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Truelearn Advanced Exam > TL block 4 > Flashcards

TL block 4 Flashcards

1
Q

Benefits of prone positioning

A

-improved ventilation perfusion matching enter
– improved functional residual capacity
– Improve drainage of secretions

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2
Q

What are electrolytes does a trade affect?

A

Calcium and magnesium

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3
Q

What blood products contain the highest amount of citrate

A

FFP and platelets

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4
Q

How is citrate metabolize?

A

By the liver

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5
Q

What increases the likelihood of citrate toxicity?

A

– Hypothermia
– Liver disease, or transplant
– Hyperventilation
– Pediatric patients
(decrease metabolism of citrate)

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6
Q

Most common cause of acute liver failure

A

Acetaminophen overdose

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7
Q

Pathophysiology as to why there is liver failure with acetaminophen overdose

A

Acetaminophen overdose causes increased, ammonia levels, excess ammonia, combines with glutamate to form glutamine -> glutamine acts as an osmotic agent, causing swelling of astrocytes and cerebral edema

– Elevated ammonia levels are toxic to the brain -> cereal, edema, third vision, vomiting, asterixis , seizures

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8
Q

How does lactulose decrease ammonia levels?

A

Causes a decrease in intestinal pH -> traps ammonia as ammonium ion -> Can no longer cross intestinal membrane and can’t be absorbed

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9
Q

Grades of hepatic encephalopathy

A

I: short, attention, span, minor, lack of awareness, and disordered sleep
II: asterixis, lethargy, and behavioral change
III: confusion, disorientation bizarre behavior, and tiredness
IV: coma

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10
Q

What should be screened for preoperatively and Duchenne and Becker muscular dystrophy?

A

Heart, commonly associated with dilated cardiomyopathy

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11
Q

Why do patients with the Shane and Beck are muscular dystrophy get hyper kalemia?

A

No association with malignant hyperthermia, but when exposed to volatile anesthetics and succinylcholine, can get hyperkalemia from rhabdomyolysis -> cardiac arrhythmias and arrest

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12
Q

Treatment for hyperkalemia

A

Calcium, hyperventilation, insulin, bicarb, and albuterol

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13
Q

Why do patients with spinal cord injury get succinylcholine induced hyperkalemia

A

Extra junctional acetylcholine receptors

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14
Q

Where is the mutation in hyperkalemic periodic paralysis?

A

Sodium channel mutations

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15
Q

Where is the mutation and hypokalemic periodic paralysis?

A

Calcium channels

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16
Q

Why do you get bradycardia with carotid, stent application?

A

Afferent limb of carotid sinus baroreceptor reflex disease (glossopharyngeal) -> stimulation of the nucleus tractus solitarius in medulla -> vagal nuclei activation -> bradycardia and hypotension

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17
Q

Carotid body chemoreceptors

A

Monitors partial pressure of oxygen, secondarily monitors pH and PaCO2

** after carotid endarterectomy chemoreceptors lose innervation, and have a decreased response to hypoxia **

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18
Q

Alveolar partial pressure of O2

A

PAO2 = FiO2 * (Patm - PH2O) - (PaCO2/.8)

FiO2 is % at ambient air

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19
Q

Risk factors for the development of postherpetic neuralgia

A

– Older age
– Female gender
– Increased pain or sensory abnormalities during acute phase
– Severe skin lesion
-Presence of prodrome

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20
Q

How to decrease incidence of postherpetic neuralgia

A

Vaccines

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21
Q

Where does herpes zoster remain after primary infection to cause shingles?

A

Dorsal root ganglia

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22
Q

Contraindications to shockwave lithotripsy

A

– Pregnancy
– Anticoagulation
– Uncorrected bleeding disorders
– Large abdominal aortic aneurysm

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23
Q

Shunt fraction equation

A

Qs/Qt = (1-SaO2)/ (1-SvO2)

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24
Q

Ex of anatomical shunts

A

thebesian veins (valveless veins in walls of cardiac chambers that drain directly into cardiac chambers they are on)
bronchial veins (into pulm veins)

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25
Q

Normal shunt

A

5% in healthy pts

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26
Q

Def of oliguria

A

< 0.5 cc/kg/hr in adults

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27
Q

ADH and surgery

A

inc in surgical stress -> inc ADH -> contributes to postop oliguria

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28
Q

hemodynamic changes in ECT

A

parasym immediately -> sympathetic lasts for 10 minutes

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29
Q

Absolute CI to ECT

A

pheochromocytoma
MI w/i 4-6 weeks
stroke < 3 months
intracranial surgery < 3 months
Intracranial mass lesion
Unstable cervical spine

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30
Q

Why is intracranial mass lesion a CI for ECT?

A

CBF inc 100-400% in ECT due to inc CMR and in BP -> inc ICP -> at risk for stroke or herniation

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31
Q

MCC of maternal death in pts with preeclampsia

A

Hemorrhagic stroke
-commonly postpartum
-best predictor: high systolic pressure

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32
Q

preeclampsia w /severe features

A

plts < 100
Cr > 1.1
baseline Cr x2
LFTs x2
pulm edema
cerebral or visual symp

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33
Q

Leading cause of maternal death in USA

A

cardiac dx

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34
Q

Leading cause of maternal death worldwide

A

PPH

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35
Q

Goal for BP dec in preeclampsia

A

< 160 systolic, and if dec no more than 15-25%

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36
Q
A

1 noncoronary cusp
2 L coronary cusp
3. R coronary cusp
4. RA
5. RV
6. LA
**noncoronary cusp at interatrial septum

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37
Q

How does uremia affect plt aggregation?

A
  1. interferes w/ vWF formation and release (impaired plt activation at injury site)
  2. function of glycoprotein IIb-IIIa abnormal
  3. prostacyclin and nirtic oxide synthesis inc (plt inhibitory effects)
  4. dec factor III activity (can’t bind to factor VII to activate factor X)
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38
Q

what does vWF do?

A

subendothelial vWF binds plts, activates plts and helps plts aggregate

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39
Q

what does glycoprotein IIb-IIIa do?

A

on surface of plts -> receptor for fibrinogen, fibronectin, vWF
-helps w/ plt activation and aggregation

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40
Q

acid-base status hyperparathyroidism

A

-prevents reabsorption of bicarb -> non-AG metabolic acidosis
-inhibits Na-Cl cotransporter in DCT -> hyperCl

**same as excessive NS admin in OR

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41
Q

RV appears large on echo w small lLV, cause? shock

A

PE, obstructive shock

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42
Q

small RV and LV, dilated IVC, dx? shock

A

cardiac tamponade, obstructive

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43
Q

dilated ventricles and dec contractility, shock?

A

cardiogenic

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44
Q

normal ventricular sizes, tachycardia inc contractility, shock?

A

distributive sepsis

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45
Q

small LV and RV, contracility inc, shock?

A

hypovolemic

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46
Q

MOA MH

A

d/o ryanodine receptor -> uncontrolled release of Ca -> sustained m contraction, hypermetabolic state, hyperthermia -> myoglobinuria, rhabdo, organ failure cardiac arrest

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47
Q

acid-base MH

A

mixed resp and metabolic acidosis

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48
Q

bolus dose of acute MH

A

Dantrolene 2.5 mg/kg

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49
Q

maintenance dose of dantrolene

A

1 mg/kg every 6 hours for 24-48 hours

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50
Q

Monitoring for MH

A

CK (peak 12-24 hrs later)
Liver enzymes
Coag studies (monitor for DIC)
Blood gas (looking for resolution of acidosis)
Electrolytes (esp K)

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51
Q

MC SE dantrolene

A

skeletal m weakness > thrombophlebitis > GI upset

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52
Q

earliest symp of MH in peds

A

tachycardia and rapid inc in EtO2

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53
Q

Dantrolene MOA

A

muscle relaxant restores Ca homeostasis

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54
Q

Lab monitoring for long term use of dantrolene

A

LFTs

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55
Q

What pain medication works through the inhibitors of VG Ca channels?

A

gabapentin and pregabalin

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56
Q

MOA inhaled nitric oxide

A

inc cGMP prod -> selective pulm vasodilator -> dec pulm artery pressures and red RV afterload
**primarily arterial dialtor

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57
Q

Nitric oxide function in body

A

-nitric oxide prod by vascular endothelium: is a neurotransmitter, prevents plt aggregation, and smooth m relaxant (vasodilatory)

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58
Q

Nitric oxide and tissue damage

A

tissue damage, less nitric oxide -> plt aggregation at damaged tissue, vasoconstriction/spasm to dec bleeding and start coag cascade

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59
Q

Why does inhaled nitric oxide not have systemic effects?

A

erythrocytes w/i pulm circulation rapidly inactivate the gas

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60
Q

Max dose of lidocaine w/ epi

A

7 mg/kg

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61
Q

Max lidocaine dose w/o epi

A

5 mg/kg

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62
Q

Max bupi dose

A

2.5 mg/kg

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63
Q

Max bupi dose w/ epi

A

3

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64
Q

Max mepivacaine dose

A

5 mg/kg

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65
Q

Max mepivacaine dose w/ epi

A

7 mg/kg

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66
Q

Max dose of ropi

A

3 mg/kg

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67
Q

Max dose of ropi w/ epi

A

3.5 mg/kg

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68
Q

CI to sugammadex

A

hypersensitivity to cyclodextrins

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69
Q

What NMB can be reversed by sugammadex

A

roc and vecuronium

70
Q

What is incompatible w/ sugammadexx?

A

Ondansetron and Verapamil
**flush adequately b/w admin

71
Q

increase in K after succ in healthy pts

A

0.5 mEq/L

72
Q

How long after burns, trauma, denervation should you avoid succ?

A

after 24 hours no succ!

73
Q

How is sugammadex dosed? Actual, lean, or ideal body weight?

A

ACTUAL

74
Q

Triad of sodium nitroprusside toxicity

A

CN toxicity
elevated mixed venous O2, sodium nitroprusside tachyphylaxis, and metabolic acidosis, flushing

75
Q

types of toxicity with sodium nitroprusside

A

CN and thiocyanate

76
Q

Increased risk of toxicity w/ sodium nitroprusside

A

renal failure
diets low in sulfur or Vit B12

77
Q

sodium nitroprusside after: hypoxia, nausea, tinnitus, m spasm, disorientation, psychosis

A

thiocyanate toxicity (usually several days after SNP)
levels 5-10 mg/dL

78
Q

When does CN toxicity w/ sodium nitroprusside occur?

A

blood levels > 100 mg/dL
SNP > 1mg/kg in less than 2 hours
> 0.5 mg/kg over 24 hours

79
Q

Antidote for cyanide poisoning

A

Amyl nitrite
-converts Hg to met-Hg -> binds CN -> nontoxic cyanometHg

80
Q

How is vecuronium metabolized?

A

hepatically then renally cleared

81
Q

succ dosing in infants

A

increased compared to kids due to increased volume of distribution

82
Q

Bioavailability

A

IV > subq > IM > sublingual/buccal > intranasal > rectal > oral

83
Q

Phases of liver transplant

A

preanhepatic
anhepatic
neohepatic

84
Q

What is the preanhepatic phase liver transplant?

A

incision to cross clamping of the major vessels of the liver

85
Q

What is the anhepatic phase? liver transplant

A

starts w/ cross clamping and continues until anastomosis made and perfusion restarts

86
Q

What is the neohepatic phase? liver transplant

A

unclamping of portal vein when reperfusion starts until abd closure

87
Q

postreperfusion syndrome (liver transplant)

A

systemic hypoTN
pulm HTN
possible emboli

88
Q

What causes postreperfusion syndrome?

A

Build up of K, lactate, H+ into circulation -> lack of ATP and glycogen -> Na/K pump stops working -> extracellular Na moves into cells causing swelling
-vascular permeability also inc due to lack of ATP

89
Q

Metabolism of chloroprocaine

A

plasma cholinesterase
**b/c ester local anesthetic, same as all esters!

90
Q

Metabolism of amide local anesthetics

A

hepatic metabolism

91
Q

Why chloroprocaine for OB emergency sections?

A

-metabolized by plasma cholinesterase, little availabily to cross placenta
-does not participate in ion trapping, so useful w/ acidotic in distress fetus
-fast onset

92
Q

What local anesthetics most likely to cross placenta?

A

Lidocaine! less protein bound
-Bupi and Ropi more protein bound, so harder
-Amides more likely than esters (Chloroprocaine least likely)

93
Q

What dx associated w/ MH?

A

Central core dx
Multiminicore Dx
King Denborough Syndrome
Hyper/hypokalemic periodic paralysis

94
Q

Central core dx

A

Auto Dom mutation in ryanodine receptor
-spine and pelvic weakness w/ foot deformities
**assoc w/ MH!

95
Q

Duchenne muscular dystrophy

A

X linked recessive, dystrophin gene
-hyperK to succ
-rhabdo w/ volatile anesthetics
**no MH assoc

96
Q

Treatment of neuroleptic malignant syndrome

A

bromocriptine (DA agonist)

97
Q

Diagnostic test for MH

A

caffeine halothane contracture test

98
Q

tx for benzo OD

A

flumazenil

99
Q

What OD: AMS, nausea, tachypnea, ringing in the ears

A

salicylate (ASA)

100
Q

acid-case for salicylate OD

A

combined anion gap metabolic acidosis and resp alk
-salicylates act on resp drive in medulla to inc RR

101
Q

Treatment of salicylate toxicity

A
  1. supportive (ABCs)
  2. activated charcoal and/or gastric lavage if recent
  3. dextrose to avoid CSF hypoglycemia
  4. IV fluids to replace losses from tachypnea and vomiting
  5. Bicarb: inc pH to dec tissue distribtuion and raises urine pH to inc renal clearance

**if severe symptoms: HEMODIALYSIS

102
Q

OD: abd pain, N/V, sweating

A

Acetaminophen tox
liver failure
**don’t show many symptoms in first 24 hours, but have worse liver failure

103
Q

tx for acetaminophen OD

A

N-acetylcysteine

104
Q

What pressor should not be given IM?

A

Norepi

105
Q

Tx for area of necrosis caused by Norepi in a PIV?

A

Phentolamine

106
Q

Best lab test to determine if someone in end stage liver failure is in DIC

A

***factor VII! b/c inc/normal in end stage liver dx, but dec in DIC
-in endstage liver dx, fibrinogen will already be dec, so will a lot of other factors, and if pt had surgery d-dimer will be inc

107
Q

Primary signs of acute liver failure

A

inc in INR
encephalopathy
elevated AST/ALT
*no symp of portal HTN b/c rapid progression

108
Q

What causes hepatic encephalopathy?

A

Ammonia!
-ammonia metabolized to glutamine by astrocytes in CNS -> swelling of astrocytes and cerebral edema
-untreated can cause inc ICP, herniation, death

109
Q

postop shivering, then rigidity, hyperthermia, N/V, hyperreflexia, dx? tx?

A

Serotonin Syndrome
tx: Cyproheptadine (antihistamine)

110
Q

Treatment of acute dystonia likely 2/2 antipsychotics

A

benztropine
diphenhydramine
benzos

111
Q

AMS, hypthermia, rigitidity, dysautonomia w/ antipsychotics dx? tx?

A

NMS
tx: bromocriptine, amantadine, dantrolene

112
Q

Methadone MOA

A

full agonist at mu receptors
NMDA antag
monoamine reuptake inh

113
Q

Safest opioids in ESRD

A

fent
methadone (metabolites inactive, metabolized by liver cytochrome P450)

114
Q

SE methadone

A

resp depression
QTc prolongation (caution if > 450, d/c if > 500)
N/V
constipation
biliary spasms*

115
Q

What drugs increase conc of methadone?

A

Alcohol
Benzos
Ciprofloxacin
Fluconazole
Urinary alkalinizers

116
Q

What drugs dec methadone conc?

A

Anti-retroviral therapy
Phenobarb
Phenytoin
Urinary acidifiers

117
Q

Inhaled anesthetics QTc?

A

causes prolongation

118
Q

tx of torsades de points

A

IV Mg

119
Q

Metabolized by butylcholinesterase

A

succ
ester local anesthetics
heroin
cocaine
mivacurium
ASA

120
Q

If information submitted to National Anesthesia Clinical Outcomes Registry, what other registry does the data go to?

A

Multicenter Perioperative outcomes Group
-both get data from AIMS: anesthesia information management systmes

121
Q

Where does anesthesia closed claims project get its data?

A

case summaries submitted by ASA from malpractice insurance claim files -> goal of pt safety

122
Q

where does society for thoracic surgery w/ society of cardiovascular anesthesiologist get its info?

A

it’s own anesthesia module -> checkboxes to collect info about pts underoing cardiothoracic surgery -> research purpose

123
Q

PCWP PE

A

deceased! b/c circulation to the L atrium is limited

124
Q

PCWP tamponade

A

increased

125
Q

PCWP tension PTX

A

increased

126
Q

severe pulm HTN PCP

A

decreased
circulation to LA is limited

127
Q

MC type of shock

A

distributive

128
Q

What type of shock is neurogenic shock?

A

Distributive
-dec BP and dec HR -> discruption in CNS that regulate circulation
**SC injuries

129
Q

Cardiac index for cardiogenic shock

A

< 2.2 L/min/m^2

130
Q

def of shock

A

life-threatneing emergncy where tissues of body not getting adequate BF

131
Q

Hemodynamics for cardiogenic shock

A

HypoTN for > 30 minutes w/ systolic < 90 (or decrease from baseline by 40)
-PCWP > 18
-CI < 2.2

132
Q

Which measure of ABG is calculated not measured?

A

base excess
bicarbonate
SaO2

133
Q

How is PCO2 measured ABG?

A

Severinghaus electrode

134
Q

Blood PO2 measured how ABG?

A

Clark electrode

135
Q

How is blood pH measured?

A

pH electrode, optical absorbance technique
-difference b/w known and measuring sample

136
Q

What to do if d/c TPN?

A

start IV glucose and freq monitoring of blood glucose
-body inc insulin production during constant TPN

137
Q

Who is more likley to get refeeding syndrome

A

pts who have had poor or no nutrition for >72-96 hours
-low levels of prealbumin (<10)

**hypophos severe

138
Q

Septic shock pathophys

A

Exposure to certain microbial components -> activate cytokine cascade -> upregulation of tissue factor (prothrombotic state) -> release of TNF alpha from macrophages -> enhance release of other cytokins (interferon gamma, IL 1, 2, 6, 8, 10) and plt activating factor
-activation of complement -> promotes vascular permeability, leukocyte chemotaxis, inc inflammatory resp

139
Q

Which NMB has the most potent metabolite?

A

Vecuronium 3-desacetyl vec is 90% as potentn -> can accumulate w/ infusions and in pts w/ renal failure

140
Q

Difference between alpha and pH stat for CPB

A

in hypothermia w/ CPB -> total CO2 content the same, but partial pressure CO2 decreases
-pH corrects this and adds CO2 into the circuit to correct alkalosis
-alpha stat doesn’t do this

141
Q

Advantages of pH stat during CPB

A

-increased speed of homogenous cerebral cooling (cerebral vasodilation)
-inc cerebral blood flow
-improved O2 delivery (corrects alkalosis, counteracts L shift of oxy-Hg curve)

142
Q

Disadvantages of pH stat

A

-inc delivery of embolic load to brain
-loss of cerebral autoregulation

143
Q

Goals for brain dead organ donors

A

MAP 60-120
CVP 4-12
Na < 155
ideally low dose pressor
PaO2/FiO2 ratio > 300
pH 7.25-7.5
Glucose < 150
UOP .5-3 cc/kg/hr
LV EF > 50%
Hg > 10

144
Q

for brain dead organ donors best pressor?

A

Vasopressin
-dec catecholamine req and effective for diabetes insipidus (80% of pts following brain death)

145
Q

CVP tracing tamponade

A

exaggerated x descent (initial ventricular ejection and atrial relaxation)

146
Q

normal CVP tracing

A
147
Q

CVP pericartiditis

A

-change in compliance during diastole w/o inc pericardial pressure

148
Q

hemodynamic goals for cardiac tamponade

A

tachycardia
hypervolemia
inv SVR
full, fast, strong
** cardiac output HR dept**

149
Q

what blood test should be monitored w/ inhaled NO?

A

Met-Hg

150
Q

tx for CN tox

A

amyl nitrite

151
Q

what dyes cause a dec in SpO2?

A

methylene blue, indocyanine green, indigo carmine

152
Q

what type of adrenal insuff w/ exogenous glucocorticoids?

A

tertiary

153
Q

type of adrenal insuff in ICU

A

Functional
-inadequate synthesis of cortisol due to cellular dysfunction and change sin adrenal gland
-peripheral glucocorticoid resistance
-transport of cortisol to organs reduced
-resp to cortisol impaired

154
Q

Hemodynamic changes in cirrhosis

A

build up of nitric oxide and carbon monoxide (vasodilators) -> dec SVR and decreased afterload -> increased cardiac output
-inc renin b/c kidneys see vasodilation as depleted state
-inc mixed venous O2 saturation due to inc cardiac output and arteriovenous collaterals

155
Q

Platypnea

A

dyspnea and hypoxia while sitting that is relieved while laying flat
**hepatopulm syndrome

156
Q

exposure to pt w/ unknown HIV status at low risk for HIV

A

no post exposure ppx

157
Q

ppx if exposed to known HIV pt and exposure is superficial or exposure w/ solid needle

A

2 drug ppx

158
Q

ppx if pt has HIV w/ high viral load or AIDS

A

3 drug ppx

159
Q

It provider exposed to hep B and unvaccinated or vaccine nonresponder

A

Hepatitis B immunoglobulin

160
Q

when to give hydrocortisone in pt w/ septic shock

A

unresponsive to fluids and vasopressors

161
Q

How does hydrocortisone help w/ septic shock?

A

inhibits nitric oxide synthesis

162
Q

intubated pt on TPN having difficulty vent weaning, how to fix?

A

increase percentage of lipid content in TPN
-lipid content has a lower resp quotient than protein or carbs -> limiting CO2 production

163
Q

MC adverse event in peds propofol sedation

A

apnea or airway obstruction

164
Q

how long after no PO should parenteral nutrition be started?

A

7 days

165
Q

enteral vs parenteral nutrition

A

enteral helps to maintain gut integrity > prevents inc in gut permeability, provides nutrition support for lymphoid tissue
-dec risk of infxn, no IV needed

parenteral: inc infxn risk, cholestasis (no stimulus for GB contraction)

166
Q

complications of enteral nutrition

A

inc risk of aspiration (esp if bed not above 30 degrees)
-sinusitis
-diarrhea
-hypophosphatemia

167
Q

Normal mixed venous blood jugular bulb sat

A

55-75%

168
Q

change in jugular bulb venous O2 saturation monitoring w/ stroke

A

none (only global, not focal)

169
Q

change in jugular bulb venous O2 saturation monitoring w/ barbiturate infusion

A

increased!
dec CMRO2 -> dec O2 consumption

170
Q

change in jugular bulb venous O2 saturation monitoring w/ severe anemia

A

dec b/c dec hgb -> dec O2 deliver

171
Q

change in jugular bulb venous O2 saturation monitoring w/

A

increased b/c dec O2 extraction by cerebral tissue
(inc cardiac output)

172
Q

oculogyric crisis

A

spasmodic movements of eyeballs into fixed upwardsposition
-acute dystonia

Truelearn Advanced Exam (15 decks)

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