Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

USMLE Step 1 > HemeOnc > Flashcards

HemeOnc Flashcards

You may prefer our related Brainscape-certified flashcards:
USMLE® Step 1 flashcards
1
Q

membrane of RBC contains what channel?

A

chloride bicarbonate antiport which is imp for allowing it to transport CO2 from periphery to lungs for elimination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

anisocytosis vs poikilocytosis

A

varying sizes vs varying shapes of the RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

platelets contain

A

dense granules (ADP, calcium), and alpha granules (vWF, finbrinogen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how much of platelets is stored in the spleen?

A

one third

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

life span of platelets

A

8-10 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

vWF receptor

A

Gp1b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Fibrinogen receptor

A

Gp11b/111a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

neutrophils

A

phagocytic, multilobed nucleus, large, spherical, azurophilic granules contain hydrolytic enzymes , lysozyme, myeloperoxidase, and lactoferrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is lactoferrin used for?

A

binds iron and inhibits growth of phagocytosed bacteria and some fungi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

monocyte

A

large kidney shaped nucleus; extensive frosted glass cytoplasm; differentiates into macrophages in tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

macrophages are activated by

A

gamma-interferon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

cell surface marker for macrophages

A

CD14

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

eosinophil

A

bilobate nucleus, defends against helminthic infxns (major basic protein), produces histaminase and arylsulfatase (helps limit rxn following mast cell degranulation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

causes of eosinophilia

A

NAACP: neoplastic, asthma, allergic processes, collagen vascular diseases, parasites (invasive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

basophil

A

mediates allergic rxn, bilobate nucleus, densely basophilic granules containing heparin, histamine, and leukotrienes (LTD4); MN: basophilic - staining readily with BASIC stains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Mast cell

A

mediates allergic rxn, degranulation - histamine, heparin, and eosinophil chemotactic factors; can bind the Fc portion of igE to membrane; involved in type 1 hypersensitivity rxns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what prevents mast cell degranulation?

A

cromolyn sodium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

dendritic cells

A

professional APCs; express MHC II and Fc Receptor on surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

lymphocyte

A

round densely staining nucleus; small amt of pale cytoplasm; B lymphocytes produce antibodies; T lymphocytes manifest the cellular immune response as well as regulate B lymphocytes and macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

plasma cell histo

A

off center nucleus, clock face chromatin distribution, abundant RER and well developed golgi apparatus; produced from B cells; will then produce large amts of antibody specific to a particular antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

costimulatory signal necc for t cell activation

A

cd28

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

AB blood group

A

has both A and B antigens on RBC surface; no antibodies in plasma; universal recipient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

O blood group

A

neither A nor B antigen on RBC surface; both antibodies in plasma; universal donor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

treatment for mom at first delivery

A

Rho (D) immunoglobulin to prevent future erythroblastosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

vit K deficiency causes

A

decreased synthesis of factors 2, 7, 9 and 10; proteins C and S

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how is vit K activated?

A

epoxide reductase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

role of activated protein C (APC) and protein S

A

cleaves and inactivates 5a and 8a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

vWF carries what factor?

A

factor 8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is the extrinsic pathway of coagulation?

A

7 –> 10 –> 5 –>2 –> fibrinogen—> fibrin mesh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

role of 5a and 8a

A

5a converts 10a to 2a; 8a converts 9a to 10a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

antithrombin inactivates what factors?

A

inhibits thrombin and factors 7a, 9a, 10a, 11a, and 12a; activated by heparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

role of tPA

A

converts plasminogen to plasmin –> cleavage of fibrin mesh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

platelet plug formation

A

vWF binds to exposed collagen upon damage; platelets then bind to vWF via Gp1b receptor at injury site; platelets then release ADP and Ca2+; ADP helps platelets adhere to endothelium; ADP binding induces GpIIb/IIIa expression at platelet surface; fibrinogen binds to these receptors and links platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

ticlopidine and clopidogrel inhibit

A

ADP induced expression of GpIIb/IIIa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

proaggregation factors

A

TXA2 (released by platelets) to decrease blood flow and increase platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

antiaggregation factors

A

PGI2 and NO (released by endothelial cells) to increase blood flow and decrease platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

aspirin inhibits

A

cyclooxygenase (TXA2 synthesis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

abciximab inhibits

A

GpIIb/IIIa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

decreased ESR can be indicative of

A

polycythemia, sickle cell anemia, congestive heart failure, microcytosis, hypofibrinogenemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

acanthocyte

A

spur cell; asso with liver disease, abetalipoproteinemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

howell jolly bodies

A

basophilic nuclear remnant found in RBCs, seen in pts with functional hyposplenia or asplenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

ddx for microcytic anemia

A

IDA, ACD, thalasssemias, lead poisoning, sideroblastic anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

nonmegaloblastic anemia

A

liver disease, alcoholism, reticulocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

extrinsic hemolytic anemias

A

autoimmune, AIHA, MAHA, infxns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

intrinsic hemolytic anemias

A

rbc membrane defect; hereditary spherocytosis; rbc enzyme def: G6PD, PK; HbC, sickle cell anemia, paroxysmal nocturnal hemoglobinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

intravascular hemolysis findings

A

decreased haptoglobin, increased LDH, hemoglobin in urine (PNH), mechanical destruction (aortic stenosis, prosthetic valve)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

extravascular hemolysis findings

A

macrophage in spleen clears RBC, increased LDH plus increased UCB which causes jaundice; examples are hereditary spherocytosis, sickle cell anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

nonhemolytic anemias

A

Anemic of chronic disease, aplastic anemia, kidney disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

pancytopenia, normal cell morphology but hypocellular bone marrow with FATTY infiltration, dx?

A

aplastic anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

causes of aplastic anemia

A

radiation and drugs (benzene, chloramphenicol, alkylating agents, antimetabolites); viral (parvo, EBV, HIV, HCV), fanconi’s anemia ; idiopathic (may follow acute hepatitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

treatment of aplastic anemia

A

withdrawal of offending agent, immunosuppressive regimens (antihyymocyte globulin, cyclosporine), allogeneic bone marrow transplanation, RBC and platelet transfusion, G-CSF or GM-CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

anemia of chronic disease

A

inflammation causes increased hepcidin (released by liver, binds ferroportin on intestinal mucosal cells and macroophages thus inhibiting iron transport) caused decreased release of iron from macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

anemia of chronic disease lab findings

A

decreased iron, decreased TIBC, increased ferritin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

pathogenesis of hereditary spherocytosis

A

less membrane causes small, round RBCs with no central pallor –> premature removal of RBCs by spleen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

findings of iron def

A

microcytosis, hypochromia –> plummer vinson syndrome (IDA, esophageal web, atrophic glossitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

4 gene deletion in alpha thalassemia causes

A

Hb Barts, incompatible with life (hydrops fetalis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

3 gene deletion in alpha thalassemia causes

A

HbH disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

beta thalassemia defect

A

point mutation in splice sites and promoter sequences; decreases beta globin synthesis;

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

beta thalassemia is prevalent where?

A

in mediterranean populations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

how to confirm diagnosis of beta thalassemia minor?

A

increased HbA2 on electrophoresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

dif between beta thalassemia minor vs major

A

heterozygote, beta chain is underproduced vs homozygote, beta chain is absent , severe anemia requiring blood transfusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

both major and minor beta thalassemias cause an increase in what kind of hemoglobin

A

HbF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

chipmunk facies

A

assso with beta thalassemia major due to marrow expansion (crew cut on skull xray ) –> skeletal deformities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

why is lead toxic?

A

inhibits ferrochelatase and ALA dehydratase causing a decrease in heme synthesis; inhibits rRNA degradation;

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

etiologies of megaloblastic anemia caused by folate deficiency

A

malnutrition (alcoholics), malabsorption, impaired metabolism (methotrexate, trimethoprim), hemolytic anemia, pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

findings of megaloblastic anemia caused by folate def

A

hypersegmented neutrophils, glossitis, decreased folate, increased homocysteine but normal methylmalonic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

etiologies of megaloblastic anemia caused by b12 def

A

insufficient intake (vegans), malabsorption (crohn’s dz), pernicious anemia, D latum (fish tapeworm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

findings of megaloblastic anemia

A

increased homocysteine AND methylmalonic acid; peripheral neuropathy with sensorimotor dysfunction, posterior columns (vibration/proprioception); lateral corticospinal (spasticity); dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

MN for lead poisoning

A

Lead lines on gingivae (burton’s lines) and on epiphyses of long bones; Encephalopathy and Erythrocyte basophilic stippling, Abdominal colic and sideroblastic ANEMIA, DROPS (wrist and foot drop),

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

treatment for lead poisoning

A

Dimercaprol and EDTA are 1st line of treatment; use succimer for kids (“it sucks to be a kid who eats lead)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

hereditary spherocytosis

A

defect in proteins interacting with RBC membrane skeleton and plasma membrane (ankyrin, band3, protein 4.2, or spectrin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

clinical findings of hereditary spherocytosis

A

splenomegaly, aplastic crisis, howell jolly bodies after splenectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

hereditary spherocytosis lab findings

A

positive osmotic fragility test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

G6PD deficiency

A

x linked, defect in g6pd causes a decrease in glutathione which causes increased RBC susceptibility to oxidant stress–> hemolytic anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

fava beans

A

causes hemolytic anemia:oxidant stress –> G6PD deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

G6PD deficiency lab findings

A

blood smear with RBCs with Heinz bodies and bite cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

pt presents with back pain followed by hemoglobinuria a few days later, what do you think it is?

A

g6pd deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

pyruvate kinase deficiency

A

autosomal recessive, defect in PK causes decrease in ATP which causes rigid RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

hemolytic anemia in a newborn think

A

pyruvate kinase def

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

crew cut on skll x ray due to marrow expansion from increased erythropoiesis caused by 2 conditions

A

sickle cell anemia and thalassemias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

pathogenesis OF sickle cell anemia

A

deoxygenated HbS polymerizes. Low O2 or dehydration precipitates sickling –> anemia + venoocclusive disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

complications in homozygotic SCD

A

aplastic crisis, autosplenectomy, salmonella osteomyelitis, painful crisis (vaso-occlusive), dactylitis (painful hand swelling), acute chest syndrome, renal papillary necrosis, microhematuria, splenic sequestrations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

defect in sickle cell anemia

A

HbS point mutation causes a single amino acid replacement in beta chain (substitution of glutamic acid with valine) at pos 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

heterozygotic SCD has resistance to

A

malaria

85
Q

treatment for SCD

A

hydroxyurea (increases HbF) and bone marrow transplantation

86
Q

HbC defect

A

glutamic acid to lysine mutation at position 6 in chain mutation

87
Q

paroxysmal nocturnal hemoglobinuria

A

increased complement - mediated RBC lysis from Impaired synthesis of GPI anchor, decay accelerating factor in the RBC membrane; increased urine hemosiderin

88
Q

autoimmune hemolytic anemia (warm agglutinin)

A

IgG; chronic anemia seen in SLE, in CLL, and with certain drugs (methyldopa); MN: Warm weather is GGGGreat

89
Q

cold agglutinin autoimmune hemolytic anemia

A

acute anemia triggered by cold, seen in CLL, mycoplasma pneumoniae, mononucleosis; MN: Cold ice cream…MMMM

90
Q

erythroblastosis fetalis

A

autoimmune hemolytic anemia seen in newbornes due to Rh or other blood antigen incompatibility

91
Q

direct coomb’s test

A

anti-Ig antibody added to patient’s RBCs agglutinate if RBCs are coated with Ig

92
Q

indirect coomb’s test

A

normal RBCs added to pt’s serum agglutinate if serum has anti-RBC surface iG

93
Q

microangiopathic anemia pathogenesis

A

RBCs are damaged when passing thru obstructed or narrowed vessel lumina, seen in DIC, TTP-HUS, SLE, malignant HTN

94
Q

schistocytes (helmet cells) seen in

A

microangiopathic anemia and macroangiopathic anemia

95
Q

macroangiopathic anemia

A

prosthetic heart valves and aortic stenosis can cause hemolytic anemia secondary to mechanical destruction

96
Q

increased serum iron can be seen in what conditions

A

hemochromatosis, lead poisoning

97
Q

in anemia of chronic disease

A

decrease in serum iron, decrease in TIBC, increase in ferritin

98
Q

iron deficiency lab values

A

decreased serum iron, increased transferrin/TIBC, decreased ferritin , major decrease in % transferrin saturation

99
Q

dif bw lab values for hemochromatosis vs lead poisoning

A

both will have increased serum iron, decreased transferrin/TIBC and increased % transferrin saturation but there is an increase in ferritin in hemochromatosis

100
Q

lead poisoning affects what enzymes that are needed for heme synthesis

A

ferrochelatase, ALA (aminolevulinic acid) dehydratase

101
Q

lab findings for anemia caused by pregnancy or OCP use

A

will only see an increase in transferrin and a decrease in % transferrin saturation

102
Q

transferrin vs ferritin

A

transport iron in blood vs primary iron storage protein of body

103
Q

what is the accumulated substrate of lead poisoning?

A

protoporphyrin (blood)

104
Q

acute intermittent porphyria: affect enzyme, accumulated substrate

A

porphobilinogen deaminase; accumulated substrates are porphobilinogen, ALA, uroporphyrine (urine)

105
Q

symptoms of acute intermittent porphyria

A

painful abdomen, red wine colored urine, polyneuropathy, psychological disturbances,

106
Q

treatment of acute intermittent porphyria

A

glucose and heme,w hich inhibit ALA synthase

107
Q

porphyria cutanea tarda: affected enzyme and accumulated substrate

A

uroporphyrinogen decarboxylase; uroporphyrin (tea colored urine)

108
Q

porphyria cutanea tarda symptoms

A

blistering cutaneous photosensitivity, most common porphyria

109
Q

decreased heme causes what to ALA synthase activity

A

increases ALA synthase activity and vice versa

110
Q

PT

A

tests function of factors 1, 2, 5, 7, and 10

111
Q

PTT

A

tests function of all factors except 7 and 13

112
Q

hemophilia A or B causes prolonged

A

PTT but not PT

113
Q

vit K deficiency causes prolonged

A

PT and PTT

114
Q

clinical manifestations of hemophilia a or b

A

macrohemorrhage, hemarthroses (bleeding into joints), easy bruising

115
Q

platelet abnormalities can result in

A

microhemorrhage: mucous membrane bleeding, epistaxis, petechiae, purpura, increased bleeding time, possible decreased platelet count

116
Q

bernard soulier disease

A

decrease in platelet count, increase in bleeding time, defect in platelet plug formation, decrease in Gp1b which causes a defect in platelet to vwf adhesion

117
Q

Glanzmann’s thrombasthenia

A

increase in bleeding time, defect in platelet plug formation, decrease GPIIb/IIIa –> defect in platelet to platelet aggregation

118
Q

idiopathic thrombocytopenic purpura

A

decrease in platelet count, increase in bleeding time, decrease platelet survival

119
Q

ITP defect

A

anti GpIIb/IIIa antibodies –> platelet/Ab complex is consumed by splenic macrophages ; labs show an increase in megakaryocytes

120
Q

thrombotic thrombocytopenic purpura

A

decrease platelet survival; defect in ADAMTS 13 (vWF metalloprotease) which decreases degradation of vWF multimers

121
Q

pathogenesis of TTP

A

increase large vWF multimers –> increased platelet aggregation and thrombosis

122
Q

symptoms of TTP

A

pentad: neurologic and renal symptoms, fever, thrombocytopenia, microangiopathic hemolytic anemia

123
Q

labs of TTP

A

schistocytes, increased LDH

124
Q

most common inherited bleeding disorder

A

von willebrand’s disease

125
Q

mechanism of von willebrand’s disease

A

defect in platelet plug formation: decreased vWF causing a defect in platelet to collagen adhesion

126
Q

treatment for von willebrand’ disease

A

DDAVP (desmopressin) which releases vWF stored in endothelium

127
Q

DIC levels for PC, BT, PT and PTT

A

decrease in platelet count, increase bleeding time, increase in PT and PTT as well

128
Q

causes of DIC

A

MN: STOP Making New Thrombi = sepsis (gram neg), trauma, obstetric complications, acute Pancreatitis, Malignancy, Nephrotic syndrome, Transfusion

129
Q

DIC labs

A

schistocytes, increased fibrin split products (D-dimers), decreased fibrinogen, decreased V and VIII

130
Q

factor V leiden disease

A

production of mutant factor V that cannot be degraded by protein C.

131
Q

most common cause of inherited hypercoagulability

A

factor V leiden

132
Q

prothrombin gene mutation

A

mutation in 3’ untranslated region associated with venous clots –> hypercoagulability

133
Q

Antithrombin deficiency

A

inherited deficiency of antithrombin –> hypercoaguability, reduced increase in PTT after administration of heparin so cannot give heparin bc it works to activate antithrombin

134
Q

protein C or S deficiency

A

decreased ability to inactivate factors V and VIII; increase risk of thrombotic skin necrosis with hemorrhage following adminstration of warfarin

135
Q

cryoprecipitate contains

A

fibrinogen, factor 8 and factor 13, vWF

136
Q

blood transfusion risks

A

hypocalcemia (citrate is a calcium chelator) and hyperkalemia (RBCs may lyse in old blood units)

137
Q

when to give FFP

A

DIC cirrhosis, warfarin over-anticoagulation; will increase coagulation factor levels by about 20%

138
Q

leukemoid reaction

A

increase WBC count with left shift and increase leukocyte alkaline phosphatase usually due to infection

139
Q

reed sternberg cells characteristic of what neoplasm

A

hodgkin’s lymphoma; binucleate/bilobed mirror images that look like “owl’s eyes”

140
Q

B symptoms

A

low grade fever, night sweats, weight loss

141
Q

incidence of hodgkin’s lymphoma vs nonhodgkin’s lymphoma

A

hodgkin = bimodal (young and old, men) vs 20-40 years of age

142
Q

viruses associated with hodgkin and nonhodgkin’s lymphoma

A

EBV (50%) vs HIV

143
Q

mediastinal lymphadenopathy is seen in hodgkin’s or nonhodgkin’s

A

hodgkin’s lymphoma

144
Q

hodgkin’s vs nonhodgkins in terms of nodes and spreading

A

localized single group of nodes; contiguous spread vs multiple peripheral nodes; extranodal is common; noncontiguous spread

145
Q

Reed Sternberg cell markers

A

CD30+ and Cd15+ B cell origin

146
Q

nodular sclerosing hodgkin’s lymphoma

A

(65-75% of all hodgkin’s lymphoma); excellent prognosis, collagen banding, lacunar cells, found in M<W, primarily young adults!

147
Q

lymphocyte predominant type of hodgkin’s lymphoma

A

excellent prognosis, 5% of all hodgkin’s lymphoma, occurs in <35 yo men

148
Q

lymphocyte depleted type of hodgkin’s lymphoma

A

poor prognosis, occurs in older males with disseminated disease

149
Q

burkitt’s lymphoma occurs in

A

adolescents or young adults

150
Q

genetics of burkitt’s lymphoma

A

t(8,14) c-myc gene

151
Q

starry sky appearance

A

sheets of lymphocytes with interspersed macrophages = burkitt’s lymphoma

152
Q

diffuse large B cell lymphoma occurs in

A

older adults, 20% in children (a type of nonhodgkin’s lymphoma)

153
Q

most common adult NHL

A

diffuse large B cell lymphoma

154
Q

mantle cell lymphoma occurs in

A

older males

155
Q

genetics of mantle cell lymphoma, prognosis, marker

A

t(11,14), overexpression of cyclin D regulatory gene, poor prognosis, CD5+

156
Q

follicular lymphoma occurs in whom? Prognosis?

A

adults, difficult to cure, indolent course, bcl-2 inhibits apoptosis

157
Q

genetics of follicular lymphoma

A

t(14, 18), bcl-2 expression

158
Q

adult T cell lymphoma caused by what virus?, clinical manifestations? Where is it most common?

A

HTLV-1 lesion, adults present with cutaneous lesions , in Japan, west africa, caribbean, aggressive

159
Q

mycosis fungoides/Sezary syndrome occurs in whom? And what is the clinical manifestation?

A

adults; cutaneous patches/nodules

160
Q

marker on mycosis fungoides/sezary syndrome

A

indolent Cd4+

161
Q

fried egg appearance

A

multiple myeloma

162
Q

multiple myeloma

A

monoclonal plasma cell cancer that arises in marrow and produces large amts of IgG or IgA

163
Q

primary amyloidosis, lytic bone lesions, M spike on protein electrophoresis, Ig light chains in urine are associated with that?

A

multiple myeloma

164
Q

bence jones protein

A

Ig light chains in urine, associated with multiple myeloma

165
Q

rouleaux formation

A

RBCs stacked like poker chips in blood smear

166
Q

mnemonic for clinical manifestations of multiple myeloma

A

CRAB: hypercalcemia, renal insufficiency, anemia, bone lytic lesions/back pain

167
Q

multiple myeloma vs waldenstrom’s macroglbulinemia

A

both have M spike = IgM (–> hyperviscosity) , but no lytic bone lesions in waldenstrom’s

168
Q

MGUS

A

monoclonal gammopathy of undetermined significance, monoclonal plasma cell expansion without the symptoms of multiple myeloma

169
Q

Acute lymphoblastic leukemia/lymphoma occurs in

A

children

170
Q

ALL markers

A

TdT+ (marker of pre-T and pre-B cells), CALLA+

171
Q

where can ALL spread to?

A

CNS and testes

172
Q

genetics of ALL that provides a better prognosis

A

t(12, 21)

173
Q

small lymphocytic lymphoma/chronic lymphocytic leukemia occurs in whom? And what are the differences?

A

adults >60 yrs of age; SLL same as CLL except CLL has an increase in peripheral blood lymphocytosis

174
Q

smudge cells on PBS indicate

A

SLL/CLL

175
Q

hairy cell leukemia

A

mature B cell tumor in the ELDERLY, cells have filamentous hairlike projections,

176
Q

what kind of leukemia stains TRAP (tartrate, resistant acid phosphatase) +?

A

hairy cell leukemia

177
Q

acute myelogenous leukemia seen in whom? PBS characteristic?

A

adults, auer rods

178
Q

t(15,17)

A

M3 AML subtype

179
Q

how to treat AML M3 type

A

ATRA (all-trans retinoic acid (vit A) which induces differentiation of myeloblasts

180
Q

CML presentation

A

increased neutrophils, metamyelocytes, basophils, splenomegaly, may transform to aml or all, very low leukocyte alkaline phosphatase due to immature granulocytes

181
Q

genetics of CML

A

philadelphia chromosome (t9,22, bcr-abl); MN: PHILADELPHIA CreaML cheese = CML

182
Q

CML responds to what treatment

A

imatinib (anti-bcrabl antibody) which inhbiits bcr-abl tyrosine kinase

183
Q

blast crisis is associated with what condition and why?

A

CML bc it may accelerate and transform to AML or ALL

184
Q

ages of the four leukemias

A

ALL = 60

185
Q

auer rods

A

peroxidase+ cytoplasmic inclusions in granulocytes and myeloblasts, commonly seen in acute promyelocytic leukemia (M3)\

186
Q

why do you get DIC in AML M3

A

release of Auer rods

187
Q

Ewing’s sarcoma genetics

A

t(11,22)

188
Q

langerhans cell histiocytosis

A

proliferative disorders of dendritic (langerhans) cells. Defective cells express S-100 and Cd1a; cells immature and cannot stimulate T lymphocytes via antigen presentation

189
Q

birbeck granules/tennis rackets on EM

A

langerhans cell histiocytosis

190
Q

polycythemia vera in relation to RBC, WBC, platelet levels

A

increase in all, positive JAK2 mutation

191
Q

essential thrombocytosis

A

increase in platelets, possible Jak2 mutation (30-50%)

192
Q

myelofibrosis

A

decrease in RBCs , psotive JAK2 mutation (30-50%)

193
Q

CML (RBC, WBC, Platelet levels)

A

decrease in RBC, increase in white cell and platelets; philadelphia chromosome!

194
Q

polycythemia vera ?

A

abnormal clone of hematopoietic stem cells that are increasingly sensitive to growth factors

195
Q

tear drop cell

A

bone marrow infiltration as seen in myelofibrosis: MN: bone marrow is crying bc it is fibrosed

196
Q

appropriate absolute polycythemia and associate diseases

A

increase in RBC mass, decrease in O2 sat, increase in EPO; lung disease, congenital heart disease, high altitude

197
Q

inappropriate absolute polycythemia and associated cause

A

increase in RBC mass and EPO; due to RCC, wilms’ tumor, cyst, HCC, hydronephrosis; ectopic erythropoietin

198
Q

plasmin’s role

A

converts fibrinogen to degradation products or fibrin to to fibrin split products (d dimers)

199
Q

leucovorin

A

used to “rescue” bone marrow if methotrexate is given too much

200
Q

3 pathologies that will give basophilic stippling of RBCs

A

MN: Baste the ox TAIL: thalassemias, anemic of chronic disease, Lead Poisoning

201
Q

bite cell RBC is caused by what pathology

A

G6PD deficiency

202
Q

schistocytes and helmet cells can be seen in what pathology?

A

DIC, TTP/HUS, traumatic hemolysis

203
Q

target cells are seen in what conditions?

A

MN: HALT -said the hunter to his target: HbC disease, Asplenia, Liver Disease, Thalassemia

204
Q

heinz bodies seen in what pathologies?

A

alpha thalassemia, G6PD deficiency, oxidation of iron from ferrous to ferric form leads to denatured Hb precipitation and damage to RBC membrane which leads to formation of BITE CELLS

205
Q

sideroblastic anemia

A

defect in heme synthesis

206
Q

treat sideroblastic anemia with

A

pyridoxine (b6 therapy)

207
Q

sideroblastic anemia etiology

A

x linked defect in aminolevulinic acid (ALA) synthase gene; reversible etiologies are alcohol and lead

208
Q

lab findings for sideroblastic anemia

A

increased iron, normal TIBC, increased ferritin

209
Q

thrombotic thrombocytopenic purpura

A

decreased platelet survival due to deficiency of ADAMTS 13 (vWF metalloprotease) that decreases degradation of vWF multimers

USMLE Step 1 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions