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ESA 2 > MOD > Flashcards

MOD Flashcards

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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
What is the main leukocyte of chronic inflammation?
Lymphocytes (T and B)
26
What is the generic formation of a giant cell?
The fusion of many macrophages
27
What is granulation tissue?
The walling off of the injured site with macrophages with central necrosis due to avascularisation
28
Describe the appearance of Langhan's giant cells
Crescent shape of marginalised nuclei. Seen in TB
29
Describe the histological appearance of foreign body giant cells
Central, disorganised nuclei that overlap. Seen in foreign body invasion
30
Describe the histology of a Touton giant cell
Completely encapsulated by a ring of marginalised nuclei. Often seen in areas with a high lipid content e.g. fat necrosis
31
What are permanent cells and give an example
These are cells that have completely arrested and are unable to divide further. Skeletal muscle, brain neurones
32
What is Hayflick's number?
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
Give one physiological and one pathological case of hyperplasia
Endometrial hyperplasia in menstrual cycle | Thyroid hyperplasia in gone formation
34
Give one physiological and one pathological cause of hypertrophy
Muscle bulk in exercise training | Cardiac hypertrophy in cardiomyopathy
35
Give a physiological and pathological cause of atrophy
Ovarian atrophy in post-menopause is physiological | Denervation atrophy is pathological
36
What is metaplasia? Give an example condition
Change of one cell type to another. E.g. Barrett's oesophagus
37
What is the fatty streak?
Lipid infiltration in the intimal lining of arteries
38
Describe a simple plaque
Propagation of the fatty streak so that it has an irregular outline and is widely distributed
39
Describe the complicated plaque and give a condition it predisposes to
Calcification of the atheroma surface to form a fibrous cap. Can predispose to aneurysm
40
What are foam cells?
Macrophages that have ingested too much lipid in the artery intima that they now contribute to the plaque
41
Give some risk factors for atheroma
High cholesterol, male, age, hypertension, diabetes
42
Give the benign and malignant tumour name of a gland
Adenoma is benign | Adenocarcinoma is malignant
43
Give some structural changes seen in malignant cells
Poor differentiation Increased nuclear:cytoplasmic ratio Mitotic figures
44
Give some behavioural changes of malignant cells
Immortality - as seen in HeLa cells Loss of contact inhibition Loss of anchorage dependence Low requirement for growth factors
45
Give some functional changes seen in malignant cells
Decreased adhesion between cells | Tissue factor production, increasing clotting
46
What are foci of necrosis?
A central portion of necrosis seen in malignant tumours. Associated with a poor prognosis
47
Give the ways that metastases can spread
Blood Lymph Direct spread
48
Describe the seed and soil hypothesis
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
What factors must a metastasis do to become a new tumour?
``` Separate itself from the primary Digest through the basement membrane Escape systemic defences Penetrate the new endothelium Induce angiogenesis to create a secondary ```
50
Give the two commonest paraneoplastic syndromes
Small cell carcinoma of the lung producing ADH | Squamous cell carcinoma of the lung producing PTH
51
Why are many cancer patients in a hypercoagulable state?
Platelets are activated by tumour secreted ADP | Tumours secrete tissue factor
52
Give some chemical carcinogens
Pollution Smoking Alcohol (promotes turnover of cells) Diet
53
What are the Japanese and American common GI cancers?
Japanese have stomach cancers, Americans have colon. This is due to diet
54
How do tumours divide indefinitely?
By stimulating proto-oncogenes and switching off tumour suppressor genes
55
Give the most commonly changed tumour suppressor gene
P53
56
Give the staging of Dukes classification and the cancer assessed
``` 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
Give the staging of Ann Arbor classification and the cancer involved
``` 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
Give the cancers that the following markers correlate to; bence-jones protein, PSA, CEA, Alpha-fetoprotein
BJP - multiple myeloma PSA - prostate ca CEA - colon ca AFP - hepatoma and germ cell tumours
59
Describe TNM staging
Tumour size 0-4 Nodal involvement 0-3 Metastases 0 or 1
60
Give the three stages of haemostasis
Artery contracts Platelet plug formation Fibrin infiltrate to stabilise the platelet plug
61
Give some platelet activators
Thrombin Collagen surfaces ADP
62
Give the function of thrombin
Cleaves fibrinogen to fibrin
63
How is a blood clot dissolved?
Dilution of clotting factors by the blood flow | Natural anticoagulants produced by the liver
64
Give the function of plasmin
Enzyme responsible for fibrinolysis | Circulates as plasminogen and is activated by tissue plasminogen activator (tPA)
65
What is the function of Von Willebrand factor?
Found on the endothelial wall to favour clotting
66
What is Virchow's triad of thrombus formation?
Changes to vascular wall Changes in blood flow Changes in the blood
67
How would you differentiate between a thrombus and a post-mortem clot?
Thrombi are laminated with lines of Zahn | Post-mortem clots are shiny and never laminated
68
What is disseminated intravascular coagulation?
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
Give some forms of emboli
``` Thrombo-embolus Gas Fat Amniotic Foreign body ```

ESA 2 (2 decks)

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