Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

vascular injury response (3)?

A
  1. vasoconstriction
  2. plt adhesion
  3. thrombin generation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

intrinisic pathway?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

extrinisic pathway?

A

tissue factor + 7
10 add 5
2
1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how is thrombin key to coagulation?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what does fibrin actually do?

A

plt plug to bind plt via Gp2BA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

factor with shortest half life?

A

7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

whose activity is lose in stored blood but not FFP?

A

due to lability….
5 and 8.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

which factor not synth’d in liver?

A

8 with vonWillebrand factor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Vit K factors?

A

2, 7, 9, 10, C, S

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Vit K vs FFP onset?

A

Vit K 12 hours (IV), FFP is immediate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

half life RBC, plt, PMN?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

function of prostacyclin PGI2?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

pGE2

A

in hypothalamus; induce FEVER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

cryoprecipitate contents?

A

vWF-8 and fibrinogen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

indication for cryoprecipitate?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

FFP contents?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

DDAVP and conjugated estrogen effect on clotting

A

cause release of 8 and vWF from endothelium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

prothrombin time measures?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

partial thromboplastin time measures?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

activated clotting time goal

A

150-200 routine AC
>480 for bypass.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

vWB disease AD vs AR?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

vWF role?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Type I vWB disease?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Type 2 vWB disease?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Type 3 vWB disease?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

hemophilia A deficiency?

A
  1. sex linked recessive.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

how does hemophilia A present?

A

hemarthrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

coag abnormality in hemophilia A?

A

PTT prolonged, PT normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

newborns with hemophilia A?

A

might be OK because factor 8 crosses placenta.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

if bleeding, hemophilia A? how to treat.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

hemophilia B deficiency?

A
  1. sex linked recessive.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

coag abnormality in hemophilia B?

A

PTT prolonged
PT normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

treat hemophilia B bleeding?

A

recombinant 9 or FFP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

factor 7 deficiency bleeding? how to treat.

A

prolonged PT
normal PTT
treat wiht recombinant 7 or FFP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

acquired thrombocytopenia Rx-related etiology?

A

heparin
H2 blockers famotidine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

glanzmann’s thrombocytopenia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Bernard Soulier thrombocytopenia?

A

Gp1b-R deficiency on plt.
treat: plt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

HIT Ab

A

IgG heparin-PF4 Ab causing plt destruction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

HIT pathogenesis

A

plt die… causing plt aggregation and thrombosis***

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

HIT 1 vs 2

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

how to dx HIT?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

treat HIT?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

DIC lab abnormalities

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

DIC etiology

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

ASA MOA?

A

inhibit COX, decrease TXA2.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

when to stop ASA and plavix and coumadin?

A

7 days preop.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

plavix/clopidogrel MOA?

A

ADP-R antagonist.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

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

A

bridge with eptifibatide (integrilin) Gp2B3A inhbitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

plt goal for periop?

A

50K preop
20K postop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

bleeding issues after prostate surgery?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

factor V leiden MC what?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

how to treat Factor V leiden?

A

heparin, warfarin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

how to treat hyperhomocysteinemia?

A

folic acid, B12.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

G20210A

A

prothrombin gene defect causing hypercoagulability
treat: AC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

protein C/S deficiency tx?

A

AC.n

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

antithrombin 3 deficiency?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Polycythemia vera treat?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

APLS

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

dx APLS?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

treat APLS?

A

heparin, warfarin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

MC acquired hypercoagulable state?

A

tobacco.w

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

why anticoagulate on bypass?

A

Factor 7 (Hageman factor) is activated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Virchow’s triad?

A
  1. stasis
  2. endothelial injury
  3. hypercoagulability.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

postop DVT tx?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

amicar indication? = a-FIBRINOLYTIC

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

inhibits PLASMIN.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

warfarin MOA

A

inhibits Vit K dependent carboxylation of glutamic residues on VKORC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

heparin MOA

A

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

lovenox does not neutarlize 2a. just X.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

half life of heparin?

A

60-90 min.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

lovenox half life

A

6 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

heparin clearance

A

by reticuloendothelial system (spleen, macrophages)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

half life warfarin

A

40 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

heparin vs warfarin placental barrier?

A

heparin does not cross; warfarin does.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

SE long term heparin?

A

osteoporosis, alopecia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

protamine reaction?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

dabigatran MOA

A

direct thrombin inhibitors

half life: 12 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

reversal dabigatra (pradaxa)

A

praxbind = idarucizumab

or HD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

eliquis and xarelto half lives

A

eliquis (apixaban) 12 hours

xarelto (rivaroxaban) 6 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

argatroban MOA

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

bivalrudin MOA

A

direct 2 inhibitor REVERSIBLE
half life 25 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

argatroban vs bivalrudin metabolized by?

A

argatroban: liver
bivalrudin: proteinase enzymes in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

hirudin MOA

A

direct 2 inhibitor IRREVERSIBLE. leeches.
most potent.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

hirudin / hirulog half life

A

40 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

ancrod?

A

malayan pit viper venom. stimulates TPA release.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

absolute CI for uro/strepto/tpa?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

which blood products do not have HIV risk?

A

albumin, serum globulins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

what is screened for in blood

A

HIV
HBV
HCV
HTLV
syphilis
West Nile Virus

97
Q

how to treat warfarin coagulopathy?

A

IV Vit K with PCC (faster than FFP)

98
Q

4 factor vs 3 factor PCC

A

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

99
Q

Why does stored blood have higher affinity for oxygen?

A

Low 2,3 DPG causes increase affinity.

100
Q

What type of hypersensitivity is ABO incompatibility?

A

Type II. Ab mediated.

101
Q

Dx of acute hemolysis from ABO incompatibility?

A

Haptoglobin < 50
Free Hgb > 5
Increase IndBili

102
Q

sx of acute hemolytic transfusions reaction?

A

chills, lightheadedness, back pain
stop the transfusion!

103
Q

What is the most common transfusion reaction?

A

Febrile nonhemolytic transfusion reaction.

= urticaria, fever within 60 seconds

104
Q

Febrile nonhemolytic transfusion reaction pathogenesis?

A

Recipient Ab against donor WBCs. (Cytokine release).

105
Q

Mgmt febrile nonhemolytic transfusion reaction?

A

Stop transfusion, WBC filter and antihistamines for future transfusions.

106
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

107
Q

MC cause of death from transfuions reaction?

A

TRALI.

108
Q

MOA hypocalcemia in large transfusion?

A

Citrate in blood products binds Ca.

109
Q

calcium required for coagulation

A

ca is required in the clotting cascade (hypocalcemia; relative coagulopathy)

110
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.

111
Q

how do NK cells work?

A

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

112
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

113
Q

Ab mediated immunity (humoral) cytokines, cells?

A

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

114
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

115
Q

Which Ab are opsonins?

A

IgM and IgG

116
Q

Which Abs fix complement?

A

2 IgG adn 1 IgM

117
Q

Primary lymphoid organs?

A

Liver, bone, thymus.

118
Q

Secondary lymphoid organs?

A

Spleen and lymph nodes.

119
Q

How to manage nontetanus prone wounds, not UTD?

A

Give tetanus toxoid.

120
Q

How to manage tetanus prone wound if UTD?

A

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

121
Q

Tetanus prone wound not UTD.

A

Tetanus toxoid with tetanus Ig.

122
Q

MC anaerobe in colon? MC aerobe?

A

Anaerobe Bacteroides. Aerobe E. Coli.

123
Q

How to treat candiduria?

A

Just remove foley; watch. No antifungal.

124
Q

ART for HIV PEP

A

AZT zidovudie and ritonavir (recall ribavirin is HCV)

within 1-2 hours of exposure

125
Q

MC neoplasm in AIDS?

A

Kaposi sarcoma

126
Q

MC lymphoma in HIV?

A

Stomach > rectum; mostly B cell non-Hodgkins

2nd mC reason for laparotomy in HIV (1st is CMV)

127
Q

MC causes of UGI and LGI bleeds in HIV?

A

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

128
Q

Primary SBP tx?

A

IV CTX

129
Q

Dx primary SBP?

A

Ascites > 250 PMN or positive Cx

130
Q

How to tx Hep C

A

Sofosbuvir and ribavirin

131
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%)

132
Q

MC infection in txp pt? Q

A

CMV

colitis, pneumonitis (MC deadly infection of it )

133
Q

What cell transmits CMV?

A

Leukocytes.

134
Q

CMV dx

A

Serology and stain: leukocyte inclusion bodies.

135
Q

Tx cmv

A

Ganciclovir (CMV Ig if severe infection or + donor liver)

136
Q

MC aspiration PNA spot?

A

Sup seg

bug = S.pneumo (cover for poly anaerobe too though)

137
Q

Brown recluse spider bite?

A

Tx: dapsone

138
Q

which nucleotide do sulfonamides effect?

A

purines; PABA analogue.

139
Q

which nucleotide does trimethoprim TMP effect?

A

purine; inhibits DHF reductase (dihydrofolate).

140
Q

bacteriostatic abx?

A

tetracycline, clindamycin, erythromycin, bactrim

141
Q

most common method of antibiotic resistance?

A

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

142
Q

MRSA resistance mechanism

A

mutation of cell wall binding protein.

143
Q

VRE resistance MOA?

A

mutation in cell wall binding protein. like MRSA.

144
Q

genamicin resistance MOA?

A

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

145
Q

vanc peak and trough?

A

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

146
Q

gentamicin peak and trough?

A

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

147
Q

what to do if peak too high?

A

decrease AMOUNT of each dosei

148
Q

what to do if trough too high?

A

decrease FREQUENCE of dose

149
Q

ampicillin coverage vs pencillins?

A

GPCs but also includes ENTEROCOCCI.

150
Q

augmentin and unasyn vs penicillins?

A

also includes GNRs and some anaerobic.

151
Q

anti-pseudomonals?

A

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

152
Q

generations of cephs.

A

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

153
Q

MOA cilastin with carbapenems?

A

prevents renal hydrolysis and increases half life

154
Q

aminoglycoside SE (rev and irrev)

A

reversible nephrotoxicity
irreversible ototoxicitya

155
Q

macrolide coverage

A

GPCs (think: PNA) and is prokinetic…

156
Q

MOA amphotericin

A

bind ergosterols in wall and laters membrane permeability

157
Q

SE of amphotericin (decreased by liposomal type)

A

nephrotoxicity, hypokalemia, anemia, fevers.

158
Q

MOA azoles

A

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

159
Q

MOA micafungins

A

inhibit synthesis of cell wall GLUCAN.

160
Q

MOA amphotericin B

A

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

liposomal = less nephrotoxicity

161
Q

TB Rx?

A

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

162
Q

ganciclovir side effect (give for CMV)

A

myelotoxicity, CNS toxicity

163
Q

-cyclovir MOA

A

inhibit viral DNA polymerase.

164
Q

enterococcus and cephalosporins?

A

resistant to ALL CEPHALOSPORINS.

165
Q

Methotrexate and 5-FU nucleotide effect?

A

Purine.

166
Q

Leucovorin effect on methotrexate and 5-FU?

A

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

167
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

168
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

169
Q

significant BAL Cx?

A

10,000+ CFU

170
Q

HAART in elective surgery

A

Continue through surgery; don’t stop.

171
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.

172
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.

173
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

174
Q

C diff pathogenesis

A

toxin A (ELISA)

175
Q

mucor vs aspergillus on GMS stain

A

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

176
Q

GVHD

A

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

177
Q

leukotrienes

A

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

178
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

179
Q

HCV needlestick exposure

A

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

180
Q

HCV treatment

A

sofosbuvir and ribavirin = TREATMENT CURE

181
Q

HCV to ca vs cirrhosis

A

cirrhosis 15%
chronic infection 60%
HCC 1-5%

182
Q

liver txp #1 reason

A

US: HCV
world: HBV

183
Q

HBV needlestcik

A

give PEP ASAP (even if pregnant)

184
Q

HIV needlestick

A

give PEP ASAP
then PEP x 4 wks

(but if not confirmed patient, just w8 (like HBV)

185
Q

HIV exposure risk

A

blood transfusion 70%
infant form positive 30%
needle 0.3%
mucous 0.1%

186
Q

B cells can secrete what without helper T

A

IgM

187
Q

B cells need what to become plasma

A

IL5 and IL 6

IL4 from helper T stimulate B to become plasma

188
Q

what labs to get in vWB disease suspicion?

A

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

189
Q

SCDs MOA

A

TPA release; reduce fibrinolysis
improve veous return

190
Q

type and screen vs crossmatch

A

screen also looks for preformed Abs to minor antigens

191
Q

what bug can be transmitted with blood transfusion??

A

Chagas disease

192
Q

HBV pathogenesis destruction

A

CD8s bind MHC I receptors on the virus; majority of liver injury

193
Q

MHC class I A B C architecture

A

single chain with 5 domains

194
Q

MHC class II DR DP DQ architecture

A

2 chains with 4 domains each

195
Q

most important APC

A

dendrites

196
Q

most common overall Ig

A

IgG

197
Q

MC Ab in spleen

A

IgM

198
Q

travels thru breast milk

A

IgA

199
Q

crosses placenta

A

IgG

200
Q

basophil vs mast cell

A

basophil in plasma
mast cell in tissue

201
Q

IL2 in cancer

A

converts lymphocytes to
LYMPHOKINE ACTIVATED KILLER cells (enhance tumor response)
or TUMOR INFILTRATING LYMPHOCYTES (TILs)

for melanoma!

202
Q

E. coli pathogenesis sepsis

A

LPS lipid A (endotoxin)&raquo_space; activate macs , complement, coag cascade

203
Q

MC bug SSI

A

S. aureus

204
Q

exoslime in Staph is what kind of matrix

A

exopolysaccharid matrix

205
Q

MC GNR in SSI

A

E. coli

206
Q

MC anaerobe in SSI

A

Bacteroids (also MC anaerobe in the gut)

207
Q

how many bug is a wound infaction

A

10^5

208
Q

what produces ENDOtoxin

A

C. perfringens (alpha toxin) and B-hemolytic strep

209
Q

MC infection postop

A

UTI

210
Q

MC infectious death postop

A

HAP/VAP

211
Q

MC HAP/VAP bug

A

S. aureus > Pseudomonas > E. coli

212
Q

MC line bug

A

S. epi > S. aureus > YEAST

213
Q

necrotizing fasciitis bugs

A

GAS (b hemolytic) > MRSA (both have exotoxin)

214
Q

invasive aspergillosis

A

voriconazole

215
Q

invasive candidiasis

A

mica vs anidulafungin

216
Q

SBP in cirrhosis is moslty what bug

A

mostly monobacterial E. coli

217
Q

SBP SECONDARY mostly what bug

A

polymicrobial POO bugs

218
Q

DFI bugs

A

need to cover for PSA too (include staph, strep, anaerobes)

tx = ZOsyn, Unasyn

219
Q

Septic arthritis bugs

A

include VANC…. cuz staphs, strep, gonococcal, H flu

220
Q

cat dog human bite bug

A

MC - GAS

also cover…. human (Eikenella for joint injury)… cat/dog (pasturella multocida)

tx = Augmentin

221
Q

skin infection (impetigo, erysipelas, cellulitis, follicutisi) bug

A

STAPH > strep

222
Q

PD cath infection MC bug

A

STAPH EPI**»»> S aureus, PSA

223
Q

PD cath infectoin tx

A

IP vanc + gentamicin

remove if > 4-5 days or if fungal/TB/PSA

224
Q

iodofors for what bugs

A

GNR
GPC

not fungal

225
Q

chlorhexidine gluconate for what bugs

A

GNR
GPC
FUNGUS

226
Q

50S ribosome subunits (protein synth)

A

macrolides
linezolid
Synercid

227
Q

30S ribosome subunits (protein synth)

A

aminoglycosides (gentamycin, tobra) – which are bacteriocidal
tetracycline - is the only bacteriostatic one

228
Q

RNA polymerase inhbiitors

A

RIFAMPIN

229
Q

makes oxygen radicals to break DNA

A

Flagyl

230
Q

IL-1 and fever

A

macrophages release

cause PGE2 mediated fever
can release IL1 in alveolar macs during atelectasis

231
Q

selectins

A

L: leukocytes
E: endothelial
P: platelets

for rolling adhesion

232
Q

B2 integrins (CD 11/18)

A

on WBCs… .bind ICAMs

for anchoring adhesion

233
Q

ICAM, VCAM, PECAM, ELAM

A

on endothelial cells… bind B2 on WBCs and plts

for tranesndothelial migration (diapedesis- foot)

234
Q

leukotrienes

A

LTC4, LTD4, LTE4: slow reacting substrate for anaphylaxs

LTB4: chemotactic for inflammatory cells

235
Q

cxc chemokinds

A

cysteine - something - cysteine

IL8 and PF4

for chemotaxis, angiogenesis, wound healing

236
Q

oxidant and reagant

A

superoxide anion - NADPH oxidase

hydrogen peroxide - xanthine oxidase

237
Q

cellular defense to oxidation

A

SOD
glutathione peroxidase or catalase for H2O2ri

238
Q

primary mediator of reperfusion injury

A

PMN ss

239
Q
A

ABSITE (37 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions