Exam 3 - Foster Flashcards

1
Q

how is oral absorption affected in critically ill patients?

A

impaired/unpredictable due to alterations in gastric emptying and gastric motility

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2
Q

how is distribution affected in critically ill patients?

A

-alterations vary, relates to fluid/hydration status
-decreased albumin = decreased protein binding of many drugs
-increased protein binding of drugs that bind to a1-acid glycoprotein

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3
Q

how is metabolism affected in critically ill patients?

A

hepatic enzyme expression and activity may be decreased - some degree of hepatic impairment in critically ill patients

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4
Q

how is renal elimination affected in critically ill patients?

A

-renal dysfunction common in critical illness
-we detect changes in renal function through urine output
-dialysis of continuous renal replacement therapy is common in ICU

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5
Q

What is sepsis? Where does it occur?

A

-life threatening organ dysfunction caused by dysregulated response to infection
-can occur in response to any pathogen
-most common sites of infection are lungs, bloodstream, and urinary tract

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6
Q

Sepsis treatment options

A

-no specific drug therapy - broad spectrum IV antibiotics + source control
-early detection and supportive care is critical

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7
Q

Septic shock treatment options

A
  1. fluids - crystalloids, colloids
  2. vasopressors - norepinephrine
  3. Corticosteroids if refractory
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8
Q

What is the MAP goal in septic shock?

A

> 65mmHg

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9
Q

What is the preferred treatment for thromboprophylaxis in ICU patients?

A

LMWH - enoxaparin, dalteparin

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10
Q

UFH dosing

A

5000 U SC q8h

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11
Q

Enoxaparin dosing (+ renal dosing)

A

30mg SC q12h or 40mg SC once daily

CrCl < 30: 30mg SC once daily

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12
Q

Blood glucose target in ICU patients

A

144-180 mg/dL

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13
Q

stress ulcer risk factors

A

shock
coagulopathy
chronic liver disease
mechanical ventilation
neurotrauma
drugs: NSAIDS, anticoags

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14
Q

When should you d/c stress ulcer prophylaxis?

A

when risk factors are no longer present

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15
Q

What type of insulin should you avoid in unstable patients? Why?

A

long-acting insulin, because they might be on and off tube feeds

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16
Q

What type of NMBA is depolarizing?

A

Succinylcholine

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17
Q

What is the only indication for succinylcholine?

A

Rapid sequence intubation (RSI) - placement of endotracheal tube

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18
Q

Succinylcholine ADRs

A
  1. Apnea (must be ready to intubate)
  2. Muscle fasciculations - deep aching muscle pain
  3. Hyperkalemia
  4. intracranial pressure elevation
  5. Increased intraocular pressure
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19
Q

Which NMBAs do NOT activate Ach receptors?

A

Non-depolarizing NMBAs:
(aminosteroidal: vecuronium, rocuronium, pancuronium)
(benzylisoquinolinium: cisatracurium, atracurium)

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20
Q

In patients with acute respiratory distress syndrome (ARDS), how should NMBA be administered?

A

as a continuous infusion

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21
Q

Are NMBAs required in all mechanically ventilated patients?

A

No

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22
Q

NMBAs do NOT provide ___________, ___________, or ____________ effects

A

analgesic, sedative, or anxiolytic

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23
Q

What must be done prior to initiation of NMBA?

A

optimize sedative and analgesic drugs

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24
Q

NDNMBAs ADRs

A

prolonged paralysis/muscle weakness or ICU-acquired muscle weakness

25
Q

What is the toxicity endpoint of NMBAs?

A

peripheral nerve stimulation - avoid 0/4 twitches!
(adjust dose to 1-2 twitches)

26
Q

What is the gold standard for pain assessment?

A

Patient self-reported pain

27
Q

What does the Behavioral Pain Scale (BPS) look for?

A
  1. facial expression
  2. upper limb movements
  3. compliance with mechanical ventilation
28
Q

What does the Critical Care Pain Observation Tool look for?

A
  1. facial expressions
  2. body movements
  3. muscle tension
  4. compliance with mechanical ventilation
  5. vocalization
29
Q

What is generally preferred for non-neuropathic pain in critically ill patients?

A

IV opioids

30
Q

In what patients might the Bispectral Index (BIS) be used?

A

In patients in whom other measures are not feasible - deep sedation and neuromuscular blockade

31
Q

Benzodiazepines adverse effects

A
  1. respiratory depression
  2. CV effects
  3. withdrawal/risk of seizures - TAPERING REQUIRED
  4. delayed emergence from sedation
  5. association with delirium
32
Q

Which BZD has delayed onset and prolonged duration of action?

A

Lorazepam

33
Q

Which one is more titratable: midazolam or lorazepam?

A

Midazolam

34
Q

What toxic component do IV formulations of lorazepam contain? What should you monitor for this?

A

Propylene glycol - monitor Osm gap

35
Q

Osm gap > ________ may indicate PG toxicity

A

10

36
Q

Lorazepam is the least _______ _______ of the commonly used BZDs, but it is also the least prone to _______ ________

A

lipid soluble
drug interactions

37
Q

Midazolam has high _______ _______ so it has _______ onset of action

A

lipid solubility
rapid

38
Q

Midazolam is __________ metabolized, so t1/2 is increased in hepatic disease

A

hepatically

39
Q

Which is more likely to accumulate in elderly patients: midazolam or lorazepam?

A

Midazolam

40
Q

Midazolam may be a good option for what situations?

A
  1. rapid sedation of acutely agitated patients
  2. short-term use
  3. procedural sedation
    NOT LONG TERM
41
Q

Does propofol have analgesic properties?

A

NO

42
Q

Propofol has _______ onset and _______ offset

A

RAPID

43
Q

Propofol is ____________ metabolized

A

hepatically

44
Q

Propofol is __________ protein bound and has a ________ Vd

A

highly
large

45
Q

Propofol adverse effects (7)

A
  1. apnea
  2. hypotension + bradycardia
  3. pain upon infusion
  4. hypertriglyceridemia
  5. elevated pancreatic enzymes
  6. Electrolyte abnormalities with preservative EDTA (Diprivan)
  7. Withdrawal possible - tapering required
46
Q

How does propofol infusion syndrome present?

A

metabolic acidosis, bradycardia, lipidemia

47
Q

Why might propofol be preferred in neurosurgical/neurotrauma patients?

A

It may aid in decreasing intracranial pressure

48
Q

When should triglycerides be checked after starting propofol?

A

after 48h

49
Q

What type of drug is dexmedetomidine?

A

selective a2 agonist

50
Q

Precedex should not be used for _______ sedation

A

deep

51
Q

T/F: Precedex can cause respiratory depression

A

FALSE

52
Q

Precedex pharmacokinetics:
1. ________ protein-bound
2. _________ t1/2
3. __________ metabolized

A
  1. highly
  2. short
  3. hepatically
53
Q

Why should you avoid a loading dose of Precedex?

A

associated with more severe side effects - mostly CV effects like transient increased BP followed by bradycardia and hypotension

54
Q

What are the two subtypes of delirium?

A
  1. hyperactive (agitated, delusions)
  2. hypoactive (calm, confusion)
    patients can go between the two
55
Q

Is pharmacological treatment recommended for prevention of delirium?

A

NO

56
Q

When is dexmed recommended for delirium?

A

when agitation is preventing extubation

57
Q

Haloperidol adverse effects

A
  1. QTc prolongation - potential torsades de pointes
  2. decreased seizure threshold
  3. EPS
58
Q

Of the typical antipsychotics used for delirium, which one causes the highest rate of QTc prolongation?

A

Ziprasidone

59
Q

What other properties does dexmed have besides sedating?

A
  1. anxiolysis similar to BZDs
  2. analgesic-sparing effects