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ABSITE > hematology & infectious disease > Flashcards

hematology & infectious disease Flashcards

1
Q

initial thrombus formation steps?

A

plt adhesion > shape change (flat), ADP TXA2 granule release > recruitemnt > aggregation.

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2
Q

vascular injury response (3)?

A
  1. vasoconstriction
  2. plt adhesion
  3. thrombin generation
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3
Q

intrinisic pathway?

A

collagen + prekallikrein + HMW kininogen + 12
activate 11
activate 9
add 8
activate 10
add 5
2
1 (fibrin)

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4
Q

extrinisic pathway?

A

tissue factor + 7
10 add 5
2
1

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5
Q

how is thrombin key to coagulation?

A

2 (thrombin) activate 1a to 1, 5 and 8, activates plt

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6
Q

what does fibrin actually do?

A

plt plug to bind plt via Gp2BA

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7
Q

normal anticoagulation (3)?

A
  1. AT3 antithorombin 3; binds and inhibits 2 (thrombin), 9, 10, and 11
    activated by heparin
  2. protein C: degrades 5 and 8 and fibrinogen (1)
  3. protein S: protein C cofactor
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8
Q

normal fibrinolysis (2)

A
  1. tissue plasminogen activator (TPA) released from endothelium and converts plasminogen to plasmin
  2. plasmin: degrades 5, 8, fibrinogen, and fibrin
    * alpha 2 antiplasmin: inhibitor of plasmin (released from endothelium)
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9
Q

factor with shortest half life?

A

7

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10
Q

whose activity is lose in stored blood but not FFP?

A

due to lability….
5 and 8.

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11
Q

which factor not synth’d in liver?

A

8 with vonWillebrand factor.

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12
Q

Vit K factors?

A

2, 7, 9, 10, C, S

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13
Q

Vit K vs FFP onset?

A

Vit K 12 hours (IV), FFP is immediate

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14
Q

half life RBC, plt, PMN?

A

RBC 120 days, plt 7 days, PMN 1-2 days.

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15
Q

function of prostacyclin PGI2?

A

from endothelium. PREVENT CLOT.
decrease plt aggregation, promote vasodilation (antagonizes TXA2) increases cAMP in plt

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16
Q

function of thromboxane TXA2?

A

from platelets. INCREASE CLOT.
increase plt aggregation, promote vasoconstriction.
triggers Ca release in plt. exposes Gp2B3A-R and causes plt-plt bind, plt-collagen (GpIb-R).

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17
Q

cryoprecipitate contents?

A

vWF-8 and fibrinogen.

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18
Q

indication for cryoprecipitate?

A

von Willebrand’s disease, hemophilia A (8), low fibrinogen.

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19
Q

FFP contents?

A

ALL coagulation factors, C, S, AT-3**.

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20
Q

DDAVP and conjugated estrogen effect on clotting

A

cause release of 8 and vWF from endothelium.

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21
Q

prothrombin time measures?

A

extrinsic pathway… 2, 5, 7, 10, fibrinogen.
best to see liver synthetic function

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22
Q

partial thromboplastin time measures?

A

measures intrinsic (cannot see 7 and 13 fibrin stabilizing factor).
70-90 AC

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23
Q

activated clotting time goal

A

150-200 routine AC
>480 for bypass.

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24
Q

vWB disease AD vs AR?

A

Type 3 is AR. Type 1 and 2 are AD.

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25
Q

vWF role?

A

GpIb-R on plt link to GpIb on collagen*.

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26
Q

Type I vWB disease?

A

mild bleeding, most common*
issue: reduced vWF
treat: recomb 8-vWF, DDVP, cryo.

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27
Q

Type 2 vWB disease?

A

issue: defect in vWF molecule; doesn’t work
treat: recomb 8-vWF, cryo, DDAVP.

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28
Q

Type 3 vWB disease?

A

AR. rare. complete deficiency.
treat: recomb 8-vWF, cryo (DDAVP won’t work).

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29
Q

DDAVP

A

desmopressin; stim release of vWF from endothelium.

use in uremic pts 2/2 ESRD as well

use in Hemophilia A and vWB disease

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30
Q

hemophilia A deficiency?

A
  1. sex linked recessive.
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31
Q

how does hemophilia A present?

A

hemarthrosis.

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32
Q

coag abnormality in hemophilia A?

A

PTT prolonged, PT normal

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33
Q

newborns with hemophilia A?

A

might be OK because factor 8 crosses placenta.

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34
Q

if bleeding, hemophilia A? how to treat.

A

ice/immobilize (if joint) +++ factor 8 concentrate, or cryoprecipitate.

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35
Q

hemophilia B deficiency?

A
  1. sex linked recessive.
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36
Q

how to preop 8 and 9 levels in hemophilia pre and postoperatively?

A

100% preop.
A/8: 80-100% for 2 wks after OR.
B/9: 30-40% 2-3 days after OR.

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37
Q

coag abnormality in hemophilia B?

A

PTT prolonged
PT normal

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38
Q

treat hemophilia B bleeding?

A

recombinant 9 or FFP.

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39
Q

factor 7 deficiency bleeding? how to treat.

A

prolonged PT
normal PTT
treat wiht recombinant 7 or FFP.

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40
Q

acquired thrombocytopenia Rx-related etiology?

A

heparin
H2 blockers famotidine.

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41
Q

glanzmann’s thrombocytopenia

A

G2B3A-R deficiency on plt
cannot bind together via fibrin
treat: plt

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42
Q

Bernard Soulier thrombocytopenia?

A

Gp1b-R deficiency on plt.
treat: plt

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43
Q

what level of uremia causes plt dysfxn

A

BUN > 60-80.
inhibits by inhibiting release of vWF.
treat: HD, DDAVP for acute reversal, cryo (if bleeding)

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44
Q

HIT Ab

A

IgG heparin-PF4 Ab causing plt destruction.

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45
Q

HIT pathogenesis

A

plt die… causing plt aggregation and thrombosis***

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46
Q

HIT 1 vs 2

A

1: non-immune (don’t treat)
2: IgG Abx - Factor 4

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47
Q

clinical manifestation of HIT?

A

plt < 100 but >20, plt drop > 50% from admission, thrombosis on heparin.
WHITE clot. ALL WITHIN 5-10 DAYS OF EXPOSURE.

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48
Q

how to dx HIT?

A

ELISA for Ab’s, SRA (serotonin release assay).

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49
Q

treat HIT?

A

stop heparin, start argatroban (direct 2 inhibitor); don’t give plt

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50
Q

DIC lab abnormalities

A

thrombocytopenia
low fibrinogen
high fibrin split products (high D dimer)
prolonged PT
prolonged PTT

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51
Q

DIC etiology

A

intiated by tissue factor. but multifactorial (treat the cause).

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52
Q

ASA MOA?

A

inhibit COX, decrease TXA2.

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53
Q

when to stop ASA and plavix and coumadin?

A

7 days preop.

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54
Q

plavix/clopidogrel MOA?

A

ADP-R antagonist.

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55
Q

what if new stent (need plavix) and need to go to OR?

A

bridge with eptifibatide (integrilin) Gp2B3A inhbitor

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56
Q

plt goal for periop?

A

50K preop
20K postop

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57
Q

bleeding issues after prostate surgery?

A

release of UROKINASE can activate plasminogen causing thrombolysis.
treat: amicar (inhibit fibirnolysis by inhibiting plasmin)

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58
Q

factor V leiden MC what?

A

MC congenital hypercoagulability d/o
resistance to activated protein C (defect is on factor V)

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59
Q

how to treat Factor V leiden?

A

heparin, warfarin

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60
Q

how to treat hyperhomocysteinemia?

A

folic acid, B12.

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61
Q

G20210A

A

prothrombin gene defect causing hypercoagulability
treat: AC

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62
Q

protein C/S deficiency tx?

A

AC.n

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63
Q

antithrombin 3 deficiency?

A

hypercoagulable.
heparin doesn’t work…
treat: recombinant AT-3 concentrate, FFP, warfarin

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64
Q

Polycythemia vera treat?

A

keep Hct < 48, plt < 400 before OR
treat: phlebotomy, ASA, hydroxyurea

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65
Q

APLS

A

antiphospholipid antibody syndrome .
ass’d SLE
PTT prolonged but HYPERCOAGULABLE
Ab to phospholipids: cardiolipin (mitochondria) and lupus anticoagulant (cell membrane)

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66
Q

dx APLS?

A

PTT prolonged, not better with FFP
positive Russell viper venom time
false positive RPR test for syphilis

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67
Q

treat APLS?

A

heparin, warfarin

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68
Q

MC acquired hypercoagulable state?

A

tobacco.w

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69
Q

why anticoagulate on bypass?

A

Factor 7 (Hageman factor) is activated

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70
Q

who is most susceptible to warfarin skin necrosis?

A

protein C deficient ppl
because C and S short half life so have a relatively hyperTHROMBOTIC state.

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71
Q

Virchow’s triad?

A
  1. stasis
  2. endothelial injury
  3. hypercoagulability.
72
Q

postop DVT tx?

A

1st: coumadin 6 mos
2nd coumadin 1 yr
3rd or PE: lifetime coumadin

73
Q

amicar indication? = a-FIBRINOLYTIC

A
  1. urokinase bleeding after prostate
  2. DIC
  3. persistent bleeding after bypass
  4. thrombolytic overdoses

inhibits PLASMIN.

74
Q

warfarin MOA

A

inhibits Vit K dependent carboxylation of glutamic residues on Vit K factors

75
Q

heparin MOA

A

antithrombin 3 activator
increase neutralization of 2a prothrombin and Xa (pre X)

lovenox does not neutarlize 2a. just X.

76
Q

half life of heparin?

A

60-90 min.

77
Q

heparin vs warfarin placental barrier?

A

heparin does not cross; warfarin does.

78
Q

SE long term heparin?

A

osteoporosis, alopecia.

79
Q

protamine reaction?

A

hypotension, bradycardia, decreased heart function (cross reacts with NPH insulin or previous protamine exposure).

80
Q

argatroban MOA

A

direct 2 inhitor REVERSIBLE.
half life 50 min
good for HIT.

81
Q

bivalrudin MOA

A

direct 2 inhibitor REVERSIBLE
half life 25 min

82
Q

argatroban vs bivalrudin metabolized by?

A

argatroban: liver
bivalrudin: proteinase enzymes in blood

83
Q

hirudin MOA

A

direct 2 inhibitor IRREVERSIBLE. leeches.
most potent.

84
Q

ancrod?

A

malayan pit viper venom. stimulates TPA release.

85
Q

absolute CI for uro/strepto/tpa?

A

active internal, recent CVA/NSGY < 3 mos, intracranial pathology, recent GI bleed

86
Q

major CI for u/s/tpa?

A

recent < 10 day surgery, organ Bx, OB delivery, LV thrombus, active peptic ulcer, recent major trauma, uncontrolled HTN, recent eye surgery

87
Q

which blood products do not have HIV risk?

A

albumin, serum globulins

88
Q

how to treat warfarin coagulopathy?

A

IV Vit K with PCC (faster than FFP)

89
Q

4 factor vs 3 factor PCC

A

3: 2, 9, 10
4: 2, 7, 9, 10 + C/S

90
Q

Why does stored blood have higher affinity for oxygen?

A

Low 2,3 DPG causes increase affinity.

91
Q

What type of hypersensitivity is ABO incompatibility?

A

Type II. Ab mediated.

92
Q

Dx of acute hemolysis from ABO incompatibility?

A

Haptoglobin < 50
Free Hgb > 5
Increase IndBili

93
Q

sx of acute hemolytic transfusions reaction?

A

chills, lightheadedness, back pain
stop the transfusion!

94
Q

What is the most common transfusion reaction?

A

Febrile nonhemolytic transfusion reaction.

= urticaria, fever within 60 seconds

95
Q

Febrile nonhemolytic transfusion reaction pathogenesis?

A

Recipient Ab against donor WBCs. (Cytokine release).

96
Q

Mgmt febrile nonhemolytic transfusion reaction?

A

Stop transfusion, WBC filter and antihistamines for future transfusions.

97
Q

MOA TRALI?

A

Donor Ab against recipient WBCs causing clot in pulmonary capillaries.
Leads to pulmonary edema < 6… very fast.

causes hypotension and respiratory sx

98
Q

MC cause of death from transfuions reaction?

A

TRALI.

99
Q

MOA hypocalcemia in large transfusion?

A

Citrate in blood products binds Ca.

100
Q

Cell mediated immunity includes what cytokines and cells?

A

IL 2, IL 4, IFN-gamma
MHC class I on all nucleated cells to activate CD8
also CD4, NK cells, macrophages.

101
Q

how do NK cells work?

A

recognize non-self-MHC
recognize anything bound by a bunch of Abs

102
Q

MHC-II

A

DR DP DQ

on all APCs.
activates CD4 to then activate helper T cells
stimulates Ab formation after B cell interaction

103
Q

Ab mediated immunity (humoral) cytokines, cells?

A

IgM, IgG, IgA, IgD (on B cells), IgE

104
Q

what does helper T cell CD4 release? = cell mediated immunity

A

IL2, IL4 (mature to plasma), IFN y (activate macrophage) cytotoxic T cells CD8

105
Q

Which Ab are opsonins?

A

IgM and IgG

106
Q

Which Abs fix complement?

A

2 IgG adn 1 IgM

107
Q

Primary lymphoid organs?

A

Liver, bone, thymus.

108
Q

Secondary lymphoid organs?

A

Spleen and lymph nodes.

109
Q

How to manage nontetanus prone wounds, not UTD?

A

Give tetanus toxoid.

110
Q

How to manage tetanus prone wound if UTD?

A

Give tetanus toxoid still unless 3 doses have been within past 5 years.

111
Q

Tetanus prone wound not UTD.

A

Tetanus toxoid with tetanus Ig.

112
Q

MC anaerobe in colon? MC aerobe?

A

Anaerobe Bacteroides. Aerobe E. Coli.

113
Q

How to treat candiduria?

A

Just remove foley; watch. No antifungal.

114
Q

ART for HIV?

A

AZT zidovudie and ritonavir

115
Q

MC neoplasm in AIDS?

A

Kaposi.

116
Q

MC lymphoma in HIV?

A

Stomach > rectum; mostly B cell non-Hodgkins

117
Q

MC causes of UGI and LGI bleeds in HIV?

A

UGI: Kaposi, lymphoma
LGI: CMV, bacterial, HSV

118
Q

Primary SBP tx?

A

IV CTX

119
Q

Dx primary SBP?

A

Ascites > 250 PMN or positive Cx

120
Q

How to tx Hep C

A

Sofosbuvir and ribavirin

121
Q

exposure to unknown blood if not Hep B Vax’d

A

PEP within 72 hours of exposure (0.3%)

And HBIG and Hep B vaccine (23-37%)

Continue serology testing for Hep C don’t need to tx though (1.8%)

122
Q

MC infection in txp pt? Q

A

CMV

123
Q

What cell transmits CMV?

A

Leukocytes.

124
Q

CMV dx

A

Serology and stain: leukocyte inclusion bodies.

125
Q

Tx cmv

A

Ganciclovir (CMV Ig if severe infection)

126
Q

MC aspiration PNA spot?

A

Sup seg

127
Q

Brown recluse spider bite?

A

Tx: dapsone

128
Q

which nucleotide do sulfonamides effect?

A

purines; PABA analogue.

129
Q

which nucleotide does trimethoprim TMP effect?

A

purine; inhibits DHF reductase (dihydrofolate).

130
Q

bacteriostatic abx?

A

tetracycline, clindamycin, erythromycin, bactrim

131
Q

most common method of antibiotic resistance?

A

transfer of plasmids (I.e. of B-lactamase)

132
Q

MRSA resistance mechanism

A

mutation of cell wall binding protein.

133
Q

VRE resistance MOA?

A

mutation in cell wall binding protein. like MRSA.

134
Q

genamicin resistance MOA?

A

modifying enzymes leads to decrease in active transport of gentamicin into the bacteria.

135
Q

vanc peak and trough?

A

peak: 20-40 ug/mL
trough 5-10 ug/mL

136
Q

gentamicin peak and trough?

A

peak 6-10 ug/mL
trough <1 ug/mL

137
Q

what to do if peak too high?

A

decrease AMOUNT of each dosei

138
Q

what to do if trough too high?

A

decrease FREQUENCE of dose

139
Q

ampicillin coverage vs pencillins?

A

GPCs but also includes ENTEROCOCCI.

140
Q

augmentin and unasyn vs penicillins?

A

also includes GNRs and some anaerobic.

141
Q

anti-pseudomonals?

A

ticarcillin, piperacillin, cefepime, cipro, levo, ceftazidime, (+aminoglycodies… gentamicin)

142
Q

generations of cephs.

A

1st: GPC
2nd: GPC + GNR + little anaerobic
3rd: GNR some Pseudo.

143
Q

MOA cilastin with carbapenems?

A

prevents renal hydrolysis and increases half life

144
Q

aminoglycoside SE (rev and irrev)

A

reversible nephrotoxicity
irreversible ototoxicitya

145
Q

macrolide coverage

A

GPCs (think: PNA) and is prokinetic…

146
Q

MOA amphotericin

A

bind ergosterols in wall and laters membrane permeability

147
Q

SE of amphotericin (decreased by liposomal type)

A

nephrotoxicity, hypokalemia, anemia, fevers.

148
Q

MOA azoles

A

inhibit ergosterol synthesis. (for cell wall) via inhibiting cytochrome p450 14a-demethylase

149
Q

MOA micafungins

A

inhibit synthesis of cell wall GLUCAN.

150
Q

MOA amphotericin B

A

prevent fungal growth by binding cell membrane sterols and causing cell death via LYSIS.

liposomal = less nephrotoxicity

151
Q

TB Rx?

A

RIPE.
rifampin (RNA polymerase) - hepatotox, GI sx
Isoniazid (inhibit mycolic acid) + B6 - hepatotox
pyrazinamide - hepatotox
ethambutol - retrobulbar neuritis

152
Q

ganciclovir side effect (give for CMV)

A

myelotoxicity, CNS toxicity

153
Q

-cyclovir MOA

A

inhibit viral DNA polymerase.

154
Q

enterococcus and cephalosporins?

A

resistant to ALL CEPHALOSPORINS.

155
Q

Methotrexate and 5-FU nucleotide effect?

A

Purine.

156
Q

Leucovorin effect on methotrexate and 5-FU?

A

MTX: Reverse effects by re-supplying folate.
5-FU: increases toxicity

157
Q

TEG thromboelastography

A

clot formation and lysis to identify abnormalities at multiple points in the coagulation process

guide resuscitation efforts and selection of products to give coagulopathic patients

158
Q

how to treat the TEG

A

a-angle high - cryo
Lysis% high - TXA
Max amplitude low - plt
K time (20 mm clot) - cryo
R time (start clot) - FFP

159
Q

significant BAL Cx?

A

10,000+ CFU

160
Q

HAART in elective surgery

A

Continue through surgery; don’t stop.

161
Q

Dosing considerations (MIC) for B-lactam abx

A

β-Lactam antibiotics are most effective when drug levels exceed the MIC (minimum inhibotry concentration)

Therefore, dosing should keep the drug level above the MIC for more than 50% of the time between doses. In addition, frequent doses or continuous infusions have also been shown to increase effectiveness.

162
Q

VAP dx and mgmt

A

Obtain Cx.
Start broad-spectrum abx
**Therapy should be narrowed or stopped in about 48 to 72 hours based on the culture results rather than automatically continued for the full 8-day course.

Don’t need to wait for CT scan necessarily.

163
Q

duration of C diff tx

A

10 days

vancomycin or fidaxomicin over metronidazole. The dosage of vancomycin is 125 mg orally 4 times daily or fidaxomicin 200 mg orally twice a day for 10 days. If access to vancomycin or fidaxomicin is limited, metronidazole can be used, 500 mg orally 3 times a day

164
Q

mucor vs aspergillus on GMS stain

A

Aspergillus: septated hyphae with narrow branching angles.
Mucor: nonseptated hyphae with broad, branching angles

165
Q

GVHD

A

after stem cell/BM txp
transplanted immune WBCs attack host body cells
T and B
palm and sole rash, GI distress

166
Q

leukotrienes

A

from arachidonic
PRO INFLAMMATORY…
chemoattraction of adhesion, bronchoCONSTRICTION, MUCUS production, increased cap PERMEABILITY

167
Q

vancomycin infusion reaxtion

A

hypersensitivity with rapid infusion
direct degranulation mast cells/basophils
so stay awy from relaxants/opioids (fentanyl/tramadol OK) and other abx to prevent more histamine

168
Q

HCV needlestick exposure

A

0.1-1.8% infection..
so just wait and only treat if YOUR blood is infected

169
Q

HCV treatment

A

glecaprevir/pibrentasvir x 8 wk

or

sofosbuvir/velpatasvir x 12 wks

170
Q

HBV needlestcik

A

give PEP ASAP (even if pregnant)

171
Q

HIV needlestick

A

give PEP ASAP
then PEP x 4 wks

172
Q

B cells can secrete what without helper T

A

IgM

173
Q

B cells need what to become plasma

A

IL5 and IL 6

174
Q

what labs to get in vWB disease suspicion?

A

PTT
plasma levels of vWF antigen
vWF activity (ristocetin cofactor)
factor VIII activity

175
Q
A

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