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Hemetology and oncology > Pathology > Flashcards

Pathology Flashcards

(73 cards)

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1
Q

Acanthocyte RBC

A

Spur cell
Abetalipoproteinemia
Due to disruption of the membrane (cholesterol dysregulation)

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2
Q

Basophilic stippling RBC

A

Lead poisoning

Seen in other conditions too

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3
Q

Degmacyte

A

Bite cell.

G6PD deficiency

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4
Q

Elliptocyte

A

Hereditary elliptocytosis

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5
Q

Macro-ovalcyte

A

Megaloblastic anemia, marrow failure

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6
Q

Ringed sideroblast

A

Excess iron-deposits in the mitochondria, can’t be incorporated into Hb

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7
Q

Schistocyte

A

Helmet cell
DIC, TTP, HUS
HELLP syndrome
Trauma induced

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8
Q

Target cell

A

HbC disease, liver disease, Thalassemias, asplenia

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9
Q

Heinz bodies

A

Oxidation of Hb-SH groups to S-S–>Hb precipitation

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10
Q

Howell-Jolly bodies

A

Asplenic or hyposplenic patients

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11
Q

Microcytic anemia

A 
Iron deficiency
ACD
Sideroblastic anemia
Thalassemias
Lead poisoning (basophilic stippling)
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12
Q

Normocytic-non-hemolytic anemia

A

Reticulocyte count: normal or decreased
Iron deficiency and ACD (early stages)
Aplastic anemia
Chronic kidney disease

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13
Q

Normocytic-hemolytic-intrinsic

A 
RBC membrane defect: hereditary spherocytosis
RBC enzyme defect: G6PD, pyruvate kinase
HbC defect
Paroxysmal nocturnal hemoglobinuria
Sickle cell anemia
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14
Q

Normocytic-hemolytic-extrinsic

A

Autoimmune
Micro/macroangiopathic
Infection

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15
Q

Macrocytic anemia-megaloblastic

A

B12 deficiency
Folate deficiency
Orotic aciduria

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16
Q

Macrocytic anemia-non-megaloblastic

A

Liver disease
Alcoholism
Reticulocytosis

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17
Q

Hydrops fetalis

A

Hb-g4 no alpha globin

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18
Q

What do you call Hb-g4 (4 allele deletion a-thalassemia)

A

Hb Barts

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19
Q

Plummer-vinson syndrome

A

Iron deficiency, esophageal webs, atrophic glossitis

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20
Q

3 allele deletion- a thalassemia

A

Hb-b4 with a little a chain

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21
Q

a thalassemia vs. b thalassemia

A

a=a globin gene deletion, cis deletion: asians trans deletion: africans
b=b globin point mutation in splice site and promoter sequences–>decrease in B globin synthesis
Prevalent in Mediterraneans

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22
Q

B thalassemia minor

A

Heterozygous
B chain is underproduced
Usually asymptomatic
Diagnosis confirmed with ^hBA2>3.5%

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23
Q

B thalassemia major

A

B chain is absent–>severe anemia requiring a blood transfusion
Marrow expansion–>skeletal deformities “chipmunk facies”
Extramedulllary hematopoiesis–>hepatosplenomegaly/^ risk of parvovirusB19-induced aplastic crisis

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24
Q

How is B thalassemia major protected?

A

Increase in HbF (a2f2), and infants do not become symptomatic until 6 months of age

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25
Lead poisoning mneumonic
``` LEAD: Lead lines Encephalopathy and erthyrocyte basophilic stippling Anemia Drops (wrist and foot drops) ```
26
First line treatment for lead poisoning
Dimercaprol and EDTA, succimer can be used for chelation for kids
27
Lead poisoning mechanism
Inhibits ferrochelatase and ALA dehydratase (leads to a decrease in heme synthesis and increases RBC protoporphyrin
28
Causes of ringed sideroblast
``` Alcohol (most common reversible cause), B6 deficiency, cooper deficiency, lead poisoning, isonazid. Myelodysplastic syndrome (acquired) ```
29
Orotic aciduria pathology and presentation
Deficiency in UMP synthase-->increase in orotic acid in the urine Presents as failure to thrive, developmental delay, megaloblastic anemia refractory to folate and B12
30
Orotic aciduria treatment
urdine monophosphate to bypass mutated enzyme
31
Anemia of chronic disease
Normochromic-non-hemolytic anemia Increase in hepcidin (released by liver)-->Iron stays stored in macrogphages RA, SLE, neoplasms Chronic kidney disease (treat with EPO)
32
Hereditary spherocytosis: pathology and findings
Intrinsic normochromic anemia Defect in the skeleton (ankyrkin, band 3, protein 4.2, spectrin)-->small, spherical, no central pallor RBCs ^MCHC/RDW-->premature degradation by spleen-->aplastic crises (parvovirus19), splenomegaly
33
Hereditary spherocytosis: treatment
Splenectomy
34
G6PD: pathology and findings
Intrinsic normocytic anemia | Deficiency in G6PD-->no regeneration of glutathione (RBCs can't be properly reduced and precipitate Hb)
35
HbC defect
Glutamic acid to lysine mutation in B globin | Patients have milder symptoms with HbCS than HbSS
36
Paroxysmal nocturnal hemoglobinuria: classic triad
MISNOMER 1. Negative Coombs hemolytic anemia (non-immune mediated) 2. Pancytopenia 3. Venous thrombosis
37
Paroxysmal nocturnal hemoglobinuria: lab findings and treatment
CD55/59 - RBC on flow cytometry | Eculizumab (terminal complement inhibitor)
38
Paroxysmal nocturnal hemoglobinuria: pathology
Increased complement-mediated RBC lysis (imparied synthese of GPI anchor to protect from complement) Acquired mutation in hematopoietic stem cell
39
What are you at risk for with paroxysmal nocturnal hemoglobinuria?
Acute leukemias
40
What infection are sickle cell patients particularly at risk for?
Salmonella osteomyelitits
41
What type of bacteria can sickle cell patients not fight off due to splenic injury?
Encapsulated bacteria SHINE SKiS Strep pneumo, H. influenzae, Neisseria, E. Coli, Salmonella, Klebsiella, Group B Strep
42
Autoimmune hemolytic anemia
``` Warm agglutinin(IgG)-Chronic anema trigger by SLE and CLL and certain drugs (a-methyldopa) Cold agglutinin(IgM)-anemia triggered by cold seen in CLL, Mycoplasma pneumonia infections and mono Positive Coombs test ```
43
Lead poisoning affected enzymes
Ferrochelatase and ALA dehydratase
44
Lead poisoning accumulated substance
Protoporphyrin, G-ALA (blood)
45
Acute intermittent porphyria affected enzyme
porphobilinogen deaminase | "pay your BILLs intermittently"
46
Acute intermittent porphyria presentation
``` 5 P's Painful abdomen Port-wine red urine Polyneuropathy Psychological disturbances Precipitated by drugs (p450 inducers), alcohol, starvation ```
47
Acute intermittent porphyria treatment
Glucose and heme-->leads to inhibition of ALA synthase
48
Acute intermittent porphyria affected enzyme
Porphobilinogen deaminase
49
Acute intermittent porphyria accumulated substance
Porphobilinogen, G-ALA, coporphobilinogen (urine)
50
Iron poisoning mechanism
Cell death due to peroxidation of membrane lipids
51
Which of the hemophilias is not X linked?
Hemophilia C (factor XI)
52
All hemophilias increase what test?
PTT
53
What does Ristocetin test for?
It activates vWF, if there is a vWF or GpIB deficiency (von Willebrand disease/Bernard-Soulier) than there will not be agglutination
54
Thrombotic thrombocytopenia purpura: symptoms
FAT RN: | Fever, anemia (microangiopathic hemolytic), thrombocytopenia, renal symptoms, neurologic symptoms
55
Thrombotic thrombocytopenia purpura: pathology
Deficiency of ADAMTS 13 causing a deficiency of vWF multimers-->many vWF multimers-->platelet adhesion/clotting/thrombosis *ADAM effed the FAT RN
56
Thrombotic thrombocytopenia purpura: treatment
Steroids, plasmapheresis
57
DIC pathology
Widespread activation of clotting-->Deficiency in clotting factors-->bleeding state
58
DIC labs
Schistocytes, Increased d-dimer, decreased fibrinogen, decreased factors V and VIII
59
Protein C/S deficiency
Associated with skin necrosis and hemorrhage following warfarin administration
60
Waldenstrom macroglobulinemia
M spike=IgM-->hyperviscosity syndrome (blurred vision, Raynaud phenomenon) No CRAB findings (like in multiple myeloma)
61
Pseudo-Pelger-Huet anamoly
Bilobed PMN's, typically seen after chemotherapy
62
How do you treat Hairy cell leukemia
Cladribine or pentostatin | 5(pento) hairy (leukemia) claddys TRAPped on the Bed (b cell tumor)
63
What is a common presentation of Acute myeloid leukemia?
DIC
64
Auer rods
Peroxidase + cytoplasmic inclusions seen mostly in M3 AML (PML)
65
t(8:14)
Burkitt lymphoma (c-myc activation)
66
t(9:22)
CML (BCR-ABL hybrid)
67
t(11:14)
Mantle cell (cyclin D1 activation)
68
t(14:18)
Follicular lymphoma (BCL-2 activation)
69
t(15:17)
M3 type of AML (responds to all-trans retinoic acid)
70
Langerhaan cell histiocytosis
Proliferative disorders of dendritic cells-->lytic bone lesions, skin rash, recurring otitis media Mass in the mastoid bone Cells expression S-100 (mesoderm) Tennis racket rod shaped on EM
71
Three disorders that involve JAK2 gene mutation
Polycythemia vera Essential thrombocytopenia Myelofibrosis
72
Polycythemia vera
Increased hemotocrit. Intense itching after how shower Rare but classic: red-blue coloration with burning pain Increased in RBC WBC and platelets
73
Hereditary spherocytosis defect?
RBC membrane skeleton and plasma membrane interaction: ankyrin, band 3, protein4.2, spectrin

Hemetology and oncology (6 decks)

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