Hematology Flashcards
1
Q
Plasma versus serum
A
Only plasma has clotting factors
2
Q
Ankyrin
A
Anchors RBC microfilaments to plasma membrane. One of proteins that car be mutated in hereditary spherocytosis.
3
Q
Band neutrophils
A
Immature, notfully segmented
Seen in bm and active infection whenthere is mass neutrophil release
4
Q
Hypersegmented neutrophils
A
Abnormal maturati due to B 12 and folate deficiencies
5
Q
Basophilicspecific granules contain…
A
Histamine and heparin
6
Q
Basophilia in which cancer
A
. CM L
7
Q
Bernard soulier syndrome
A
Platelet disorder
Loss of gpib ie adhesion to vessel walls
Bleeding
8
Q
Glanzmann thrombasthenin /
A
Platelet disorder
Loss ofGP2b/3a receptors ie platelet aggregation
Bleeding
9
Q
Myeloid toerythroid range in bm
A
2-4 m: 1 e
10
Q
Blast cells are replaced with… At a rate of about… % per decade in bm
A
Adipose
10%
11
Q
First differentiated stage myeloid
A
Promyelocyte
12
Q
First stage of specificgranulation myeloid
A
Myclocyte
13
Q
Para-aortic lymph nodes
A
Kidneys, ovaries, uterus, testes
14
Q
Cervical lymph nodes
A
Head and neck
15
Q
Hisar lymphnodes
A
Lungs
16
Q
Mediastinaltymphnodes
A
Trachea andesophogus
17
Q
Axillazy lymph nodes
A
/ Upper limbbreast and skin aboveembilicus
18
Q
Celiac lymph nodes
A
Liver stomachspleen pancreas upper duodenum
19
Q
Sm lymph nods
A
Lover duodenum, jejunum, ileum, colon thrusplenic-feare
20
Q
I’m lymph nodes
A
Colon from splenic plexure upper rectum
21
Q
Internal iliaclymphnores
A
Lower rectum, bladder, vagina, cervix,prostate
22
Q
Superficial inguind lymph nodes
A
Anal canal, skin below umbilicus, scrotum, vulva
23
Q
Popliteal lymphnodes
A
Dorsolateral foot and posterior calf
24
Q
Stave cells
A
Physicallyform filter in red pulp to remove damaged or aged RB Cs
25
Pentose phosphate pathway
Detour fromglycolysic
To make nadph
Membrane antioxidant
26
2,3- bpg
Glycolysis detour
Enhances O2 release
27
G6pd
Glucose 6 phosphate dehydrogenase
Involved in reduction of nadp+ to nadph
Mutation —> RBC damage
28
Porphyria
Family ofdisorders related to interruptedheme metabolism
29
Sideroblastic anemia
Defect in heme synthesis at Ala synthase first step
Due to B6deficiency
Possible sfx ofisoniazid For TB
30
Bilirubin
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
31
Gilbert syndrome
Decreased activity of UDP glucuronyltransferase ie bilirubinconjugation leading to jaundice on physical stress illness orexertion
32
Hepcidin
' Iron transportmolecule
Mutation leads to uncheckedexport from enterocytes and macrophages ie iron overload inblood
Hereditary hemochromocjosis
33
Ferritin
BindsFerricironinside of enterocyes and macrophages
Catalyst neutralizer and storage reservoir
34
Ferroportin
Transports iron across enterocyte or macrophage membrane into blood
35
Transferrin
Binds ferric iron for transport in blood
36
Deferoxamine
Iron Che later
37
Fanconi anemia
Hereditary aplasticanemia
Short stature, cafe an laïi spots,radial and thumb defects
38
Hydroxyurea
' Sickle cell t x
Increases fetalhemogeobin
39
Infective stagemalaria
Sporozite
40
Feeding stage malaria
Trophozite
Lives in RBCand feeds on hemoglobin
41
Shizont
Replication phase of malaria in liver cells
42
Chloroquine
Malaria drug
Preventsconversion of toxic hemoglobin . breakdown product fpix into neutral hemozoin by malarial heme polymerase
Thus fpix kills malaria
43
Relapsing malarias
Vivax and ovale
Dormant phase inliver
Need autimalarialthat enters liver
44
Most common malaria
Falciparum
Also must dangerous
But no dormant phase
45
Fever intervalsmalarias
Falciparum 24h
Vivax and ovals 48h
Malariae 72h
46
Ring insideesythrocyte
Malarial trophozite
47
Basopbilia
Usually cml
48
Reactive lymphocytosis with Downey 2 cells
Usually mono
49
Steroids Leukocytosis
Fairly common and benign response tosteroids if mature cells but ro infection important
50
Left shiftblood smear
More immatureveutrophits
51
Steps ofdot formation
Vessel constrict
Platelet plu g
Fibrin seal - thrombin fibrin fibrinogen
52
Intrinsic pathway
11
9
8
Common 10 (5 cofactor) 2 1
53
Extrinsic pathway
7 t tissue factor tf
Common 10/5 = 2 > 1
54
Anticoagsnatural
Turn off:
Antithrombin
C + S
Dissolve:
Plasmin
55
Inhibitors ofplatelet adhesion
No
Endothelial atpase
Prostacyclin pgi2
Sterrically; intactendothelial cells
56
Plate let chemoattracte.
VWF
Also tethers
57
Vw f bindingpartner
GPIb
Tethers and activates
58
Gpiii a /Iib
Binds fibrinogen
59
Thromboxane az
Arachadonicaciddevivatire
Activates otherplatelets
Induces vasoconstriction
60
Fibrinogen and thrombin
Fibrinogen bridgesplatelets andthrombin stabilizes via conversion of fibrin ogen to fibrin
61
Tissue factor
Released fromdamaged tissue, and vitiatescoagulationcascade
62
Intrinsic and extrinsic
T f initiates extrinsic shut off quickly intrinsic finishes
E=7
I=11-9_8
63
Factor 7 deficiency
Asymptomatic
64
Heparin
Potentates antithrombin to inhibit all serine proteases i.e. New or continuedclotting
Does not dissolve c lots
65
Plasmin
Breaks down clots
Potentate by t PA
66
D dimers
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
Ristocetin
Assay
If no aggreg action problem w/ VwF GPIb interaction
Von willebranddisense or Bernard soulierrespectively
68
Platelet threshold severe bleeding
30000
69
Thrombopoetin
Constituitivelysccreteel by lifer
70
Warfarin
Vitamins K antagonist
2 7 9-10
Intrinsic and extrinsic so pt and ptt,
7 most sensitive so effects monitoredw/ pt/inr
71
Antiphospholipid coa g assays
Clinicallyensymptomatic or cause thrombosis
Bind reagent in test so false positivefor bleeding
72
Thrombocytopenia vs factor bleeding sites
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
Hemophilia A
Factor 8
X linked
74
Hemophilia B
Factor 9 x linked
Less common
75
Vwf tests
Ptt ie intrinsic decreased as vWF normally prevents degradation offactor 8
Ristocetin platelet aggregationabnormal
76
Thromboticthrombocytopenic purpor a
Opposite of vwf disease.
Impaired breakdown of vwf
Thrombosis with eventual platelet consumption and bleeding
77
vWD genetics
Autosomal dominant most common with homozygous more severe
Can be recessive depending on subtype
78
Coags in hemophilia
Normal because extrinsic arm is normal
PTT prolonged
79
Dic causes
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
Adamts 13
Cleaves large VWF
Defective in ttp
81
Hemolyticuremic syndrome
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
coags in TTP/HUS and DIC
elevated PT and PTT in DIC
NORMAL in TTP/HUS since clots are primarily platelet only without much consumption of coagulation factors
83
TTP clinical
neuro abnormalities
microangiopathic hemolytic anemia
thrombocytopenia purpura
fever
abnormal renal fx
typically adults
84
HUS clinical
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
Bernard soulier sx
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
bernard soulier tx
recombinant 7a
eltrombopag - thrombopoeitin agonist
platelet transfusions
87
glanzmann thrombasthenia sx
GPIIb/IIIa - fibrinogen can't bind platelets together
autosomal recessive
severe
normal platelet morphology but no clumping
may cooccur w/ leukocyte adhesion deficiency
88
Glanzmann thrombasthemia tx
7a
HSCT
platelet or blood transfusion
common presentation:
- infant w/ severe infection
- delayed detachment of umbilical cord
- easy bruising/bleeding
- Fix
89
gray platelet syx
reduction or absence of alpha granule - minimal to no platelet plug formation
giant, pale platelets
inheritance depends on genes
90
uremia coags
decreased platelet aggregation
decreased granule secretion i.e fx
91
factor 5 leiden
most common thrombotic disorder
constitutively active F5
hereditary - because it cannot bind and be cleaved by protein C
92
APLS
most common acquired thrombotic disorder
93
heparin resistant thrombotic disorder
antithrombin deficiency
heparin potentiates antithrombin so does nothing if it's deficient
high doses might still work
very uncommon
94
budd chiari syx
obstruction of hepatic vein
abd pain - hepatomegaly
as an uncommon site for clotting raises suspicion of a thrombotic disorder
95
AT deficiency test
heparin cofactor assay first
AT antigen levels next
rarely genetic testing
96
reasons to test for thrombotic disorders
at least one unprovoked DVT/other clot
Recurrent clotting episodes
Unusual locations
97
warfarin induced skin necrosis
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
purpura fulminans
acute rapid widespread coagulability including hemorrhagic necrosis and skin infarction
usually d/t C+S deficiency
99
-xaban
direct factor "Xa" inhibitors
oral
api-, riva-, edo-
100
direct thrombin inhibitors e.g.
dabigatran PO
argatroban
bivalirudin
lepirudin
101
reversal warfarin
immediate: fresh frozen plasma (FFP)
then vitamin K
102
reversal heparin
protamine sulfate
103
clopidegrel
antiplatelet
used when aspirin c/I or as second agent in dual therapy
P2Y12/ADP receptor blocker
104
abciximab
anti platelet
anti-GPIIb/IIIa receptor
105
dipyridamole
antipltelet
phosphodiesterase inhibitor
vasodilator
indic`ated in prior stroke
106
-eplase
thrombolytics
e.g. alteplase aka tPA
tenecteplase now first choice d/t long t/12 and most specificity
all activate plasmin
107
thrombolytic antidote
aminocaproic acid
transexamic acid
reserve for life threatening d/t sfx
if less severe just d/c-ing should be sufficient
