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ESA 2 > MOD > Flashcards

MOD Flashcards

1
Q

Give the function and an example of a heat shock protein

A

Work to mend the misfolded proteins in the cell. An example is uniquitin

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2
Q

Oncosis is cell death with swelling, what are the three stages of oncosis?

A

Pyknosis - shrinkage of the nucleus
Karyorrhexis - nuclear fragmentation
Karyolysis - resorption of the nuclear membrane

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3
Q

Give four types of necrosis

A

Coagulative
Liquefactive
Caseous
Fat

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4
Q

Give the difference between coagulative and liquefactive necrosis

A

Coagulative - protein denaturation dominates enzyme release

Liquefactive - enzyme release dominates protein denaturation

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5
Q

Describe the ghost outline and give the type of necrosis it occurs in

A

The preservation of the cellular architecture seen in coagulative necrosis

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6
Q

Which condition is closely associated with caseous necrosis?

A

Tuberculosis

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7
Q

Which disease is closely associated with fat necrosis?

A

Acute pancreatitis and breast trauma

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8
Q

Name an organ that undergoes white infarction

A

Heart
Kidney
Spleen
All have dense tissue to stem the bleeding

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9
Q

Name two organs that undergo red infarcts and the reason why they show this

A

Brain - poor stromal support

Lungs- numerous anastomoses

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10
Q

What is the main regulator of apoptosis (cell death with shrinkage)?

A

P53

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11
Q

Which complex, created in the mitochondria, induces the destruction of the cell in apoptosis?

A

Caspases

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12
Q

What is the difference between stable and labile cells?

A

Stable cells have arrested in G0 but can divide again if they leave this phase.
Labile cells continuously divide e.g. epidermal cells

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13
Q

Describe the process of fibrous repair

A

Fibroblasts release collagen into the area, myofibroblasts contract to reduce the area of injury, angiogenesis occurs to vascularise the area

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14
Q

What is the difference between primary and secondary intention healing?

A

Primary - the edges are opposed and the epidermis can regenerate with granulation in the dermis
Secondary - the edges are unopposed and myofibroblasts must response them. Keloid scarring in the epidermis and eschar formation in the dermis

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15
Q

Give the four cardinal signs of acute inflammation

A

Dolor (pain), rubor (redness), calor (heat) and tumor (swelling)

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16
Q

Histamine is secreted from which cells?

A

Mast cells

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17
Q

Give the effects of histamine

A

Vasodilation and increasing vascular permeability

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18
Q

Give the difference between transudate and exudate

A

Transudate is due to a hydrostatic pressure disturbance and so has a low specific gravity
An exudate is the secretions seen in inflammation and so has protein inside and has a higher specific gravity

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19
Q

Give the four stages of neutrophil infiltration at an inflammation site

A

Margination, rolling, adhesion and emigration

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20
Q

What are the effects of endogenous pyrogens and give an example

A

Stimulate the thermoregulatory centre in the hypothalamus to induce a fever. IL-1 and TNF-α

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21
Q

What is the primary leukocyte of acute inflammation?

A

Neutrophil

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22
Q

Which cell can the monocytes differentiate into?

A

Macrophages

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23
Q

Describe the resolution process of acute inflammation

A

Lymphatic drainage of exudate, phagocytosis of foreign bodies and regeneration of damaged tissue

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24
Q

Define chronic inflammation

A

Inflammation lasting more than 12 weeks with associated fibrosis

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25
Q

What is the main leukocyte of chronic inflammation?

A

Lymphocytes (T and B)

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26
Q

What is the generic formation of a giant cell?

A

The fusion of many macrophages

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27
Q

What is granulation tissue?

A

The walling off of the injured site with macrophages with central necrosis due to avascularisation

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28
Q

Describe the appearance of Langhan’s giant cells

A

Crescent shape of marginalised nuclei. Seen in TB

29
Q

Describe the histological appearance of foreign body giant cells

A

Central, disorganised nuclei that overlap. Seen in foreign body invasion

30
Q

Describe the histology of a Touton giant cell

A

Completely encapsulated by a ring of marginalised nuclei. Often seen in areas with a high lipid content e.g. fat necrosis

31
Q

What are permanent cells and give an example

A

These are cells that have completely arrested and are unable to divide further. Skeletal muscle, brain neurones

32
Q

What is Hayflick’s number?

A

The maximum number of divisions that a cell can undergo before the telomere length is too short to allow further growth. Quoted at 61.3

33
Q

Give one physiological and one pathological case of hyperplasia

A

Endometrial hyperplasia in menstrual cycle

Thyroid hyperplasia in gone formation

34
Q

Give one physiological and one pathological cause of hypertrophy

A

Muscle bulk in exercise training

Cardiac hypertrophy in cardiomyopathy

35
Q

Give a physiological and pathological cause of atrophy

A

Ovarian atrophy in post-menopause is physiological

Denervation atrophy is pathological

36
Q

What is metaplasia? Give an example condition

A

Change of one cell type to another. E.g. Barrett’s oesophagus

37
Q

What is the fatty streak?

A

Lipid infiltration in the intimal lining of arteries

38
Q

Describe a simple plaque

A

Propagation of the fatty streak so that it has an irregular outline and is widely distributed

39
Q

Describe the complicated plaque and give a condition it predisposes to

A

Calcification of the atheroma surface to form a fibrous cap. Can predispose to aneurysm

40
Q

What are foam cells?

A

Macrophages that have ingested too much lipid in the artery intima that they now contribute to the plaque

41
Q

Give some risk factors for atheroma

A

High cholesterol, male, age, hypertension, diabetes

42
Q

Give the benign and malignant tumour name of a gland

A

Adenoma is benign

Adenocarcinoma is malignant

43
Q

Give some structural changes seen in malignant cells

A

Poor differentiation
Increased nuclear:cytoplasmic ratio
Mitotic figures

44
Q

Give some behavioural changes of malignant cells

A

Immortality - as seen in HeLa cells
Loss of contact inhibition
Loss of anchorage dependence
Low requirement for growth factors

45
Q

Give some functional changes seen in malignant cells

A

Decreased adhesion between cells

Tissue factor production, increasing clotting

46
Q

What are foci of necrosis?

A

A central portion of necrosis seen in malignant tumours. Associated with a poor prognosis

47
Q

Give the ways that metastases can spread

A

Blood
Lymph
Direct spread

48
Q

Describe the seed and soil hypothesis

A

The seed is an opportunistic portion of the primary tumour that enters a serosal surface. The soil is a distant tissue site that supports the seed for growth as a metastasis. The seed must be slippery enough to pass in the blood/lymph but adhesive enough to adhere to the new soil

49
Q

What factors must a metastasis do to become a new tumour?

A 
Separate itself from the primary
Digest through the basement membrane
Escape systemic defences 
Penetrate the new endothelium
Induce angiogenesis to create a secondary
50
Q

Give the two commonest paraneoplastic syndromes

A

Small cell carcinoma of the lung producing ADH

Squamous cell carcinoma of the lung producing PTH

51
Q

Why are many cancer patients in a hypercoagulable state?

A

Platelets are activated by tumour secreted ADP

Tumours secrete tissue factor

52
Q

Give some chemical carcinogens

A

Pollution
Smoking
Alcohol (promotes turnover of cells)
Diet

53
Q

What are the Japanese and American common GI cancers?

A

Japanese have stomach cancers, Americans have colon. This is due to diet

54
Q

How do tumours divide indefinitely?

A

By stimulating proto-oncogenes and switching off tumour suppressor genes

55
Q

Give the most commonly changed tumour suppressor gene

A

P53

56
Q

Give the staging of Dukes classification and the cancer assessed

A 
Colon cancer
A - not through bowel wall
B - invasion through bowel wall but not including lymph nodes
C - lymph node involvement
D - widespread metastases
57
Q

Give the staging of Ann Arbor classification and the cancer involved

A 
Lymphoma
1 - one lymph node involved
2 - two regions on one side of the diaphragm
3 - both sides of the diaphragm involved
4 - diffuse involvement of lymph nodes
58
Q

Give the cancers that the following markers correlate to; bence-jones protein, PSA, CEA, Alpha-fetoprotein

A

BJP - multiple myeloma
PSA - prostate ca
CEA - colon ca
AFP - hepatoma and germ cell tumours

59
Q

Describe TNM staging

A

Tumour size 0-4
Nodal involvement 0-3
Metastases 0 or 1

60
Q

Give the three stages of haemostasis

A

Artery contracts
Platelet plug formation
Fibrin infiltrate to stabilise the platelet plug

61
Q

Give some platelet activators

A

Thrombin
Collagen surfaces
ADP

62
Q

Give the function of thrombin

A

Cleaves fibrinogen to fibrin

63
Q

How is a blood clot dissolved?

A

Dilution of clotting factors by the blood flow

Natural anticoagulants produced by the liver

64
Q

Give the function of plasmin

A

Enzyme responsible for fibrinolysis

Circulates as plasminogen and is activated by tissue plasminogen activator (tPA)

65
Q

What is the function of Von Willebrand factor?

A

Found on the endothelial wall to favour clotting

66
Q

What is Virchow’s triad of thrombus formation?

A

Changes to vascular wall
Changes in blood flow
Changes in the blood

67
Q

How would you differentiate between a thrombus and a post-mortem clot?

A

Thrombi are laminated with lines of Zahn

Post-mortem clots are shiny and never laminated

68
Q

What is disseminated intravascular coagulation?

A

This is a complication of another condition (commonly sepsis) where all the clotting factors are used up and so the person is at risk of haemorrhage

69
Q

Give some forms of emboli

A 
Thrombo-embolus
Gas
Fat
Amniotic
Foreign body

ESA 2 (2 decks)

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