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Phase 2a Stuff > ICS Pathology > Flashcards

ICS Pathology Flashcards

1
Q

Define Inflammation

A

Local physiological response to tissue injury

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2
Q

In what ways can inflammation be beneficial?

A
  • Destruction of invading microorganisms

- Walling off an abscess cavity

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3
Q

In what ways can inflammation be harmful?

A
  • Over-reaction to stimulus
  • Autoimmune diseases
  • Abscesses can act as space-occupying lesions in the brain
  • Fibrosis
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4
Q

Define acute inflammation

A

Initial and transient series of tissue reactions to injury

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5
Q

Define chronic inflammation

A

Subsequent and/or prolonged tissue reactions following initial response

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6
Q

Steps of acute inflammation

A
  1. Initial reaction
  2. Vasodilation
  3. Vascular leakage of protein-rich fluid
  4. Neutrophil polymorph recruited
  5. Outcomes
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7
Q

Outcomes of Acute Inflammation

A
  • Resolution
  • Suppuration (formation of pus e.g. abscess)
  • Organisation
  • Chronic Inflammation
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8
Q

Acute Inflammation causes

A 
Microbial Infections
Hypersensitivity reactions
Physical agents
Chemical
Bacterial toxins
Tissue necrosis
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9
Q

Appearance of Acute Inflammation

A

Rubor - Redness
Calor - Heat
Tumor - Swelling
Dolor - Pain

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10
Q

What cells are required for histological diagnosis of inflammation?

A

Neutrophil polymorphs

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11
Q

Describe Neutrophil Polymorphs

A

Contain cytoplasmic granules full of bacteria-killing enzymes. Usually die at scene of inflammation. Attracts macrophages.

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12
Q

Describe Macrophages

A

Phagocytic properties, ingesting bacteria and debris. Last weeks to months, can present antigen to lymphocyte

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13
Q

Describe lymphocytes

A

Live for years, attract other inflammatory cells, immunological memory etc.

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14
Q

Describe endothelial cells in areas of inflammation

A

Become sticky so inflammatory cells stick to them, become porous to allow inflammatory cells into tissues.

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15
Q

Describe fibroblasts in inflammation

A

Long-lived, form collagen in areas of chronic inflammation and repair.

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16
Q

Example of Acute Inflammation

A

Acute Appendicitis

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17
Q

Example of Chronic Inflammation

A

Tuberculosis

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18
Q

Treatment for acute inflammation

A

RICE
Aspirin
Ibuprophen (NSAIDs)
Analgesics

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19
Q

What is a granuloma?

A

A collection of epithelioid histocytes (macrophages) - a small area of inflammation

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20
Q

What is granulation tissue?

A

Important component of healing and comprises small blood vessels in a connective tissue matrix with myofibroblasts

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21
Q

What are the two types of autopsy and how common are they?

A

Hospital autopsies - 10%

Medico-legal autopsies - 90% (coronial or forensic)

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22
Q

What types of deaths are referred to coroners?

A
  • Natural
  • Iatrogenic
  • Unnatural
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23
Q

Causes of Chronic Inflammation

A

Primary chronic inflammation (most common)
Transplant rejection
Progression from acute
Recurrent episodes of acute

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24
Q

Is a granuloma a form of acute or chronic inflammation?

A

Chronic (type IV hypersensitivity)

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25
Q

What is Rheumatoid Arthritis?

A

Inflammatory arthritis with granulomatous features with no overt cause

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26
Q

Define resolution of an injury

A

Initiating factor removed and tissue is undamaged or able to regenerate

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27
Q

Define repair of an injury

A

Initiating factor still present, tissue damaged and unable to regenerate. Usually results in fibrous scarring.

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28
Q

Lobar Pneumonia

A

Affects 1 lung lobe. Alveoli filled with polymorphs. Pneumocytes can regenerate so can be resolved.

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29
Q

Lung damage in COVID

A

Interstitial pneumonia, alveolar walls cannot regenerate so fibrosis occurs.

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30
Q

Describe healing of abrasions

A

Abrasion -> scab formed -> epidermis growing out from adnexa protected by scab -> thin confluent epidermis -> final epidermal regrowth

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31
Q

Describe healing of skin by 1st intention

A

Incision causes little damage to surrounding tissues. two sides brought together and healing can proceed quickly.

Incision -> exudation of fibrinogen -> weak fibrin joint -> epidermal regrowth and collagen synthesis -> strong collagen joint

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32
Q

Describe healing of skin by 2nd intention

A

Tissue loss injury, granulation tissue forms -> organisation -> early fibrous scar -> scar contraction

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33
Q

What is granulation tissue?

A

Loops of capillaries supported by myofibroblasts. Actively contracts to reduce wound size.

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34
Q

Examples of cells that DO regenerate

A
  • Hepatocytes
  • Pneumocytes
  • All blood cells
  • Gut epithelium
  • Skin epithelium
  • Osteocytes
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35
Q

Examples of cells that DON’T regenerate

A
  • Myocardial cells

- Neurones

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36
Q

What is fibrosis in the brain called?

A

Gliosis

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37
Q

Why are blood clots rare?

A

Laminar flow

Endothelial cells aren’t sticky when healthy

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38
Q

Define thrombosis

A

Solid mass of blood constituents formed within vascular system

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39
Q

Steps of thrombus formation

A
  1. Damage to endothelial cells exposes collagen
  2. Platelets begin to stick to exposed collagen – platelet aggregation
  3. Red blood cells get trapped within aggregating platelets
  4. Clotting factors join the RBCs and platelets, clotting cascade forms fibrin which is deposited and forms a clot
  5. Positive feedback loop -> can end up causing a thrombus – blocking the artery
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40
Q

What can reduce risk of thrombosis?

A

Low-dose aspirin

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41
Q

Causes of thrombosis

A
  1. Changes in vessel wall
  2. Changes in blood flow
  3. Changes in blood constituents
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42
Q

What is an embolism?

A

Process of a solid mass in the blood being carried to a place where it gets stuck

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43
Q

Types of embolus

A
  • Broken off thrombus (most common)
  • Air
  • Tumour
  • Amniotic fluid
  • Fat
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44
Q

What happens if an embolus enters the venous system?

A

Travels to the vena cava and lodges in pulmonary arteries

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45
Q

What happens if an embolus enters the arterial system?

A

Can travel ANYWHERE downstream of entry

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46
Q

Define ischaemia

A

Reduction in blood flow to tissue without other implications

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47
Q

Define infarction

A

Reduction in blood flow causing lack of nutrients to tissue causing tissue death

48
Q

What is an end artery supply

A

Organ that only receives blood supply from 1 artery (problematic with thrombus)

49
Q

Examples of organs with multiple arterial supplies

A

Lungs
Liver
Brain

50
Q

What is in a plaque?

A
  • Fibrous tissue
  • Lipids (cholesterol)
  • Lymphocytes
51
Q

Is atherosclerosis found in low or high pressure systems?

A

High pressure systems e.g. systemic arteries

52
Q

Risk factors of atherosclerosis

A

Age, smoking, hypertension, poorly-controlled diabetes, hyperlipidaemia

53
Q

Formation of atheroma

A

Endothelial damage causes thrombus formation, endothelial cells grow over thrombus and this happens a lot causing build up.

54
Q

What can be used to prevent platelet aggregation?

A

Low-dose aspirin

55
Q

Complications of atherosclerosis

A

Cerebral infarction, MI, gangrene, carotid atheroma, aortic aneurysms, peripheral vascular disease

56
Q

What is apoptosis?

A

Programmed cell death to get cells no longer functioning

57
Q

Process of apoptosis

A

Nucleus condenses, cell shrinkage, cell breaks into apoptotic bodies

58
Q

Trigger of apoptosis

A

DNA damage in dividing cells

59
Q

Apoptosis in disease

A

Cancer (too little)

HIV (too much)

60
Q

What are the effector molecules of apoptosis?

A

Caspases

61
Q

What is necrosis?

A

Traumatic cell death of functioning cells

62
Q

Causes of necrosis

A

Disease, injury or blood supply

63
Q

Clinical examples of necrosis

A
  • Toxic spider venom
  • Frostbite
  • Cerebral Infarction
  • Avascular necrosis of bone
  • Pancreatitis
64
Q

Define Hypertrophy

A

Increase in tissue size due to increase in size of constituent cells

65
Q

Define Hyperplasia

A

Increase in tissue size due to increase in number of cells

66
Q

Define Atrophy

A

Decrease in size of tissue caused by decrease in constituent cell number OR size

67
Q

Define Metaplasia

A

Change in differentiation of a cell from one fully-differentiated type to a different fully-differentiated type (reversible)

68
Q

Define Dysplasia

A

Morphological changes seen in cells in the progression to becoming cancerous

69
Q

What occurs to telomeres as we age?

A

Telomeres get shorter after each cell division – limiting the amount of division that can occur

70
Q

Dermal elastosis in ageing

A

Accumulation of abnormal elastic in dermis. Result of prolonged exposure to UV light (causing cross-linking)

71
Q

Osteoporosis in ageing

A
  • Loss of coupling in the bone remodelling process – due to increased bone resorption or decreased bone formation due to a lack of oestrogen
  • Can cause osteopenia
  • Bone matrix mineralised as usual but trabeculae thinned
  • Leads to hypercalciuria
72
Q

Cataracts in ageing

A
  • Result of the formation of opaque proteins within the lens resulting in loss of lens elasticity
  • UV-B light causes protein cross-linking
73
Q

Senile dementia in ageing

A

Plaques and neurofibrillary tangles occur in brain

74
Q

Sarcopenia in ageing

A

Decreased GH, decreased testosterone, increased catabolic cytokines

75
Q

Deafness in ageing

A

Hair cells cannot divide/regenerate so cannot recover once damaged

76
Q

Pathology of Basal cell carcinoma

A

Only invades locally, never metastasises - local excision = cure

77
Q

Basic pathology of Leukaemia

A

Malignant tumour of WBCs so circulates, so needs a systemic treatment e.g. chemotherapy

78
Q

Where can carcinomas spread?

A
  • Lymph nodes draining site of carcinoma
  • Bone (breast, prostate, lung, thyroid and kidney)
  • Rest of the body
79
Q

Breast cancer care plan

A
  • Core needle biopsy to confirm
  • Axillary nodes ultrasound (then biopsy)
  • CT scan/radio nucleotide scan of rest of body
  • Surgery
80
Q

What is adjuvant therapy?

A

Extra treatment given after surgical excision to eliminate micro-metastases

81
Q

What can oestrogen-receptor positive breast cancers be combated with?

A

Anti-oestrogen therapy

82
Q

Define carcinogenesis

A

The transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations

83
Q

Define oncogenic

A

tumour causing

84
Q

Define carcinogenic

A

cancer causing (only malignant neoplasms)

85
Q

Why are carcinogens hard to identify?

A

Long latent periods, complexity of environment, ethical issues with research

86
Q

Occupational cancer risks

A

Lung cancer - smoking
Bladder cancer - aniline dye and rubber
Scrotal cancer - chimney sweeps

87
Q

5 classes of carcinogens

A 
Chemical
Viral
Ionising and non-ionising radiation
Hormones, parasite and mycotoxins
Misc.
88
Q

What percentage of cancer risk is inherited

A

15% (rest is environmental)

89
Q

How long is the latent period typically between exposure and cancer?

A

VERY LONG

90
Q

Define neoplasm

A

o A lesion resulting from the autonomous or relatively autonomous abnormal growth of cells which persists after the initiating stimulus has been removed

91
Q

What makes up neoplasms?

A

Neoplastic cells and stroma

92
Q

What cells are present in the stroma of a neoplasm?

A

Fibroblasts

93
Q

Tumour angiogenesis

A

Blood supply growth to tumour, needed for growth. Malignant neoplasm too fast so has central necrosis.

94
Q

Characteristics of a benign neoplasm

A
  • Localised
  • Non-invasive
  • Grow slowly (low mitotic activity)
  • Close resemblance to normal tissue
  • Necrosis and ulceration rare
  • Nuclei often normal looking
95
Q

How can benign neoplasms cause morbidity/mortality

A

Pressure on adjacent structures, hormone production, transformation into malignant, anxiety

96
Q

Characteristics of a malignant neoplasm

A
  • Invasive and can metastasise
  • Rapid growth rate
  • Variable resemblance to normal tissue
  • Poorly defined or irregular border
  • E.g. prostate cancer, squamous cell carcinoma
  • Hyperchromatic and pleomorphic nuclei
  • Increased mitotic activity
  • Necrosis and ulceration common
  • Encroach upon and destroy surrounding tissues
97
Q

Suffix of all neoplasms

A

-oma

98
Q

What do you call a benign tumour of non-glandular or secretory epithelium?

A

Papilloma

99
Q

Name of benign tumour of glandular/secretory epithelium

A

Adenoma

100
Q

Name of malignant epithelial neoplasm

A

Carcinoma

101
Q

Name of carcinoma of glandular epithelium

A

Adenocarcinoma

102
Q

Benign connective tissue neoplasm

A 
Lipoma
Chondroma
Osteoma
Angioma
Leiomyoma
Rhabdomyoma
Neuroma
103
Q

Malignant connective tissue neoplasms

A

Sarcoma

104
Q

What is an anaplastic tumour?

A

Cell-type of origin is unknown

105
Q

Exceptions to neoplasm naming rules (long list)

A 
Granuloma
Tuberculoma
Melanoma
Mesothelioma
Lymphoma
Burkitt's lymphoma
Ewing's sarcoma
Grawitz tumour
Kaposia's sarcoma
Teratoma
Blastomas
Mixed Tumours
APUDomas
Carcinosarcoma
106
Q

Example of granulomatous inflammation

A

Chron’s disease

107
Q

Chronic inflammatory process never going through acute stage

A

Infectious mononucleosis

108
Q

Pattern of differentiation of metaplastic cells in bronchi of smokers

A

Ciliated columnar to squamous

109
Q

What is a carcinoma in situ?

A

A malignant epithelial neoplasm that has not yet invaded through the original basement membrane

110
Q

Define invasive carcinoma

A

A carcinoma that has breached the original basement membrane. Needs proteases and cell motility

111
Q

Define metastasis

A

A malignant tumour spreads from its primary site to produce secondary tumours at distant sites.

112
Q

Steps of the metastatic cascade

A
  1. Detachment
  2. Invasion through basement membrane
  3. Intravasation
  4. Evasion of host immune defence
  5. Extravasation
  6. Growth at metastatic site
  7. Angiogenesis
113
Q

Routes of metastasis

A

Haematogenous - blood
Lymphatic
Trans-coelomic - pericardial and peritoneal cavities

114
Q

Tumours which commonly metastasise in the lungs

A

Sarcomas and any common cancers

115
Q

Tumours which commonly metastasise in the liver

A

Colon, stomach, pancreas and carcinoid tumours of intestine

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