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

Therapeutics Exam 3 (Acute/Critical Care) Flashcards

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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
Stress ulcer prophylaxis is warranted in critically ill patients such as?
Mechanical ventilation Coagulopathy Chronic liver disease Shock Others
26
What is the target blood glucose for ICU patients?
144-180 mg/dl
27
At what BG level do we initiate insulin for ICU patients?
>180 mg/dl
28
What is the purpose of a spontaneous awakening trial/ spontaneous breathing trial?
Helps to prevent oversedation Promotes weaning from mechanical ventilation
29
When neuromuscular blockers are not present, how does neuromuscular signaling typically occur?
Synaptic vesicles release acetylcholine Acetylcholine binds receptors on muscle cell, causes depolarization and ultimately muscle contraction
30
What are the 2 types of neuromuscular blockers?
Depolarizing Nondepolarizing
31
What drug is the only depolarizing neuromuscular blocker available?
Succinylcholine
32
How does succinylcholine work?
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)
33
What do we use succinylcholine for?
Rapid sequence intubation (RSI) **this is its only use, not used for sustained neuromuscular blockade
34
What are the side effects of succinylcholine?
Apnea (*need to be ready to intubate) Muscle fasciculations (muscle ache, may last days) Hyperkalemia
35
When is succinylcholine contraindicated?
Major burns Crush injury Upper motor neuron disease ***risk of life-threatening hyperkalemia
36
How do nondepolarizing neuromuscular blockers work?
Competitively block the action of acetylcholine (block receptors) ***Do not activate receptors -this means there are no initial muscle contractions
37
What are the 2 classes of nondepolarizing neuromuscular blockers?
Aminosteroidal Benzylisoquinolinium
38
What are the aminosteroidal neuromuscular blockers?
Pancuronium Vecuronium Rocuronium
39
What are the benzylisoquinolinium neuromuscular blockers?
Atracurium Cisatracurium
40
True or False: Neuromuscular blockers are required in all mechanically ventilated patients
FALSE -only those with Acute Lung Injury or Acute Respiratory Distress Syndrome (ARDS)
41
What are the side effects associated with non-depolarizing NMBs?
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
What drugs interact with non-polarizing NMBs?
Corticosteroids -potentially cause long-term muscle weakness
43
What is the toxicity endpoint for neuromuscular blockers?
Peripheral nerve stimulation -Stimulate the nerve 4 times and record the number of muscle twitches
44
When assessing peripheral nerve stimulation with neuromuscular blockers, what do the different amounts of twitches recorded mean?
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
How many peripheral nerve twitches do we normally hope to see when dosing neuromuscular blockers?
Adjust dose to 1-2 twitches **avoid 0 twitches
46
What are the 2 scales used for pain assessment?
Behavioral Pain Scale (BPS) Critical Care Pain Observation Tool (CPOT)
47
In critically ill patients, what is the preferred analgesia used for non-neuropathic pain?
IV opioids *note that these also have sedative effects
48
What is the role of non-opioid analgesics in critically ill patients?
May be used to decrease opioid requirements
49
What are the most commonly used opioids and how do we dose these?
Fentanyl Morphine Burn patients: Methadone (due to long-term needs) *these can be administered as continuous infusions and bolus doses
50
What is the first thing we try when trying to treat agitation?
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
What are the indications for sedatives?
*Poorly defined -Adjunct for anxiety and agitation -Reduce anxiety -Many patients needing mechanical ventilation (reduce stress) -Prevent agitation-related harm
52
Sedation should not be used for what?
Restraint Coercion Discipline Convenience Retaliation
53
The degree of sedation in a patient is dependent on what?
Need/ability to protect their airway
54
Why is over-sedation problematic?
-Increases time on mechanical ventilation -Increases ICU and hospital length of stay -Obscures neurological function testing
55
What are the goals of sedation treatment?
-Adequate but not over sedation -Less is best -Obtain a calm, arousable patient able to follow simple commands
56
What 2 scales are used to assess agitation in patients and consequently to titrate their sedation?
Richmond-Agitation-Sedation Scale (RASS) Sedation-Agitation Scale (SAS)
57
What objective assessment can be used to assess sedation?
Bispectral Index (BIS)
58
When would we use the Bispectral Index (BIS) to assess patient sedation?
When using the other measures are not feasible in a patient (deep sedation, neuromuscular blockade)
59
True or False: BIS monitoring is recommended in all sedated ICU patients
FALSE
60
What are the sedative drugs used in the ICU?
Benzodiazepines (lorazepam, midazolam) Propofol Dexmedetomidine
61
What is the moa of benzodiazepines?
Bind + activate the GABA receptor Inhibit GABA action on neuronal impulse transmission (this hyperpolarizes the cell and makes them more resistant to excitation)
62
What are the adverse effects of benzodiazepines (lorazepam + midazolam)?
-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
What is the reason why benzodiazepines are not used as commonly anymore?
They cause delirium!
64
How do we dose benzodiazepines?
Continuous or bolus doses
65
What are some points specific to lorazepam?
-Less lipid soluble than midazolam -Crosses BBB slowly -Has a delayed onset with prolonged duration of effect (less titratable)
66
How is lorazepam metabolized and what effect can this have?
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
***What does lorazepam contain that is important to remember?
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
An osmol gap of what may indicate potential propylene glycol toxicity?
>10
69
When is lorazepam not a good option?
If rapid awakening is required
70
What is the onset of midazolam?
Rapid onset *Has increased lipid solubility at physiological pH
71
How is midazolam metabolized and what effect can this have?
Hepatically metabolized by CYP450 3A -Half-life increased in the elderly and hepatic disease -Numerous drug interactions
72
What is an important thing to remember about midazolam's half-life?
It is short, but not reliably short -Prolonged use makes the half-life more unpredictable
73
When could we consider using midazolam?
-Rapid sedation of acutely agitated patients -Short-term use only (<48-72 h) -Rapid titration needed -Procedural sedation
74
What is the maximum amount of time midazolam can be used for?
48-72 hours
75
What are some benefits to using propofol for sedation?
Rapid onset (1-2min) and Rapid offset (highly titratable) No changes reported with renal or hepatic dysfunction
76
What are some side effects of propofol?
Some antegrade amnesia CNS depression! Withdrawal (titrate off) "Propofol Infusion Syndrome" -acidosis, bradycardia, lipidemia -leads to asystole and death -33% mortality
77
What is the drug of choice for sedation of neurosurgical patients and why?
Propofol -may reduce elevated intracranial pressure (ICP) -rapid resolution of sedative effects when stopped
78
What does propofol contain that is important to remember?
Phospholipid vehicle (contains fat) 1.1 kcal/mL (need to account for in nutritional assessment)
79
What labs do we need to check when propofol is administered?
Triglycerides (after 48h) *because propofol may cause hypertriglyceridemia
80
What side effects are associated with Propofol Infusion Syndrome?
acidosis bradycardia lipidemia
81
What preservatives are present in propofol and how do these affect how we give the drug?
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
When is propofol preferred?
-Rapid awakening wanted -Neurotrauma *Recommended over benzodiazepines*
83
What kind of drug is Dexmed?
Selective a-2 agonist -activation of these receptors in the CNS inhibits noradrenalin release
84
What are the side effects of Dexmed?
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
How does sedation from dexmed vary from the other agents?
-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
What is the half-life of dexmed?
Short
87
How is dexmed metabolized?
Hepatically metabolized -eliminated in urine as glucuronide -some impaired metabolism in hepatic dysfunction
88
What quirk should you be aware of with dexmed dosing?
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
How long can dexmed be used?
Only approved for <24h *Experience with longer durations but just remember to use this drug short-term
90
Which sedation meds should we use first and second line?
First Line: -Propofol -Dexmed (limited by duration and CV effects) Second Line: -Benzodiazepines (lorazepam + midazolam)
91
What are the 2 subtypes of delirium?
Hyperactive (agitated) --associated with hallucinations/delusions Hypoactive (calm/lethargic) --associated with confusion/sedation
92
What are the modifiable risks for delirium?
Benzodiazepines Blood transfusions
93
What 2 assessment tools do we use for delirium?
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
How do we prevent/treat delirium?
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
What are our 2 choices when patients require antipsychotics for delirium relating to significant stress?
Haloperidol Atypical Antipsychotics (risperidone, olanzapine, quetiapine)
96
What medication would we administer for delirium when agitation is precluding weaning of vent/extubation?
Dexmedetomidine
97
What are some important points about haloperidol?
-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
What are the side effects of haloperidol?
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
What are the side effects of atypical antipsychotics? (risperidone, olanzapine, quetiapine)
-Generally better tolerated than haloperidol -Fewer EPS -Still associated with prolonged Qt interval and torsades de points
100
In what case is propofol preferred over dexmed?
Cardiac surgery

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