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PHRM 864 therapeutics > Acute Care Therapeutics > Flashcards

Acute Care Therapeutics Flashcards

1
Q

How is absorption of drugs altered in critical care

A

impaired/unpredictable due to:
-gastric emptying/motility
-interactions w/ tube feeds

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2
Q

How is distribution of drugs altered in critical care?

A

Fluid and hydration status is altered
Alterations in plasma protein binding

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3
Q

How is metabolism of drugs altered in critical care?

A

Hepatic enzyme expression may be decreased

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4
Q

How is renal elimination altered in critical care patients

A

Kidney may not work so drugs will build up in system

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5
Q

what is sepsis

A

life threatening organ dysfunction caused by dysregulated response to infection

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6
Q

how to treat sepsis

A

no specific drug therapy
antibiotics and source control

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7
Q

what is septic shock?

A

sepsis associated with CV collapse/hypotension

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8
Q

how do you treat septic shock?

A

fluids (LR)
vasopressors (norepi)
steroids (hydrocortisone)

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9
Q

What is Acute Respiratory Distress Syndrome (ARDS)

A

Life threatening respiratory failure that is acute with lung injury
often requires ventilation and sedation

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10
Q

what is FASTHUGSBID

A

Feeding/fluids
Analgesia
Sedation
Thromboprophylaxis
HOB elevation
Ulcer prophylaxis
Glycemic control
Spontaneous waking
Bowel regimen
Indwelling catheters
Delirium assessment

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11
Q

who in the ICU should receive thromboprophylaxis

A

majority of ICU patients should unless sufficiently mobile and very low risk or a contraindication

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12
Q

what are the factors that ICU patients have that make them candidates for thromboprophylaxis

A

immobility
trauma, hypercoagulable states
cancer/obesity/prior VTE

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13
Q

what are the preferred agents for thromboprophylaxis

A

LMWH (enoxaparin, dalteparin) over UFH

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14
Q

what is the dosing of UFH for thromboprophylaxis

A

5000 U SC q8h or q12h

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15
Q

what is the dose of enoxaparin for thromboprophylaxis

A

30mg SC q12h, 40mg SC q24h

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16
Q

what is the dose of dalteparin for thromboprophylaxis

A

5000 U SC q24h

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17
Q

what is the monitoring for all thromboprophylaxis agents

A

s/s bleeding, CBC for HIT

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18
Q

what thromboprophylactic agents need renal adjustments

A

Enoxaparin

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19
Q

what are risk factors for stress ulcers

A

shock, coagulopathy
mechanical ventilation
neurotrauma
burns
life support
drugs: antiplatelets, anticoag, NSAIDs

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20
Q

what should you do for stress ulcer prophylaxis

A

H2RAs or PPIs and encourage enteral feeding

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21
Q

which is better for stress ulcer prophylaxis

A

H2RA and PPI are same

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22
Q

when to d/c SUP

A

when risk factors no longer present

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23
Q

what are ADRs of H2RAs

A

potential thrombocytopenia
adjust for renal dysfunction

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24
Q

what are the ADRs of PPIs

A

increased risk for C. diff and pneumonia

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25
Q

why do we care about glycemic control in the ICU?

A

hyperglycemia is associated with increased ICU mortality

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26
Q

what is the BG target in the ICU

A

144-180

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27
Q

when to initiate insulin in ICU and with what formulations

A

initiate insulin if BG > 180
avoid long acting insulin in unstable patients

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28
Q

MOA of succinylcholine

A

binds and activates Ach receptors to induce sustained depolarization of neuromuscular junctions (muscle cant contract)

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29
Q

what are ADRs of succinylcholine

A

may cause initial muscle contractions
APNEA
Hyperkalemia
increased intracranial pressure (ICP)

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30
Q

when to use succinylcholine

A

Rapid sequence intubation
NOT for sustained NMB

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31
Q

when is succinylcholine contraindicated

A

major burns
crash injury
upper motor neuron disease

32
Q

what is the MOA of nondepolarizing NMBAs

A

competitively block the action of Ach

33
Q

what are the 2 general classes of nondepolarizing NMBAs

A

aminosteroidal
benzylisoquinolinium

34
Q

when are NDNMBAs indicated

A

immediate and sustained paralysis
mechanical ventilation (ARDS)
manage increased ICP

35
Q

what are ADRs of NDNMBAa

A

paralysis of respiratory muscles/apnea
Inadequate pain and sedation (must be optimized prior to sedation)
prolonged paralysis/muscle weakness

36
Q

how to monitor sustained NMB

A

can’t really monitor
goal is lowest dose possible and minimize ADRs

37
Q

what is a toxicity endpoint for NMB

A

peripheral nerve stimulation

38
Q

what is peripheral nerve stimulation

A

test 4 muscles to determine how deeply someone is suppressed. adjust to 1-2 twitches

39
Q

what is PADIS

A

Pain
Agitation
Delirium
Immobility
Sleep

40
Q

how is agitation characterized

A

increased motor activity and autonomic arousal
agitation!!!

41
Q

How is delirium characterized

A

fluctuation or change in baseline mental status
disturbed consciousness

42
Q

what are the two major pain scales

A

BPS or CPOT

43
Q

what pain meds are preferred in the ICU

A

IV opioids

44
Q

what IV opioids are most common

A

fentanyl
morphine

45
Q

when should sedatives be introduced

A

when adequate analgesia is not enough to keep patient calm and resting

46
Q

why is oversedation bad

A

increased time on ventilator
increased ICU stay
obscure neuro testing

47
Q

what is the goal of sedatives

A

LESS IS BEST!
keep sedation light for spontaneous awakening to improve outcomes

48
Q

what are the 2 sedation assessments called

A

RASS and SAS

49
Q

is the bispectral index indicated?

A

not recommended in sedated ICU patients

50
Q

what are the common sedative drugs used in the ICU

A

benzos (lorazepam, midazolam)
propofol
dexmedetomidine

51
Q

what are ADRs of benzos

A

respiratory depression
CV effects
withdrawal could lead to seizures
delayed emergence from sedation
delirium

52
Q

what are the cons of using lorazepam

A

delayed onset, prolonged duration of effect
less titratable

53
Q

what is an advantage of lorazepam

A

metabolite does not linger in elderly
less prone to DDIs

54
Q

what do some IV lorazepam agents contain that is toxic

A

propylene glycol solvent

55
Q

how to track propylene glycol toxicity

A

calculate osmol gap

56
Q

what is the onset of midazolam

A

rapid onset and short half life
titratable

57
Q

what is the onset of propofol

A

rapid onset
rapid offset

58
Q

what should be checked before starting propofol

A

egg or soybean allergy

59
Q

how long can you hand propofol

A

no more than 12hrs risk of infection

60
Q

what are the ADRs of propofol

A

apnea
Hypotension, bradycardia
pain
inc TGs
seizures neuroexcitory system

61
Q

what limits high doses of propofol

A

CV effect/propofol infusion system

62
Q

how to dc propofol

A

gradual tapering of dose especially if greater than 7 days of therapy

63
Q

what is the MOA of dexmedetomidine

A

selective alpha-2 agonist

64
Q

how is dexmed different than other sedatives

A

patients readily arousable with gentle stimulation
no respiratory depression
no anticonvulsant activity
less delirium than BZDs

65
Q

PK of dexmed

A

short half life
hepatically metabolized

66
Q

what is the dose of dexmed

A

maintenance infusion: 0.2-0.7 ug/kg/h
AVOID LOADING DOSE

67
Q

what are LDs of dexmed associated with

A

increased CV effects

68
Q

how long can dexmed be used

A

only approved for short term, but can go longer if other options too risky

69
Q

what are the ADRs of dexmed

A

increased CV effects such as bradycardia, hypotension

70
Q

when should dexmed be used over benzos

A

for critically ill mechanically ventilated adults

71
Q

what are non pharm treatments/prevention of delirium

A

early mobilization
improving cognition
optimizing sleep, hearing, and vision

72
Q

what are pharm treatments/prevention of delirium

A

NO DRUGS
antipsychotics may be used for short term but associated w/ significant stress
dexmed may be option

73
Q

when can haloperidol be used

A

in acute delirium situations

74
Q

what are ADRs of haloperidol

A

prolongation of QT interval on ECG
decreases seizure threshold

75
Q

when to dc haloperidol

A

if QTc exceeds 450msec or increases >25 % from baseline?

76
Q

what are the PAD guidelines

A

best way to avoid over sedation
encourage regular assessment of ICU patient

PHRM 864 therapeutics (14 decks)

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