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MRCS PART B > Past questions - Pathology > Flashcards

Past questions - Pathology Flashcards

1
Q

What is acute inflammation?

A

Bodys response to tissue injury.
Innate and immediate.

Heat, pain, redness, swelling

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2
Q

What are the stages of wound healing?

A
  1. Vasoconstriction
  2. Hemostasis - vasodilation, increased vascular permeability, platelet activation
  3. Inflammatory - migration of white cells - neutrophils
  4. Phagocytosis - macrophages
  5. proliferative - fibroblasts
  6. resolution or progression
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3
Q

Chemical mediators

A

Platelets - prostaglandins, leukotriene, histamine, serotonin

plasma - plasmin, bradykinin

complement

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4
Q

Gastric cancer

A

CDH mutation

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5
Q

Polyp

A

Abnormal growth of tissue form mucous membrane

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6
Q

What is an oncogene

A

A muted gene that has the potential to cause cancer. Stimulates growth when not required.

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7
Q

Adenoma cancer sequence

A

Stepwise pattern of Mutations of oncogenes and TSG

  • APC - tumour supressor gene - mutation
  • K-Ras - oncogene
    P53 - TSG - inactivated
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8
Q

Dysplasia

A

Disordered cellular development characterised by increased mitosis and pleomorphism but unable to invade basement membrane

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9
Q

What is the APC gene?

A

Tumour supressor gene
Negatively regulates WNT pathway
degrades beta catenin

mutation - beta catenin not degraded - WNT stimualted - overgrowth

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10
Q

RHD pathophysiology

A

Group A strep - cross reacts with host abs -complement - T cell - recurrent inflmaation - stenosis

Ashcoff bodies

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11
Q

Steroids

A

Opportunisitic bacteria
CIshings - obesity, stria muscle weakness
cardio-fluid retention
DM

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12
Q

GCA Eye

A

Anterior ischeamic optic neuropathy

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13
Q

How do steroids cause bone disease

A

Inhibitiion of GIT calcium
Dircet stimulation of osteoclast
Decrease of renal reabsorption

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14
Q

Neutrophils

A

Margination and rolling
Adhesion
Transmigration
Migration

Bone marrow - HEAMTOPOEITC STEM CELLS

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15
Q

Parathyroid hyperplasia

A

Chief cell - MEN
Water clear cell

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16
Q

What is IHC?

A

lOCALISING SPECIFIC ANITGENS IN TISSUES based on antigen aby

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17
Q

How does a malignant tumour survive in LN/ lymphatic spread

A

Release growth factors such as VGEF - Lymphactic vessel explanison

18
Q

How does cancer spread?

A
  1. Direct or continuous extension
  2. Penetrates into lymph, blood or body
  3. Transport into circulation
  4. ARREST IN THE CAPILLARY BEDS
  5. Growth of tumour
18
Q

Carcinoid tumour

A

Enterchomofin cells

Cutaneous flushing, diarrhoea, malabsorption

Beta catain allows spread

18
Q

Why renal stones in crohns?

A

Increased intestinal fat -> binds to calcium -> leaving oxalates

19
Q

Chronic changes in IBD

A

laminia propira
paneth cell meteplasia

20
Q

Role of TNF in IBD

A

Cytokine involved in systemic inflammation.
Regulates the innate immune response

Increases tight junction epithelia
Increase flux of luminal
Causes acute inflammation

TNF alpha inhibition by monoclonal antibodies

21
Q

Biofilms

A

Viscous layer of extracellular polysaccharides that adhere to host

22
Q

Why pus yellow

A

Myeloperoxidase

23
Q

Granuloma

A

Aggregation of macrophages

24
Q

Heart carcinoid

A

Libman sacks endocardis (non bacterial endocardis)

25
Q

What to look out for on report

A

Malignant features
- Histological grade and differentiation
- Size
- Margin status
- Immunohistochemistry

26
Q

Grading

A

Microscopic differentiaiton

27
Q

Staging

A

extent and spread

28
Q

Lung cancer parneoplastic

A
  • (ADH), inducing hyponatremia due to inappropriate ADH secretion
  • (ACTH), producing Cushing syndrome
  • Parathormone, parathyroid hormone-related peptide, prostaglandin E, and somecytokines, all
    implicated in the hypercalcemia
  • Calcitonin, causing hypocalcemia
  • Gonadotropins, causing gynecomastia
  • Serotonin and bradykinin, associated with the carcinoid syndrome
29
Q

What is amyloid

A

Fibril protein

30
Q

Why Hyper coagulable

A

Tumor cells to produce and secrete procoagulant/fibrinolytic substance which activate coagulation cascade
stimulation of tissue factor production by host cell.

31
Q

What is an ulcer

A

local defect of mucus membrane due to loss of surface epithelial cells

32
Q

H.pylori

A

Spiral heix microareophilic gram negative bacteria

33
Q

What is gangrene

A

Necoris caused by critically insufficent blodd supply

34
Q

Tb tests

A

sputum - ziehl neelson
mantoux
PCR
quantiferon
FNAC

35
Q

What are giant cells?

A

Multinucleated cells comprising of macrophages often forming granuloma
e.g. Langerhans’ giant cells, Reed sternberg cells

36
Q

Granuloma

A

Organised collection of macrophages IN REPSOSNE TO CHRONIC INFLAMMATION

37
Q

Cracinoma

A

Malignat neoplasm of epithelial cells

38
Q

Hamartoma

A

Disorganised arrangements of different amounts of tissue normally found at that site

39
Q

PMC

A

abx - disrupt microbe - allow c.diff to colonise - release toxins - eruption of neutrophils - mucopurulent psudeomemrbanes

40
Q

GCA

A

Tunica media

Intimal thickening
granulmotosis inflamamtion - lamina destruciton
Tcells and macrophages
Skip lesions

MRCS PART B (10 decks)

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