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Physiology > Coagulation > Flashcards

Coagulation Flashcards

1
Q

How do you treat Hemophilia A?

A

Factor 8 deficiency

If severe, < 1% = Factor 8 concentrate @ home, factor 8 prior to surgery (12 hour half life in adults)

If mild, 6 - 30% = Microdeletion, underdiagnosed until adulthood - DDAVP 30 - 90m prior to surgery

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2
Q

How long do you give factor 8 to severe hemophilia a patients

A

days - weeks post surgery

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3
Q

what else can be used to treat hemophilia a

A

ffp, cryo, txa

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4
Q

15 - 20 mL/kg of FFP =

A

20 - 30% increase in any factor

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5
Q

how do you dx hemophilia a/b

A

prolonged aptt, gene, factor testing

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6
Q

anesthesia & hemophilia b

A
  1. hemoc consult
  2. replacement therapy (recombinant F9, purified F9, PCCs)
  3. continue replacement therapy for 18-24h
  4. txa
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7
Q

anesthesia & hemophilia a

A
  1. hemoc consult
  2. factor 8 at least > 50 % prior to surgery
  3. mild = ddvap 30m prior vs moderate = f8
  4. ffp/cryo/txa
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8
Q

hemophilia b mild vs severe

A

mild 5- 40%

severe < 1%

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9
Q

vwf antigen

A

antigenic determinant on VWF measured by immunoassay; usually low in type 1 & 2, absent in 3

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10
Q

ristocetin cofactor activity

A

functional assay of vwf activity based on plt aggregation with ristocetin. greatest decrease in type 2

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11
Q

type 1 vw dx

A

most common
mild - moderate reduction in level of VWF
mild symptoms - bruising, nosebleeds

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12
Q

type 1 vw dx labs

A

vwf-rco & vwf-ag < 30

factor 8 low or normal

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13
Q

type 2 vw

A

9 - 30 % of patients
qualitative defect of vwf
4 subtypes

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14
Q

type 2 vw labs

A

vwf-rco < 30
vwf-ag <30 - 200
factor 8 low or normal

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15
Q

type 3 vw dx

A

< 1 % of patients

nearly undetectable - severe quantitative phenotype

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16
Q

type 3 vw labs

A

vwf-rco & vwf-ag < 3

< 10 factor 8 (very low)

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17
Q

platelet pseudo type

A

defect in platelets g1b receptor, normal everything

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18
Q

type 1 tx

A

desmopressin

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19
Q

type 2 or type 3 tx

A

factor 8 concentrate, or platelets

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20
Q

replacement goals in vw dx - major dx

A

maintain factor 8 >/= 50 % for 1 week

prolonged tx in type 3 patients (> 1 week)

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21
Q

minor surgery & vw dx goals

A

factor 8 >/= 50% for 1 - 3 days pre and post > 20 - 30% for 4 - 7 days

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22
Q

dental extraction & vw dx goals

A

one infusion to achieve factor 8 > 50% or desmopressin for type 1

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23
Q

spontaneous bleeding

A

transfuse 20 - 40 units/kg

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24
Q

1 unit/kg of factor 8 =

A

2% increase

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25
Q

what is factor 8 called

A

antihemophilic factor
1/2 life 12 - 15h
source: FFP, FC, cryo

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26
Q

what is factor 9 called

A

christmas factor
1/2 life 18 - 30
source: FFP, PCC, FC

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27
Q

what causes DIC?

A

thrombin (which normally stays at the site of vascular injury), is generated in response to endotoxins, amniotic fluid embolism

leads to intravascular clotting which then disseminates

coagulation factors and platelets are used up

fibrinolysis is activated = bleeding

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28
Q

symptoms of DIC

A

chest pain. SOB, leg pain, can’t move
clotting/bleeding/both
hemorrhage IV sites, catheters, drains

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29
Q

name 9 causes of DIC

A 
sepsis, surgery, or snake bites
trauma or transfusion rx 
cancer
burns
frostbite
pregnancy complications
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30
Q

tell me about tissue factor & DIC

A

TF is present in cell surfaces like endothelium, macrophages, monocytes and lung, brain, placenta

it is exposed, released, binds with F8 = 9 & 10 activation = thrombin = fibrin = boom, clot

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31
Q

what does fibrinolysis do

A

creates fibrin degredation products that

  1. inhibit plts aggregation
  2. have antithrombin activity
  3. impair fibrin polymerization
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32
Q

thrombin & DIC

A

have lots of thrombin generation leading to consumption of coags, leading to more bleeding

consumption of anticoag proteins indicued by thrombin can also lead to clots

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33
Q

blood tests in DIC

A

DIC panel
low platelets, low fibrinogen
high INR, PT, PTT, D-dimer (DVP)

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34
Q

DIC progression

A 
non-overt = hypercoagulable
overt = hypocoagulable
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35
Q

how to treat DIC

A

infection? abx
trauma? resuscitation

supportive: plt, cryo, fibrinogen, FFP, heparin, TCA, PCCs

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36
Q

procoagulant DIC tx

A

monitor tests

start LMWH

37
Q

hyperfibrionlytic DIC tx

A

txa

blood products

38
Q

what is thrombin

A

potent proinflammatory protein and platelet aggregator

neutralizing thrombin in DIC is crucial

39
Q

how. to neutralize thrombin

A

thrombomodulin - limited by clinical tirals

direct thrombin inhibitors - no RCTs yet (ie dabigatrin bilavalirudin argatroban lepirudin)

40
Q

blood products in dic

A

plt –> cryo or fibrinogen –> FFP

41
Q

name the 6 aa in hgb beta chain

A

valine = histidine = leucine = thre = proline = glutamic acid

glutamic acid = sc dx

42
Q

formation of hgb

A
  1. proerythroblast –> reticulocyte
  2. 2 succinyl-CoA (from kreb’s cycle) + 2 glycine –> pyrrole
  3. 4 pyrrole combine = protoporphyrin
  4. protoporphyrin + irone = heme
  5. heme + globin combine
  6. 4 subunit chains possible (alpha, beta, gamma, delta)
43
Q

what is the most common hgb

A

hgb a = 2 alpha/2beta

44
Q

genesis of rbc (7)

A
  1. pluripotent hematopoietic stem cell
  2. proerythroblast
    erythroblast hgb synthesis starts
  3. bosphil erythroblast
  4. polychromatophil erythroblast
  5. orthochromatic erythroblast
    loses nucleus, organelles –> into blood
  6. retic (3 days in marrow, 1 day in blood)
  7. erythrocyte
45
Q

name 3 common d/o of hgb

A
  1. methemoglobin - altered affinity
  2. thalassemia - quantitative d/o of globin chain
  3. sickle cell - qualitative d/o of globin structure
46
Q

cause of methemoglobinemia

A

iron in hgb is oxidized from ferrous (fe 2+) to ferric (fe 3+)

  1. congenital (globin chain mutation) or (methemoglobin reductase system mutation)
  2. acquired (toxic exposure that oxidizes hgb iron)
47
Q

symptoms of methemoglobin

A

left shift in oxy/hgb curve
pt can tolerate up to 30%, < 1 % is normal
30 - 50% = muscle weakness, nausea, tachycardia
> 50 % = death

48
Q

globin chain mutation in methhgb

A

mutations that stabilize heme iron in the ferric state, making it resistant to reduction by methemoglobin reductase system

asymptomatic b/c levels don’t exceed 30%

49
Q

impaired reductase system

A

causes methemoglobinemia
mutations impair NADH and cytochrome b methemoglobin reductase resulting in methemoglobinemia < 25%

slate gray pseudocyanosis despite normal pao2

50
Q

acquired methemoglobinemia

A

rare
infants have lower levels of reductase (nitrates in well water, or oragel)
topical anesthetics (benzocaine)

51
Q

anesthesia & methemoglobinemia

A
  1. avoid hypoxia and acidosis
  2. supplemental oxygen won’t help
  3. pulse ox won’t work
  4. a-line. EKG. blood sample (chocolate)
  5. avoid LA, nitrates, nitric oxide
52
Q

treatment of methemoglobinemia

A

oxygen
1-2 mg/kg methylene blue over 3-5 m
repeat q30m if needed

METHYLENE BLUE NEEDS G6PD B/C USES REDUCTASE SYSTEM

53
Q

HOW does methylene blue work

A

acts as an electron donor for the nonenzymatic reduction of methemoglobin

nadph converts methylene blue - leukomethylene using nadph

54
Q

b-thalassemia =

A

an inherited defect in globin chain synthesis
contributes to anemia by :
1. inadequate formation of hba = microcytic rbcs
2. excess unpaired a-globin chains form toxic stuff that damage baby erythroids

55
Q

a-thalassemia

A

deletion of one or more a-globin genes

ineffective erythropoiesis and hemolysis less pronounced than b but ineffective oxygen tissue delivery remains

56
Q

thalassemia major & 3 defects

A

life-threatening - tx for the first few years
3 defects that depress oxygen-carrying capacity
1. ineffective erythropoiesis
2. hemolytic anemia
3. hypochromia and microcytosis

57
Q

s/s thalassemia major (4)

A

damaged rbcs
bone hyperplasia
splenomegaly
death d/t chf & arrhythmias

58
Q

anesthesia & thalassemia

A

mild = chronic, compensated anemia (preop tx for a hgb 10)
severe = spleno/hepatomegaly, skeletal malformations, chf, iron overload, cirrhosis, rshf
infection - abx
dvt prophylaxis
difficult intubation
tell blood blank the thalassemia

59
Q

pathophjys sickle cell

A

hgb s, genetic defect of hgb synthesis
precipitated hgb damages membranes = sickling crisis of ruptured cells = further decrease in oxygen tension = more sickling

severe anemia, painful episodes

60
Q

transfusion goal scd

A

increase ratio of normal hgb to sickle hgb

61
Q

anesthesia & scd

A

avoid 3h’s

  1. hypothermia
  2. hypoxia
  3. hypovolemia

anxiolytics
lots of narcs
t&c (hard if you had lots of txs)
tourniquet - c/i?

62
Q

acute chest syndrome

A 
pna on cxr
2-3 days postop
hypoxemia, analgesia, blood tx
nitric oxide?
decrease if preop hct > 30%
63
Q

where are rbcs made

A

bone marrow

stimulated by erythropoietin (glycoprotein formed in the kidneys)

64
Q

what is anemia

A

reduced number of rbcs

hgb < 12 for girls, 13 for boys

65
Q

3 causes of anemia

A

blood loss, decreased production, increased destruction

66
Q

s/s anemia

A 
yellow eyes
pale, cold skin
SOB
weak
changed stool color
dizzy, fainting
chest pain/angina/heart attack
enlarged spleen
67
Q

acute blood loss anemia

A

body replaces fluid part of plasma in 1-3 days leaving low concentration of rbcs

rbc normalizes in 3 - 6 weeks

68
Q

chronic blood loss anemia

A

can’t absorb enough iron from gut to make hgb as rapidly as it is lost

rbcs are produced smaller, with smaller hgb inside microcytic anemic

69
Q

transfusion trigger

A

10/30 rule (no evidence)

< 6 = evidence

70
Q

ebl < 15 %

A

rarely need transfusion

71
Q

ebl 30%

A

crystalloids/albumins

72
Q

ebl 30 - 40%

A

rbc tx

73
Q

ebl > 50%

A

massive tx
ffp and plt as well
ratio 1/1/1

74
Q

name 4 types of anemia based on mechanism

A
  1. decreased production (iron, autoimmune)
  2. increased destruction (thalassemia, hemolytic anemia, SCD)
  3. blood loss
  4. infectious (malaria, babesia, parvo)
75
Q

what causes iron deficiency anemia

A

nutritional
chronic gi bleeds/ menstraution
pregnancy

-mild anemia, 9 - 12-

76
Q

iron deficiency anemia causes (2)

A

impaired rbc maturation and diminishes rbc production

microcytic hypochromic anemia

77
Q

tx iron deficiency anemia

A

oral iron & postpone 2-4mo
IV iron & postpone 1-2w
RBC tx

78
Q

hemolytic anemia labs (4)

A

increased retics
unconjugated hyperbilirubinemia
increased lactate dehydrogenase
decreased haptoglobin

79
Q

scd affects what globin

A

b –> which leads to polymerization of sickle hgb (hb s) into long, stiff chains when its deoxygenated

80
Q

scd tx

A

hydroxyurea which rasies hbF

stem cell transplants

81
Q

autoimmune anemia tx

A

immunosupression & steroids

82
Q

causes of autoimmune anemia (5)

A 
igg/igm
idiotpathic
leukemia
mono
drug induced (pcn, quinidine)
83
Q

hemolytic dx of newborn

A

fetus rhd antigen +
mother rhd antigen -

igg mediated

84
Q

rh factor

A

rhesus factor - a protein found on the surface of rbcs
genetically inherited
factor refers to the rh (D) antigen only (there are several Rh antigens)

the rh (D) antigen is the most immunogenic of all the non-ABO antigens

85
Q

g6pd deficiency & drugs to avoid

A 
metoclopramide
pcn & sulfa
methylene blue
hypothermia
acidosis
hyperglycemia
infection
86
Q

polycythemia s/s

A

hct > 55 - 60%
PCV

cyanosis, HA, dizzy, GI symptoms, hematemesis, melena
hepatic/coronary/cerebral thrombosis
leukemia
engorged vessels
bluish/ruddy skin
marrow fibrosis

usually see in the 6th/7th decade

87
Q

types of polycythemia

A 
physiologic d/t low atmospheric oxygen
polycythemia vera (hct @ 60 - 60%)
88
Q

PCV treatment

A

phlebotomy
myelosuppressive drugs (hydroxyurea)
anticoags to decrease thrombosis risk

these ppl die within months from vascular complications if not treated

Physiology (5 decks)

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