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Phase 2a Gold Standard > ICS - Pathology > Flashcards

ICS - Pathology Flashcards

1
Q

Give 2 benefits and 2 limitations of inflammation in the body

A

Benefit - Destruction of invading microorganisms and walling off of an abscess, preventing spread of infection.

Limitations - Acts as a space occupying lesion, compressing surrounding structures. Fibrosis after chronic inflammation may distort tissues and permanently alter function.

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2
Q

Characteristic inflammation cell

A

Neutrophil polymorph

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3
Q

4 outcomes of inflammation

A

Resolution - goes away
Suppuration - abscess or pus formation
Organisation - Healing by fibrosis (scarring)
Progression to chronic inflammation

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4
Q

Describe organisation (inflammation outcome)

A

Substantial tissue damage means tissue cant regenerate specialised cells. Dead tissues and inflammatory exudate removed from damaged areas by macrophages. Defect becomes filled by specialised granulation tissue, which contains fibroblasts that produce collagen.

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5
Q

What are the 3 stages of inflammation?

A

Increased vessel calibre (inflammatory cytokines mediate vasodilation)
Fluid exudate
Cellular exudate

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6
Q

5 causes of acute inflammation

A

Microbial infection
Hypersensitivity reactions
Physical agents (trauma, ionising radiation, heat/cold)
Tissue necrosis
Bacterial toxins

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7
Q

5 macroscopic features of acute inflammation

A

Redness (Rubor)
Heat (Calor)
Swelling (Tumour)
Pain (Dolor)
Loss of function

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8
Q

Explain why macroscopic features of acute inflammation occur

A

Redness - Dilation of small blood vessels in damaged area
Heat - Vascular dilation and increased blood flow. Systemic fever due to chemical mediators of inflammation.
Swelling - swelling due to oedema from fluid exudate
Pain - Stretching and distortion of tissues due to inflammatory oedema.
Loss of function - fibrosis distorts tissue.

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9
Q

What is fluid exudate?

A

Exudate is fluid that leaks out of blood vessels into surrounding tissues. Fluid made up of cells, proteins and solid materials.

Is also known as pus.

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10
Q

Stages in neutrophil polymorph emigration

A

Margination - Vascular dilation = slowing of blood flow and oedema = increase in plasma viscosity.
Adhesion - Pavementing occurs at site of inflammation, Adhesion molecules expressed on endothelial surface and neutrophils adhere and roll along endothelium.
Neutrophil emigration - Neutrophils, eosinophil polymorphs and macrophages all insert pseudopodia between endothelial cells and migrate through gap.
Diapedesis - RBC also escape from vessels - passive process depending on hydrostatic pressure.

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11
Q

Role of histamine and TNF-a in inflammation

A

Histamine and TNF-a released mast cells cause expression of adhesion molecules on surface of endothelial cells. = very firm neutrophil adhesion to endothelial surface.

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12
Q

4 effects of endogenous chemical mediators of inflammation

A

Vasodilation
Chemotaxis
Increased vascular permeability
Itching and pain

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13
Q

Diagnostic criteria for acute inflammation

A

Presence of neutrophil polymorphs

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14
Q

3 endogenous chemical mediators of acute inflammation

A

Bradykinin
Histamine
Nitric oxide

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15
Q

5 systemic effects of acute inflammation

A
  1. Fever
  2. Weight loss
  3. Fatigue
  4. Reactive hyperplasia
  5. Tachycardia

(There are loads - tachypnoea, hypotension, depression, athralgia etc etc)

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16
Q

Benefits and drawbacks of fluid exudate in inflammation

A

Benefits
- Dilution of toxins
- Entry of antibodies
- Fibrin formation

Drawbacks
- Digestion of normal tissues
- Swelling
- Inappropriate inflammatory response (hypersensitivity)

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17
Q

Define chronic inflammation, and what cells is it characterised by?

A

Subsequent and prolonged tissue reactions to injury following initial response.

Characterised by lymphocytes, plasma cells and macrophages. Some macrophages form multinucleated giant cells. Not many neutrophils.

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18
Q

4 causes of chronic inflammation

A

Primary chronic inflammation
Transplant rejection
Recurrent acute inflammation (e.g. cholecystitis due to gallstones)
Progression from acute (suppurative most common)

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19
Q

4 causes of primary chronic inflammation

A

Resistance of infective agent to phagocytosis (TB)
Granulomatous disease (e.g. sarcoidosis, crohns)
Autoimmune disease
Exogenous material (silica, asbestos)

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20
Q

5 Macroscopic features of chronic inflammation

A

Chronic ulcers
Chronic abscess cavity
Thickening of hollow organ wall
Granulomatous inflammation
Fibrosis

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21
Q

Define granuloma

A

An aggregate of epithelioid histocytes. (horseshoe shape)

(where immune system walls off substance but is unable to eliminate it)

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22
Q

Why do you get exudate in inflammation?

A

Capillary hydrostatic pressure increases and plasma proteins are pushed into extravascular space, increasing osmotic pressure there. Results in much more fluid leaving vessels than is returning.

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23
Q

4 changes to local blood vessels in inflammation

A
  1. Vascular Dilation (causing redness and warmth)
  2. Increased permeability (causing oedema and pain)
  3. Endothelial cells activate (express cell-adhesion molecules, allowing binding of circulating leukocytes)
  4. Clotting in small blood vessels (prevents circulation of pathogens)
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24
Q

What cell is the most important source of histamine?

A

Mast cells

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25
Q

What stimulates histamine release in inflammation?

A

C5a causes histamine and TNF-a release from mast cells.

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26
Q

7 microscopic features of chronic inflammation

A

Lymphocytes
Plasma cells
Macrophages
Multinucleate giant cells
New fibrous tissue
Tissue necrosis may be present
Eosinophil polymorphs

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27
Q

What enzyme acts as a marker of granulomatous disease?

A

Angiotensin converting enzyme (secreted by granulomas)

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28
Q

What cells regenerate? (5)

A

Hepatocytes
Pneumocytes
All blood cells
Gut and skin epithelium
Osteocytes

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29
Q

What cells don’t regenerate? (2)

A

Myocardial cells
Neurones

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30
Q

Define abscess

A

Acute inflammation with a fibrotic wall

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31
Q

What is the difference between repair and resolution?

A

In resolution, initiating factor removed and tissue can regenerate.

In repair, initiating factor still present and tissue can’t regenerate

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32
Q

What 2 properties of blood flow mean thrombosis formation is uncommon?

A
  1. Laminar flow (cells travel in centre of vessels)
  2. Non sticky endothelial cells
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33
Q

Describe Virchows triad

A

3 factors that could contribute to thrombosis
1. Endothelial injury (cellulitis, trauma, HTN, smoking)
2. Venous stasis (Immobility, pregnancy, AF)
3. Hypercoagulability (Major surgery, malignancy, pregnancy, sepsis)

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34
Q

Treatment of arterial and venous thrombosis

A

Arterial - Antiplatelets
Venous - DOAC/Warfarin

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35
Q

What are alpha and dense granules in platelets?

A

Alpha granules contain substances that aid adhesion to damaged vessel
Dense granules contain substances that cause platelets to aggregate

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36
Q

Fates of thrombi

A

Resolution
Organisation
Decreased blood flow

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37
Q

Define cytokine and chemokine

A

Cytokines are secreted by cells of the immune system and affect other cells
Chemokines induce directed movement of cells

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38
Q

Define thrombosis

A

Solid mass of blood constituents formed within intact vascular system during life

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39
Q

6 constituents of an atherosclerotic plaque

A
  1. Lipids (e.g. cholesterol)
  2. Smooth muscle
  3. Macrophages
  4. Foam cells (macrophages that phagocytose LDL)
  5. Platelets
  6. Fibroblasts
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40
Q

6 risk factors for atherosclerosis

A
  1. Cigarette smoking
  2. Hypertension
  3. Hyperlipidaemia
  4. Uncontrolled diabetes mellitus
  5. Lower socioeconomic status
  6. Old age
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41
Q

5 stages of atherosclerosis

A
  1. Fatty streak (10 years precursor)
  2. lipid accumulation
  3. Platelet aggregation
  4. Fibrin mesh and RBC trapping
  5. Fibrous cap formation
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42
Q

What is granulation tissue composed of?

A

Fibroblasts/myofibroblasts
New thin walled capillaries
Endothelial cells
Keratinocytes

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43
Q

Healing by first intention vs second

A

First - wound edges approximated (e.g. by glue, staples, plasters, sutures) so healing begins top down. Reduces tissue loss, allowing body to heal smaller area than initial wound.

Second - wound edges cant be approximated. Larger tissue loss occurs and wound heals from bottom up. Higher risk of infection. Relies on body’s own mechanisms. Needed in cases of large burns or ulcers, where approximation would reduce mobility or function.

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44
Q

Pathogenesis of atherosclerosis

A
  • High LDL causes them to deposit and oxidise in tunica intima, activating endothelial cells which present leukocyte adhesion molecules.
  • Leukocytes move into intima and attract monocytes (macrophages/T helper cells)
  • Macrophages take up oxidised LDL and form foam cells, which release IGF-1 causing smooth muscle to migrate to intima from media.
  • Smooth muscle proliferation forms fibrous cap.
  • As foam cells die they release lipid content, growth factors and cytokines, growing plaque.
  • Plaque either occludes vessel or ruptures, triggering platelet aggregation and clotting.
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45
Q

Causes of outcomes of inflammation

A

Resolution - normal
Suppuration - excessive exudate
Repair and organisation - excessive necrosis
Chronic - persistent causal agent

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46
Q

Define Atrophy with example

A

Decrease in tissue size due to reduction in number of constituent cells or cell size.

Example: Loss of innervation, or under usage = muscle atrophy
OR
Thyroid gland atrophy in Hashimotos thyroiditis.

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47
Q

Define hyperplasia with example

A

Increase in tissue size due to increase in number of constituent cells (by mitosis)

Physiological: Ductal hyperplasia in pregnancy
Pathological: BPH/ Endometrial hyperplasia

CANT OCCUR IN MYOCARDIAL OR NERVE CELLS (dont divide)

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48
Q

Define hypertrophy with physiological and pathological examples

A

Increase in cell size without division

Physiological: Skeletal muscle hypertrophy in athletes. Uterine smooth muscle in puberty and pregnancy.
Pathological: RV Hypertrophy in pulmonary hypertension

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49
Q

Define metaplasia with example

A

The change in differentiation from one fully differentiated cell type to another.

Example: Squamous to columnar in Barrett’s oesophagus
OR
Ciliated respiratory epithelium to squamous in smokers

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50
Q

Define dysplasia with example

A

Imprecise term for morphological (cell shape, structure, form) differences in cell on way to becoming cancerous.

E.g. Barrett’s oesophagus, Gastritis (chronic inflammation = epithelial metaplasia)

51
Q

Define Carcinogenesis

A

Transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations (only applies to malignant (invasive) neoplasms)

52
Q

6 steps of metastasis

A
  1. Detachment of tumour cells from neighbours
  2. Invasion of surrounding tissues to reach metastasis conduits (blood/lymphatics)
  3. Intravasation into lumen of vessels
  4. Evasion of host defence mechanisms
  5. Adherence to endothelium at remote location
  6. Extravasation of cells from lumen to surrounding tissue
53
Q

Which cancers metastasise to bone and how do they spread

A

Lung
Breast
Kidney
Thyroid
Prostate

Haematogenous spread

54
Q

Invasion vs metastasis

A

Invasion is ability of cancer cells to directly extend and penetrate into surrounding cells, whilst metastasis uses lymphatic or blood vessels to form a secondary tumour elsewhere

55
Q

How is basal cell carcinoma treated?

A

Complete local excision is curative (basal cell carcinoma is locally invasive but doesn’t metastasise)

56
Q

Name a drug that inhibits platelet aggregation

A

Aspirin, can be prescribed low dose to prevent thrombosis

57
Q

3 disease causing processes of atherosclerosis

A
  1. Vessel stenosis - more than 50-70% occlusion = critical reduction of blood flow. Tissue ischaemia reversible at first with pain only at exertion. Severe stenosis = pain at rest
  2. Plaque rupture = Activation of coagulation cascade, leading to thrombosis which can occlude vessels
  3. Ruptured atherosclerotic aneurysm
58
Q

Define infarction

A

Local cell and tissue death due to obstruction of blood supply

59
Q

5 preventative measures against atherosclerosis

A
  1. Smoking cessation
  2. Blood pressure control
  3. Weight reduction
  4. Low dose aspirin (inhibits platelet aggregation)
  5. Statins
60
Q

5 possible complications of atherosclerosis

A

Cerebral infarction
Myocardial infarction
Aortic aneurysm
PVD
Gangrene

61
Q

How does smoking damage arteries?

A

Free radicals oxidise LDL
Nicotine and CO damage endothelial cells

62
Q

What protein detects DNA damage in cells, leading to apoptosis?

A

P53 protein

63
Q

Where is apoptosis found physiologically?

A

In tissues with high cell turnover (Skin. gut)

64
Q

Give an example of apoptosis in disease?

A

HIV

65
Q

Define necrosis and give a pathological example

A

Traumatic cell death, which induces inflammation and repair, for example frostbite, cerebral infarction.

66
Q

apoptosis vs necrosis

A

Apoptosis is non inflammatory and controlled. Organelles retailed and chromatin unaltered. Apoptosis affects single cells. Cells shrink and fragment into apoptotic bodies.

Necrosis is inflammatory and traumatic. Cells burst, organelles spread, chromatin altered. Necrosis affects groups of cells. Cells swell and lysis.

67
Q

Inducers and inhibitors of apoptosis (3 each)

A

Inducers - DNA damage, glucocorticoids, loss of matrix attachment

Inhibitors - Growth factors, Extracellular cell matrix, Sex steroids

68
Q

Intrinsic apoptosis pathway

A

Intrinsic - Responds to biochemical stress or growth factors. P53 gene responds and activates either: Bcl-2 which responds to apoptosis inhibitors or Bax which enhances apoptotic stimuli. More Bax or less Bcl-2 stimulates Caspases, leading to apoptosis.

69
Q

Extrinsic apoptosis pathway

A

Extrinsic - Apoptosis activated by ligand binding at death receptors on cell surface, e.g. TNFR1 (tumour necrosis factor receptor) or Fas. Initiates signal transduction cascade and activates caspases.

70
Q

What do caspases do?

A

Caspases are proteases that cause apoptosis through degradation of cytoskeletal framework and nuclear proteins.

71
Q

Why is apoptosis non inflammatory?

A

Dead cells are arranged into apoptotic bodies, which are eventually phagocytosed.

72
Q

Why is necrosis inflammatory?

A

Spillage of cell contents provoke inflammatory response

73
Q

Give the 4 types of necrosis

A

Coagulative - Caused by ischaemia, causes proteins to coagulate and tissue is digested by macrophages, making firm tissue soft. Necrotic tissue = inflammation.
Liquefactive - Brain liquifies due to lack of supporting stroma (blood, lymph, connective tissue, nerves)
Caseous - e.g. TB. Tissue structureless
Gangrene - Tissue rots, appears black due to iron sulphide deposition from degraded haemoglobin. Usually due to bacteria.

74
Q

Acquired vs inherited

A

Acquired - No DNA involvement, result from environmental factors

Inherited - Caused by changes in DNA, passed genetically

75
Q

What syndromes are trisomy 21, 18 and 13

A

Trisomy 21 - Down’s
Trisomy 18 - Edwards
Trisomy 13 - Patau’s

All are spontaneous mutations

76
Q

Define neoplasm

A

New, autonomous, abnormal, persistent growth. Only occurs from nucleated cells

77
Q

Define tumour

A

Any abnormal growth (neoplasm + inflammation + hypertrophy + hyperplasia)

78
Q

Arterial vs venous thrombosis: Clinical effects

A

Arterial:
Pale, pulseless, paralysis, paraesthesia, perishingly cold, painful

Venous:
Area becomes tender, warm, red, swollen. (95% in legs (DVT)). Superficial veins distended. Oedematous.

79
Q

How might you differentiate an arterial ulcer from a venous ulcer?

A

Arterial: Distal extremities. hairless, pale/ necrotic wound tissue, skin shiny pale taut, minimally exudative

Venous: Gaiter area, lower calf to medial malleolus. Irregular shape, granular appearance, more exudative, firm odoema, thick skin.

80
Q

Arterial vs venous thromobosis: causes

A

Arterial: atherosclerosis (See card on process)

Venous: grow by successive deposition via propagation. When BP low, blood flow is less laminar, thrombi can grow near valves.

81
Q

Why dont you get atheroma in veins

A

They have a lower blood pressure

82
Q

Pharmacological ways to prevent thrombosis

A

Aspirin - inhibits platelet aggregation
Warfarin (severe) - inhibits vitamin K (clotting factor)

83
Q

What clotting factors are Vit K dependant

A

K-10,9,7,2

84
Q

Possible complications of arterial embolism passing through heart

A

Cerebral infarct (stroke)
Renal infarct
Bowel ischaemia
Foot ischaemia (dry gangrene)

85
Q

5 host factors that influence carcinogenesis

A

Race
Diet
Constitutional factors - age, gender etc.
Premalignant lesions
Transplacental exposure

86
Q

Naming conventions of cancers of cancers of connective tissue
- Adipocytes
- Striated muscle
- Smooth muscle
- Cartilage
- Bone
- Vascular

A

-oma and -sarcoma

  • Adipocytes: lipo-
  • Striated muscle: Rhabdomyo-
  • Smooth muscle: leiomyo-
  • Cartilage: Chondro-
  • Bone: Osteo-
  • Vascular: Angio-
87
Q

What 2 ways are cancers classified

A
  • Behaviour (benign or malignant)
  • Histogenesis (origin cells)
88
Q

What are the 2 major subdivisions of histogenic cancer classification

A

Epithelial cells: Non glandular : Papilloma/ Carcinomas
Glandular: Adenoma/adenocarcinoma

Connective tissues: -Oma/ -Sarcomas

89
Q

3 ways benign cancers can be pathological

A
  1. Can secrete hormones (e.g. prolactinoma)
  2. Can cause obstruction to flow of fluid (e.g. BPH - urinary issues)
  3. Pressure on adjacent structures (e.g. pituitary adenoma pressing on optic chiasm)
90
Q

Benign vs malignant tumour behaviours

A

Benign
- localised (no BM invasion)
- Slow growing
- Closely resemble normal tissue
- Necrosis and ulceration is rare
- Exophytic (grow outward)

Malignant
- invasive (but not always metastatic - Basal cell carcinoma is malignant but doesnt metastasise)
- Grow fast
- Irregular border and dont resemble parent cell as much
- Hyperchromatic nuclei that stain dark
- Necrosis common
- Endophytic (grow inward)

91
Q

Organs with a dual artery supply

A

Liver - portal venous and hepatic artery supplies
Lung - pulmonary venous and bronchial artery supplies
Brain - circle of willis and multiple arterial supplies

Less susceptible to infarction

92
Q

How are malignant tumours pathological

A
  • Pressure on and destruction of adjacent tissue
  • Formation of metastases
  • Blood loss (ulcerated surfaces)
  • Obstruction of flow (malignant tumor of colon = intestinal obstruction)
  • Paraneoplastic effects (SIADH/ Cushings)
93
Q

Why is cell differentiation important in malignant cancers?

A

A tumour with poorly differentiated cells is more aggressive than well differentiated tumours.

Grade 1- Well differentiated (75% cells resemble parent)
Grade 2 - Moderately differentiated (10-75%)
Grade 3 - Poorly differentiated (<10%)

94
Q

What is an anaplastic cancer?

A

A cancer whose cells are so poorly differentiated they lack recognisable histogenic features. These are extremely aggressive

95
Q

What is carcinoma in situ?

A

A tumour presenting all the features of a malignant cancer but has not yet penetrated the basement membrane. In these cases, excision is a cure.

96
Q

Tumours which commonly metastasise to liver

A

Colon
Stomach
Pancreas
Intestine

97
Q

3 ways neoplastic cells are adapted to differentiate so much

A
  1. Growth stimulation due to oncogene overexpression and tumour suppressor gene inactivation
  2. Reduced apoptosis due to abnormal expression of apoptosis inhibiting genes (bcl-2)
  3. Telomerase - Prevents telomeric shortening, so cell cycles are not restricted - can divide forever.
98
Q

What 6 cancers are caused by alcohol?

A

Oropharynx
Larynx
Oesophagus
Liver
Breast
Colorectal

99
Q

3 ways alcohol causes cancer

A
  • Ethanol makes it easier for cells in oropharynx to absorb other carcinogens
  • Ethanol increases oestrogen levels
  • Alcohol’s metabolite, acetaldehyde, is a mutagen
100
Q

What cancers can be caused by these chemicals:
1- polycyclic aromatic hydrocarbons?
2- aromatic amines?
3- nitrosamines?
4- alkylating agents?

A

1- lung or skin cancer
2- Bladder
3- Gut
4- Leukaemia

101
Q

What cancers are caused by Epstein Barr virus

A

Burkitt’s Lymphoma
Hodgkin’s lymphoma
Nasopharyngeal carcinoma

102
Q

What cancers are caused by Human papillomavirus (HPV)

A

Squamous cell carcinomas of cervix, penis, anus, head, neck

103
Q

What cancers are caused by human herpes virus 8

A

Kaposi sarcoma
Primary effusion lymphoma

104
Q

3 lifestyle risk factors for cancer

A

Excess alcohol causes cancer
Obesity increases risk of some cancers
Unprotected sex increases risk of HPV related cancer

105
Q

Define oncogenesis

A

Development of benign or malignant tumour

106
Q

What 2 types of cells do tumours consist of?

A

Neoplastic cells
Stroma

107
Q

Function of stroma

A

Mechanical support
Intercellular signalling
Nutrition to neoplastic cells

108
Q

What does stroma consist of

A

Fibroblasts
Collagen
Blood vessels

109
Q

Major categories of origin for cancers

A
  • Epithelial cells (carcinomas)
  • Connective tissues (sarcomas)
  • Lymphoid (lymphoma/leukaemia - ALWAYS MALIGNANT)
110
Q

3 genetic alterations that transform a normal cell to neoplastic

A
  1. expression of telomerase - avoids shortening of telomeres, meaning cell can divide perpetually
  2. Loss or inactivation of both copies of a tumour suppressor gene, remove inhibitory control
  3. Activation or abnormal expression of oncogenes to stimulate cell proliferation
111
Q

3 mutations that can cause abnormal oncogene activation

A
  1. Translocation
  2. Point mutation
  3. Amplification
112
Q

Why should a wide margin be removed when excising tumours

A

To ensure tumour cells that could cause a local recurrence arent left behind

113
Q

Factors influencing tumour invasion

A
  1. Decreased cellular adhesion
  2. Secretion of proteolytic enzymes
  3. Abnormal/increased cellular motility
114
Q

Tumour grading vs staging

A

Grading is an assessment of malignancy/aggressiveness

Staging is an extent of spread

115
Q

3 main features when assessing grading

A
  1. Mitotic activity
  2. Nuclear size, hyperchromasia (dark staining), pleomorphism
  3. Resemblance to normal tissue
116
Q

Explain the staging system for tumours

A

TNM
T - Tumour size
N - Degree of lymph Node involvement
M - Extent of distant Metastases

117
Q

4 characteristics of a neoplastic cell

A
  1. Autocrine growth stimulation (overexpression of GF, mutations of tumour suppressor genes)
  2. Evasion of apoptosis
  3. Telomerase
  4. Sustained angiogenesis and ability to invade BM
  5. Invasive growth
118
Q

Explain the disease/ mutation involved in colorectal cancer.

Oncogenes implicated.
Inheritance pattern.

A

FAP (familial adenomatous polyposis) - caused by mutation in APC gene (adenomatous polyposis coli).
Causes multiple adenomas at early age in large intestine. KRAS and c-MYC oncogenes.

Autosomal dominant inheritance.

119
Q

Define germline mutation

A

A mutation in sex or germ cells (egg or sperm). Can be passed onto child and mutation will present in all cells of childs body.

120
Q

Define somatic mutation

A

Spontaneously arise in any cell except germ cells in life. Limited to that cell and its descendants. No inheritance.

121
Q

What cancers are screened for in the UK

A

Breast
Bowel
Cervical

122
Q

What cancers are caused by BRCA1 and BRCA2 mutations

A

BRCA1 - Breast and ovarian
BRCA2 - Breast, prostate, pancreatic

123
Q

How are the 3 screened cancers screened for

A

Cervical - Cervical swab
Breast - Mammogram
Colorectal - Faecal occult blood

124
Q

What does the heel prick test screen for

A

Sickle cell
Cystic fibrosis
Hypothyroidism

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