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USMLE REVIEW > Hemeotology > Flashcards

Hemeotology Flashcards

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USMLE® Step 1 flashcards
1
Q

What kicks off extrinsic pathway of coagulation cascade?

A

Tissue Factor (from damage) activates Factor 7

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2
Q

What kicks off the intrinsic pathway of coag cascade?

A

Factor 12

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3
Q

Hemophilia A is deficient in…

A

Factor 8

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4
Q

Hemophilia B is deficient in…

A

Factor 9

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5
Q

Accelerating factors?

A

Factors 5 and 8

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6
Q

What cation is essentialnfor the coagulation cascade?

A

Ca+

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7
Q

What molecule breaks down fibrin mesh?

A

Plasmin

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8
Q

Functions of kallikrein

A

Converts plasminogen to plasmin

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9
Q

PT

A

Prothrombin Time

**test how effectively tissue factor activates

Extrinsic and common pathway

Always reported as an INR

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10
Q

PTT

A

Partial thromboplastin time (PTT)

Intrinsic and common pathway

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11
Q

Bleeding time

A

Measuring platelet function

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12
Q

Lab results of hemophilia

A

Increase PTT

**NO EFFECT on PT/INR

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13
Q

Normal bleeding time but increased PT and PTT

A

Vitamin K deficiency

Co factor for carboxylation of factor 10, 9, 7, 2, C and S

Inadequate Vit. K intake
Newborns
Warfarin
End-stage liver disease

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14
Q

Most common cause of hypercoaguability in whites?

A

Factor V Leiden = Mutant factor 5 that is resistant to degradation by activated protein C

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15
Q

Heparin reversal

A

Protamine sulfate

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16
Q

Warfarin reversal

A

Oral or IV Vitamin K (takes days)

Fresh frozen plasma, if unstable

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17
Q

Preferred anticoagulant for immediate anticoagulation?

A

Heparin

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18
Q

Preferred anticoagulant for long term?

A

Warfarin

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19
Q

Preferred anticoagulant during pregnancy?

A

HEPARIN!!

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20
Q

Anisocytosis

A

RBCs of varying sizes

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21
Q

Poikilocytosis

A

RBCs of varying shapes

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22
Q

Too many RBCs

A

Polycythemia/ erythrocytosis

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23
Q

Immature erythrocytes in circulation?

A

Reticulocytes

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24
Q

Basophilic stippling

A

clumps of denatured RNA

Lead Poisoning

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25
Q

Acanthocyte “spur cell”

A

Irregular spikes
Abetalipoproteinemia
Liver Disease

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26
Q

Schistocytes

A

Chopped up parts of RBC, pathologic intravascular clotting

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27
Q

Target cells

A

“HALT” said the hunter to its target

Hemoglobin C disease
Asplenia
Liver Disease
Thalassemia

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28
Q

Howell-Jolly body

A

Basophilic remnant of nucleus in red cell

Asplenic

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29
Q

Heinz Body/ Bite Cells

A

Oxidized hemoglobin = G6PD deficiency

Normally removed from RBCs by splenic macrophages resulting in bite cells

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30
Q

Drugs that cause oxidative damage with G6PD deficiency

A

“Spleen purges nasty inclusions from damaged cells”

Sulfonamides
Primaquine
Nitrofurantoin
Isoniazide
Fava beans*****
Dapsone
Cloroquine
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31
Q

How to differentiate a heinz body from a howell-jolly body?

A

RBC can only have 1 howell-jolly body (nuclear remnant)

Can have many heinz bodies (oxidized hemoglobin)

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32
Q

What allows RBCs to change shape as they pass through vessels?

A

Spectrin creates biconcave & flexible

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33
Q

Immature erythrocytes in circulation

A

Reticulocytes

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34
Q

Where does hematopoesis take place in the embryo?

A

“Young Liver Synthesizes Blood”

Yolk Sac (3-8 weeks)
Liver
Spleen
Bone Marrow (28 weeks)

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35
Q

Defect in sickle cell hemoglobin

A

2 alpha and 2 beta chains but one amino acid substitution in B chain (glutamic acid is replaced by valine)

Hemoglobin polymerize with in red cell and creates the sickle shape

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36
Q

Rate limiting step in heme synthesis

A

ALA-synthase, requires B6

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37
Q

Enzyme defective in lead poisoning

A

ALA dehydratase and ferrochelatase

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38
Q 
Painful abdomen
Port-wine urine
Polyneuropathy
Psychological disturbances
Precipitated by Drugs
A

Acute intermittent porpyria

Defect in prophobilinogen deaminase

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39
Q 
Blistering cutaneous photosensitivity
Tea colored urine
Hyertrichosis
Associated with hep C/ alcoholism
High LFTs
A

Porphyria cutanea tarda

Defect in uroporphyrinogen decarboxylase

*Most common porphyria

40
Q

Malignancies with high epo leading to polycythemia

A

“Potentially Really High Hematocrit”

Pheochromocytoma
Renal Cell Carcinoma
Hepatocellular Carcinoma
Hemangioblastoma

41
Q

alpha globin gene deletions

A

alpha thalassmia

African and asian

1 abnormal allele = no anemia
2 abnormal alleles = alpha thalassemia minor, no anemia
3 abnormal alleles = HgH disease, little alpha globin, and the excess B globin forms B4
4 abnormal alleles = incompatible with life, hydrops fetalis

42
Q

Defect in beta globin gene most common in what populations?

A

Mediterannean

43
Q

B chain is underproduced

A

B-thalassemia minor
Usually asymptomatic
Increased HbA2

44
Q

Absent beta globin

A

B-thalassemia major
Target cell
SEVERE anemia
Requires blood transfustions

45
Q

What would use a to treat a B-thalassemia major patient with hemochromatosis

A

Not phelbotomy = counter productive!!

Instead chelate the iron with deferoxamine!

46
Q

Severe anemia
Target cells
Hair on end appearance on skull extra
Chipmunk faces

A

B thalassemia major

47
Q

hypocellular bone marrow with fatty infiltration

A

Aplastic anemia

48
Q

Microcytic anemia + swallowing difficulty + glossitis

A

Plummer Vinson

49
Q

Microcytic anemia

> 3.5% HbA2

A

B-Thal minor

50
Q

Macrocytic anemia

Hypersegmented neutrophils

A

B12 or Folate

51
Q

Megaloblastic anemia

Peripheral Neuropathy

A

B12 deficiency

52
Q

Megaloblastic anemia

Basophilic stippling

A

Lead poisoning

53
Q

Microcytic anemia reversible with B6 supplements

A

Sideroblastic Anemia

54
Q

HIV-positive patient with macrocytic anemia

A

ZIdovudine

55
Q

Normocytic anemia with elevated creatinine

A

Anemia of chronic disease

56
Q

+ osmotic fragility test

A

Hereditary spherocytosis

High % of lysis of RBCs at any given concentration of NaCl

57
Q

Treatment for hereditary spherocytosis?

A

Splenectomy - will then see howell jolly bodies!

58
Q

Common causes of sickle crisis?

A

Hypoxemia
Dehydration
Acidosis

**deoxygenated HbS polymerizes!!!

59
Q

What resistance do heterozygotes for sickle cell trait have?

A

Resistance to malaria

60
Q

Treatment for sickle cell

A

Hydroxyurea - increases production of HbF

Bone Marrow transplantation

61
Q

Direct coombs test

A

Coombs reagent = anti-human antibodies (bind constant region)

Add coombs reagent to pts serum, if Abs present on RBCs they will agglutinate when coombs reagent is added

62
Q

Indirect coombs test

A

Looking for antibodies in serum….

Normal RBCs added to pts serum, then add coombs reagent and watch for agglutination

63
Q

Difference between hemoglobin S defect and hemoglobin C defect?

A 
S = glutamic acid to valine
C = glutamic acid to lysine
64
Q

What molecules are involved in platelet adhesion?

A

Endothelial damage exposes collagen

VWF binds collagen and then binds Gp1B receptor on platelets

65
Q

Describe platelet activation

A

ADP is released from platelets bound to the vWF

ADP stimulates platelets to expose Gp2b3a receptors

Fibrin connects Gp2b3a receptors and allows for aggregation to occur

66
Q

Clopidogrel

A

ADP receptor blockers

67
Q

Abciximab
Tirofibal
Eptifibatide

A

Glycoprotein 2b/3a inhibitors

68
Q 
Mucous membrane bleeding
Epistaxis
Petechiae
Increased bleeding time
Normal PT/PPT
Anti Gp2b3a antibodies
A

Immune thromobcytopenia

Abs bind platelets and complex gets eaten by splenic macrophages

LOW platelet count
Increased megakaryocytes on bone marrow biopsy

69
Q

Deficiency in metalloprotease ADAMTS`13

Fever
Anemia
Thrombocytopenia
Renal failure
Neuro symptoms
A

Thrombotic Thromocytopenic Purpura

ADAMTS13 is deficient
Less degradation of vWF multimers

More large vWF multimers
Increased platelet adhesion
Increased platelet adhesion and thrombosis

70
Q

Bernard-Soulier Syndrome

A

Defect in Gp1b (defect in platelet to vWF adhesion)

71
Q

Glanzmass thrombasthenia

A

Defect in Gp2b3a (defect in platelet to platelet aggregation)

72
Q

Most common inherited bleeding disorder

A

Von Willebrand disease

Decreased vWF

Mixed! Affects both coag casacade and platelet plug formation

73
Q

2 functions of vWF

A

Stabilize and protects factor 8

Binds to subendothelial collagen and Gp1b on platelets

74
Q

Ristocetin cofactor assay

A

Ristocetin = makes vWF aggregate

SO if no vWF then no agglutination!

75
Q

Treatment for vWF Disease

A

Desmopressin - releases vWF from stored in endothelium

76
Q 
Low fibrinogen
High D-dimer
Low platelet, high bleeding time
Schistiocytes
Bleeding
Multiorgan Failure
A

DIC

77
Q

Causes of DIC

A

“STOP making thrombi”

Sepsis (gram neg)
Trauma
Obstetric complications
Pancreatitis (acute)
Malignancy
Transfusion
78
Q

What defines Hodgkin lymphoma?

A

Presence of Reed-Sternberg cells

“Owl’s Eyes”

79
Q

Constitutional B symptoms of hodgkin lymphoma

A

Fever
Night Sweats
Wt loss

80
Q

What CDs are found on Reed Sternberg cells

A

CD15 and CD30

2 owls eyes x 15 =30

**the more reed sternberg cells the worse the prognosis

81
Q

“Starry Sky” = lymphocytes with interspersed macrophages
Associated with EBV
t(8;14)

A

Burkitt Lymphoma

82
Q

Reed Sternberg

A

Owls eyes

Hodgkin Lymphoma

83
Q

Down syndrome is associated with which hematological malignancy?

A

Acute lymphoblastic Leukemia (ALL)

“We ALL fall DOWN”

84
Q

Auer rods

A

Acute Myloid Leukemia

85
Q

Defined by philadelphia chromosome

A

Chronic Myloid Leukemia

t(9:22) = BCR-ABL

Encodes constitutively activated tyrosine kinase

“Philadelphia CreaML Cheese”

86
Q

Treatment for philadelphia chromosome

A

Imantinib = inhibits bcr-abl tyrosine kinase

87
Q

Tdt+ Leukemia

A

ALL

88
Q

Leukemia with smugde cells

A

CLL

89
Q

Anemia
Renal insufficiency
Back Pain
Hypercalcemia

A

MULTIPLE MYELOMA!

90
Q

Rouleaux formation

Punched out lytic bone lesions on x-ray

A

Multiple Myeloma

91
Q

What type of antibody is secreted in multiple myeloma?

A

IgG

92
Q

Increased red cell mass (hematocrit) without elevated erythropoietin

Plethroa
Pruritis after hot shower
Splenomegaly
Hyperviscosity of blood

A

Polycthemia vera

93
Q

Mutation associated with polycthemia vera

A

JAK2 mutation

94
Q

Teardrop RBCs

A

Myleofibrosis = obliteration of bone marrow due to increased fibroblast activity in response to proliferation of monoclonal cell lines

95
Q

Treatment for hemophilia A and Von Willibrand Disease?

A

Desmopressin… releases VWF and Factor 8 stored in endothelium

USMLE REVIEW (25 decks)

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