

What can long infusions of etomidate cause?

A

adrenal corticoid suppression

59
Q

Where is etomidate metabolized and where is it excreted?

A

liver; urine and bile

60
Q

What is a common side effect of etomidate?

A

myoclonus

61
Q

Does a standard induction dose of etomidate inhibit ventilation?

A

no

62
Q

Why is etomidate the desired induction drug for hemodynamically unstable patients?

A

it has minimal effects on the CV system- contratility and CO usually unchanged

63
Q

What are cerebral effects of etomidate?

A

decreased CMR, CBF and ICP

64
Q

What is the relationship between fentanyl and etomidate?

A

fentanyl decreases myoclonus but also increases plasma levels and prolongs elimination

65
Q

What is the MoA of barbiturates?

A

depress RAS, enhance transmission of GABA, suppress excitatory ACh

66
Q

How are barbiturates biotransformed?

A

hepatic oxidation to inactive water soluble metabolites

67
Q

What are the CV effects of barbiturates?

A

decreased BP and increased HR- peripheral pooling of blood due to vasodilation (ensure adequate volume status and baseline autonomic tone)

68
Q

What are the respiratory effects of barbiturates?

A

depress medullary ventilation, decreases response to hypercapnia and hypoxia

69
Q

What are the cerebral effects of barbiturates?

A

decreased CBF, ICP, but decrease in CPP

70
Q

What are the renal and hepatic effects of barbiturates?

A

decreased RBF and GFR; decreased HBF and can trigger porphyria

71
Q

What is the MoA of ketamine?

A

NMDA antagonist (blocks glutamate and glycine)- dissociates thalamus from limbic cortex

72
Q

What is the metabolite of ketamine?

A

norketamine- ACTIVE

73
Q

What are the CV effects of ketamine?

A

increased BP, HR, CO, increased PAP and myocardial work

74
Q

Who should you avoid ketamine in?

A

patients with CAD, uncontrolled HTN, CHF

75
Q

What are the respiratory effects of ketamine?

A

potent bronchodilator, increased salivation- minimal effect on ventilatory drive

76
Q

What are the cerebral effects of ketamine?

A

increased CMRO2, CBF, ICP

77
Q

What are some common undesired effects of ketamine?

A

emergence delirium and nausea at high doses

78
Q

Glycopyrrolate is the recommended anticholinergic for which cholinesterase inhibitors?

A

neostigmine and pyridostigmine

79
Q

What is glycopyrrolate used to offset?

A

bradycardia and increased salivation

80
Q

Prolonged duration of action of succinylcholine can occur in:

A

high doses and those with decreased psuedocholinesterase activity

81
Q

What are some meds and conditions that can decrease pseudocholinesterase activity?

A

hypothermia, pregnancy, carcinoma, hepatic disease, Reglan, neostigmine, esmolol, atypical enzyme

82
Q

What are some conditions that can increase pseudocholinesterase activity?

A

obesity, alcoholism, psoriasis, ECT therapy

83
Q

Pseudocholinesterase is synthesized by?

A

liver

84
Q

What are some contraindications to succs?

A

pseudocholinesterase deficiency, those sensitive to hyperkalemia (burns, digitalis, GBS), glaucoma

85
Q

What is the RSI dose of roc?

A

1.2 mg/kg

86
Q

What is the dose of propofol?

A

1-2 mg/kg

87
Q

What is the dose of etomidate?

A

0.2-0.3 mg/kg

88
Q

What is the dose of ketamine?

A

2-4 mg/kg

89
Q

Which non depolarizers are short acting and what is that time frame?

A

mivacurium, <30 minutes

90
Q

Which non depolarizers are intermediate acting and what is that time frame?

A

atracurium, cisatracurium, vecuronium, rocuronium 30-60 minutes

91
Q

Which non depolarizers are long acting and what is that time frame?

A

pancuronium, >60 minutes

92
Q

What is the site of action for neuromuscular blocking agents?

A

ACh receptors (alpha subunit)

93
Q

What is the dose of succinylcholine in mg/kg?

A

1-1.5 mg/kg

94
Q

What paralytics are best for those with renal failure?

A

atracurium and cisatracurium

95
Q

How are labetolol and esmolol different?

A

labetolol is beta/alpha 7/1 whereas esmolol is selective beta

96
Q

The most indirect adrenergic agonist with mixed alpha and beta effects that does not decrease uteroplacental blood flow

A

ephedrine

97
Q

List some anticholinergic medications

A

atropine, glycopyrrolate, scopolamine

98
Q

What are the intubating and maintenance doses of cisatracurium?

A

intubation 0.1 mg/kg

maintenance 0.02 mg/kg

99
Q

What is the typical final concentration of phenylephrine?

A

100 mcg/ml

Pharm 2 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions