CR histology Flashcards

1
Q

0-12h after infarct

A

No changes

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2
Q

12-24h after infarct

A

Bright pink eosinophilia of muscle fibres

Intracellular oedema

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3
Q

24-72h after infarct

A

Acute infiltration of inflammatory cells (mainly neutrophils)
Loss of nuclei and striations

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4
Q

3-10 days after infarct

A

Replacement of damaged tissue with granulation tissue

–> loose oedematous mesh with capillaries and fibroblasts

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5
Q

Weeks - months after infarct

A

Granulation tissue becomes fibrocollageous and becomes avascular and acellular

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6
Q

When is the repairing heart muscle the weakest?

A

5 days post infarct

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7
Q

Aschoff body cells

A

Central core of necrosis with macrophages

Surrounded by lymphocytes

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8
Q

Where are Aschoff bodes most commonly found?

A

Myocardium

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9
Q

Valve structure

A

Core of dense irregular CT
Lined by endothelial cells
CT from cusps merges around the edges to form the fibrous skeleton of the heart

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10
Q

Oat cell tumour

A

20-25% of lung carcinomas
Small cell carcinoma
Small, densely packed, dark staining cells
Highly malignant

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11
Q

Non-small cell lung carcinomas

A

Squamous cell = 25-40%
Adenocarcinoma
Large cell

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12
Q

Lung squamous cell carcinoma

A

Mainly arises in main or major bronchi
Associated the squamous metaplasia due to cigarette smoking and other irritant exposure
Evidence of keratin –> stains orange

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13
Q

Granuloma layers

A

Central core of necrosis
Ring of macrophages with some giant cells
Collar of lymphocytes
Ring of fibroblasts forming a fibrous wall
Calcification of this wall may occur

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14
Q

Gohn focus

A

Occurs after primary infection
Lesions the mid zone close to the pleura
May be hilar lymph node involvement

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15
Q

Assmann focus

A

Occurs after reactivation of primary lesion or exogenous infection
Bilateral apical nodules
Erosion of bronchi and blood vessels may cause haemopytsis

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16
Q

Define anisocytosis

A

= RBCs are different sizes

17
Q

Define poikilocytosis

A

= RBCs are different shapes

18
Q

Abnormal cells seen in megaloblastic macrocytic anaemia

A

Megaloblasts

Neutrophils with hypersegmented (>5) nuclei

19
Q

Features of haemolytic anaemia

A

Premature RBC destruction
Increase in catabolic products of haemoglobin, e.g. jaundice
Increased rate of erthyropoiesis –> reticulocytosis

20
Q

Hereditary spherocytosis abnormality

A

Spectrin mutation

21
Q

G6PD function

A

Prevents oxidative damage

22
Q

Triggers of G6PD symptoms

A

Drugs, fava beans, infection

= times of oxidative stress

23
Q

Cell types seen in sickle cell disease

A

Sickle shaped cells
Target cells
Cells with Howell-Jolley bodies

24
Q

What causes fragmentation haemolytic anaemia?

A

Prosthetic cardiac valves

Microvascular narrowing/obstruction

25
Q

Cell types seen in G6PD deficiency

A

Heinz body formation

Basket/bite/blister cells

26
Q

Cell types seen in fragmentation haemolytic anaemia

A

Schistocytes (helmet cells)
Burr cells (echinocytes)
Blister cells

27
Q

Autoimmune haemolytic anameia

A

Non-hereditary spherocytosis

Autoantibodies against RBC membrane components