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Truelearn Advanced Exam > TL block 3 > Flashcards

TL block 3 Flashcards

1
Q

Guidelines for reducing the incidence or severity of TURP

A

-suspending irrigating fluid < 30cm above pt
=draining bladder regularly to avoid inc in bladder pressure
-limit resection time to < 1 hr
-avoid hypotonic IV fluids
-use vasopressors to tx hypoTN from regional -> regional dec venous pressures and inc absorption of irrigation

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2
Q

why coagulopathy from TURP?

A

rare unless lenthy resection -> prostatic tissue plasminogen activator
-expediates conversion of plasminogen to plasmin promoting fibrinolysis
-tx: supportive blood product transfusion, incl cryo

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3
Q

complications of glycine irrigation in TURP

A

glycine resembles GABA -> transient blindness
-metabolized to ammonia -> encephalopathy, N/V

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4
Q

Complications of TURP

A

hypothermia (room temp irrigation)
transient blindness and hyperammonia (glycine)
intraperiteoneal bladder perf
extraperitoneal prostatic capsular perf
cardiopulm compromise
coagulopathy (fibrinolysis)

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5
Q

landmarks for the infragluteal sciatic nerve block

A

greater trochanter of the femur
ischial tuberosity
sciatic groove

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6
Q

infragluteal sciatic n block

A
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7
Q

When to use a Mann-Whitney test for data analysis

A

nonparametric interval data
-compare data that is skewed towards a high or low value in an unpaired group

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8
Q

Where are cardiac myxomas usually found?

A

Left atrium most commonly
interatrial septum

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9
Q

more common: primary cardiac malignancy or mets of lung cancer to heart?

A

Mets

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10
Q

Most common benign cardiac tumor in adults

A

myxoma

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11
Q

Complications w/ cardiac tumors

A

arrhythmias
ventricular obstruction
heart failure
pulm edema
pulm HTN
arterial hypoxemia
dyspnea
positional hemodynamic compromise
embolism

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12
Q

RF for placenta accreta

A

prior uterine surgery
placenta previa
adv maternal age
smoking
multiparity

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13
Q

How is CO2 partial pressure measured w/ built-in gas analyzer?

A

Intensity of light detected by infrared spectrophotometer is inversely proportional to CO2 partial pressure
-b/c higher CO2 absorbs more of the infrared -> less reachs the analyzer

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14
Q

which gases use infrared spectrophotometry to be analyzed?

A

CO2
volatile anesthetics
N2O

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15
Q

How is O2 measured in gas analyzer?

A

paramagnetic analysis

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16
Q

Why can an infrared spectrophotometry be used to measure CO2?

A

b/c CO2 is polar, asymmetric, and polyatomic

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17
Q

Winter’s formula

A

PCO2 = (1.5 * bicarb) + 8 +/- 2
-if not within expected range -> more than 1 acid/base disturbance

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18
Q

what causes a hyperchloremic hypokalemic non-anion gap metabolic acidosis

A

diarrhea

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19
Q

pH changes w/ vomiting and diarrhea

A

vomiting goes up so does pH (met alk)
diarrhea goes down, so does pH (met acidosis)

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20
Q

Why do we get histamine release from rapidly giving vancomycin?

A

Histamine release

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21
Q

Why does cefepime cause worsening hypoTN in pt w/ E Coli

A

abx tx of gram negative bacteria -> release of lipopolysaccharide -> significant immune response -> release of multiple cytokines incl nitric oxide -> worsens sepsis response

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22
Q

several hrs after uneventful spinal, weakness on plantar flexion of L ankle, red sensation on L posterior thigh, perineal paresthesias, no back pain, able to void, dx?

A

conus medullaris injury
-assoc w/ multiple peripheral n unilateral or b/l

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23
Q

post spinal paraplegia, saddle anesthesia, and urinary/fecal retention

A

cauda equina syndrome

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24
Q

contraindications for spinal cord stimulator

A

untreated psychological dx
substance abuse
lack of social support

sepsis
coagulopathy
prev surgery/trauma obliterating spinal canal
localized infection
spina bifida

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25
Q

Indications for SC stimulator

A

-thoracic and lumbar post-laminectomy syndrome
-post-herpetic neuralgia
-phantom limb pain
-cauda equina syndrome
-CRPS I and II
-cardiovascular angina
-lower extremity ischemic pain
-chronic cervical radiculopathy
-n root injury

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26
Q

Which coronary vessels are most likely to vasospasm?

A

right coronary artery and its branches

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27
Q

Physiologic effects of hypothermia

A

confusion and sedation
inc sz threshold

dec RR, inc pulm vascular resistance

dec cardiac output, QT prolongation, arrhythmias, vasoconstriction

cold diuresis

coagulopathy, thrombocytopenia

dec granulocyte count, dec monocyte activity

hyperglycemia, dec drug metabolism and clearance

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28
Q

at what temp do bradycardia and hypoTN occur 2/2 hypothermia

A

< 28C

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29
Q

why concern for shivering in PACU?

A

inc O2 consumption by 400% -> puts pts w/ coronary artery dx at risk of MI

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30
Q

Recommendations for TBI ICU pts

A

ICP < 20
SaO2 > 95%
Glucose < 180
CPP 50-70
PaCO2 35-40
Temp < 37

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31
Q

ppx needed for TBI ICU pts

A

sz, stress ulcer, DVT

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32
Q

Two most common causes of postop jaundice

A

hemolysis
breakdown of extravasated blood or hematoma

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33
Q

How to eval postop jaundice

A

pre-hepatic, intra-hepatic, post-hepatic

pre-hepatic: inc indirect bili (hemolysis, resolution hematoma)

intra-hepatic: hypoTN, TPN, hypoxia, ischemia, drugs, hepatitis, sepsis (inc AST/ALT)

post-hepatic: inc direct bili: gallstones, biliary stricture, bile leaks

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34
Q

tx for HIT

A

stop heparin and start argatroban or bivalirudin

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35
Q

heparin-induced thrombocytopenia caused by what Ab?

A

Ab against complexes of platelet-factor 4 and heparin
-ab bind to plts -> activate plts -> thrombosis and consumptive thrombocytopenia

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36
Q

4T score for HIT

A
  1. thrombocytopenia (30-50%)
  2. timing of thrombocytopenia (5-10 d after heparin start)
  3. thrombotic complications
  4. lack of other causes of thrombocytopenia
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37
Q

dx of HIT

A

serotonin-release assay is the gold standard
-ELISA for plt factor 4 antibody

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38
Q

hemophilia A factor def and inheritance pattern

A

VIII
X-linked recessive

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39
Q

hemophilia B factor def and inheritance pattern

A

IX
X-linked recessive

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40
Q

Hemophilia C factor def and inheritance pattern

A

XI
autosomal recessive

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41
Q

symptoms in hemophilia A and B

A

spontaneous bleeding in joints, m, orangs

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42
Q

symptoms in hemophilia C

A

NO spontaneous bleeding -> initial steps in hemostasis unaffected -> amplification of thrombin response and resistance of clot affected
**more clinically relevant in trauma or surgery

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43
Q

Acquired hemophilia: how? dx? tx?

A

assoc w/ pregnancy, cancer or connective tissue d/o
-antibodies against factor VIII
-symp: subcutaneous bleeding w/ soft tissue hemoatomas
-labs: prolonged PTT, no correction of low factor VIII mixing study
-tx: bypass agent recombinant activated factor VII, or prothrombin complex concentrate
long term: immunosuppression

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44
Q

What’s in prothrombin complex concentrate

A

factors II, VII, IX, X
Vitamin K dpt clotting factors

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45
Q

Promote sickling intraop

A

hypothermia
hyperthermia
hypoxemia
hypotension
hypovolemia
acidosis

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46
Q

Hct goal for Sickle cell dx prior to surgery

A

30-40%

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47
Q

Recs for sickle cell dx prior to surgery

A

-have baseline hct and hg -> ideally w/ hematologist
-exchange transfusion recommended to get HbS proportion < 30%
-advanced type and cross due to large titer of antibodies, can take hours

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48
Q

lupus anticoagulant effect on blood test

A

increase in PTT (b/c phospholipid in test binds with it)
**actually prothrombotic

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49
Q

clotting cascade

A
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50
Q

What’s in cryo?

A

fibrinogen
fibronectin
vwF
factors VIII and XIII

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51
Q

liver dx what lab changes first?

A

Prolonged PT due to dec in factor VII

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52
Q

what type of transfusion reaction is assoc w/ leukopenia

A

TRALI

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53
Q

pathophys in TRALI

A

antibodies from donor attack neutrophils/leukocytes in recipient -> agglutination of leukocytes in pulm circulation => TRALI

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54
Q

RF for TRALI

A

critically ill pts
-chronic alcohol or tobacco abuse
-s/p liver transplant
-mechanical vent w/ high peak airway pressures
-pts with positive fluid blanace

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55
Q

How to dec incidence of TRALI?

A

leukoreduction
-having male plasma donors (less risk of HLA antibodies)

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56
Q

Timeframe for TRALI

A

new acute lung injury/ARDS w/i 6 hours of transfusion

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57
Q

What blood components most assoc w/ TRALI

A

apheresis plt conc
high plasma-volume plasma
whole blood
plasma or whole blood from female donors higher

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58
Q

Blood tests for TRALI

A

CBC
bili
haptoglobin
direct antiglobulin test (Coombs)
HLA antigen typing

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59
Q

r value: TEG measurement and how to tx

A

initial clot formation
tx: clotting factors (FFP)

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60
Q

K value: TEG measurement and how to tx

A

time to reach certain clot strength
tx: clotting factors or fibrinogen

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61
Q

alpha angle value: TEG measurement and how to tx

A

speed of clot formation
tx: clotting factors or fibrinogen

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62
Q

Max amplitude value: TEG measurement and how to tx

A

strength of clot
tx: plt count, plt function, and/or fibrinogen

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63
Q

LY30 value: TEG measurement and how to tx

A

fibrinolysis
tx: TXA or aminocaproic acid

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64
Q

Coagulation by hypothermia on TEG

A

will show up normal b/c blood sample is heated to 37!

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65
Q

what does vWF do”?

A

forms linkages b/c plts and subendothelial structures, and acts as a carrier for factor VIII

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66
Q

How does desmopressin work for vWD?

A

most effective for mild bleeding or bleeding ppx for minor surgeries
-causes release of vWF from endothelial cells -> improves plt function and shortens bleeding time

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67
Q

PPx for major surgery for vWD type 1, bleeding despite desmopressin, or significant bleeding tx

A

factor VIII-vWF concentrate

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68
Q

First like ppx and tx for vWD type 2 and 3

A

factor VIII-vWF concentrate

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69
Q

Difference b/w types of vWD

A

vWD type 1: quanitative, dec vWF production, shorted factor VIII 1/2 life

type 2: qualitative, issues w/ plt binding

type 3: quantitative, complete absence of vWF, severe factor VIII def

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70
Q

1st line for treatment of hemophilia A w/ minor bleeding or minor surgery

A

Desmopressin

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71
Q

Tx for active bleeding in hemophilia A

A

Cryo
-high concn of factor VIII and fibrinogen

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72
Q

tx for Hemophilia A pts if they do not respond to exogenous human factor VIII infusions

A

-have anti-factor VIII antibodies
-tx: porcine factor VIII, recominant factor VIIa or recombinant factor IIa
(b/c it will activate the extrinsic and common pathway)

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73
Q

Def of heparin resistance

A

-ACT < 480 after 500U/kg IV heparin
-ACT < 400 at anytime during CPB

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74
Q

Which coag factors does antithrombin III inactivate

A

IIa (thrombin)
VII, IX, X, XI, XII

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75
Q

Tx for heparin resistance

A

FFP
antithrombin 3 (cocentrate or recombinant)

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76
Q

RF for heparin resistance

A

AT levels < 60^ of normal
plts > 300k
preop heparin therapy
use of LMWH
age > 65

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77
Q

What is HgA made of?

A

2 alpha and 2 beta
adult Hg

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78
Q

What is HgF made of?

A

2 alpha and 2 gamma
fetal Hg

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79
Q

what causes febrile nonhemolytic transfusion reaction?

A

release of cytokines due to WBC leakage (IL-1)

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80
Q

way to prevent febrile nonhemolytic transfusion rxn?

A

leukoreduction

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81
Q

MOA acute hemolytic transfusion reaction

A

Recipient antibodies targeting donor RBCs

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82
Q

how quickly does acute hemolytic transfusion rxn occur and symp?

A

immediately or w/i a few minutes
-fever, chills, flank and back pain, hypoTN -> renal failure, jaundice, DIC

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83
Q

dx post transfusion HTN, elvated CVP, resp distress, no fever

A

TACO
-give diuretics

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84
Q

what blood product most likely to give citrate toxicity?

A

FFP

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85
Q

hypocalcemia EKG

A

prolonged QT
narrow QRS
flattened T waves

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86
Q

How does Hg compensate w/ anemia

A

R shift of oxy-Hg dissocation curve
-due to inc 2,3 DPG
-inc acidosis (lactic)

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87
Q

Body compensations for chronic anemia

A

inc cardiac output (inc SV due to dec afterload b/c dec blood viscosity)
-inc symp tone (inc HR and contractility)
-R shift of oxy-Hg dissocation curve

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88
Q

Teardrop shape on TEG indicates

A

inc fibrinolysis

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89
Q

Parts of a TEG

A
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90
Q

What is LY30 on TEG

A

percent lysis at 30 minutes

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91
Q

What does R value represent on TEG

A

initial clot formation

92
Q

K on TEG

A

time to certain clot strength (20 mm)

93
Q

alpha angle on TEG

A

speed of clot formation

94
Q

MA on TEG

A

strength of clot
-maximum width

95
Q

A1c for DM dx

A

higher than 6.5%

96
Q

What is fructosamine?

A

test in DM that is a shorter time span than Hg A1c (only 1-2 weeks compared to 3 months)
-used in pts with dec RBC lifespan (hemolytic anemia, SCD)

97
Q

Inheritance pattern for vWD type I

A

autosomal dominant

98
Q

Inheritance pattern for vWD type II

A

auto dom

99
Q

Inheritance pattern for vWD type III

A

auto rec

100
Q

severe vWD PTT

A

prolonged due to insuff factor VIII

101
Q

SE of desmopressin admin for vWD

A

hypoNa and water retention b/c structurally similar to ADH

102
Q

Timing of desompressin admin

A

-takes 30 minutes to work, can only repeat dosing every 12 hrs or risk of tachyphylaxis (depletion of stores)

103
Q

tx of type I vWD

A

DDAVP

104
Q

tx of type II vWD

A

trial of DDAVP, avoid if known type IIB

105
Q

tx of type III vWD

A

vWF concentrate

106
Q

tx of acquired vWF def

A

trial DDAVP -> if nothing vWF concentrate

107
Q

tx of Ab-mediated acquired vWF def

A

IVIG

108
Q

if unable to acquire concentrated vWF, what is tx for extensive bleeding w/ vWD?

A

cryo! much more vWF than FFP

109
Q

Acquired met-Hg causes

A

topical anesthesics (esp benzocaine)
-dapsone (tx leprosy)
-antimalarials
-inhaled nitric oxide
-rasburicase (dec uric acid)
-nitrate and nitrites
-aniline dyes

110
Q

tx for metHg

A

methylene blue

111
Q

tx for metHg if G6PD def

A

ascorbic acid
(vit C)

112
Q

tx for metHg if taking serotonergic meds

A

ascorbic acid
(vit C)

113
Q

MOA Met-Hg

A

ferrous iron (Fe2+) converted to ferric (Fe3+) -> reduces O2 carrying capacity of Hg and dec delivery to tissues

114
Q

awake pt with blood loss acid-base status

A

metabolic acidosis (lactate from dec perf)
compensatory resp alk (hyperventilate! awake person lol)

115
Q

MOA Factor V Leiden d/o

A

resistance to activated protein C -> protein C can’t cleave factor V or VIII -> factor V procoag inc production of thrombin -> hypercoagulable

116
Q

1st clot w/ factor V Leiden tx

A

unfractionated heparin or LMWH immediately -> warfarin or DOAC for minimum 3-6 months
INR goal: 2-3

117
Q

When do pts with factor V Leiden need long-term therapy?

A

-2 or more spontaneous thromboses
-1 spontaneous thrombosis if pt has factor V Leidin + another prothrombotic mutation
-one spont life-threatening thrombosis (near fatal PE)
-one spot thrombosis at unusual side (cerebral or mesenteric v)

118
Q

Prothrombotic mutations

A

Antithrombin Def
protein S def
factor V Leiden

119
Q

Type I HIT symp and timiing

A

mild thromboctopenia, no thrombosis
-2-5 days of heparin
-heparin binds to plts at GPIb receptors -> release of ADP -> plt aggregation

120
Q

Type II HIT

A

5-9 days after heparin admin
-more severe, pts < 100k, thrombosis
-antibodies to heparin-plt factor 4 complex

121
Q

gold standard for HIT dx

A

heparin-induced serotonin release assay

122
Q

MOA bivalirudin

A

direct thrombin inhibitor

123
Q

CI to bivalirudin

A

renal failure (20% renally cleared)

124
Q

treatment for CN toxicity

A

amyl nitrate and sodium nitrate
hydroxocobalamin

125
Q

goal for factor replacement for hemophilia before mild and major surgery

A

mild > 40%
major 100%

126
Q

in pts with hemophilia A but factor VIII inhibition antibodies, tx?

A

PCC or recombinant factor VII

127
Q

Hemophilia: PTT, PT, bleeding time, plt count

A

PTT prolonged
PT norm
bleeding time norm
plts norm

128
Q

vWD PTT, PT, bleeding time, plt count

A

PTT prolonged
PT normal
bleeding time prolonged
plts normal

129
Q

DIC PTT, PT, bleeding time, plt count

A

PTT prolonged
PT prolonged
bleedging time prolonged
plts dec

130
Q

Vit K def PTT, PT, bleeding time, plt count

A

PTT prolonged
PT prolonged
bleeding time normal
plts normal

131
Q

Multiple myeloma MOA

A

cancer of plasma cells (WBC resp for Ab prod)
-proliferation of tumor cells in bone marrow inhibit RBC prod -> normocytic normochromic anemia
-inc expression of RANKL -> activates osteoclasts and causes bone destruction -> bone pain, fx, hyperCa
-renal failure from hyperCa, excretion of Ab light chains
-neuro symp: infiltration in peripheral n, hyperCa lethargy and confusion, damage to vertebrae cause compression
-freq infxns (overprod ineffective Ab and immunosupp from chemo)

132
Q

When does monitoring with enoxaparin need to occur?

A

extreme BMIs (high or low)
renal impairment
pregnant patients

**factor Xa activity

133
Q

tx for antithrombin III def

A

ATP3 or FFP (incl AT3)

134
Q

4T’s for HIT

A
  1. Thrombocytopenia
  2. Timing of reduced plt count
  3. presence of Thrombosis
  4. exclusion of other causes of thrombocytopenia
135
Q

MCC of mortality from transfusion

A

TACO

136
Q

signs of TACO

A

new onset resp distress
inc brain natriuretic peptide
inc CVP
L heart failure
pulm edema on radiology

137
Q

How to confirm acute hemolytic transfusion reactions

A

direct antiglobulin test

138
Q

How to prevent anaphylaxis w/ blood

A

for pts with IgA def
-washed RBCs

139
Q

morbidly obese pts have inc risk of

A

bioactive mediators -> abnormal lipids, insulin resistance, inc inflammation, coagulopathies

140
Q

obese pts coagulopathy

A

higher levels of fibrinogen, factor VII, factor VIII, vWF, plasminogen activator inh 1 -> hypercoag

141
Q

obese pts cardiac output

A

higher cardiac output -> blood volume must also reach adipose tissue

142
Q

what does vWF do??

A

plasma protein that assists plts to adhere to sites of vascular injury and stabilizes clotting factor VIII

143
Q

which factor interacts w/ vWF?

A

factor VIII -> vWF prevents degradation of factor

144
Q

Which meds promote stabilization of clots?

A

aminocaproic acid
tranexamic acid
topical clotting products (oxidized regenerated cellulose or topical thrombin)

145
Q

What’s in cryo?

A

factor VIII
factor XIII
fibrinogen
vWF

146
Q

Hemorrhage in vWD

A

vWF-factor VIII concentrates
DDAVP
Cryo
antifibrinolytics
topical clotting products

147
Q

best way to reduct cerebral ischemia during circulatory arrest

A

hypothermia
-dec cerebral metabolic consumption of O2 -> longer ischemic time

148
Q

target temp w deep hypothermic circulatory arrest

A

15-19 C

149
Q

Dec in brain metabolism w/ change in temp

A

dec 1 C -> 6-7% dec in CMRO2

150
Q

Butyrylcholinesterase responsible for metabolism of what

A

succinylcholine, mivacurium, ester local anesthetics

151
Q

Dibucaine number

A

% of inhibition of butyrylcholinesterase enzyme by dibucaine
-normal: 80% activity should be inhibited
-heterozygous atypical: inhibit 60% activity
-butylcholinesterase def inhibits 20% of activity

152
Q

how do opioids dec ventilation

A

activation of mu receptors in ventrolateral medulla

153
Q

renal compensation for acute resp acidosis

A

10 CO2 = 1 bicarb

154
Q

renal compensation for chronic iresp acidosis

A

10 CO2 = 4-45 bicarb

155
Q

N/V intrathecal v IV opioids

A

same

156
Q

pruritis intrathecal v IV opioids

A

higher pruritis w/ intrathecal

157
Q

what fibers to intrathecal opioids affect

A

C and A-fibers

158
Q

which inhaled anesthetic potentiates NMB most?

A

DES
Des > sevo > iso > nitrous oxide

159
Q

which abx prolong roc?

A

aminoglycosides
clindamycin
polymyxins
tetracyclines

160
Q

affect of anticonvulsants on NMB?

A

phenytoin AND carbamazepine
acute: potentiation
chronic: attenuation

161
Q

Lithium and effect on NMB

A

potentiate

162
Q

local anesthetics and effect on NMB

A

potentiate

163
Q

Why changes w/ roc from phenytoin/carbamazepine?

A

acutely: potentiates roc b/c dec ACh release
chronically: causes upregulation of ACh receptors

164
Q

Which NMB are unaffected by phenytoin?

A

Mivacurium and Atracurium
(metabolized by pseudocholinesterase)

165
Q

Pancuronium metabolism

A

excreted renally , minor metabolism from liver

166
Q

Effects of pancuronium besides NMB

A

metabolite 3-OH-pancuronium -> vagolytic and sympathomimetic effects
-counteract bradycardia effects w/ high-opioid dosing
-blocks reuptake of NE

167
Q

What to do if Ace inh hypoTN after induction

A
168
Q

Methylene blue and SSRIs

A

CI! methylene blue is an MAO inhibitor -> serotonin syndrome

169
Q

Methylene blue and vasoplegia

A

methylene blue can block vasodilatory effects of nitric oxide (inhibits guanylate cyclase)

170
Q

Best way to avoid protamine reactions

A

infuse it slowly for greater than 5 minutes

171
Q

Why do get protamine reactions?

A

release of nitric oxide from endothelial cells
mast cell degranulation
histamine release
-rapid infusion causes formatino of large protamine-heparin complexes that deposit in pulm circulation

172
Q

Type I protamine rxn

A

mild hypoTN w/ normal filling and airway pressures
-give volume, vasoactive meds, and slow infusion

173
Q

Type II protamine rxn

A

mod-severe hypoTN w/ anaphylactoid features

174
Q

Type III protamine rxn

A

complexes deposit in pulm circulation -> release of vasoactive mediators -> severe hypoTN, inc pulm a pressures, and possible RV failure

175
Q

Which class of local anesthetic more likely to give allergic reaction?

A

Esters b/c PABA

176
Q

If allergic to amide local anesthetic, what is pt most likely allergic to?

A

Methylparaben (preservative)

177
Q

Preservative in lidocaine w/ epi vials that can elicit allergic rxn?

A

Sulfites: Na metabisulfite

178
Q

if pt has -caine allergies but needs sutures what to give?

A

1% diphenhydramine

179
Q

Normal dibucaine number

A

70-80

180
Q

homozygous atypical dibucaine number

A

50-50

181
Q

pseudocholinesterase def dibucaine number

A

20-30

182
Q

Why is thiopental so quick on and off?

A

Highly lipid soluble
highly protein bound
high nonionized fraction
redistributes rapidly from central to peripheral compartments

183
Q

Why prolonged effect of thiopental in elderly pts?

A

slower redistribution
reduction in hepatic metabolism and renal clearance

184
Q

What would cause thiopental to have a larger heart and brain conc in a single dose?

A

volume depletion
low serum albumin (less protein bound)
acidosis (nonionized fraction increases)

185
Q

How are barbiturates biotransformed?

A

hepatic oxidation -> inactive water soluble metabolite excreted in urine

186
Q

Methohexital v thiopental which cleared my liver faster?

A

Methohexital (greater hepatic extraction)

187
Q

CI to barbiturates

A

acute intermittent porphyria b/c hepatic enzyme induction
(exp phenobarbital b/c renally excreted unchanged)

188
Q

half life of barbiturates and children

A

shorter 1/2 life b/c inc hepatic clearance

189
Q

why can’t you use liposomal bupi and licocaine together?

A

will disrupt liposomal barrier in bupi -> LAST

** can be done if lidocaine injxn 20 minutest before liposomal bupi

190
Q

what affects duration of action of local anesthetics?

A

drugs lipophilicity
degree of tissue protein-binding
co-admin of additives (epi)

191
Q

dilution of liposomal bupi

A

avoid w/ water or hypotonic solution (disrupts liposome)

192
Q

Ketamine effect on chronically ill pts

A

ketamine has direct negative inotropic effects -> hypoTN and dec cardiac output b/c no compensatory sympathetic response

193
Q

What meds to avoid during pheochromocytoma surgeries?

A

ketamine
ephedrine
meperidine
desflurane
(all cause inc catecholamine release)

194
Q

Selective alpha 1 antagonists

A

Prazosin
Doxazosin
Terazosin

195
Q

Phenoxybenzamine MOA

A

non-selective alpha 1 and alpha 2 blocker
-long acting
**can get worsening tachycardia and HTN due to alpha 2 effects blocked

196
Q

Phentolamine MOA

A

non-selective alpha 1 and 2 blocker
short acting (10-15 min)
**can get worsening tachycardia and HTN due to alpha 2 effects blocked

197
Q

Mirtazapine MOA

A

selective alpha 2 blocker
tx depression

198
Q

how long after sugammadex does a pt need a 2nd form of BC?

A

7 days

199
Q

Possible SE of sugammadex

A

-bradycardia!
-anaphylaxis/hypersentivity rxn
-inactivation of hormonal contraceptives
-inc PT/INR, PTT (1 hr)
-

200
Q

Hypocalcemia EKG changes

A

narrow QRS duration
prolonged QT

201
Q

Hypercalcemia EKG changes

A

wide QRS, short QT
-J waves in severe hyperCa

202
Q

HypoK EKG

A

narrow QRS, prolonged QT
flattened/inverted T and U waves

203
Q

hyperK EKG

A

wide QRS
peaked T waves
prolonged PR

204
Q

acid-base changes from acetazolamide

A

hyperchloremic metabolic acidosis
-can’t reabsorb bicarb -> wasting of Na and bicarb -> inc reabsorption of Cl

205
Q

What dose of methadone inc risk of prolonged QT most likely

A

> 120 mg/day

206
Q

What abx can’t be used w/ methadone?

A

Ciprofloxacin (fluoroquinolone) -> prolongs QT

207
Q

What antiemetics can be used w/ methadone?

A

Dexamethasone
Aprepitant
Palonosetron
-don’t prolong QT

208
Q

codine to morphine

A

0.15

209
Q

Hydrocodone to morphine

A

1

210
Q

Oxycodone to morphine

A

1.5

211
Q

Fentanyl mcg/hr to morphine

A

2.4

212
Q

Hydromorphone to morphine

A

4
(2mg hydromorphone = 8 morphine)

213
Q

Methadone to morphine

A

1-20mg/day : 4
21-40mg/day: 8
41-60mg/day: 10
>61-80: 12

214
Q

Remifentanil metabolism

A

nonspecific tissue and blood esterases

215
Q

Esmolol metabolism

A

RBC esterases

216
Q

What does pseudocholinesterase metabolize?

A

succ
mivacurium
ester local anesthetics
cocaine
heroin

217
Q

What can lower pseudocholinesterase activity?

A

severe liver dx
plasmapheresis
ACE inh
pregnancy
organophosphates

218
Q

What medication can cause significant prolongation of succ?

A

Echothiophate
-up to 2 weeks after d/c

219
Q

What medications for ventricular tachycardia?

A

Phenytoin or Lidocaine
-binds to VG Na channels -> prolongs phase 0 of ventricular depolarization -> prolong QRS and shortens repolarization

220
Q

Phenytoin effects other than anti-epileptic

A

-termination of ventricular arrhythmias
-induce P450 in liver
-gingival hyperplasia
-at start enhance NMB
-chronic dec NMB

221
Q

Class 1 antiarrhythmics work where?

A

Na channel blocker
-widens QRS and targets ventricle

222
Q

Class 2 antiarrhythmics work where?

A

phase 4: K rectifier
beta blockers: propranolol, metoprolol
-slows conduction through the AV node

223
Q

Class 3 antiarrhythmics work where?

A

Phase 3
potassium channel blockers: amiodarone, sotalol

224
Q

Class 4 antiarrhythmics work where?

A

phase 2: calcium channel blocker
verapamil, diltiazem

225
Q

what block? identify structures

A

interscalene

226
Q

Common side effects of interscalene n block

A

-phrenic n blockade 100%
-horners syndrome (blockade of sympathetic chain)

rare: PTX, RCLN injury

227
Q

Most to least likely locations for last

A

IV > intercoastal > caudal > epidural > brachial plexus and sciatic

Truelearn Advanced Exam (15 decks)

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