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STEP1 > Hematology > Flashcards

Hematology Flashcards

1
Q

Plasma versus serum

A

Only plasma has clotting factors

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2
Q

Ankyrin

A

Anchors RBC microfilaments to plasma membrane. One of proteins that car be mutated in hereditary spherocytosis.

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3
Q

Band neutrophils

A

Immature, notfully segmented
Seen in bm and active infection whenthere is mass neutrophil release

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4
Q

Hypersegmented neutrophils

A

Abnormal maturati due to B 12 and folate deficiencies

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5
Q

Basophilicspecific granules contain…

A

Histamine and heparin

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6
Q

Basophilia in which cancer

A

. CM L

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7
Q

Bernard soulier syndrome

A

Platelet disorder
Loss of gpib ie adhesion to vessel walls
Bleeding

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8
Q

Glanzmann thrombasthenin /

A

Platelet disorder
Loss ofGP2b/3a receptors ie platelet aggregation
Bleeding

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9
Q

Myeloid toerythroid range in bm

A

2-4 m: 1 e

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10
Q

Blast cells are replaced with… At a rate of about… % per decade in bm

A

Adipose
10%

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11
Q

First differentiated stage myeloid

A

Promyelocyte

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12
Q

First stage of specificgranulation myeloid

A

Myclocyte

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13
Q

Para-aortic lymph nodes

A

Kidneys, ovaries, uterus, testes

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14
Q

Cervical lymph nodes

A

Head and neck

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15
Q

Hisar lymphnodes

A

Lungs

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16
Q

Mediastinaltymphnodes

A

Trachea andesophogus

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17
Q

Axillazy lymph nodes

A

/ Upper limbbreast and skin aboveembilicus

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18
Q

Celiac lymph nodes

A

Liver stomachspleen pancreas upper duodenum

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19
Q

Sm lymph nods

A

Lover duodenum, jejunum, ileum, colon thrusplenic-feare

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20
Q

I’m lymph nodes

A

Colon from splenic plexure upper rectum

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21
Q

Internal iliaclymphnores

A

Lower rectum, bladder, vagina, cervix,prostate

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22
Q

Superficial inguind lymph nodes

A

Anal canal, skin below umbilicus, scrotum, vulva

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23
Q

Popliteal lymphnodes

A

Dorsolateral foot and posterior calf

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24
Q

Stave cells

A

Physicallyform filter in red pulp to remove damaged or aged RB Cs

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25
Q

Pentose phosphate pathway

A

Detour fromglycolysic
To make nadph
Membrane antioxidant

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26
Q

2,3- bpg

A

Glycolysis detour
Enhances O2 release

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27
Q

G6pd

A

Glucose 6 phosphate dehydrogenase
Involved in reduction of nadp+ to nadph
Mutation —> RBC damage

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28
Q

Porphyria

A

Family ofdisorders related to interruptedheme metabolism

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29
Q

Sideroblastic anemia

A

Defect in heme synthesis at Ala synthase first step
Due to B6deficiency
Possible sfx ofisoniazid For TB

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30
Q

Bilirubin

A

Ultimateproduct of heme breakdown
Unconjgated travels thru body via albumin
Conjugated by liver to be water soluble
Converted tourobili nogen by gut bacteria
Re absorbed or excreted in bile, urine

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31
Q

Gilbert syndrome

A

Decreased activity of UDP glucuronyltransferase ie bilirubinconjugation leading to jaundice on physical stress illness orexertion

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32
Q

Hepcidin

A

’ Iron transportmolecule
Mutation leads to uncheckedexport from enterocytes and macrophages ie iron overload inblood
Hereditary hemochromocjosis

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33
Q

Ferritin

A

BindsFerricironinside of enterocyes and macrophages
Catalyst neutralizer and storage reservoir

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34
Q

Ferroportin

A

Transports iron across enterocyte or macrophage membrane into blood

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35
Q

Transferrin

A

Binds ferric iron for transport in blood

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36
Q

Deferoxamine

A

Iron Che later

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37
Q

Fanconi anemia

A

Hereditary aplasticanemia
Short stature, cafe an laïi spots,radial and thumb defects

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38
Q

Hydroxyurea

A

’ Sickle cell t x
Increases fetalhemogeobin

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39
Q

Infective stagemalaria

A

Sporozite

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40
Q

Feeding stage malaria

A

Trophozite
Lives in RBCand feeds on hemoglobin

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41
Q

Shizont

A

Replication phase of malaria in liver cells

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42
Q

Chloroquine

A

Malaria drug
Preventsconversion of toxic hemoglobin . breakdown product fpix into neutral hemozoin by malarial heme polymerase
Thus fpix kills malaria

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43
Q

Relapsing malarias

A

Vivax and ovale
Dormant phase inliver
Need autimalarialthat enters liver

44
Q

Most common malaria

A

Falciparum
Also must dangerous
But no dormant phase

45
Q

Fever intervalsmalarias

A

Falciparum 24h
Vivax and ovals 48h
Malariae 72h

46
Q

Ring insideesythrocyte

A

Malarial trophozite

47
Q

Basopbilia

A

Usually cml

48
Q

Reactive lymphocytosis with Downey 2 cells

A

Usually mono

49
Q

Steroids Leukocytosis

A

Fairly common and benign response tosteroids if mature cells but ro infection important

50
Q

Left shiftblood smear

A

More immatureveutrophits

51
Q

Steps ofdot formation

A

Vessel constrict
Platelet plu g
Fibrin seal - thrombin fibrin fibrinogen

52
Q

Intrinsic pathway

A

11
9
8
Common 10 (5 cofactor) 2 1

53
Q

Extrinsic pathway

A

7 t tissue factor tf
Common 10/5 = 2 > 1

54
Q

Anticoagsnatural

A

Turn off:
Antithrombin
C + S

Dissolve:
Plasmin

55
Q

Inhibitors ofplatelet adhesion

A

No
Endothelial atpase
Prostacyclin pgi2

Sterrically; intactendothelial cells

56
Q

Plate let chemoattracte.

A

VWF
Also tethers

57
Q

Vw f bindingpartner

A

GPIb
Tethers and activates

58
Q

Gpiii a /Iib

A

Binds fibrinogen

59
Q

Thromboxane az

A

Arachadonicaciddevivatire
Activates otherplatelets
Induces vasoconstriction

60
Q

Fibrinogen and thrombin

A

Fibrinogen bridgesplatelets andthrombin stabilizes via conversion of fibrin ogen to fibrin

61
Q

Tissue factor

A

Released fromdamaged tissue, and vitiatescoagulationcascade

62
Q

Intrinsic and extrinsic

A

T f initiates extrinsic shut off quickly intrinsic finishes
E=7
I=11-9_8

63
Q

Factor 7 deficiency

A

Asymptomatic

64
Q

Heparin

A

Potentates antithrombin to inhibit all serine proteases i.e. New or continuedclotting
Does not dissolve c lots

65
Q

Plasmin

A

Breaks down clots
Potentate by t PA

66
Q

D dimers

A

Clot bits
More specifically degradation products of cross-linked je. Clotted fibrin
Very sensitive but lowspecificityeven forpathogenic events in general, so used toro if negative but needs addition al to ri

67
Q

Ristocetin

A

Assay
If no aggreg action problem w/ VwF GPIb interaction
Von willebranddisense or Bernard soulierrespectively

68
Q

Platelet threshold severe bleeding

A

30000

69
Q

Thrombopoetin

A

Constituitivelysccreteel by lifer

70
Q

Warfarin

A

Vitamins K antagonist
2 7 9-10
Intrinsic and extrinsic so pt and ptt,
7 most sensitive so effects monitoredw/ pt/inr

71
Q

Antiphospholipid coa g assays

A

Clinicallyensymptomatic or cause thrombosis
Bind reagent in test so false positivefor bleeding

72
Q

Thrombocytopenia vs factor bleeding sites

A

T= skin and mucous membrane s petechia
Includesnosebeeds, heavy periods,gum bleeding

Fr excessivebleeding hours after trauma
If severe manybleed into joints. and deep issue

73
Q

Hemophilia A

A

Factor 8
X linked

74
Q

Hemophilia B

A

Factor 9 x linked
Less common

75
Q

Vwf tests

A

Ptt ie intrinsic decreased as vWF normally prevents degradation offactor 8
Ristocetin platelet aggregationabnormal

76
Q

Thromboticthrombocytopenic purpor a

A

Opposite of vwf disease.
Impaired breakdown of vwf
Thrombosis with eventual platelet consumption and bleeding

77
Q

vWD genetics

A

Autosomal dominant most common with homozygous more severe
Can be recessive depending on subtype

78
Q

Coags in hemophilia

A

Normal because extrinsic arm is normal
PTT prolonged

79
Q

Dic causes

A

Things that dump prrcoagulants into blood or things that damage entihelium
Most commonly malignancy obstetric complications sepsis and trauma
Others include snake bites and lupus.

80
Q

Adamts 13

A

Cleaves large VWF
Defective in ttp

81
Q

Hemolyticuremic syndrome

A

Thromboticmieroangiopathy similar to Ttp but caused by toxins
Most common e-coli 0157 h7
Second Shig.a toxin

Thrombocytopenia - microangiopathis hemolytic anemia -acute renal failure

82
Q

coags in TTP/HUS and DIC

A

elevated PT and PTT in DIC
NORMAL in TTP/HUS since clots are primarily platelet only without much consumption of coagulation factors

83
Q

TTP clinical

A

neuro abnormalities
microangiopathic hemolytic anemia
thrombocytopenia purpura
fever
abnormal renal fx

typically adults

84
Q

HUS clinical

A

bloody diarrhea usually
vomiting –> dehydration and hyponatremia

acute renal failure d/t direct effects of toxin on kidney
decreased urine output
uremia

thrombocytopenia
purpura, petechia, oozing blood

no fever or neuro findings usually except secondary to decompensation

usually kids <5 w/ recent diarrheal infection

85
Q

Bernard soulier sx

A

GPIb defect - no binding to vWF
autosomal recessive
severe bleeding
giant platelets

can cooccur w/ heavy chain non-muscle myosin 9 defects (glomerulonephritis, sensorineural deafness, cataracts) or filamin A defects (hemorrhage, coagulopathy, macrothrombocytopenia)

86
Q

bernard soulier tx

A

recombinant 7a
eltrombopag - thrombopoeitin agonist
platelet transfusions

87
Q

glanzmann thrombasthenia sx

A

GPIIb/IIIa - fibrinogen can’t bind platelets together
autosomal recessive
severe
normal platelet morphology but no clumping

may cooccur w/ leukocyte adhesion deficiency

88
Q

Glanzmann thrombasthemia tx

A

7a
HSCT
platelet or blood transfusion

common presentation:
- infant w/ severe infection
- delayed detachment of umbilical cord
- easy bruising/bleeding
- Fix

89
Q

gray platelet syx

A

reduction or absence of alpha granule - minimal to no platelet plug formation
giant, pale platelets

inheritance depends on genes

90
Q

uremia coags

A

decreased platelet aggregation
decreased granule secretion i.e fx

91
Q

factor 5 leiden

A

most common thrombotic disorder
constitutively active F5
hereditary - because it cannot bind and be cleaved by protein C

92
Q

APLS

A

most common acquired thrombotic disorder

93
Q

heparin resistant thrombotic disorder

A

antithrombin deficiency
heparin potentiates antithrombin so does nothing if it’s deficient
high doses might still work

very uncommon

94
Q

budd chiari syx

A

obstruction of hepatic vein
abd pain - hepatomegaly

as an uncommon site for clotting raises suspicion of a thrombotic disorder

95
Q

AT deficiency test

A

heparin cofactor assay first
AT antigen levels next
rarely genetic testing

96
Q

reasons to test for thrombotic disorders

A

at least one unprovoked DVT/other clot
Recurrent clotting episodes
Unusual locations

97
Q

warfarin induced skin necrosis

A

can occur in anyone but Protein C+S deficiency confers highest risk
should prompt evaluation for C+S deficiency

happens b/c warfarin decreases synthesis of most clotting factors including anti-coags C+S. C+S decrease fastest meaning there is a transient hypercoag period. If C+S are already deficient this is extreme.

tx: d/c warfarin
avoid by bridging w/ heparin (doesn’t work as well in C+S deficient but does help in normal)

98
Q

purpura fulminans

A

acute rapid widespread coagulability including hemorrhagic necrosis and skin infarction
usually d/t C+S deficiency

99
Q

-xaban

A

direct factor “Xa” inhibitors
oral
api-, riva-, edo-

100
Q

direct thrombin inhibitors e.g.

A

dabigatran PO
argatroban
bivalirudin
lepirudin

101
Q

reversal warfarin

A

immediate: fresh frozen plasma (FFP)
then vitamin K

102
Q

reversal heparin

A

protamine sulfate

103
Q

clopidegrel

A

antiplatelet
used when aspirin c/I or as second agent in dual therapy
P2Y12/ADP receptor blocker

104
Q

abciximab

A

anti platelet
anti-GPIIb/IIIa receptor

105
Q

dipyridamole

A

antipltelet
phosphodiesterase inhibitor
vasodilator
indic`ated in prior stroke

106
Q

-eplase

A

thrombolytics
e.g. alteplase aka tPA
tenecteplase now first choice d/t long t/12 and most specificity
all activate plasmin

107
Q

thrombolytic antidote

A

aminocaproic acid
transexamic acid
reserve for life threatening d/t sfx
if less severe just d/c-ing should be sufficient

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