Hematology Flashcards
(103 cards)
1
Q
RBC membrane transporter
A
HCO3-/Cl- to sequester bicarb and transport CO2
2
Q
Platelet lifespan
A
10 days
3
Q
platelet dense granules contents
A
ADP (A dense P), calcium (a dense mineral)
4
Q
alpha granules contents
A
vWF fibrinogen
5
Q
vWF receptor
A
GpIb (von wille BRAND)
6
Q
Fibrinogen receptor
A
GpIIb/IIIa
7
Q
Macrophages MHC class
A
II
8
Q
Dendritic cells MHC
A
II
9
Q
T cell costim signal
A
CD28
10
Q
MHC II associated with CD
A
4
11
Q
MHC I associated with CD
A
8
12
Q
Activates fibrinogen
A
thrombin
13
Q
activates thrombin
A
Va using prothrombin
14
Q
First step in clotting cascade
A
XII activation by collagen, BM, or platelets
15
Q
bradykinin actions
A
vasodilation
permeability
pain
16
Q
Major extrinsic pathway factor
A
VII activated by TF
17
Q
Prothrombin times measures extrinsic/intrinsic
A
extrinsic
18
Q
PTT time measures extrinsic/intrinsic
A
intrinsic
19
Q
Vit K and coagulation
A
procoagulation via factor formation
warfarin inhibits this production
20
Q
Protein C and coagulation
A
Anticoagulation; requires protein S to cleave and inactivate Va and VIIIa
21
Q
tPA and coagulation
A
Anticoagulation; activates plasminogen to plasmin which starts fibrinolysis
22
Q
Heparin and anticoagulation
A
Anticoagulation; activates antithrombin
23
Q
Warfarin MOA
A
inhibits epoxide reductase (reduces vitamin K in process of making factors)
24
Q
Clot formation step 1
A
Injury: vWF binds exposed collagen
25
Clot formation step 2
Adhesion: platelets bind vWF via GpIb(rand) at injury site
platelets release dense granules (ADP and Ca)
ADP increases platelet adherence via shape changes
26
Clot formation step 3
Activation: ADP binding causes GpIIb/IIIa (fibrinogen r) receptor expression on platelet surface
27
Clot formation step 4
Aggregation: fibrinogen binds and links platelets
28
Pro-aggregation platelet factors
TXA2
Low blood flow
Inc. aggregation
29
Anti-aggregation factors
PGI2 and NO (endothelium)
Inc. blood flow
Dec. platelet aggregation
30
Clopidogrel MOA
Inhibits GpIIb/IIIa expression by blocking ADP receptor
31
Abciximab MOA
GpIIb/IIIa mAb
32
Glanzmann's thrombasthenia main issue
GpIIb/IIIa defect
33
Basophilic stippling
Little specks in round RBC
BASte the ox TAiL:
Thalassemias
Anemia chronic
lead poisoning
34
Bite cells
G6PD deficiency
35
Ringed sideroblasts
Excess iron in mitochondria (sideroblastic anemia)
36
Schistocyte
DIC, TTP/HUS, mechanical hemolysis
37
Spherocyte
hereditary spherocytosis or autoimmune hemolysis
38
Teardrop cell
Bone marrow infiltration forces extramedullary hematopoiesis (sheds a tear because forced out of home)
39
Target cell
```
HALT he said to the target:
HbC
Asplenia
Liver
Thalassemia
```
Excessive RBC membrane
40
Heinz bodies
Oxidation of iron causes denatured Hgb precipitation and membrane damage -> bites taken out
G6PD
41
Howell-Jolly bodies
Nuclear remnants in RBC
Normally removed by spleen
Hypo-/asplenia or mothball ingestion (naphthalene)
looks like olive (Olive-Olly bodies)
42
Microcytic anemias
```
Iron deficiency
ACD
Thalassemia
Sideroblastic
Lead poisoning
```
43
Normocytic nonhemolytic anemias
ACD at first
CKD
Aplastic anemia
44
Normocytic hemolytic intrinsic anemias
```
Hereditaryspherocytosis
G6PD
HbC
SCD
PNH
```
45
Normocytic hemolytic extrinsic anemias
Autoimmune
Microangiopathic
Macroangiopathic
Infection
46
What is megaloblastic anemia
RBCs with high nuclear:cytoplasm ratio due to impaired DNA synthesis (think about requirements for DNA synthesis being lost as a cause)
47
Megaloblastic anemias
Folate deficiency
| B12 deficiency
48
Non-megaloblastic macrocytic anemias
Liver disease
Alcoholism
Reticulocytosis
49
What finding is always present in megaloblastic anemias?
Hypersegmented neutrophils
50
Iron deficiency lab/slide profile
Low free iron
Inc. TIBC (free transferrin)
Low ferritin
Microcytosis
51
What is Plummer-Vinson syndrome?
Iron deficiency anemia +
Esophageal webs +
Atrophic glossitis
Blood + Throat + Tongue
52
Alpha thalassemia defect
Alpha globin
53
Alpha thalassemia cis deletion common in __
Asians - ChIneSe
54
Alpha thalassemia trans deletion common in __
TRANSatlantic - Africa
55
Alpha thalassemia 4 gene deletion -->
No alpha globin --> gamma 4 globin (Hb Bart's) --> dead at birth hydrops fetalis
56
Hb Bart's is _
gamma 4 globin from no alpha
57
Alpha thalassemia 3 gene deletion
HbH
| Excess B so B4 (HbH)
58
Alpha thal 1 or 2 gene deletion
clinically insignificant
59
Alpha thalassemia is bad because it disrupts the__
Alpha:gamma globin ratio
| Gamma 4 is the worst
60
Alpha thalassemia smear
Microcytic anemia (not enough alpha globin so similar to iron deficiency)
61
Beta thalassemia major issue
Dec. B-globin synthesis from point mutations
62
Beta thalassemia major population to think of
Mediterraneans and Italians!
63
B-thal minor
Asymptomatic
Heterozygote
Diagnosis by inc. HbA2 >3.5 on gel
64
This hemoglobin is necessary from gestation on
alpha
65
B thal major smear
```
Anisocytosis
Poikilocytosis
Microcyotsis
Target cells
Schistocytes
```
66
B thal major
B chain absent so severe anemia req/ blood transfusion
Marrow expands to make up leading to crew cut skull XR and skeletal deformities
Inc. HBF (alpha 2 gamma 2)
67
Folate deficiency findings
hyperseg PMNs
glossitis
high homocysteine
68
B12 deficiency risk factors
vegans
malabs (Crohn's)
Pernicious anemia
PPIs
69
B12 deficiency findings
Neurologic symptoms!
Peripheral neuropathy
Dementia
70
Findings of intravascular hemolysis
High LDH
| Hemoglobinuria
71
Findings of extravascular hemolysis
Spleen clears RBCs
Inc. LDH
Inc. unconj bilirubin --> jaundice
72
Mechanism of ACD
Inflammation causes inc. hepcidin which binds ferroportin and inhibits iron transport
73
ACD lab findings
Low iron
Low TIBC
High ferritin
74
Hereditary spherocytosis mechanism
defective membrane-associated proteins causes round cells that get caught by spleen causing splenomegaly (ankyrin, band 3, protein 4.2, spectrin)
extravascular
75
Hereditary spherocytosis smear
No central pallor
Inc. MCHC
(Premature removal by spleen)
76
G6PD deficiency mechanism
low glutathione and inc. RBC susceptibility to oxidant stress
extravascular hemolysis
77
G6PD deficiency smear
```
Heinz bodies (oxidized iron bodies)
Bite cells
```
78
Pyruvate kinase deficiency presentation
hemolytic anemia in a newborn
| Low ATP leads to rigid RBCs
79
PNH mechanism
intravascular
| Complement-mediated RBC lysis due to low decay-accelerating factor
80
PNH triad
Hemolytic anemia
Pancytopenia
Venous thrombosis
81
SCD most common mutation
Point mutation G6V of beta chain
82
Virus to watch out for with SCD
Parvovirus B19 bc of aplastic crisis
83
Howell jolly bodies would be found after __ in SCD
Autosplenectomy
84
AIHA Warm agglutinin antibodies
IgG because from chronic anemia from SLE, CLL, drugs, etc.
85
AIHA cold agglutinin antibodies
IgM because from acute anemia by CLL, Mycoplasma, or mono
86
Microangiopathic anemia smear findings
Schistocytes
87
Microangiopathic anemias
```
DIC
TTP
HUS
SLE
Malignant hypertension
All cause mechnical destruction
```
88
Macroangiopathic anemia mechanism
Prosthetic valves and aortic stenosis, heavy running causes schistocytes and hematuria
89
Hemophilia A defect
Deficiency of factor VIII which increases PTT
90
Hemophilia B defect
Deficiency of factor IX which increases PTT also
91
PTT measures all factors except:
VII and XIII
92
Bernard-Soulier syndrome mechanism
Defective GpIb (vWF receptor) causes low platelet adhesion
93
Glanzmann's thormbasthenia mechanism
Defective GpIIb/IIIa (ADP receptor) so defective platelet-platelet aggregation
94
ITP defect
GpIIb/IIIa antibodies causes splene consumes complexes and inc. megakaryocytes
95
TTP defect
ADAMTS13 (vWF cleaver)
Multimers cause platelet aggregation and thrombosis
Labs shows schistocytes and inc. LDH (hemolysis)
96
TTP presentation
```
Pentad:
Neurologic
Renal
Fever
Thrombocytopenia
Microangiopathic hemolytic anemia
```
97
von willebrand factor is highly associated with this coagulation factor
VIII
| protects / carries it
98
Causes of DIC
```
Sepsis
Trauma
OB complications
Pancreatitis
Malignancy
Nephrotic syndrome
Transfusion
```
99
DIC labs
Schistocytes, D-dimer, low fibrinogen, low factor V and VIII
100
Factor V Leiden mutation
Mutant V resists degradation by protein C and causes hypercoagulability; MC inherited hypercoagulability in whites
101
Protein C or S deficiency
Inability to inactivate V and VIII causes inc. thrombotic skin necrosis with hemorrhage after warfarin administration
102
Main benefit of transfusing fresh frozen plasma
Coagulation factors
103
Uses of FFP
DIC, cirrhosis, warfarin overdose
