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Fall 2024 > Therapeutics Exam 3 (Acute/Critical Care) > Flashcards

Therapeutics Exam 3 (Acute/Critical Care) Flashcards

1
Q

How is oral absorption altered in critical illness?

A

Impaired/Unpredictable

-Alterations in gastric emptying and motility (this is caused by high dose opioids)

-Absorption may decrease, we would not expect increases

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2
Q

How is distribution altered in critical illness?

A

These patients have a higher fluid/hydration status
-hydrophilic drugs have a higher volume of distribution

*consider with aminoglycosides

Decreased albumin levels lead to decreased protein binding of many drugs

Increased acute phase proteins (a1-acid glycoprotein) leads to increased protein binding of drugs that bind a1-acid glycoprotein

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3
Q

How do we detect changes in renal function?

A

CrCl
-but is challenging because you may not see changes in serum creatinine immediately when renal dysfunction occurs

More immediate way is to determine using urine output

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4
Q

What is sepsis?

A

Life threatening organ dysfunction that is caused by a dysregulated/exaggerated immune response to that infection

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5
Q

What is the treatment for sepsis?

A

Antimicrobial therapy (broad spectrum IV antibiotics) and source control of the infection

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6
Q

What is septic shock?

A

Sepsis associated with cardiovascular collapse/hypotension

*decreased vascular tone is what leads to hypotension

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7
Q

How do we treat septic shock?

A

Fluids* (crystalloids and colloids)
*note that this is not enough to cure the shock

Vasopressors (increase vascular tone and cardiac output)

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8
Q

What is the target Mean Arterial Pressure (MAP) when using vasopressors?

A

> or = 65 mmHg

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9
Q

What is the preferred vasopressor to use?

A

Norepinephrine

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10
Q

Which inotrope (not vasopressor) can be added on to a vasopressor if a patient has mixed shock syndrome with declining cardiac output?

A

Dobutamine -used to increase cardiac output

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11
Q

What medication may be used as an add-on to vasopressors to provide extra benefit?

A

Vasopressin

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12
Q

If a patient with septic shock is not responding to vasopressors + add-ons (refractory), what medication can be added?

A

Corticosteroids (IV hydrocortisone)

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13
Q

What is Acute Respiratory Distress Syndrome (ARDS)?

A

Life threatening respiratory failure characterized by acute, diffuse inflammatory lung injury

**Often requires mechanical ventilation with sedation
**Potentially need a neuromuscular blockade

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14
Q

What are the elements included in General Supportive Care?

A

FAST HUGS BID

F: Feeding, Fluids
*A: Analgesia
*S: Sedation
*T: Thromboprophylaxis

H: HOB elevation
*U: Ulcer (stress ulcer) prophylaxis
*G: Glycemic control
*S: Spontaneous Awakening Trial,

B: Bowel regimen
I: Indwelling catheters
*D: Delirium assessment

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15
Q

What is the preferred agent to use in the ICU for thromboprophylaxis?

A

Low molecular weight heparin (LMWH)

*preferred over unfractionated heparin (UFH)

*use mechanical prophylaxis in patients with contraindications to pharmacological prophylaxis

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16
Q

What is the dosing of UFH thromboprophylaxis?

A

5000 units Subq q8h or q12h

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17
Q

What is the dosing of Enoxaparin thromboprophylaxis?

A

30 mg Subq q 12h or 40 mg Subq q24h

CrCl< 30: 30mg subq q24h

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18
Q

Which thromboprophylaxis drug must be renally adjusted?

A

Enoxaparin (for CrCl <30)

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19
Q

What do we monitor when using thromboprophylaxis?

A

S/S of bleeding

Complete Metabolic Panel (CPC)

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20
Q

What are the risk factors for getting stress ulcers?

A

-Shock, coagulopathy, chronic liver disease

-Mechanical ventilation/respiratory failure

-Neurotrauma, burn injury, life support

-Drugs: antiplatelets, anticoagulants, NSAIDs

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21
Q

What drugs should be used for stress ulcer prophylaxis?

A

Histamine-2 Receptor Antagonists (H2RAs)

Proton Pump Inhibitors (PPIs)

*many people choose PPI’s but no evidence exists to suggest one is better

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22
Q

What are the H2RAs used for stress ulcer prophylaxis?

A

Famotidine
Ranitidine

*enteral or parenteral

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23
Q

What are the PPIs used for stress ulcer prophylaxis?

A

Omeprazole
Lansoprazole
Pantoprazole
Esomeprazole
Rabeprazole

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24
Q

PPIs may increase the risk for which disease states?

A

Clostridium difficile colitis

Nosocomial pneumonia

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25
Q

Stress ulcer prophylaxis is warranted in critically ill patients such as?

A

Mechanical ventilation
Coagulopathy
Chronic liver disease
Shock

Others

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26
Q

What is the target blood glucose for ICU patients?

A

144-180 mg/dl

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27
Q

At what BG level do we initiate insulin for ICU patients?

A

> 180 mg/dl

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28
Q

What is the purpose of a spontaneous awakening trial/ spontaneous breathing trial?

A

Helps to prevent oversedation

Promotes weaning from mechanical ventilation

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29
Q

When neuromuscular blockers are not present, how does neuromuscular signaling typically occur?

A

Synaptic vesicles release acetylcholine

Acetylcholine binds receptors on muscle cell, causes depolarization and ultimately muscle contraction

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30
Q

What are the 2 types of neuromuscular blockers?

A

Depolarizing

Nondepolarizing

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31
Q

What drug is the only depolarizing neuromuscular blocker available?

A

Succinylcholine

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32
Q

How does succinylcholine work?

A

Physically resembles acetylcholine

-Binds and activates Ach receptors on the muscle
-Causes sustained depolarization which ultimately leads to a loss of muscle contraction

*Note that this drug may initially cause muscle contraction

*Rapid onset (1 min) and short duration (3-5 mins)

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33
Q

What do we use succinylcholine for?

A

Rapid sequence intubation (RSI)

**this is its only use, not used for sustained neuromuscular blockade

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34
Q

What are the side effects of succinylcholine?

A

Apnea (*need to be ready to intubate)

Muscle fasciculations (muscle ache, may last days)

Hyperkalemia

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35
Q

When is succinylcholine contraindicated?

A

Major burns
Crush injury
Upper motor neuron disease

***risk of life-threatening hyperkalemia

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36
Q

How do nondepolarizing neuromuscular blockers work?

A

Competitively block the action of acetylcholine (block receptors)

***Do not activate receptors
-this means there are no initial muscle
contractions

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37
Q

What are the 2 classes of nondepolarizing neuromuscular blockers?

A

Aminosteroidal
Benzylisoquinolinium

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38
Q

What are the aminosteroidal neuromuscular blockers?

A

Pancuronium
Vecuronium
Rocuronium

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39
Q

What are the benzylisoquinolinium neuromuscular blockers?

A

Atracurium
Cisatracurium

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40
Q

True or False: Neuromuscular blockers are required in all mechanically ventilated patients

A

FALSE
-only those with Acute Lung Injury or Acute Respiratory Distress Syndrome (ARDS)

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41
Q

What are the side effects associated with non-depolarizing NMBs?

A

Paralysis of muscles/apnea

Inadequate pain care and sedation
***note that these drugs DO NOT provide analgesia, sedative, or anxiolytic effects (patients still feel pain but cannot communicate)
-patients must be optimized on sedatives+analgesia before administration

Prolonged paralysis/Muscle weakness

42
Q

What drugs interact with non-polarizing NMBs?

A

Corticosteroids
-potentially cause long-term muscle weakness

43
Q

What is the toxicity endpoint for neuromuscular blockers?

A

Peripheral nerve stimulation

-Stimulate the nerve 4 times and record the number of muscle twitches

44
Q

When assessing peripheral nerve stimulation with neuromuscular blockers, what do the different amounts of twitches recorded mean?

A

4/4: <75% suppression (no saturation)
3/4: 75% suppression
2/4: 80% suppression
1/4: 90% suppression
0/4: 100% suppression (complete saturation)

45
Q

How many peripheral nerve twitches do we normally hope to see when dosing neuromuscular blockers?

A

Adjust dose to 1-2 twitches

**avoid 0 twitches

46
Q

What are the 2 scales used for pain assessment?

A

Behavioral Pain Scale (BPS)

Critical Care Pain Observation Tool (CPOT)

47
Q

In critically ill patients, what is the preferred analgesia used for non-neuropathic pain?

A

IV opioids
*note that these also have sedative effects

48
Q

What is the role of non-opioid analgesics in critically ill patients?

A

May be used to decrease opioid requirements

49
Q

What are the most commonly used opioids and how do we dose these?

A

Fentanyl
Morphine

Burn patients: Methadone (due to long-term needs)

*these can be administered as continuous infusions and bolus doses

50
Q

What is the first thing we try when trying to treat agitation?

A

Nonpharmacologic efforts

-Maintain patient comfort
-Provide adequate analgesia
-Frequent reorientation
-Optimize environment to maintain normal sleep

Note that MANY (not most) patients needing mechanical ventilation will require pharmacological sedation

51
Q

What are the indications for sedatives?

A

*Poorly defined

-Adjunct for anxiety and agitation
-Reduce anxiety
-Many patients needing mechanical ventilation (reduce stress)
-Prevent agitation-related harm

52
Q

Sedation should not be used for what?

A

Restraint
Coercion
Discipline
Convenience
Retaliation

53
Q

The degree of sedation in a patient is dependent on what?

A

Need/ability to protect their airway

54
Q

Why is over-sedation problematic?

A

-Increases time on mechanical ventilation
-Increases ICU and hospital length of stay
-Obscures neurological function testing

55
Q

What are the goals of sedation treatment?

A

-Adequate but not over sedation
-Less is best

-Obtain a calm, arousable patient able to follow simple commands

56
Q

What 2 scales are used to assess agitation in patients and consequently to titrate their sedation?

A

Richmond-Agitation-Sedation Scale (RASS)

Sedation-Agitation Scale (SAS)

57
Q

What objective assessment can be used to assess sedation?

A

Bispectral Index (BIS)

58
Q

When would we use the Bispectral Index (BIS) to assess patient sedation?

A

When using the other measures are not feasible in a patient (deep sedation, neuromuscular blockade)

59
Q

True or False: BIS monitoring is recommended in all sedated ICU patients

A

FALSE

60
Q

What are the sedative drugs used in the ICU?

A

Benzodiazepines (lorazepam, midazolam)
Propofol
Dexmedetomidine

61
Q

What is the moa of benzodiazepines?

A

Bind + activate the GABA receptor

Inhibit GABA action on neuronal impulse transmission (this hyperpolarizes the cell and makes them more resistant to excitation)

62
Q

What are the adverse effects of benzodiazepines (lorazepam + midazolam)?

A

-Respiratory depression
-CV effects (hypotension, tachycardia)
-Withdrawal
risk of seizures
doses need to be tapered off
-Delayed emergence from sedation
*especially with midazolam in hepatic/renal
insufficient patients
-Longer duration of mechanical ventilation
-Delirium**

63
Q

What is the reason why benzodiazepines are not used as commonly anymore?

A

They cause delirium!

64
Q

How do we dose benzodiazepines?

A

Continuous or bolus doses

65
Q

What are some points specific to lorazepam?

A

-Less lipid soluble than midazolam
-Crosses BBB slowly
-Has a delayed onset with prolonged duration of effect
(less titratable)

66
Q

How is lorazepam metabolized and what effect can this have?

A

Metabolized to inactive form by glucuronidation

*It is not expected to accumulate in the elderly
*Half-life may be prolonged in liver disease and end-stage renal disease

67
Q

***What does lorazepam contain that is important to remember?

A

IV form contains propylene glycol solvent (PG)

*this is a common ingredient in antifreeze
*with high doses, patients could get toxic amounts of this
-there is no easy way to get serum concentrations of thus

Need to calculate an osmol gap qd or qod to detect toxicity

68
Q

An osmol gap of what may indicate potential propylene glycol toxicity?

A

> 10

69
Q

When is lorazepam not a good option?

A

If rapid awakening is required

70
Q

What is the onset of midazolam?

A

Rapid onset

*Has increased lipid solubility at physiological pH

71
Q

How is midazolam metabolized and what effect can this have?

A

Hepatically metabolized by CYP450 3A

-Half-life increased in the elderly and hepatic disease
-Numerous drug interactions

72
Q

What is an important thing to remember about midazolam’s half-life?

A

It is short, but not reliably short

-Prolonged use makes the half-life more unpredictable

73
Q

When could we consider using midazolam?

A

-Rapid sedation of acutely agitated patients
-Short-term use only (<48-72 h)
-Rapid titration needed
-Procedural sedation

74
Q

What is the maximum amount of time midazolam can be used for?

A

48-72 hours

75
Q

What are some benefits to using propofol for sedation?

A

Rapid onset (1-2min) and Rapid offset
(highly titratable)

No changes reported with renal or hepatic dysfunction

76
Q

What are some side effects of propofol?

A

Some antegrade amnesia
CNS depression!
Withdrawal (titrate off)

“Propofol Infusion Syndrome” -acidosis, bradycardia, lipidemia
-leads to asystole and death
-33% mortality

77
Q

What is the drug of choice for sedation of neurosurgical patients and why?

A

Propofol
-may reduce elevated intracranial pressure (ICP)
-rapid resolution of sedative effects when stopped

78
Q

What does propofol contain that is important to remember?

A

Phospholipid vehicle (contains fat)

1.1 kcal/mL
(need to account for in nutritional assessment)

79
Q

What labs do we need to check when propofol is administered?

A

Triglycerides (after 48h)

*because propofol may cause hypertriglyceridemia

80
Q

What side effects are associated with Propofol Infusion Syndrome?

A

acidosis
bradycardia
lipidemia

81
Q

What preservatives are present in propofol and how do these affect how we give the drug?

A

EDTA: give patient a drug holiday after 7 days of treatment to avoid electrolyte abnormalities

Sodium metabisulfate: Allergic reactions (especially asthmatics)

Benzyl alcohol: unknown ADR

82
Q

When is propofol preferred?

A

-Rapid awakening wanted
-Neurotrauma

Recommended over benzodiazepines

83
Q

What kind of drug is Dexmed?

A

Selective a-2 agonist

-activation of these receptors in the CNS inhibits noradrenalin release

84
Q

What are the side effects of Dexmed?

A

Bradycardia and Hypotension (from agonism of a-2 receptors in the vagus nerve)

**Do not use in patients with low BP or who are on BP meds

85
Q

How does sedation from dexmed vary from the other agents?

A

-Patients are readily arousable with gentle stimulation
-Analgesic-sparing effects
-Anxiolytics (similar to BZDs)
*No respiratory depression (can continue post-extubation)
-No anticonvulsant activity

86
Q

What is the half-life of dexmed?

A

Short

87
Q

How is dexmed metabolized?

A

Hepatically metabolized
-eliminated in urine as glucuronide

-some impaired metabolism in hepatic dysfunction

88
Q

What quirk should you be aware of with dexmed dosing?

A

The maintenance infusion dose is 0.2-0.7 BUT higher doses are often used

-Drug was originally designed to be given as a loading dose followed by maintenance
-*LOADING DOSE SHOULD BE AVOIDED because of cardiovascular effects

-Alternative: administer over longer time or with lower loading dose

89
Q

How long can dexmed be used?

A

Only approved for <24h

*Experience with longer durations but just remember to use this drug short-term

90
Q

Which sedation meds should we use first and second line?

A

First Line:
-Propofol
-Dexmed (limited by duration and CV effects)

Second Line:
-Benzodiazepines (lorazepam + midazolam)

91
Q

What are the 2 subtypes of delirium?

A

Hyperactive (agitated)
–associated with hallucinations/delusions

Hypoactive (calm/lethargic)
–associated with confusion/sedation

92
Q

What are the modifiable risks for delirium?

A

Benzodiazepines
Blood transfusions

93
Q

What 2 assessment tools do we use for delirium?

A

ICDSC
(score >4 is delirium)

CAM-ICU
(2-step approach: first assess level of sedation and then delirium. When at least 3-4 diagnostic criteria are present delirium is diagnosed)

94
Q

How do we prevent/treat delirium?

A

Non-pharm:
-Assess intrinsic/environmental causes
***Early mobilization of patient (PT/OT)
-Optimize sleep
-Optimize vision and hearing
-Improve cognition (reorientation, cognitive stimulation, music, clocks)

Pham:
not recommended for prevention
not recommended for routine treatment
-Antipsychotics can be used short-term for delirium associated with stress
-Dexmed (used when agitation is precluding weaning of vent/extubation)

95
Q

What are our 2 choices when patients require antipsychotics for delirium relating to significant stress?

A

Haloperidol

Atypical Antipsychotics (risperidone, olanzapine, quetiapine)

96
Q

What medication would we administer for delirium when agitation is precluding weaning of vent/extubation?

A

Dexmedetomidine

97
Q

What are some important points about haloperidol?

A

-Mild sedation but no analgesia or amnesia

-Long half-life

-Parenteral and PO

-Intermittent dosing (used for acute aggression with delirium so it is dosed aggressively)

**Not shown to reduce delirium duration

98
Q

What are the side effects of haloperidol?

A

QT interval prolongation -> *Torsades de points

*note that haloperidol has never been approved as an IV drug so the parenteral dose being used is not approved

Decreased seizure threshold

EPS (involuntary dyskinetic movements) *Contraindicated in parkinson’s disease

99
Q

What are the side effects of atypical antipsychotics? (risperidone, olanzapine, quetiapine)

A

-Generally better tolerated than haloperidol
-Fewer EPS

-Still associated with prolonged Qt interval and torsades de points

100
Q

In what case is propofol preferred over dexmed?

A

Cardiac surgery

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