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System Path I > Heme - Ewwwww > Flashcards

Heme - Ewwwww Flashcards

1
Q

precursor of granulocytes

A

myeloblast

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2
Q

immediate precursor to neutrophil

A

band cell

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3
Q

precursor to platelets

A

megakaryocyte

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4
Q

kidney shaped nucleus

A

monocyte (macrophage in blood)

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5
Q

releases major basic protein

A

eosinophils

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6
Q

WBC where granules cover nucleus

A

basophil

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7
Q

Wright - Giemsa stain stains what?

A

AT rich segments of DNA

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8
Q

mutation in ankyrin, spectrin, or band 3 - disease and type of hemolysis

A

hereditary spherocytosis - extravascular

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9
Q

increased osmotic fragility of RBCs (disease and morphological finding)

A

Hereditary spherocytosis - Howell Jolly body

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10
Q

Heinz bodies (2 diseases stain used)

A

G6PD Deficiency and alpha thalassemia - supravital (methylene blue or bromocresol green)

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11
Q

Hb values for men and women in anemia

A

male: < 13.5 female: < 12.5

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12
Q

MCV: microcytic, normal, macrocytic

A

micro: < 80 normal: 80-100 macro: >100

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13
Q

Name components of Hb and diseases from the deficiencies

A

Heme (iron + protoporphyrin): iron def. anemia, anemia of chronic disease (Fe stuck in macrophages)
Protoporphyrin: sideroblastic anemia
Globin: thalassemia

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14
Q

most common nutrional deficiency in the world

A

iron

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15
Q

where is iron absorbed

A

duodenum

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16
Q

molecule that transports iron in blood

A

transferrin

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17
Q

molecule that stores iron and where?

A

ferritin in liver and bone marrow macrophages

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18
Q

what is TIBC

A

total iron-binding capacity, measures transferrin molecules in blood (%saturation tells % of transferrin bound by iron)

always opposite of ferritin

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19
Q

common iron deficiencies by age group: infant/children, adults, elderly

A

infants/children: diet

adults: peptic ulcer disease (males) and menorrhagia (females)
elderly: colon polyps/carcinoma (developed) hookworms in (developing)

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20
Q

consequences on gastrectomy on iron absorption

A

decreased acid production, more iron in Fe+3 state, less absorption

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21
Q

signs of iron deficiency

A

paleness, koilonychia, pica

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22
Q

RDW and what is it called when its high?

A

red cell distribution width (spectrum of size of RBCs)

wide distribution is called anisocytosis

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23
Q

esophageal web, atrophic glossitis, beefy-red tongue

A

Plummer-Vinson syndrome - iron deficiency anemia

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24
Q

anemia assoc. with chronic inflammation (disease, type of anemia, and most common population)

A

anemia of chronic disease - microcytic - hospitalized pts

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25
Q

acute phase reactant from liver that sequesters iron (name and why)

A

hepcidin - to prevent bacteria from accessing iron

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26
Q

ringed sideroblasts: disease - enzyme - causes

A

sideroblastic anemia - ALA synthase - alcoholism, lead poisoning, vit B6 def

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27
Q

ferritin: low
TIBC: high
serum iron: low
% sat: low

A

iron def. anemia

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28
Q

ferritin: high
TIBC: low
serum iron: low
% sat: low

A

anemia of chronic disease

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29
Q

ferritin: high
TIBC: low
serum iron: high
% sat: high

A

sideroblastic anemia

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30
Q

protection from plasmodium falciparum (3 diseases)

A

thalassemia
sickle cell trait
G6PD Deficiency

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31
Q

HbA

A

alpha2,beta2

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32
Q

HbA2

A

alpha2, delta2

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33
Q

HbF

A

alpha2, gamma2

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34
Q

HbH - structure and disease and chromosome (# and mutation)

A

Beta tetramer - alpha thalassemia (3 genes deleted) - chromosome 16 - deletion

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35
Q

Hb Barts - structure and disease and chromosome (# and mutation)

A

Gamma tetramers - alpha thalassemia (4 genes deleted) hydrops fetalis - chromosome 16 - deletion

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36
Q

B0 and B+ (disease, type of mutation, chromosome # - meaning)

A

Beta thalassemia - point mutation in promotor or splicing site - chromosome 11 - B0: absent production, B+: diminished production

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37
Q

target cell: disease(s) and type of anemia

A 
B-thalassemia minor (B/B+) - microcytic, hypochromic
Sickle Cell (intravascular hemolysis)
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38
Q

aplastic crisis with parvo B19 (3)

A

B-thalassemia major
Hereditary spherocytosis
Sickle cell

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39
Q

crewcut appearance on x-ray

A

B-thalassemia major, sickle cell

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40
Q

chipmunk facies

A

B-thalassemia major, sickle cell

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41
Q

no HbA, inc HbA2, inc HbF

A

B-thalassemia major

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42
Q

hypersegmented neutrophil

A

macrocytic anemia >5 lobes

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43
Q

magaloblastic anemia (deficiencies)

A

B12 and folate

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44
Q

where is folate absorbed?

A

jejunum

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45
Q

macrocytic anemia, glossitis, inc. homocysteine, normal methylmalonic acid (disease and neural state)

A

folate deficiency - no neuro symptoms

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46
Q

where is B12 absorbed?

A

ileum

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47
Q

pernicious anemia: most common cause of what? diease and explanation

A

vit B12 deficiency - autoimmune destruction of parietal cells, less intrinsic factor, less B12 absorption

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48
Q

Schilling test

A

tests for pernicious anemia - can’t absorb labeled B12 and it gets excreted

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49
Q

diphyllobothrium latum leads to?

A

vit B12 deficiency

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50
Q

inc. methylmalonic acid - disease and consequences

A

vit B12 deficiency - cant be converted to succinyl CoA, builds up and integrates into spinal cord myelin - loss of proprioception and vibratory sense - also spastic paresis

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51
Q

2 causes of normocytic anemia

A

inc peripheral destruction or underproduction

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52
Q

reticulocyte - what is it, what does it look like?

A

young RBC released from bone marrow - larger cells with bluish cytoplasm (due to residual RNA)

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53
Q

high reticulocyte count (>3%) in anemia, explain why and how to fix it

A

RC falsely elevated due to decrease in total mature RBCs (so % of RC goes up) - correct it by multiplying RC by (hematocrit/45)

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54
Q

unconjugated bilirubin is the breakdown product of what? (specifically)

A

protoporphyrin

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55
Q

Bone marrow erythroid hyperplasia, increased unconj. bilirubin, decreased serum haptoglobin, hemoglobinuria

A

hemolytic anemia

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56
Q

Howell-Jolly Bodies

A

hereditary spherocytosis
sickle cell
hemolytic anemias

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57
Q

mutation in sickle cell: gene, type, products

A

B chain of Hb - point mutation - glutamic acid replaced by valine

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58
Q

poikilocytosis: shape and disease

A

pencil cells - severe iron deficiency anemia and beta major thalassemia

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59
Q

HbS

A

two abnormal Bchain Hb genes - sickle cell

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60
Q

how does hydroxurea work? (mechanism and disease)

A

raises HbF levels, helps with sickle cell and beta thalassemia major

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61
Q

dactylitis, autosplenectomy, howell jolly bodies, hematuria and proteinuria

A

sickling crisis

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62
Q

most common cause of death in children with sickle cell

A

infection from encapsulated organisms (strep penumonia and H. influenzae) due to autosplenectomy

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63
Q

most common cause of death in adults with sickle cell?

A

acute chest syndrome: chest pain, pneumonia, lung infiltrates, SOB from thrombosis

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64
Q

affects of sickle cell TRAIT on kidney?

A

only sickles in renal medulla (microinfarcts) leading to microscopic hematuria and decreased ability to concentrate urine

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65
Q

what is the metabisulfite screen used for?

A

causes HbS to sickle in any amount, positive in disease and trait

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66
Q

HbC crystals on blood smear: mutation in what gene and what products?

A

Beta chain of Hb - glutamic acid replaced by lysine (Ly-C-ine)

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67
Q

RBCs more susceptible to destruction by complement, episodic intravascular hemolysis, hemoglobinuria and -emia (disease, underlying problem, explanation of episodic)

A

Paroxysmal nocturnal hemoglobinuria (PNH)
mutation in PIGA gene (makes GPI: anchoring protein for DAF) DAF protects against complement-mediated damage by inhibiting C3 convertase - no GPI, no DAF
Happens at night because of shallow breathing in sleep, drop in pH from CO2 which activates complement

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68
Q

sucrose test screens for what disease?

A

Paroxysmal nocturnal hemoglobinuria (PNH)

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69
Q

acidified serum test confirms what disease?

A

Paroxysmal nocturnal hemoglobinuria (PNH)

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70
Q

CD55 is also known as? absent in what disease?

A

DAF (decay accelerating factor) and PNH

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71
Q

complications of PNH?

A

iron deficiency anemia

AML (10%)

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72
Q

Forms of G6PD: name, severity, type of hemolysis

Also normal form

A

African: G6PDA- mild intravascular hemolysis
Mediterranean: severe intravascular hemolysis
Normal: G6PD B

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73
Q

exacerbated with fava beans, sulfa drugs

Disease and common complaint

A

G6PD deficiency - back pain (Hb is nephrotoxic)

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74
Q

enzyme studies for G6PD deficiency should be performed when? why?

A

weeks after hemolytic episode. During crisis all cells without G6PD are destroyed so all the cells screened during the crisis have the enzyme

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75
Q

IgG mediated destruction of RBCs is what kind of hemolysis?

A

Extravascular

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76
Q

IgM mediated destruction of RBCs is what kind of hemolysis?

A

Intravascular

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77
Q

IgG mediated destruction of RBCs is what kind of agglutinin?

A

warm

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78
Q

IgM mediated destruction of RBCs is what kind of hemolysis?

A

cold

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79
Q

what disease do you treat with IVIG and why?

A

IgG mediated hemolytic anemia so spleen eats foreign IgG instead of IgG deposited on native RBCs

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80
Q

IgG mediated hemolytic anemia is associated with what other diseases/drugs? (3)

A

SLE (most common)
CLL
penicillin

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81
Q

IgM mediated hemolytic anemia is associated with what disease?

A

Mycoplasma pneumonia

infections mononucleosis

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82
Q

Direct Coombs test: method, what it confirms, disease

A

Anti-IgG added to patient’s RBC (agglutination if RBCs are coated with Ab)
presence of antibody-coated RBCs
Immune hemolytic anemia

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83
Q

Indirect Coombs test: method and disease

A

Anti-IgG and test RBCs are mixed with pt serum (agglutination occurs if serum Abs are present)
presence of Ab’s in pt’s serum
Immune hemolytic anemia

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84
Q

bite cell: how is it formed?

A

macrophages in spleen remove Heinz bodies from RBCs

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85
Q

schistocytes: how are they formed? Name a few diseases

A

shearing forces in circulation

DIC, prosthetic heart valves, aortic calcification (stenosis)

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86
Q

parvovirus B19 infects what cells? leading to what?

A

Progenitor red cells - halts erythropoiesis - aplastic crisis in people with preexisting marrow stress

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87
Q

Diseases leading to dry tap

A

aplastic anemia
Hairy cell
myelophthisic process

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88
Q

viruses leading to aplastic anemia

A

Hepatitis (not A B C G)
CMV
EBV
herpes zoster

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89
Q

Outcome of primary hemostasis

A

weak platelet plug

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90
Q

Outcome of secondary hemostasis

A

stabilization of platelet plug by coagulation cascade

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91
Q

step of primary hemostasis mediated by reflex neural stimulation and endothelin release

A

step 1: transient vasoconstriction

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92
Q

Weibel-Palade bodies contain what substances?

A

vWF

P-selectin

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93
Q

what does von willebrand factor (vWF) bind to and with what receptor?

A

exposed subendothelial collagen

GP1b receptor

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94
Q

where does vWF come from? (2 locations)

A

Weibel-Palade bodies in endothelial cells

alpha-granules of platelets

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95
Q

dense granules in platelets release what to expose what?

A

ADP to expose GPIIb/IIIa

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96
Q

what is the role of TXA2 in primary hemostasis and how is it made?

A

platelet aggregation

made by COX

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97
Q

what molecule binds platelets in a platelet plug?

A

fibrinogen

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98
Q

petechiae are a sign of?

A

thrombocytopenia (they are not seen in qualitative disorders)

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99
Q

mucosal and skin bleeding, hemoptysis, hematuria are features of what?

A

disorder in primary hemostasis

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100
Q

autoimmune production of IgG against platelet antigens, what disease?

A

Immune thrombocytopenic purpura (ITP)

most common cause of thrombocytopenia in adults and children

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101
Q

acute Immune thrombocytopenic purpura (ITP)

who? cause? outcome?

A

children
viral infection or immunization
self-limited

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102
Q

chronic Immune thrombocytopenic purpura (ITP) who? cause? outcome?

A

adults (women)
assoc with SLE
shortlived thrombocytopenia in offspring (IgG can cross placenta)

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103
Q

decreased platelets
normal PT/PTT
increased megakaryocytes

A

Immune thrombocytopenic purpura (ITP)

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104
Q

treatment of Immune thrombocytopenic purpura (ITP)?

A

IVIG to raise platelet count

splenectomy (removes source of Ab and site of platelet destruction)

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105
Q

Decrease in ADAMTS13: disease, major system affected, and normal function of enzyme

A

thrombotic thrombocytopenia purpura (TTP)
CNS
normally cleaves vWF

106
Q

pathologic formation of platelet microthrombi in small vessels? Disease and blood smear findings

A

microangiopathic hemolytic anemia

schistocytes (from shearing across microthrombi)

107
Q

Disease associated with E. coli O157:H7 from undercooked beef? Common to see fever and renal insufficiency. Findings?

A

hemolytic uremic syndrome (HUS)

platelet microthrombi and schistocytes

108
Q

GPIb deficiency: disease, what type of platelet disorder, and blood smear findings

A

Bernard-Soulier syndrome (BS “Big Suckers”)
qualitative
thrombocytopenia (platelets destroyed because they dont have GPIb)
enlarged platelets

109
Q

GPIIb/IIIa deficiency: disease, what type of platelet disorder, and what is impaired

A

Glanzmann thrombasthenia
qualitative
platelet aggregation

110
Q

what does thrombin do and where does it come from?

A

converts fibrinogen to fibrin

end product of coagulation cascade

111
Q

what four compounds can activate the coagulation cascade?

A

Tissue Thromboplastin (VII - extrinsic)
Subendothelial collagen (XII - intrinsic)
phospholipid surface of platelets
calcium (from platelet dense granules)

112
Q

excess bleeding post surgery or wisdom tooth removal indicates what kind of disorder?

A

problem with secondary hemostasis (coagulation cascade)

113
Q

males presents with history of joint bleeding and post-surgical bleeding. Lab findings show elevated PTT and decreased levels of FVIII. What disease, what pathway is affected?

A 
Hemophilia A (8)
intrinsic
114
Q

factor IX deficiency, 2 names

A

Hemophilia B

Christmas disease

115
Q

you expect a defect with factor VIII. Upon mixing of normal plasma with patient’s plasma you see that the PTT does not return to normal. What disease? and what disease would it return to normal?

A

Anti-FVIII Ab’s - ab’s destroy new factor VIII from donor plasma too

It corrects in hemophilia A because the deficient factor is replaced

116
Q

Your pt recently had a large-volume transfusion. What effect do you except it to have on his hemostasis abilities?

A

transfusion dilutes coagulation factors, results in a relative deficiency

117
Q

which coagulation factors require vit K gamma carboxylation?

A

II VII IX X protein C and S

118
Q

what is the major source of vit K? when would this be a problem (3 instances)?

A

normal flora in the gut
newborns with sterile colon, get vit K injection at birth
long term antibiotics: disrupt vit K producing bacteria
malabsorption: vit K is a fat sol vit

119
Q

What can heparin do to platelets? Complication? What don’t you treat with and why?

A

Cause formation of IgG Ab’s that leads to platelet destruction.
fragments of destroyed platelets can activate remaining platelets leading to thrombosis
Don’t treat with warfarin -> skin necrosis

120
Q

Is DIC a primary or secondary disease process? Name 5 causes.

A

almost always secondary

  1. pregnancy complications: thromboplastin in amniotic fluid can activate coagulation
  2. sepsis: endotoxin from E coli or N meningitidis
  3. adenocarcinoma: mucin activates coagulation
  4. AML: primary granules in Auer rods can activate coagulation
  5. rattlesnake bite: venom -> coagulation
121
Q

Elevated D-dimer indicates what disease? How is it formed?

A

best screening test for DIC

degradation product of cross-linked fibrin

122
Q

How is plasmin formed and what does it do?

What inactivates it?

A

converted from plasminogen by tissue plasminogen activator (tPA)

It cleaves fibrin and serum fibrinogen, destroys coagulation factors, and blocks platelet aggregation (prevents clotting!)

alpha2-antiplasmin inactivates

123
Q

pt. has had radical prostatectomy and presents with increased bleeding. D-dimers are not present. What disease is this and what is another cause of it?

A

Disorder of fibrinolysis (removal of thrombus after damaged vessel heals)
urokinase from prostatectomy activates plasmin

resembles DIC

can also be caused by liver cirrhosis due to reduced production of alpha2-antiplasmin

124
Q

lines of Zahn are indicative of what? what are they made out of?

A

thrombosis

alternating layers of platelets/fibrin and RBCs

125
Q

Virchow’s triad (3)

A

stasis
endothelial cell damage
hypercoaguability

126
Q

prostacyclin (PGI2) does what?

A

vasodilation and inhibition of platelet aggregation

127
Q

how does thrombomodulin work and where does it come from?

A

secreted by endothelial cells to prevent thrombosis normally

it makes thrombin activate protein C which inactivates factors V and VIII

128
Q

elevated homocysteine causes what problems and how do you get it at elevated levels (2 ways, one mild, one high levels (give assoc. signs))

A

it damages endothelial cells

mild elevation seen in folate or vit. B12 deficiencies

high levels seen in cystathionine beta synthase (CBS) deficiency (thrombosis, mental retardation, lens dislocation, long slender fingers)

129
Q

3 common sites of DVTs

A

deep leg veins
hepatic vein
cerebral vein

130
Q

explain the pathogenesis of warfarin skin necrosis starting with the common deficiency that leads to it. Explain how to handle it.

A

Protein C or S deficiency (autosomal dominant)

C and S usually inactivate V and VIII. giving warfarin results in a temporary deficiency of proteins C and S relative to other factors (due to C and S having a shorter half life). Protein C is an anticoag so when it is out of balance with the coagulation factors, you clot.

If C and S deficiency, go-give heparin (to prevent clot) until old factors II, VII, IX and X degrade so all the factors are at the same level and C and S/

131
Q

Most common inherited cause of hypercoagulable state? how does it lead to hypercoaguability?

A

Factor V Leiden

mutated factor V lacks cleavage site for deactivation by proteins C and S

132
Q

what is the mutation in prothrombin 20210A and why is it a problem?

A

point mutation in prothrombin -> increased gene expression

increased prothrombin leads to increased thrombin -> thrombus formation

133
Q

explain the relationship between ATIII deficiency and heparin including mechanism of action and treatment options

A

heparin normally activates ATIII which in turn inactivates thrombin and coagulation factors

in the deficiency, PTT does not rise with standard heparin dosing (heparin normally works by activating ATIII)

treat with high heparin to activate limited ATIII then give warfarin to maintain anticoag state

134
Q

how do oral contraceptives lead to a hypercoagulable state?

A

estrogen increases production of coagulation factors

135
Q

cholesterol clefts are indicative of what?

A

atherosclerotic embolus

136
Q

pt with fracture presents with dyspnea and petechiae, why?

A

fat embolus

137
Q

what is caisson disease and how is it treated?

A

chronic form of bends with gas emobli leading to multifocal ischemic necrosis in bone

decompression chamber

138
Q

name a complication of laparoscopic sugery

A

gas embolus - air pumped into abdomen

139
Q

3 common sites for thromboembolism and where can they embolize to?

A

femoral, iliac, popliteal veins

lungs

140
Q

pt presents with SOB, hemoptysis, V/Q mismatch and elevated D-dimer. what is causing the symptoms? what is the cause of death in this pt

A

pulmonary embolism

cardiac failure due to electromechanical dissociation in heart

141
Q

pt presents with bleeding defects and has thin superficial vessels, what disease?

A

hereditary telangiectasia

142
Q

CD34 is a marker for what cells?

A

hematopoietic stem cells

143
Q

how do neutrophil numbers change in a severe infection like gram-negative sepsis?

A

neutropenia - increased movement of neutrophils into tissues

144
Q

which type of circulation cell is most sensitive to radiation?

A

WBC

145
Q

Name four instances leading to lymphopenia and give an example of each

A

immunodeficiency: DiGeorge
high cortisol: cushing syndrome
autoimmune destruction: SLE
radiation: cancer therapy

146
Q

which CD decreases in left shift and what is it?

A

CD16 - Fc receptor

147
Q

In what cells do you see Dohle bodies and under what conditions? What color are they?

A

neutrophils during sepsis

sky blue

148
Q

name two conditions leading to monocytosis

A

malignancy and SLE

149
Q

name 3 causes of eosinophilia

A 
allergic type I hypersensitivity reactions
parasitic infections
Hodgkin lymphoma (produces IL-5)
150
Q

name the most common condition leading to basophilia

A

Chronic Myeloid Leukemia (CML)

151
Q

What is the only bacteria that leads to lymphocytic leukocytosis?

A

Bordetella pertussis

152
Q

What cells (specifically) are elevated with EBV infection?

A

CD8+ T cells

153
Q

Name the 3 most common sites of EBV infection

A

oropharynx
Liver
B cells

154
Q

Describe the monospot test:
what antibodies?
how long to get a positive result?
what does a negative/positive test indicate?

A

detects IgM Abs
positive within 1 week
Negative test: CMV
Positive test: EBV

155
Q

Exposure to ampicillin creates a rash in what infection?

A

EBV

156
Q

You advise your patient to avoid contact sports for a year. What infection does he have and why would you do this?

A

EBV - increased risk for splenic rupture

157
Q

In what cells does the EBV virus lay dormant and name two risks from this.

A

Recurrence

B-cell lymphoma (usually after aquiring immunodeficiency)

158
Q

What cells are atypical in EBV infection and what do they look like?

A

Lymphocytes

Look like monocytes, but are just CD8+ cells with extra cytoplasm and enlarged nuclei

159
Q

what cells have punched out nucleoli?

A

blast cells

160
Q

Patient presents with fatigue, bleeding, and infection. What do they have and explain the mechanism

A

Acute leukemia
Increased blast cells in the marrow “crowd out” normal hematopoiesis
fatigue from anemia, bleeding from thrombocytopenia, infection from neutropenia

161
Q

What area of the lymph node contains T cells? B cells?

A

T: paracortex
B: cortex

162
Q

what cells are in the medulla of a lymph node?

A

dendrocytes, histiocytes, macrophages

163
Q

What does your WBC count look like in acute leukemia?

A

high - lots of blasts in blood

164
Q

Positive TdT staining indicates what disease? What cells are TdT negative?

A

Acute Lymphoblastic leukemia (ALL)

Negative in myeloid blasts and mature lymphocytes

165
Q

what disease is associated with Down’s syndrome and has an onset after 5 years?

A

Acute lymphoblastic leukemia (ALL)

166
Q

name the 3 CD markers in the most common form of ALL

A

B-ALL

CD10, CD19, CD20

167
Q

t(12,21) - disease, prognosis, age group

A

ALL - good - children

168
Q

t(9,22) - diseases, prognosis, age group

A

ALL - bad - adults

CML

169
Q

Name the CD markers for T-ALL

A

CD2-CD8

NOT CD10

170
Q

Patient presents with bone pain, enlargement of LN, spleen, and liver and a mediastinal mass. What is the disease and what 2 areas must be treated directly? What age group does this affect most commonly?

A

T-ALL
scrotum and CSF
teenagers

171
Q

Myeloperoxidase positive staining indicates what disease?

A

Acute myeloid leukemia

172
Q

What are Auer rods made of and in what disease are they seen?

A

crystal aggregates of MPO

AML

173
Q

What disease is associated with Down’s syndrome and has an onset before age 5?

A

AML (acute megakaryoblastic leukemia subtype)

174
Q

t(15,17) what disease? what is the protein involved? age group? treatment?

A

AML (acute promyelocytic leukemia - APL)
retinoic acid receptor (RAR) on chromosome 17
older adults 50-60
all-trans retinoic acid

175
Q

Primary granules in abnormal promyelocytes increase the risk for what?

A

DIC

176
Q

proliferation of monoblasts, lack MPO - what disease and common site of involvement?

A

AML (acute monocytic leukemia)

infiltrate gums

177
Q

Name the 3 subsets of acute myeloid leukemia and their MPO status

A

Acute promyelocytic leukemia - MPO+
Acute monocytic leukemia - MPO-
Acute megakaryoblastic leukemia - MPO-

178
Q

smudge cell

A

Chronic lymphocytic leukemia (CLL)

179
Q

CLL what cells and what CDs?

A

B cells
CD5 (normally on T cells!)
CD20

180
Q

most common adult leukemia, two names

A

CLL or SLL

181
Q

most common cause of death in CLL? why? complication?

A

infections from hypogammaglobulinemia
neoplastic cells dont produce Igs
Can make Abs against own RBCs -> autoimmune hemolytic anemia

182
Q

CLL can transform into what? signs?

A

Diffuse large B-cell lymphoma

enlarged lymph node or spleen

183
Q

CD markers for hairy cell?

A

CD11c, CD25, CD103+, CD20

184
Q

tartrate-resistant acid phosphatase

A

Hairy cell leukemia

185
Q

kidney shaped nuclei with “fried egg” appearance

A

hairy cell

186
Q

accumulation of cells in red pulp of spleen… cells and disease

A

hairy cells

hairy cell leukemia

187
Q

proliferation of naive B cells?

A

CLL

188
Q

proliferation of mature B cells?

A

hairy cell leukemia

189
Q

HTLV-1 - assoc disease and type of cell involved

A

Adult T-cell leukemia/lymphoma (ATLL)

CD4+

190
Q

Japanese patient, skin rash, lymphadenopathy, hepatosplenomegaly, hypercalcemia. Disease and 1 other common finding.

A

Adult T-cell leukemia/lymphoma (ATLL)

lytic (punched-out) bone lesions

191
Q

lytic punched out bone lesions

A 
Adult T-cell leukemia/lymphoma (ATLL) (with rash)
Multiple myeloma (vertebral column)
192
Q

Name the 4 myeloproliferative disorders and what cells are predominantly involved

A

Chronic Myeloid Leukemia (CML) - Mature granulocytes
Polycythemia Vera (PV) - RBCs
Essential Thrombocythemia (ET) - platelets
Myelofibrosis - megakaryocytes

*All mature myeloid cells are elevated, distinction based on predominant cell type

193
Q

Three complications of myeloproliferative disorders and why they happen

A

hyperuricemia and gout (high turnover of cells)
marrow fibrosis (spent phase)
transformation to acute leukemia

194
Q

BCR-ABL fusion

Translocation, disease, what cell type is predominant

A

t(9,22) - CML - basophils

195
Q

Imatinib (Gleevec) - disease it treats and how

A

CML - blocks tyrosine kinase activity (which is increased with t(9,22) BCR-ABL fusion

196
Q

3 drugs to treat CML

A

Imatinib
IFN-gamma
Hydroxyurea

197
Q

Is CML negative or positive for Leukocyte Alkaline Phosphatase (LAP) stain? Why is LAP generated and it is used to distinguish which two processes?

A

negative
LAP is generated to fight infection
raised in leukemoid reaction (absent in CML)

198
Q

CML can progress to what?

A

AML (2/3 of the time)

ALL (1/3)

199
Q

JAK2 kinase mutation (3)

A 
Polycythemia vera (PV)
Essential thrombocythemia (ET)
Myelofibrosis
200
Q

blurry vision, venous thrombosis, flushed face, itching after bathing

A

polycythemia vera (PV)

201
Q

How do you distinguish PV from reactive polycythemia?

A

Check EPO levels (decreased in PV, elevated in reactive)

202
Q

Two treatments for polycythemia vera (PV)?

A

phlebotomy: to decrease RBC count

hydroxyurea

203
Q

Budd Chiari - what is it and what is it associated with

A 
Hepatic vein thrombosis
Polycythemia Vera (PV)
204
Q

What disease shows excess PDGF?

A

Myelofibrosis

205
Q

Tear drop RBCs

A

Myelofibrosis - RBCs get stretched trying to leave fibrotic bone marrow
Beta-thalassemia major
iron deficiency anemia

206
Q

gout, splenomegaly, tear-drop RBCs, frequent infections, bleeding and thrombosis disease and why each happens

A

Myelofibrosis
splenomegaly from extramedullary hematopoiesis
tear drop RBCs: RBCs get stretched trying to leave fibrotic bone marrow
last 3: bone marrow can’t produce enough other cells, megakaryocytes crowding -> fibrosis

207
Q

painful lymphadenopathy seen in?

A

acute infection

208
Q

painless lymphadenopathy

A

chronic inflammation, metastatic carcinoma, lymphoma

209
Q

follicular hyperplasia of lymph node, what cells, what disease?

A

B-cell

rheumatoid

210
Q

paracortex hyperplasia of lymph node, what cells, what disease?

A

T-cell

viral infections

211
Q

B-cell region of cortex of lymph node: give regions

A

follicle: inner
mantle: around follicle
margin: around mantle

212
Q

hyperplasia of sinus histiocytes (in lymph node) what does it indicate

A

lymph node is draining a tissue with cancer

213
Q

What kind of cancer produces rash? (generally)

A

T cell

214
Q

which B cells are more differentiated?

A

Small

215
Q

intermediated sized B cell lymphoma

A

Burkitt

216
Q

t(14,18) disease and genes involved

A

follicular lymphoma

BCL2 on 18 and Ig heavy chain on 14

217
Q

rituximab treats what disease and what is it’s target?

A

follicular lymphoma

anti-CD20

218
Q

BCL2 inhibits what?

A

apoptosis

219
Q

tingible body macrophages are used to distinguish what from what?

A

they are present in follicular hyperplasia, absent in lymphoma

220
Q

t(11,14) what disease what genes

A

Mantle cell lymphoma

Cyclin D1 on 11, Ig heavy chain on 14

221
Q

how do you treat MALToma?

A

treat H. pylori infection

222
Q

which lymphoma is assoc with chronic inflammatory states?

A

marginal zone lymphoma like Hashimoto thyroiditis, sjogren, H pylori

223
Q

which cancers can progress to diffuse large B-cell lymphoma (2)

A

follicular lymphoma

CLL

224
Q

extranodal mass, African child. disease, translocation, genes, appearance on microscopy, associated virus

A 
Burkitt's lymphoma
t(8,14)
c-myc on 8, Ig heavy chain on 14
starry sky
EBV
225
Q

fever, weight loss, night sweats, most common form of non-Hodgkin’s lymphoma. Disease, how it grows, age group

A

diffuse large B-cell lymphoma
grows in sheets
late adulthood

226
Q

a chinese man presents with a translocation of t(8,14), where is his mass?

A

abdomen - sporadic burkitt’s lymphoma

227
Q

Reed-sternberg cells

A

Hodgkin lymphoma

228
Q

mirror imaged nuclei - cell type and disease

A

Reed-sternberg - Hodgkin

229
Q

CD15 and CD30

A

Classical Hodgkin - no 20, still B cell

230
Q

CD45+, CD20+, CD15-, CD30-

disease and common morphological finding

A

Variant Hodgkin

popcorn cell

231
Q

popcorn cell - disease and subtype

A

Variant Hodgkin - lymphocyte rich

232
Q

lacunar cells - disease, subtype, typical patient

A

nodular sclerosis Hodgkin lymphoma, young female

233
Q

Name the 4 subtypes of hodgkin lymphoma and give the best and worst prognosis

A 
Nodular Sclerosis
lymphocyte rich (variant) (best prognosis) (popcorn is the best snack evar!)

mixed cellularity
lymphocyte-depleted (worst prognosis)

234
Q

rouleaux formation (2)

A

Multiple myeloma

Polycythemia Vera

235
Q

RANK what does it do?

A

receptor on osteoclast, bone destruction “lytic lesions”

236
Q

M spike - disease (3) and what it’s made of

A

Multiple myeloma, IgG or IgA
Monoclonal Gammopathy of undetermined significance (MGUS)
Waldenstrom macroglobulinemia (IgM)

237
Q

bone pain, proteinuria, primary AL amyloidosis, rouleaux formation

A

multiple myeloma

238
Q

Name 3 complications with multiple myeloma

A

bone pain with hypercalcemia
AL amyloidosis
proteinuria - Bence Jones proteins - renal failure

239
Q

lymphadenopathy, retinal hemorrhage, M spike - disease and treatment

A

Waldenstrom macroglobulinemia

plasmapheresis removes IgM

240
Q

Birbeck granules

A

Langerhans cell histiocytosis

241
Q

CD1a, HLA-DR and S100+ disease and population

A

Langerhans cell histiocytosis

young adult smokers

242
Q

benign proliferation of Langerhans cells - disease and cells

A

eosinophilic granuloma

eosinophils

243
Q

basophilic stipling

A

sideroblastic anemia
lead poisoning
megaloblastic anemia
Beta Thalassemia major

244
Q

What are Howell-Jolly bodies made of, when do you see them, and what stain do you use to see them?

A

excess chromatin
see when spleen isn’t fully functional (usually removes the bodies)
Wright-Geimsa stain (DNA stain)

245
Q

prussian blue stains?

A

iron

246
Q

alcoholics have what common vitamin deficiency?

A

folate

247
Q

normal ratio of fat to cells in bone marrow?

A

1:1

248
Q

downy cells

A

EBV - infectious mononucleosis

249
Q

ballerina skirt (on what cells with what infection?

A

T cells - EBV

250
Q

EBV infects what cells and can progress to what cancer?

A

infects B cells

B cell lymphoma

251
Q

first lymph nodes enlarged in Hodgkin lymphoma?

A

axial

252
Q

positive PAS staining

A

Acute Lymphoblastic Leukemia (ALL)

253
Q

Hairy cell help

A

Hairy old men TRAP bloody animals (lodged in red pulp), eat fried eggs, and shoot blanks (dry tap). Hairy old men are slow -> progresses slowly

254
Q

Tamm Horsfall protein

A

Multiple myeloma

255
Q

Russel bodies (disease, what they’re made of, appearance)

A

Multiple myeloma, extended RER and Golgi due to Ig accumulation, “fried egg” and eosinophilic

256
Q

CD13 CD33

A

Acute myeloblastic leukemia (AML)

257
Q

lots of band cells

A

chronic myeloid leukemia

258
Q

dragging sensation of abdomen

A

chronic myeloid leukemia

259
Q

reticulin stain: what does it stain and its used to detect what disease?

A

stains collagen

myelofibrosis

260
Q

MPL point mutation

A

myelofibrosis

261
Q

leukoerythroblastic key word for?

A

myelofibrosis

System Path I (5 decks)

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