Pathology Flashcards

1
Q

Inflammation

A

Local physiological response to tissue injury

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2
Q

2 types of inflammation

A

Acute

Chronic

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3
Q

2 Cells involved in acute inflammation

A

Neutrophils (Day 1)

Monocytes (Day 2)

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4
Q

4 Neutrophil functions

A

Phagocytose pathogens
Pathogens ingested to form phagosome
Lysosomes released to kill pathogens
Respiratory burst

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5
Q

1 Macrophage function

A

Secrete chemical mediators for chemotaxis

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6
Q

5 Causes of Acute Inflammation

A
Microbial infections
Hypersensitivity reactions 
Physical agents
Chemicals 
Tissue Necrosis
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7
Q

4 Stages of acute inflammation

A

1) Changes in vessel calibre
2) Fluid exudate
3) Cellular exudate (accumulation of neutrophil polymorphs in extracellular space)
4) Chemotaxis

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8
Q

5 Cardinal signs of acute inflammation - SHLRP

A
Swelling (Oedema)
Redness (Dilated blood vessels)
Heat (Increased blood flow - hyperaemia)
Pain (Stretching of tissues to inflammatory oedema)
Loss of function
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9
Q

4 Outcomes of acute inflammation - ROSP

A

Resolution (Tissues restored to normal)
Suppuration (Pus formation)
Organisation (Tissue replaced by granulation tissue as part of healing process)
Progression to Chronic inflammation

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10
Q

Chronic inflammation

A

Unresolved acute inflammation

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11
Q

3 examples of chronic inflammation - AUF

A

Ulcer
Abscess
Fibrosis

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12
Q

Causes of chronic inflammation

A

Resistance of infective agent to phagocytosis
Endo/Exogenous materials
Autoimmune conditions
Primary granulomatous diseases

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13
Q

3 Cells involved in chronic inflammation - PML

A

Macrophages
Lymphocytes
Plasma cells

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14
Q

3 ways chronic is different to acute inflammation

A

Less exudative
Longer onset
Long-lasting effects

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15
Q

3 Histological features of chronic inflammation

A

Cellular infiltrate consists of PML
Tissue destruction
Tissue repair

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16
Q

Granuloma

A

Aggregate of epithelioid histiocytes

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17
Q

5 Systemic granulomatosis diseases - TCLSS

A
TB (Tuberculosis)
Crohn's disease
Leprosy 
Sarcoidosis 
Schistosomiasis
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18
Q

Special type of Granuloma cell in TB

A

Langhans giant cell

19
Q

Thrombus

A

Solid mass of blood constituents
Part of healing and repair
Physiological - Haemostasis (to prevent bleeding outside vessels)
Pathological - Imbalance in coagulation

20
Q

Virchow’s triad - SHE

A

Stasis of blood flow
Endothelial injury
Hypercoagulability

21
Q

5 Features of venous thrombosis

A

Due to stasis
Low pressure
Red thrombus (Composed of coagulation factors, RBCs)
Lead to DVT/PE
Treated with anti-coagulants (Warfarin, heparin, NOAC (New Oral Anti-Coag))

22
Q

5 Features of arterial thrombosis

A
Superimposed on atheroma
High pressure 
White thrombus (Platelets)
Lead to MI/Stroke
Treated with anti-platelets (Aspirin, clopidogerel
23
Q

Atherosclerosis - MLS

A

Accumulation of lipid, macrophages and smooth muscle cells in intimal plaques in the coronary arteries.

24
Q

5 Arteries affected by atherosclerosis - 2 Heart, 2 Brain, 1 Pelvic

A
Aorta
Coronary
Carotid 
Cerebral 
Common iliac and femoral
25
Q

3 Contents of a plaque - MLS

A

Macrophages
Lipids
Smooth muscle cells

26
Q

Pathogenesis

A

1) Endothelial cell dysfunction (lots of cholesterol damages wall)
2) High levels of LDL in blood accumulate in arterial wall.
3) Macrophages attracted to site of damage and take up lipid to form foam cells (inflammatory response)
4) Formation of a fatty streak (early stage plaque)
5) Activated macrophages release their own products (Cytokines and growth factors)
6) Smooth muscle proliferation to intima around the lipid core and formation of a fibrous cap (collagen)

27
Q

Hypertrophy

A

Increased organ/tissue size due to increased cell size
Can be via increased protein synthesis or increased size of intracellular organelles
Exercise increases skeletal muscle mass

28
Q

Hyperplasia

A

Increased organ/tissue size due to increased cell number

Uterine enlargement

29
Q

Atrophy

A

Decreased organ/tissue size due to decreased cell size
Decreased exercise
Endometrium

30
Q

Metaplasia

A

Replacement of one differentiated tissue by another

Barret’s oesophagus

31
Q

Dysplasia

A

Presence of abnormal cell types within a tissue
Increased cell growth and Decreased differentiation
Variation in size and shape of cells
High nuclear : cytoplasmic ratio
Increased nuclear DNA
Pre-cancer state

32
Q

Apoptosis

A

Programmed cell death
Non-inflammatory
Cell and its organelles are intact/undamaged/retained
Embryological development

33
Q

Necrosis

A

Morphological changes following apoptosis
Inflammatory
Cell and its organelles are destroyed/damaged/released
Gangrene
MI

34
Q

Carcinogenesis

A

Transformation of normal cells to neoplastic cells through permanent mutations (genetic alterations)

35
Q

Benign tumours

A
Does not invade basement membrane
Exophytic (grows outwards)
Low mitotic activity
Circumscribed (limited spread)
Necrosis/ulceration rare
36
Q

Malignant tumours

A
Invades basement membrane 
Endophytic (grows inwards)
High mitotic activity 
Poorly circumscribed (spread out)
Necrosis/ulceration common
37
Q

4 Effects of Benign tumours

A

Pressure on adjacent vital organs
Paraneoplastic effects
Anxiety
Transformation to malignant tumour

38
Q

4 Effects of Malignant tumours

A

Metastases
Paraneoplastic effects
Anxiety
Pain

39
Q

4 Histological features of malignant tumours

A

Poorly defined border
Hyperchromatic nuclei
High mitotic activity
Pleomorphism (altered cell size/shapes)

40
Q

Metastasis

A

Tumours spread from site of origin to form tumours at distant sites

41
Q

2 Signs of metastasis

A

Bone pain

Palpable lymph nodes

42
Q

Mechanism of metastasis

A

1) Detachment of tumour cells from neighbours
2) Invasion into surrounding connective tissue
3) Intravasation into vessel lumen
4) Evasion of host defence mechanisms (natural killer cells in blood)
5) Adherence to endothelium at remote location
6) Extravasation of cells from vessel lumen into surrounding tissue

See peer teaching pathology pres slide 39 for useful pic

43
Q

3 Routes of Metasasis - HTL

A

Haematogenous (blood)
Transcoelomic (peritoneum)
Lymphatic