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MTM > Pathology > Flashcards

Pathology Flashcards

1
Q

ASA score

A

1-5
5 being worst
Add e for emergency

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2
Q

Differ ASA 4&5

A

4 having constant threat to life
5 won’t survive without surgery

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3
Q

What is ASA 6

A

Brain death

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4
Q

Time needed to see callus on x-ray and its clinical importance

A

3 weeks
Differ new or old fracture

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5
Q

Osteoclast activity in fracture

A

Removing the trabecular bone

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6
Q

What is wallerian degeneration

A

when a nerve fiber is cut or crushed and the part of the axon distal to the injury (which in most cases is farther from the neuron’s cell body) degenerates.

Degeneration of myelin sheath and phagocytosis by macrophages

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7
Q

Relation of AIDS with CBC

A

T cell deficiency

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8
Q

Relation of neutrophils with granulomatous disease

A

N can cause granulomatous disease

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9
Q

Microscopic finding of sarcoidosis

A

Asteroid bodies

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10
Q

What forms collagen

A

Fibroblast

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11
Q

Predominant cell in wound more than 6 weeks old

A

Myofibroblast

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12
Q

What is vasculogenesis

A

Formation of new vessel from mesenchyme

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13
Q

What is angiogenesis

A

Sprouting out of vessel from an existing vessel

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14
Q

Major cell of wound healing

A

Macrophages (but it is not chr. Inflam)
Which transforms into Fibroblast
Which transforms into myofibroblast

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15
Q

Differ delayed primary closure and secondary closure

A

D.pri. is before granulation tissue
Secondary after granulation tissue

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16
Q

Pathology skin layer of hypertrophic scar

A

Dermis

17
Q

Predisposition of keloid

A

Genetic and dark skin

18
Q

Why intra lesional incision and steroid for keloid

A

To trick brain that there is a keloid

19
Q

Duke classification when lymph node got involved

A

C

20
Q

How many stages of dukes classification of colonic cancer

A

A to D

21
Q

Which disease cause brown tumor of bone

A

Hyperparathyroidism

22
Q

X-ray finding of brown tumor of bone and why

A

Radio lucent
Due to excess osteoclast activity and consumption of trabecular bone

23
Q

Why called brown bone tumor

A

Hemosiderin deposition

24
Q

Why bone pain in brown tumor

A

Post osteoclast Resorption beyond the usual shape of bone involving periosteum

25
Q

Thirst in primary hyperparathyroidism

A

Unquenchable

26
Q

Most common cause of primary hyperparathyroidism

A

Solitary adenoma of parathyroid in 80% of cases

27
Q

IGF1 gene mutation is implicated in which tumor

A

HNPCC
Hereditary nonpolyposis colorectal cancer also known as
Lynch syndrome

28
Q

genes involved in the ACS
Adenoma carcinoma sequence

A

Some of the genes involved in the ACS include:
MCC (Mutated in colorectal cancer)
DCC (deleted in colorectal cancer)
c-yes (named after the Yamaguchi sarcoma virus oncogene, which it is the cellular homolog The tyrosine kinase gene)
bcl-2 (from its original discovery in the context of B-cell lymphomas)
c-myc (cellular Myc :carried by the Avian virus, Myelocytomatosis)

APC: Located on chromosome region 5q21 (adenomatous polyposis coli, a hereditary condition that causes colon tumors)

p53: Located on chromosome region 17p13 (after its molecular mass, which is in the 53 kilodalton fraction of cell proteins)

SMAD4: A driver mutation of the ACS

KRAS: A driver mutation of the ACS (because it was first identified as a viral oncogene in the Kirsten RAt Sarcoma virus)

TP53: A driver mutation of the ACS

29
Q

What is adenoma carcinoma sequence

A

The ACS is a hypothesis that explains the evolution of colorectal cancer through a benign intermediate stage called an adenoma. The ACS is thought to be responsible for most or all colorectal cancers.

30
Q

adenoma carcinoma sequence vs hnpcc

A

The adenoma-carcinoma sequence is a morphological model for colorectal cancer, while hereditary nonpolyposis colorectal cancer (HNPCC) is a genetic syndrome that can cause colorectal adenomas or carcinomas

31
Q

Hyperopia affect osteoclast

A

Excess osteoclast activity

32
Q

APC mutations

A

In familial adenomatous polyposis coli

MTM (12 decks)

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