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1C wrong

Unlike most forms of leukemia, HCL is characterized by pancytopenia


Splenomegaly, dry tap on BMA, no lymphadenopathy
TRAP+ hairy cells in BM, spleen and PBS (CD19, 20, CD11c, CD25)
Middle aged Caucasian men
Treatment with 2-CDA (cladribine)

Birbeck granules would not be present in PBS

2A
Chronic form of ITP lasts >6 months
Secondary causes include lupus, viral infections and drugs

ITP does not cause splenomegaly


Inhibitors of cyclooxygenase (Aspirin-irreversible, and other NSAIDS-reversible)
would not cause thrombocytopenia

3C
Sickle cell pain crisis is commonly initiated by infection or exposure to cold
Splenomegaly is present in thalassemia and HS
4B eg
Follicular lymphoma is derived from the B-cell line where neoplastic cells resemble
germinal center B cells
It is the most common INDOLENT form of NHL in the US
14;18 translocation (bcl-2 which inhibits apoptosis -> IgH site on 14)
CD10, 19, 20 +. Unlike CLL/SLL and mantle cell lymphoma, CD5 is -ve.

5D
Platelet transfusion is C/I in TTP unless life-threatening bleeding is present, as
this would fuel further microthrombus formation and worsening of TTP. First line Rx
is plasmapheresis.
6A wrong
TdT is present only in extremely primitive cells of the lymphocyte lineage (VDJ
rearrangement). Cytoplasmic mu chains become positive when the cells have
successfully completed the VDJ rearrangement (pre-B cells).
Most B-ALLs are pro-B cell types, which would be CD10, TdT positive but cytoplasmic
mu marker would not be expressed yet.
If surface IgG is present then that means the B cell has already undergone class
switching. CD40 and B7 are co-stimulatory molecules.

7A
Possibly low yield:
Pappenheimer bodies are iron-containing dark blue granules found in RBCs (Wright
stained) in patients with sideroblastic anemia.
Cabot rings are present in megaloblastic anemia or lead poisoning.

-----
8A
You need to spot Auer rods. Their presence indicates AML (especially APML or M3).

9A
Neutrophils are first-line defence against extracellular bacteria. An increased TLC
with a left shift (immature forms such as band cells) almost always means an
extracellular bacterial infection.
Anemia may be present in bacterial infections since most bacteria have extremely
high nutritional requirements for iron.
Response to a systemic fungal infection is more likely to be lymphocytic than
neutrophilic.
Prions cause extracellular amyloid deposition and NO IMMUNE RESPONSE.
Viruses, intracellular bacterium -> lymphocytosis. Parasite -> eosinophilia.

10B
DIC can develop secondary to obstetric complications e.g. abruptio placentae,
retained placenta. Other causes include trauma, sepsis, malignancy.
Vitamin K deficiency can be seen with fat malabsorption (celiac disease, cystic
fibrosis) and colon resection.

11B FOLLICULAR LYMPHOMA. t(14;18) translocation produces a hybrid bcl-2 (18) /


immunoglobulin heavy chain (14) transcript.
This is a reciprocal translocation. The other type of translocation is a
Robertsonian translocation which only occurs in the acrocentric chromosomes (13,
14, 15, 21 and 22) and involves loss of the short arms and subsequent fusion of the
long arms. e.g. Down syndrome.
Learn all the translocations.. t(11;14) translocation involving bcl-1 and IgH is
seen in mantle cell lymphoma and multiple myeloma.

12C
O2 sat of 98% does not completely rule out CO poisoning because CO can give a
falsely high oxygen saturation on regular pulse oximetry. CO-Hb level would be
increased.
EPO would be reduced in polycythemia vera.
Reactive polycythemia occurs in tissue hypoxia e.g. smokers with COPD. They would
have decreased O2 sat on pulse oximetry and h/o smoking.
H/o alcohol abuse, nodular cirrhosis on P/E and elevated bilirubin suggest liver
pathology, which when combined with erythrocytosis, suggest HCC.

13A
PTT(activated) range = 25-40 sec
PT = 11-15 sec
Abnormal platelet morphology would be present in infiltration of bone marrow by
tumor or fibrosis, after splenectomy etc.

14C wrong, EBV and IM


CD10 positive cells are seen in B-ALL. CD19 positive cells are mature B cells.

15C wrong, silly mistake


Hodgkin disease & Multiple myeloma affect adults, not children.
Multiple myeloma would cause punched-out lytic bone lesions in the skull and
vertebral column.
Osteopetrosis is a rare genetic disorder (AD mild form, AR severe form)
characterised by defective osteoclast-mediated bone resorption -> thickening of the
bone. Ends of the long bones are misshapen and bulbous. (Erlenmeyer flask
deformity).
Although bone turnover is decreased, the tissue becomes weak and predisposes to
fractures. There may also be cranial nerve palsies due to decreased cranial foramen
size, extramedullary hematopoesis and increased infections and bleeding due to
reduced marrow space.

16C
Multiple myeloma is a neoplastic prolif. of plasma cells, which produce excessive
amounts of immunoglobulin, particularly IgG or IgA. ESR is high.
Decreased platelet count reflects infiltration of BM; infections common because
production of normal Ig of all types is decreased.

Lytic bone lesions are seen in multiple myeloma, lung carcinoma and breast
carcinoma. Blastic bone lesions are seen in prostate carcinoma and breast
carcinoma.
MGUS is usually asymptomatic.
Plasmacytoma is a rare, ISOLATED plasma cell neoplasm in bone or soft tissues (this
patient has MULTIPLE lytic lesions). ALways remember, primary tumors are usually
isolated, metastases are multiple.

17E
18B
Renal dysfunction can be seen with INTRAVASCULAR hemolysis (PNH, IHA or MAHA)
because excess free hemoglobin is toxic to renal tubules (similar to myoglobin).
Hemoglobinuria does not occur in extravascular hemolysis.

Possibly low yield:


Heart failure can be a complication of patients with severe thalessemia or sickle
cell anemia due to marked anemia leading to increased heart rate leading to HCM, or
repeated transfusions leading to secondary hemosiderosis -> RCM

19E
20B
21C
22C
23E
24E wrong
25C
26B wrong, silly mistake
27E wrong
28D why is WBC count not > 50000?
29A wrong
30E
31C
32E
33B
34D wrong, CML
35A
36E
37A
38C wrong
39C
40C

Amino acid metabolism, disorders


Lysosomal storage diseases DONE
Glycogen storage diseases
Fatty acid metabolism, hyperlipidemias
Anti-hyperlipidemic drugs
I cell disease
Collagen metabolism, disorders

QUESTION BANK REVIEW


THEORY: PATHOMA CHAPTER 2
ANKI: 200 NEW CARDS OF PATHOMA CH2

Growth hormone
Antimetabolites, cell cycle
Immunosuppressants
Lead poisoning
Congenital Adrenal Hyperplasia
Tumor suppressor genes
Porphyrias

Nephrocalcinosis? Calciphylaxis? Why is there metastatic calcification in multiple


myeloma? What is acute pneumonitis and why does it have metastatic calcification?

7 40 QUESTIONS
8-12 Read related theory, only the BARE MINIMUM REQUIRED TO ANSWER THAT QUESTION
CORRECTLY. Because on Sunday all you will do is the week's questions.
12-4 THEORY
4 to 7 ANKI QUESTIONS
7-8 Exercise+Dinner
8 Onwards MUSIC!!

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