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PHRM 864 Exam 3 > Acute care > Flashcards

Acute care Flashcards

1
Q

Absorption

A

Oral:
Impaired and unpredictable in critically ill patients

Alterations in gastric emptying and motility–>opioids, C.diff
Interactions with enteral feeding and tubing–>fluoroquinolines, phenytoin, GI injury/disease

IV: preferred in many of those cases

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2
Q

Distribution

A

Relates to fluid and hydration status
-Hydrophilic drugs have high Vd in critically ill patients than regular medical floor patients

Alterations in protein binding
-Decreased albumin–>less protein binding of drugs
-Increased acute phase proteins–>more protein binding of drugs
Ex: lidocaine

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3
Q

Metabolism (hepatic)

A

Enzyme expression and activity may be decreased in critically ill patients

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4
Q

Metabolism (renal)

A

Renal dysfunction and HD/CRRT is common

Decreased: shock, sepsis, nephrotoxic drugs

Increased: burn, trauma

How to assess?
CrCl–>delayed
Urine output–>immediate

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5
Q

Sepsis

A

Life threatening dysfunction caused by dysregulated response to infection
-Immune dysregulation
-Coagulation and thrombosis leading to endothelial injury

Occurs in response to any pathogen–>bacterial is most common
Occurs in any site of injection–>lungs, bloodstream, urinary tract

Treatment: early detection and supportive care + broad spectrum IV antibiotics/antifungals and source control

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6
Q

Septic shock

A

Sepsis associated with cardiovascular collapse and hypotension
-Hypotension caused by decreased vascular tone

Treatment:
Fluids
+
Vasopressors–> increase vascular tone and cardiac output via vasoconstriction
1st line: norepinephrine
others: epinephrine, phenylephrine, dopamine, add- on vasopressin, dobutamine
Target MAP > 65 mmHg

If refractory–>IV hydrocortisone

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7
Q

Respiratory failure

A

MECHANICAL VENTILATION IS COMMON

Causes: airway compromise, hypoventilation, hypoxic failure, inability to protect airways

Acute Respiratory Distress Syndrome (ARDS)
Characterized by acute, diffuse inflammatory lung injury
1st phase: mucous
2nd phase: fibrotic

Risk for ARDS: pneumonia, sepsis, trauma, aspiration

Treatment: mechanical ventilation + sedation +/- neuromuscular blockade
Corticosteroids may be used

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8
Q

Analgesia treatment

A

Preemptive analgesia in advance to painful procedures (dressing changes, chest tubes, insertion of lines)

IV opioids: Bolus or continuous infusion or both
SE: sedation, respiratory depression, do not have to worry about respiratory depression if on vent

Non-opioids: Tylenol
NSAIDS–>procedural
Ketamine–>post-surgery
Gabapentin/pregabalin/carbamazepine–>neuropathic

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9
Q

Underlying causes of agitation

A

Pain
Mechanical ventilation
Hypoxia
Delirium
Hypotension
Withdrawal

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10
Q

Non-pharmacological treatment of agitation

A

Maintain patient comfort
Provide adequate analgesia
Reorient the patient–> where and why they are in the hospital
Optimize environment for sleep patterns

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11
Q

Pharmacologic treatment of agitation

A

Sedatives
-Adjunct for anxiety and agitation
-Adjunct to non-pharmacological
-Many mechanical ventilation patients

ANALGESIA-FIRST SEDATION

Goal: Less is best–>light sedation
Desire a calm arousable patient, able to purposefully follow simple commands

Methods: spontaneous awakening trial, nursing-protocolized targeted sedation

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12
Q

Lorazepam MOA

A

Binds to the allosteric site of GABAa receptor increasing frequency of Cl- channel opening

Inhibits GABA activity on neuron impulses–>hyper-polarizes cells leading to resistance to excitation

IV contains propylene glycol solvent that can cause lactic acidosis and nephrotoxicity after high doses or prolonged infusions–>MONITOR OSMOL GAP

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13
Q

Lorazepam side effects

A

Respiratory depression

Hypotension, tachycardia

Withdrawal (seizures)–> gradually taper dose

Delayed sedation: prolonged infusion, advanced age, hepatic/renal insufficiency (midazolam)

DELIRIUM

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14
Q

Lorazepam properties

A

Anxiolysis
Sedation
Amnesia
Anticonvulsant and muscle relaxant

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15
Q

Lorazepam pearls

A

Tolerance with chronic administration

Metabolized into inactive metabolite via glucuronidation–>less accumulation

Least lipid soluble crossing the BBB more slowly leading to delayed onset and prolonged duration of action (long t1/2 life)–>LESS TITRATABLE

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16
Q

Midazolam

A

IV only

Hepatically metabolized by CYP3A4–> increased t1/2 in elderly, hepatic disease, drug interactions

At physiological pH, very high lipid solubility leading to rapid onset (short 1/2 life)–> TITRATABLE

After 48 hours, t1/2 becomes prolonged or unpredictable especially in renal disease due to metabolite accumulation

Recommended for short term use only, not for long term sedation because of unpredictable awakening time

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17
Q

Propofol MOA

A

Binds sites on multiple receptors (GABA, glycine, nicotinic, M1 muscarinic) interrupting neural transmission leading to global CNS depression

IV

Diprivan–>contains EDTA that can cause electrolyte abnormalities, recommended drug holiday after > 7 days treatment

Sodium metabisulfate–>allergic reactions in asthmatics

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18
Q

Propofol Indications

A

General anesthetic
Procedural sedation
Neurosurgical–>may reduce ICP and rapid offset of sedative effects

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19
Q

Propofol side effects

A

Hypertriglyceridemia–>check q48 hours

Apnea

Hypotension, bradycardia

Pain with infusion

Withdrawal–> gradual taper if > 7 days of therapy

Propofol Infusion Syndrome–>acidosis, bradycardia, lipidemia
**sustained treatment > 48 hours
**high doses >75-80 ug/kg/min
**metabolic acidosis
**rhabdomyolysis
**hypotension, arrhythmias
**asystole (rare)

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20
Q

Propofol PK

A

Hepatically metabolized with no active metabolite

No changes in renal or hepatic function

High protein bound

Large Vd

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21
Q

Propofol pearls

A

Easily penetrates BBB–> rapid onset
Rapidly redistributes tissues and rapid hepatic clearance–>rapid offset
Provides some amnesia
Phospholipid emulsion–>1.1 kcal/mL
DO NOT HANG > 12 hours–>risk of infection

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22
Q

Dexmedetomidine MOA

A

selective alpha-2-agonist within CNS inhibiting norepinephrine release

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23
Q

Dexmedetomidine ROA

A

IV

Avoid loading dose

May push doses higher than guidelines due to weak sedation

May use for longer than > 24 hours compared to guidelines

24
Q

Dexmedetomidine properties

A

Patients readily arousable with gentle stimulation–>not used for deep sedation

Anxiolysis

Analgesic sparing effects

No respiratory depression

No anticonvulsant

25
Q

Dexmedetomidine Side effects

A

Increase in blood pressure with rapid administration

Hypotension, bradycardia
**more common in volume depleted patients with high sympathetic tone–>AVOID IN HEMODYNAMIC UNSTABLE PATIENTS

26
Q

Dexmedetomidine PK

A

Highly protein bound
High Vd
Short t1/2

Hepatically metabolized and eliminated in urine as glucuronide
**no changes in renal dysfunction
**decrease dose by 40-70% in hepatic dysfunction

27
Q

Monitoring–>hourly assessment

A

Subjective: assessment is difficult due to inability to outward express anxiety

Richmond-agitation-sedation scale (RASS)
Sedation-agitation scale (SAS)

Objective:
Bispectral index (BIS)
-Utilizing EEG to find objective number
-Guidelines suggest using in patients who other measures are not feasible (sedation, NMBA)
NOT RECOMMENDED IN ALL PATIENTS

28
Q

Thromboprophylaxis

A

Receive unless sufficiently mobile, low risk of VTE, contraindications

29
Q

Enoxaparin

A

DOC

30 mg SQ q12h or 40 mg SQ q24h
monitor s/sx of bleeding, CBC
CrCl < 30 mL/min: 30 mg SQ q24h

30
Q

Daltaparin

A

5000 units SQ q24h
monitor s/sx of bleeding, CBC
No renal adjustment

31
Q

Unfractionated heparin

A

5000 units SQ q8-12 hours
monitor s/sx of bleeding, CBC
No renal adjustment

32
Q

Ulcer risk factors

A

Shock, coagulopathy, chronic liver dx
Neurotrauma, burn injury, extracorporeal life support
Mechanical ventilation
Drugs: antiplatelets, anticoagulants, NSAIDS

33
Q

Glycemic control

A

Causes: stress, TPN

Balance risk between hypo/hyperglycemia

BG goal: 144-180 mg/dL
> 180 mg/dL: initiate insulin

Avoid long-acting agents due to long t1/2 life

34
Q

Two subtypes of delirium

A

Hyperactive (agitated)–>hallucinations, delusions
Hypoactive (calm, lethargic)–>confusion, sedation

35
Q

Modifiable risk factors of delirium

A

Benzodiazepines
Blood transfusions

36
Q

Non-modifiable risk factors of delirium

A

Older age
Preexisting dementia
Prior coma
Pre-ICU emergency surgery or trauma
High severity of illness at admission

37
Q

Other risk factors of delirium

A

HTN
Psychoactive drugs
Prolonged physical restraint, immobility
Sepsis
Hypoglycemia, hyponatremia
Metastatic disease of the brain, head injury, CNS infections

38
Q

Assessment of delirium

A

ICDSC
CAM-ICU

39
Q

Non-pharm treatment of delirium

A

Early mobilization
Optimize sleep
Optimize hearing and vision
Improve cognition

40
Q

Pharmacological treatment of delirium

A

NOT RECOMMENDED FOR PREVENTION
NOT RECOMMENDED FOR ROUTINE THERAPY

41
Q

Haloperidol MOA

A

Short-term treatment

typical antipsychotic–>D2 antagonist

IV, PO

42
Q

Haloperidol properties

A

Mild sedation without analgesia

Minimal CV effects

43
Q

Haloperidol PK

A

long t1/2 life

44
Q

Haloperidol SE

A

QTc prolongation and TdP
-Avoid in high risk patients
-Avoid with other Qtc prolonging agents
-D/C if QTc >450 msec or > 25% increase from baseline

Lower seizure threshold
EPS
Neuroleptic Malignant Syndrome

45
Q

Atypical antipsychotics

A

Risperidone, olanzapine, quetiapine, aripiprazole, ziprasidone

MOA: 5HT2A and D2 antagonist

46
Q

Atypical antipsychotic SE

A

Lower EPS

QTc prolongation: avoid in high risk patients, avoid with other QTc prolonging agents, D/C if QTc > 450 msec

NMS–>olanzapine most common
Hypotension–>olanzapine most common

47
Q

Dexmedetomidine for delirium

A

May be used for delirium-related agitation precluding weaning off vent/extubating

48
Q

Depolarizing NMBA

A

initial inactivation of Ach receptors then inhibition

49
Q

Non-depolarizing NMBA

A

Competitively block the action of Ach

Amino steroidal
Benzylisoquinolinium

50
Q

Reversal agents

A

Pyridostigmine, neostigmine–>Ach inhibitors

Sugammadex: modified A cyclodextrin for reversal of rocuonium/vecuronium

51
Q

Succinylcholine MOA

A

physically resembles Ach to bind to Ach and activate receptors–>depolarization of neuromuscular junction–>muscle contraction blocked

52
Q

Succinylcholine indication

A

Rapid sequence intubation (RSI)

NOT USED FOR SUSTAINED NEUROMUSCULAR BLOCKAGE

53
Q

Succinylcholine SE

A

Initial muscle contractions: may pre-administer with non-depolarizing MNDA agent

APNEA–>MUST BE READY TO INTUBATE IMMEDIATELY

Prolonged apnea–>impaired pseudocholinesterase activity or lower levels

Muscle fasciculations–>deep aching muscle pain lasting for days

Hyperkalemia: contraindicated in major burns, crash injury, and upper motor neuron disease

54
Q

Succinylcholine PK

A

onset: 1 minute
Duration: 3-5 minutes
Elimination: rapidly hydrolyzed by pseudocholinesterase

55
Q

Non-depolarizing agents indications

A

Immediate/sustained paralysis

Mechanical ventilation

Muscle relaxation operations

RSI if contraindicated to succinylcholine
-Rocuonium if CI to succinylcholine

Increased ICP

Hypothermia

56
Q

Non-depolarizing NMBA SE

A

Paralysis of respiratory muscles/apnea

Inadequate pain/sedation: NMDA do not provide analgesic, sedative, or anxiolytic effects, assessment can be hard when they cannot talk, MUST BE OPTIMIZED ON SEDATIVE AND ANALGESIC DRUGS PRIOR

Prolonged paralysis: caused by accumulation of medication and chronic administration
Solution: drug holidays

Drug interactions: corticosteroids

57
Q

Toxicity endpoint–>peripheral nerve stimulation

A

Twitch monitoring or train-of-four

4/4–> < 75% suppression
3/4–> 75% suppression
2/4–> 80% suppression
1/4–> 90% suppression
0/4–> 100% suppression

Goal: 1-2 out of 4

PHRM 864 Exam 3 (10 decks)

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