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Hematology and Oncology > Pathology > Flashcards

Pathology Flashcards

1
Q

Acanthocyte

A

“Spiky” RBCs

Associated with liver disease, abetalipoproteinemia

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2
Q

Basophilic Stippling

A

See with lead poisoning, sideroblastic anemias (iron cannot be incorporated into Hb),
myelodysplastic syndrome

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3
Q

Dacrocyte

A

“Teardrop” cell
Bone marrow fibrosis

S&S: lower extremity bone pain and joint tenderness; unable to aspirate a sample from bone marrow

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4
Q

Degmacyte

A

“Bite cell”
Associated with splenic removal of ppt
Seen in G6PD deficiency

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5
Q

Echinocyte

A

“Burr cell”
Smaller and more uniform projections (looks kind of like an acathocyte though)

Associated with end-stage renal disease, liver disease, and pyruvate kinase deficiency

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6
Q

Elliptocytes

A

Hereditary elliptocytosis (usually asymptomatic)

Caused by mutations in genes encoding RBC membrane proteins (spectrin)

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7
Q

Macro-ovalocyte

A 
Megaloblastic anemia (also hypersegmented neutrophils)
Marrow failure
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8
Q

Ringed sideroblast

A

Sideroblastic anemia (excess iron in mitochondria)

Excess iron in mitochondria

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9
Q

Schistocyte

A

DIC, TTP/HUS, HELLP (HTN + hemolysis, elevated enzymes, low platelets) syndrome, mechanical hemolysis

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10
Q

Sickle cell (aka Drepanocyte)

A

Seen in sickle cell anemia

Sickling occurs with dehydration, deoxygenation, and high altitude

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11
Q

Spherocyte

A 
Hereditary spherocytosis (spectrin/ ankyrin mutation)
Drug and infection-induced hemolytic anemia
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12
Q

Target cell

A

“HALT said the hunter to his TARGET”

HbC disease (glutamic acid –> lysine)
Asplenia
Liver disease
Thalessemia (beta mainly- and alpha)

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13
Q

Heinz bodies

A

Inclusions in RBC (due to oxidation of -SH groups)

Subject to removal by spleen- causes bite cells

Seen also in G6PD (like bite cells)

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14
Q

Howell-Jolly bodies

A

Seen in sickle cell patients; patients with asplenia or hyposplenia

Inclusions are basophilic RNA remnants that are normally removed by the splenic macrophages (but impaired in people who have hypo or asplenia)

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15
Q

Microcytic (MCV < 80fL)

A 
Iron deficiency
Alpha-thalassemia
Beta-thalassemia
Lead poisoning
Sideroblastic anemia
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16
Q

Macrocytic (MCV > 100fL)

A

Megaloblastic anemia (Folate deficiency, Vitamin B12 deficiency, Orotic aciduria, Diamond-Blackfan anemia)

Non-megaloblastic anemia

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17
Q

Normocytic, normochromic anemia

A

Intravascular and extravascular hemolysis

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18
Q

Nonhemolytic, normocytic anemia

A

Anemia of chronic disease

Aplastic anemia

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19
Q

Intrinsic hemolytic anemia

A 
Hereditary spherocytosis
G6PD deficiency
Pyruvate kinase deficiency
HbC disease
Proxysmal nocturnal hemoglobinuria
Sickle cell anemia
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20
Q

Extrinsic hemolytic anemia

A

Autoimmune hemolytic anemia
Microangiopathic anemia
Macroangiopathic anemia
Infections

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21
Q

Iron deficiency

A

Decreased iron due to chronic bleeding (GI loss, menorrhagia), malnutrition, absorption disorders, or increased demand (pregnancy)

Labs: decreased iron, increased TIBC, decreased ferritin

Symptoms: fatigue, conjunctival pallor, pica (consumption of nonfood substances), spooned nails (koilonychia)

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22
Q

Plummer-Vinson syndrome

A

Triad of:

  • Iron deficiency anemia
  • Esophageal webs
  • Dysphagia
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23
Q

Alpha-thalassemia

A

Alpha-globin gene deletions –> Decreased alpha globin synthesis (cis (same chr) deletions- in Asia, trans (different chr) deletions- in Africa)

4 allele deletion: No alpha globin (hydrops fetalis- dx via presence of HbBarts- gamma4)
3 allele deletion: 1 alpha (HbH disease- presence of beta4)
2 allele deletion: 2 alpha (less severe)
1 allele deletion: 3 alpha (no anemia; clinically silent)

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24
Q

Beta-thalassemia

A

Point mutation in SPLICE SITES and PROMOTOR sequences (seen in Mediterranean populations)

Beta thal minor: B chain is underproduced; usually asymptomatic

Beta thal major: B chain is ABSENT; requires blood transfusions

S&S: severe microcytic, hypochromic anemia with target cells (anisopoikilocytosis- varying size and shape of cells)

Marrow expansion –> skeletal deformities; “Chipmunk facies”

Extramedullary hematopoiesis –> hepatosplenomegaly

Increased HbF (alpha2gamma2)- therefore kid only becomes symptomatic after 6mo

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25
Q

HbS/ beta-thalassemia heterozygote

A

Mild to moderate sickle cell disease

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26
Q

Lead poisoning

A

Lead inhibits ferrochetalase and ALA dehydratase

Leads to decreased heme synthesis and increased RBC protoporphyrin

rRNA degradation inhibited by lead –> RBCs retain aggregates of rRNA (basophilic stippling)

Consider risk in people who live in old houses

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27
Q

LEAD poisoning- symptoms

A

Lead Lines on gingivae (Burton lines) and on metaphases of long bones
Encephalopathy and Erythrocyte basophilic stippling
Abodomial colic and sideroblastic Anemia
Drops (wrist drop and foot drop); Dimercaprol and EDTA are 1st line of treatment

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28
Q

Lead poisoning- tx

A

Dimercaprol
EDTA
Succimer- used for chelation for kids

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29
Q

Sideroblastic anemia

A

Defect in heme synthesis- due to X-linked defect in delta-ALA synthase gene (NOT to be confused with ALA dehydratase that is affected in lead poisoning)

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30
Q

Sideroblastic anemia- causes

A

Can be genetic, acquired (myelodysplastic syndrome), and reversible (alcohol, lead, vitamin B6 deficiency, copper deficiency, isoniazid)

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31
Q

Sideroblastic anemia- lab findings

A

increased iron, normal/ decreased TIBC, increase ferritin

Stain: Prussian-blue

Peripheral blood smear: basophilic stippling of RBCs

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32
Q

Sideroblastic anemia- treatment

A

pyridoxine (B6- cofactor for delta-ALA synthase)

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33
Q

Megaloblastic anemia

A

Impaired DNA synthesis (maturation of nucleus is delayed relative to maturation of cytoplasm)

RBC macrocytosis, hypersegmented neutrophils, glossitis

Caused by: folate def, vitamin B12 def, orotic aciduria, Diamond-Blackfan anemia

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34
Q

Folate deficiency

A

Caused by malnutrition (alcoholics), malabsorption, drugs (methotrexate, trimethoprim, phenytoin), increased requirement (hemolytic anemia, pregnancy)

Increased homocysteine, NORMAL methylmalonic acid; NO NEUROLOGIC symptoms (vs. B12 deficiency)

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35
Q

Vitamin B12 (cobalamin) deficiency

A

Caused by insufficient intake, pernicious anemia, ileal resection/ gastrectomy, malabsorption (Crohn), Diphyllobothrium datum

Increased homocysteine and methylmalonic acid
Neurological symptoms (subacute combined degeneration- degeneration of posterior column, lateral CS tract, and spinocerebellar tract)- this is due to B12's involvement in fatty acid pathways and myelin synthesis
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36
Q

Schilling test

A

Method of diagnosing cause of B12 deficiency:

Stage I: Low levels of urinary B12
Stage II (+oral IF): If levels of urinary B12 become normal --> indicates pernicious anemia
Stage III (+antibiotics): If levels of urinary B12 become normal --> indicates small intestinal bacterial overgrowth
Stage IV (+pancreatic enzymes): If B12 levels become normal --> indicates pancreatic enzyme insufficiency
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37
Q

Orotic aciduria (AR)

A

Can’t convert orotic acid to UMP (de novo pyrimidine synthesis pathway) because of a defect in UMP synthase

IDed via orotic acid in the urine

Tx: uridine monophosphate (UMP) to bypass mutated enzyme

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38
Q

Orotic aciduria- S&S

A

S&S: children demonstrate failure to thrive, developmental delay, and megaloblastic anemia refractory to folate and B12

(NO HYPERAMMONEMIA –> vs. ornithine transcarbamylase deficiency where there is increased orotic acid WITH hyperammonemia)

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39
Q

Diamond-Blackfan anemia

A

Rapid onset anemia within 1st year of life due to defect in erythroid progenitor cells

Patients here present with anemia (vs. Fanconi anemia- where they present with pancytopenia)

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40
Q

Diamond-Blackfan anemia

A

Increase %HbF (but decrease in total Hb)

Short stature, craniofacial abnormalities and upper extremity malformations (triphalageal thumbs)

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41
Q

Non-megaloblastic anemia

A

Macrocytic anemia in which DNA synthesis is unimpaired

Causes: alcoholism, liver disease

RBC macrocytosis WITHOUT hypersegmented neutrophils

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42
Q

Normocytic, normochromic anemia

A

Can be classified in hemolytic vs. non-hemolytic

Can be classified by cause into intrinsic vs. extrinsic

Can be classified further by location into intravascular vs. extravascular

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43
Q

Intravascular hemolysis

A

Findings: decreased haptoglobin, increased LDH (lactate dehydrogenase), schistocytes, and increased reticulocytes on blood smear

Hemoglobinuria, hemosiderinuria, and urobilinogen in urine; may also see an increase in uncojugated bilirubin

Causes: mechanical- artificial heart valve, paroxysmal nocturnal hemoglobinuria, microangiopathic hemolytic anemia

44
Q

Extravascular hemolysis

A

Findings: macrophages in spleen clear RBCs

Spherocytes seen in peripheral smear, increased LDH, no hemoglobinuria/ hemosiderinuria, increased unconjugated bilirubin (can cause jaundice)

May have urobilinogen in urine

45
Q

Anemia of chronic disease

A

Inflammation –> increases hepcidin (inhibits iron txport) –> decreased release of iron from Mphages and decreased iron absorption from gut

Associated with RA, SLE, neoplastic disorders, and chronic kidney disease

46
Q

Anemia of chronic disease- findings and tx

A

Decreased iron, decreased TIBC, increased ferritin (NOT TO BE CONFUSED WITH iron deficiency- where ferritin levels decrease and TIBC increases

Generally normocytic- can become microcytic

Tx: erythropoietin

47
Q

Aplastic anemia

A

Failure or destruction of myeloid stem cells

Lots of causes: radiation and chemo, viral agents (parvo B19, EBV, HIV, hepatitis), Fanconi anemia, idiopathic

Characterized by decreased reticulocyte count, increased EPO

Pancytopenia: characterized by severe anemia, leukopenia, and thrombocytopenia (normal cell morphology, but hypo cellular bone marrow with fatty infiltration –> dry bone marrow tap (like myelodysplastic syndrome- associated with dacrocytes))

48
Q

Aplastic anemia- symptoms

A

fatigue, malais, pallor, purpura, mucosal bleeding, petechiae, infection

49
Q

Fanconi anemia- cause and symptoms

A

DNA repair defect (like XP, HNPCC, etc) causing bone marrow failure

S&S: short stature, increased risk of tumors/leukemia, cafe-au-lait spots, thumb/radial defects (e.g. polydactyly and radial hypoplasia), small testicles, and kidney malformations

Tx: Bone marrow transplant

50
Q

Aplastic anemia- tx

A

remove offending agent, give GM-CSF, bone marrow allograft, RBC/platelet transfusion

51
Q

Hereditary spherocytosis

A

Extravascular hemolysis- due to defect in proteins interacting with RBC membrane skeleton and plasma membrane (ankyrin, spectrin)

Results in small, round RBCs with less SA and no central pallor (increased MCHC) –> premature removal by spleen

52
Q

Hereditary spherocytosis- findings & tx

A

Splenomegaly, aplastic crisis (when infected with parvovirus B19)

Labs: osmotic fragility test +, normal to decreased MCV with abundance of cells

Tx: splenectomy

53
Q

G6PD deficiency (XR)

A

Defect in G6PD –> decreased glutathione –> increased RBC susceptibility to oxidant stress (sulfa drugs, antimalarials, infections, fava beans)

Drugs that induce allergy: sulfa drugs (sulfonamide– e.g. furosemide (switch pts to ethacrynic acid), dapsone, primaquine, aspirin, ibuprofen, and nitrofurantoin)

Causes intra and extravascular hemolysis

54
Q

G6PD- S&S

A

Male (generally African, Asian, or Mediterranean) with hemolysis, scleral icterus, mild splenomegaly, progressive fatigue, and exertional dyspnea

55
Q

Pyruvate kinase deficiency (AR)

A

Defect in pyruvate kinase –> decreased ATP –> rigid RBCs –> EXTRAVASCULAR hemolysis

Causes hemolytic anemia in a newborn

56
Q

HbC disease

A

Glutamic acid (-) –> lysine (+) mutation in beta globin

Causes EXTRAVASCULAR hemolysis

Labs: blood smear shows hemoglobin crystals inside RBCs and target cells

57
Q

Paroxysmal nocturnal hemoglobinuria

A

Increased complement-mediated INTRAVASCULAR RBC lysis

impaired GPI anchor that normally protects RBC membrane from complement (acquired mutation in stem cells)

Increased risk of acute leukemias

58
Q

Paroxysmal nocturnal hemoglobinuria- S&S and tx

A

Triad: Coombs negative hemolytic anemia, pancytopenia, and venous thrombosis

Morning urine is darker in color

Tx: eculizumab (terminal complement inhibitor)

59
Q

Sickle cell anemia

A

HbS point mutation: causes single AA replacement in beta chain (substitution of glutamic acid with valine)

Causes extra and intravascular hemolysis

Pathogenesis: low O2, high altitude, or acidosis –> precipitates sickling (deoxygenated HbS polymerizes) –> anemia and vaso-occlusive disease

60
Q

Complications of sickle cell disease

A

Aplastic crisis (parvovirus)
Autosplenectomy (Howell-Jolly bodies) –> increased risk of infection by encapsulated organisms (S. pneuma)
Splenic infarct/ sequestration crisis
Salmonella osteomyelitis
Painful crises: dactylitis, priapism, acute chest syndrome, avascular necrosis, stroke
Renal papillary necrosis (decreased PO2 in papilla) and microhematuria (medullary infarcts)

61
Q

Sickle cell disease- dx and tx

A

Dx: via Hb electrophoresis (will be closer to the cathode (-) than normal HbA, because of substitution of glutamic acid (-) for valine (neutral))

Tx: hydroxyurea (increases HbF), and hydration

62
Q

Autoimmune hemolytic anemia (AIHA)

A

Divided into warm and cool

Caused by antibodies against RBCs

S&S: Increased unconjugated (indirect) bilirubin and elevated LDH and low haptoglobin levels

Generally Coombs +

63
Q

Warm AIHA

A

IgG mediated; triggered by heat

Causes: SLE, CLL, alpha-methyldopa (alpha 2 agonist)

64
Q

Cool AIHA

A

IgM mediated; triggered by cold

Causes: Mycoplasma pneumo infection, infectious Mononucleosis, CLL)

65
Q

Direct Coombs test

A

Test blood + antibodies with anti-Ig (Coombs reagent) (to see if antibodies are present on the blood –> will agglutinate with the addition of Coombs reagent)

66
Q

Indirect Coombs test

A

Test serum for antibodies with RBCs (to see if RBCs agglutinate once Coombs reagent is added- if antibodies are present in the serum)

67
Q

Microangiopathic anemia

A

RBCs are damaged when passing through obstructed/ narrow vessel lumen

Seen in DIC, TTP/HUS, SLE, and malignant HTN

Schistocytes seen on blood smear due to mechanical destruction

68
Q

Macroangiopathic anemia

A

RBCs damaged when passing through mechanical valves

Schistocytes also seen

69
Q

Iron deficiency

A

Serum iron: decrease
Ferritin (iron stores): decrease
Transferrin (transports): increase (because body needs more iron)
TIBC (saturation of transferrin): decrease (because less iron)

70
Q

Anemia of chronic disease

A

Serum iron: decreases
Ferritin (iron stores): increases
Transferrin (transports iron): decreases (less is circulating so pathogens do not get access to iron)
TIBC (sat of transferrin): normal (because both iron levels and transferrin levels are decreasing)

71
Q

Hemochromatosis

A

Serum iron: increases
Ferritin (stores): increases
Transferrin (transport): decreases (tissue has too much iron)
TIBC (total iron/ transferrin): increases (too much iron relative to what is needed)

72
Q

Pregnancy/ OCP use

A

Serum iron: (same)
Ferritin: (same)
Transferrin: increases
TIBC (stored/ transported): decreases (because iron is the same while the amount that is being transported is increasing)

73
Q

Conditions that deplete eosinophils

A

Cushing syndrome, corticosteroids

74
Q

Left shift

A

More neutrophil precursors/ bands (immature cells)

75
Q

Leukoerythroblastic response

A

When left shift occurs with RBCs

Occurs when there is fibrosis/ bone marrow failure/ tumor

76
Q

Lead poisoning

A

Due to deficiency in ALA dehydratase and ferrochetalase; causes accumulation of protoporphyrin

Symptoms:
Lead Lines
Encephalopathy
Anemia (sideroblastic) and abdominal pain
Drop (wrist and foot); tx with dimercaprol and EDTA

77
Q

Acute intermittent porphyria

A

Due to deficiency in prophobilinogen deaminase; causes accumulation of porphobilinogen

Port-wine colored urine (urine darkens when exposed to light)
Painful abdomen
Polyneuropathy
Psychological disturbances
Precipitated by drugs (CYP-450 induces, alcohol, etc.)

Tx with glucose and heme

78
Q

Porphyria Cutanea Tarda

A

Due to deficiency in uroporphyrinogen decarboxylase; causes buildup of uroporphyrinogen

Causes cutaneous lesions/ blistering photosensitivity

“Ur skin is affected by uroporphyrinogen deficiency”

79
Q

Iron poisoning

A

Tx with deferoxamine, deferasirox (oral), dialysis

S&S: metabolic acidosis, nausea, vomiting, gastric bleeding, lethargy, etc

80
Q

Coagulation disorders- hemophilia

A

Hemophilia A- VIII and B- IX (XR) and C- XI (AR)

Treat with cryoprecipitate (contains factors VIII, IX, XIII, etc.)

Pts with demonstrate elevated PTT, normal PT

S&S: bleeding into joints, easy bruising, trauma after dental procedure

81
Q

Coagulation disorder- vit K deficiency

A

Depletion of Factors II, VII, IX, X, C and S (C first to go- hyper coagulable state); of factors: VII first to go, II last to go

S&S: elevated PT and PTT; easy bleeding

Normal bleeding time

82
Q

Platelet disorders- Bernard-Soulier

A

Deficiency in GpIb (normally binds to vWF –> helps platelet adhere to endothelium); increased bleeding time

Ristocetin assay identifies (vWD and BS; if BS- with the aden of plasma- problem will still not be corrected)

83
Q

Platelet disorders- Glanzmann

A

Deficiency in GpIIb/IIIa (fibrinogen binds to this to stabilize clot)

Causes increased bleeding time

84
Q

HUS (hemolytic uremic syndrome)

A

Classified by triad of: thrombocytopenia, hemolysis (microangiopathic), and renal failure

Seen in children– often after exposure to Shiga-like toxin (in EHEC/ Shigella)

85
Q

Immune thrombocytopenia

A

Antibodies against GpIIb/IIIa

Causes splenic macrophage consumption of splenic-macrophage complex

Tx with steroids, IVIG, splenectomy

86
Q

Thrombotic Thrombocytopenic Purpura

A

Inhibition or deficiency of ADAMTS –> causes decreased degradation of vWF

Increased vWF causes increase platelet clumping; therefore causing triad of: thrombocytopenia, microangiopathic hemolysis, and renal failure –> also see neurological disturbances and fever

Will see increased LDH and low haptoglobin

Tx: steroids, plasmapheresis

87
Q

von Willebrand disease

A

Does not generally bleed into joints

Will see increased bleeding time and PTT (because of its effect on increasing VIII half life)

Ristocetin assay (platelets will not clump until plasma is added)

Desmopressin- used to release vWF from the endothelial cells

88
Q

DIC

A

Caused by sepsis, trauma, pregnancy, pancreatitis, nephrotic syndrome, AML

All coag factors and platelets randomly clump in some places, causing hemorrhage in other places

Causes increase in PT, PTT, and bleeding time

89
Q

Hypercoagulable states

A

Antithrombin III def (normally inhibits factors IIa and Xa- vs. Protein C- which inhibits V and VIII)

Factor V Leiden- too active, not able to be inactivated by protein C

Protein C or S def- normally inactivates V and VIII

Prothrombin gene mutation: mutation in 3’ untranslated region –> causes increased prod of factor II

90
Q

Blood transfusion therapy- RBCs

A

Used for acute blood loss, anemia

91
Q

Platelets

A

Used for low platelet ct/ platelet defects, bleeding caused by thrombocytopenia

92
Q

Fresh frozen plasma

A

Contains coagulation factors

Used for warfarin excess, Vit K def, DIC, cirrhosis

93
Q

Cryoprecipitate

A

Contains factors I, VIII, XIII, vWF, fibronectin

Used for hemophilia A, coag defects involving factors II and VIII

94
Q

Non-Hodgkin vs. Hodgkin lymphoma

A

Hodgkin: characterized by mass, Reed-Sternberg cells, localized (generally single group of nodes with contiguous spread), strong association with EBV, bimodal distribution, demonstrates constitutional “B” symptoms

Non-hodgkin: more common, can present as lymphoma/mass or in blood (extra nodal), not contiguous; most involve B cell lineages, occurs in children and adults

95
Q

Reed Sternberg cells

A

CD 15 and CD 30 positive

B cell origin

Secrete cytokines that attract lymphocytes

96
Q

Non-Hodgkin lymphoma- B cell origin

A

B-cell origin
Burkitt: 8:14 (c-myc); kid from Africa presents with enlarging jaw mass
Follicular: 14:18 (bcl-2–> anti-apoptosis); waxing and waning presentation, slower growing
Mantle: 11:14 (cyclin D1); occurs in adult males, aggressive
Diffuse large B cell: aggressive, (can progress into this from mantle cell and SLL/CLL)
Adult lymphoma: associated with HIV, round and enhancing lesions on CT –> distinguished from Toxo via CSF analysis

97
Q

Non-Hodgkin lymphoma- T cell origin

A

Adult T cell lymphoma: preceded by infection with HTLV-1 (also causes myelin degradation in brain and spinal cord/ myelopathy); adult Asian presents with cutaneous lesions (resembling seborrhic keratoses); Bone lytic lesions and hypercalcemia are unique to this
Mycosis fungoides: Presents with skin plaques (cutaneous T cell lymphoma and may progress to T cell leukemia)

98
Q

Multiple myeloma

A

Plasma cell proliferation (generally causes M spike in IgG or IgA); rouleaux formation; Bence-Jones proteins (Ig in urine); plasma cells with “clock-face” chromatin
CRAB findings: hyperCalcemia, Renal failure, Amyloidosis and Anemia, Bone/lytic lesions

99
Q

Waldenstrom Macroglobulinemia

A

Increase in IgM

Causes hyper viscosity and blurred vision

No observed CRAB findings

100
Q

Myelodysplastic syndrome

A

Ineffective hematopoiesis –> causes defects in ALL myeloid lineages

Can progress to AML

101
Q

Leukemias- lymphoid

A

ALL: Seen in kids, better if you have the 12:21 translocation; precursor mc stain + for TdT+, CD10 (if pre-B)
CLL/SLL: seen in adults (CD20+, CD5+, B-cell origin), can progress into DLBL (Richter); crushed little lymphocytes seen on smear
Hairy cell: mature B cell tumor, dry tap on aspiration, +TRAP, tx with cladribine and pentostatin

102
Q

Leukemias- myeloid

A

CML- generally assoc. with Philadelphia chromosome (9:22); causes over activation of BCR-ABL (tyrosine kinase); responds well to imatinib; pts present with chronic weakness and increased myeloid cells (generally mature) on blood smear; can progress to AML/ALL in a process known as “blast crisis” –> wherein pts often present with DIC as well
LAP (leukocyte alkaline phosphatase) is low in these patients as opposed to those who are undergoing a normal leukemoid reaction

AML: dysregulated proliferation of myeloblasts; one subtype (APML- 15:17) –> presents with Auer rods; treat with all trans retinoic acid (forces T cells to differentiate); DIC is a common presentation

103
Q

Langerhan cell histiocytosis

A

Presents with proliferation of dendritic/ Langerhan cells (which are predominantly in the skin)
Cell are immature, do not effectively stimulate T cells, and express S-100 (like Schwannoma) and CD1a

Kids present with lytic bone lesions (as opposed to adults in MM)

Pathoma’s helpful tips:
if two names in title: happens in kids <2
if three names in title: happens in kids>3
if named after someone –> presentation involves cutaneous lesions/ skin rash and is malignant

104
Q

Chronic myeloproliferative disorders

A

General: associated with mutations in JAK2 receptor (causing chronic activation of cytoplasmic tyrosine kinases)

Polycythemia vera- increased RBCs, WBCs, and platelets; presents with erythromelalgia (itching, pain, and red-blue coloration) –> due to blood clots in vessels of extremities (responds to ASPIRIN)

Essential thrombocythemia- increased proliferation platelets and megakarycytes; may also present with erythromelalgia, and increased thrombosis and bleeding

Myelofibrosis- fibrosis of marrow (due to increased fibroblast activity) –> causes dacrocytes and dry bone marrow tap

105
Q

Polycythemia- normal and abnormal causes/ classifications

A

Relative: decreased plasma volume –> due to dehydration/ burns

Appropriate absolute: increased RBCs, increased EPO; due to decreased O2 sat –> caused by high altitude, congenital heart disease etc.

Inappropriate absolute: increased RBCs, increased EPO; due to malignancy

Polycythemia vera: increased RBCs, decreased EPO (because of negative feedback)

Hematology and Oncology (3 decks)

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