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Phase 2A Med Concise > Pathology > Flashcards

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
3 Contents of a plaque - MLS
Macrophages Lipids Smooth muscle cells
26
Pathogenesis
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
Hypertrophy
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
Hyperplasia
Increased organ/tissue size due to increased cell number | Uterine enlargement
29
Atrophy
Decreased organ/tissue size due to decreased cell size Decreased exercise Endometrium
30
Metaplasia
Replacement of one differentiated tissue by another | Barret's oesophagus
31
Dysplasia
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
Apoptosis
Programmed cell death Non-inflammatory Cell and its organelles are intact/undamaged/retained Embryological development
33
Necrosis
Morphological changes following apoptosis Inflammatory Cell and its organelles are destroyed/damaged/released Gangrene MI
34
Carcinogenesis
Transformation of normal cells to neoplastic cells through permanent mutations (genetic alterations)
35
Benign tumours
``` Does not invade basement membrane Exophytic (grows outwards) Low mitotic activity Circumscribed (limited spread) Necrosis/ulceration rare ```
36
Malignant tumours
``` Invades basement membrane Endophytic (grows inwards) High mitotic activity Poorly circumscribed (spread out) Necrosis/ulceration common ```
37
4 Effects of Benign tumours
Pressure on adjacent vital organs Paraneoplastic effects Anxiety Transformation to malignant tumour
38
4 Effects of Malignant tumours
Metastases Paraneoplastic effects Anxiety Pain
39
4 Histological features of malignant tumours
Poorly defined border Hyperchromatic nuclei High mitotic activity Pleomorphism (altered cell size/shapes)
40
Metastasis
Tumours spread from site of origin to form tumours at distant sites
41
2 Signs of metastasis
Bone pain | Palpable lymph nodes
42
Mechanism of metastasis
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
3 Routes of Metasasis - HTL
Haematogenous (blood) Transcoelomic (peritoneum) Lymphatic

Phase 2A Med Concise (18 decks)

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