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PPE Revision > MoD > Flashcards

MoD Flashcards

1
Q

What are the 4 types of hypoxia? Explain what causes them

A

Hypoxaemic - arterial content of O2 too low (e.g. high altitudes, decreased perfusion due to lung disease) Anaemic - Decreased ability of Hb to carry oxygen (e.g. anaemia, CO poisoning) Ischaemic - Interruption to blood supply (e.g. atheroma, heart failure) Histiocytic - Inability to utilise oxygen in cells due to disabled oxidative phosphorylation (e.g. cyanide poisoning)

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2
Q

What are the reversible changes due to hypoxia?

A
  1. Oxidative phosphorylation decreases due to low O2, low ATP
  2. Increased amount of anaerobic respiration, produces lactate, decreases pH
  3. Low ATP means Na accumulates in cell (Na+/K+-ATPase), so water drawn into cell by osmosis, cell swells
  4. Detatchment of ribosomes, as energy required to keep them attached
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3
Q

What are the structural changes seen in reversible hypoxic injury?

A
  • Swelling
  • Clumps of chromatic in nucleus
  • Blebs
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4
Q

What are the irreversible changes due to hypoxia?

A
  • Massive accumulation of cytosolic Ca2+ due to reversal of NCX
  • Activates enzymes resulting in cell death
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5
Q

What are the stuctural changes seen in irreversible hypoxic cell injury?

A
  • Lysosomes rupture
  • Breakdown of ER
  • Defects in the membrane
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6
Q

What is the difference between oncosis, necrosis and apoptosis?

A

Oncosis - Cell death with swelling, changes occur in cell prior to death. See pyknosis, karryohexis and karryolysis of nucleus.

Necrosis - morphological chnages that occur after a cell has been dead for some time (damage to see membranes, leaking of contents, inflammation)

Apoptosis - programmed cell death with shrinkage (no inflammation because there is no leaking of contents)

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7
Q

What is the difference between coagulative necrosis and liquefactive necrosis?

A

Coagulative = protein denaturation > release of enzymes (cell architecture preserved)

Liquefactive = enzyme release > protein denaturation (tissue is lysed)

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8
Q

What is caseous necrosis?

A

Structural debris causing cheese-like appearance surrounded by franulomatous inflammatory process

Linked with infection - especially TB, syphilis

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9
Q

What is fat necrosis?

A

Cell death in adipose tissue. Lipases cause the release of fatty acids, which bind calcium to form calcium soaps

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10
Q

What is gangrene and what is the difference between wet and dry gangrene?

A

Gangrene = grossly visible necrosis

Wet = liquefactive necrosis (tissue infected with anaeobic bacteria)

Dry = coagulative necrosis (e.g. umbilical cord)

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11
Q

What is an infarct and what is the difference between and red and white infarct?

A

Necrosis due to ischaemia

Red - occulsion of a blood vessel causing smaller blood vessels to haemorrhage into area (occurs in places with collateral supply)

White - occulsion of end arteries (e.g. kidney, spleen, heart)

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12
Q

What is ischaemia-reperfusion injury?

A

Following ischaemia, if blood flow is increased this will cause further damage due to mass production of free radicals.

Number of neutrophils also increase causing more inflammation and more injury

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13
Q

What is the difference between intrinsic and extrinsic initiation of apoptosis?

A

Intrinsic = DNA damages/growth factor withdrawal or hormone withdrawal, activates p53 making mitochondria more permable releasing cytochrome C. This forms apoptosome which activates more caspases (proteases that mediate apoptosis)

Extrinsic = External ligands (e.g. TRAIL, FAS) bind to ‘death receptors’ causing caspase activation

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14
Q

What is acute inflammation?

A

Response of living tissue to injury to limit tissue damage

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15
Q

Describe what happens in acute inflammation

A
  • Transient vasoconstriction of arterioles
  • Vasodilation to increase blood flow
  • Histamine release causes leaking of protein due to increased permability of caprillaries = oedema = increases lymphatic drainage
  • This causes slowing of circulation and stasis
  • Infiltation of neutrophils
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16
Q

Explain recruitment of neutrophils in acute inflammation

A
  1. Stasis causes neutrophils to move to the periphery of blood vessels (loss of laminar flow) = margination
  2. Roll along endothelium and weakly attach
  3. Neutrophils then more firmly attach = adhesion
  4. Migrate to blood vessel wall
  5. Move by chemotaxis
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17
Q

What are the killing mechanisms of neutrophils?

A
  • Oxygen-dependent - reactive oxygen species
  • Oxygen-independent - lysozymes and hydrolyses
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18
Q

What us the acute phase response?

A

Decreased appetite, raised pulse rate, altered sleep pattern, changes in plasma concentration of acute phase proteins

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19
Q

What are the possible events after acute inflammation?

A
  • Resolution
  • Abscess (continued acute inflammation with chronic inflammation)
  • Chronic inflammation and fibrous repair
  • Death
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20
Q

Define chronic inflammation

A

Chronic response to injury with associated fibrosis

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21
Q

What is granulomatous inflammation?

A

Inflammation with granulomas (accumulation of epitheliod histiocytes and lymphocytes)

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22
Q

What are the consequences of chronic inflammation?

A
  1. Fibrosis/scarring
  2. Impaired function
  3. Atrophy
  4. Stimulation of immune response
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23
Q

What is fibrous repair?

A

Replacement of functional tissue by scar tissue in response to injury or inflammation

24
Q

What are the stages of fibrous repair?

A
  1. Haemostasis - blood clot
  2. Inflammation - phagocytosis and clearning of wound
  3. Proliferation - angiogenesis, collagen deposition, granulation formation, re-epithelisation and wound contraction
  4. Maturation - cell population falls, collagen increases
25
Q

Describe the difference in content of thrombi arising from arteries and those arising from veins?

A

Arteries = paler, granular structure, lines of Zahn, fewer red cells

Veins = soft, gelatinous, deep red, higher cell content

26
Q

What can happen to a thrombus?

A
  1. Resoluation (lysis)
  2. Propagation (progressive spread)
  3. Organisation (reparative process leading to fibrous scar on vessel wall)
  4. Re-canalisation (blood flow re-established but not completely)
  5. Embolism
  6. Partial calcification
27
Q

What is disseminated intravascular coagulation?

A

Pathological activation of coagulation mechanisms resulting in blood clots throughout circulation.

  • Thromboemboli causing compromised blood supply to organs
  • Uses up all clotting factors
28
Q

What is the difference between atherosclerosis and arteriosclerosis?

A

Atherosclerosis = thickening and hardening of arterial walls

Arteriosclerosis = arterial and arterioles (usually as a result of HTN and DM)

29
Q

Define hyperplasia. Give an example

A

Increase in tissue or organ size due to increase in number of cells

Endometrium, eczema

30
Q

Define hypertrophy. Give an example

A

Increase in tissue or organ size due to increase in cell size (occurs in permanent cells), caused by increased functional demand or hormone stimulation

Skeletal muscle, right ventricular hypertrophy

31
Q

Define atrophy. Give an example

A

Shrinkage of tissue or organ due to acquired decrease in size and number of cells

Ovarian atrophy in post-menopausal women, muscle atrophy due to deinnervation

32
Q

Define metaplasia. Give an example

A

Reversible change from one differentiated cell type to another.

Oesophagus due to acid reflux - statified squamous to simple columnar

Bronchi due to smoking - pseudostratified ciliated to stratified squamous

33
Q

Define dysplasia. Give an example

A

A reversible, pre-neoplastic alteration in which cells show disordered tissue organisation.

34
Q

Define benign neoplasm

A

Abnormal growth of cells that persists after the initial stimulus is removed

35
Q

Define malignant neoplasm

A

Abnormal growth of cells that persists after the initial stimulus is removed and is capable of invading into surrounding tissues and spreading to distant locations

36
Q

Describe appearance of a benign neoplasm

A
  • Remain confined to site of origin
  • Pushing outer margin
  • Cells closely resemble parent tissue - well differentiated
37
Q

Describe appearance of malignant neoplasm

A
  • Potential to metastasise
  • Irregular outer margin and shape - may show areas of necrosis and ulceration
  • Range from well to poorly differentiated
38
Q

What are the features of poorly differentiated cells?

A
  • Increasing nuclear size, and nuclear to cytoplasm ratio
  • Increased staining of nucleus - hyperchromasia
  • More/abnormal mitotic figures
  • Increasing variation in size and shape of cells - pleomorphism
39
Q

What does the grade of a tumour signify?

A

Differentiation of cells

  • G1 = well differentiated
  • G2 = moderately differentiated
  • G3 = poorly differentiated
  • G4 = Undifferentiated/aplastic
40
Q

What are the general names for:

  • Benign epithelial neoplasm
  • Malignant neoplasm
  • Other benign
  • Other malignant of connective tissue or non-epithelial tissue
A
  • Benign epithelial neoplasm = -papilloma
  • Malignant neoplasm = -carcinoma
  • Other benign = -oma
  • Other malignant of connective tissue or non-epithelial tissue = -sarcoma
41
Q

What changes occur for a neoplasm to grow and invade at primary site? What are these changes referred to as?

A
  1. Altered adhesion - reduction in e-cadherin
  2. Stromal proteolysis - changes in integrin expression, altered expression of proteases
  3. Motility - changes in actin cytoskeleton

Epithelial-to-mesenchymal transition

42
Q

What does the site of a secontary tumour depend on?

A
  • Regional drainage of blood, lymoh or coelemic fluid
  • Seed and soil phenomenon
43
Q

Explain the seed and soil phenomenom

A

Explains the unpredictable distribution of blood-borne metastases - due to interaction between malignant cells and local environment at secondary site

44
Q

What are the common site for metastases?

A

Lung, bone, liver, brain

45
Q

What are common neoplasms that spread to the bone?

A

Bronchus, thyroid, kidney, prostate, breast

46
Q

What are pro-carcinogens?

A

Substances that are converted into carcinogens by CYP450 system in liver

47
Q

What are complete carcinogens?

A

Carcinogens that act as both intiators and promoters

48
Q

Explain initation and promotion with regards to chemical carcinogens

A

For neoplasm to develop initation and promotion of chemical carcinogen needs to occur

  • Initiation - causes mutations, capable of producing a tumour (permanent DNA damage)
    • Not sufficient enough for tumour formation
  • Promotion - cause sustained proliferation, induce tumours in initiated cells, exposure must follow initiation
    • They enhance proliferations in mutated cells and increse incidence of further mutations
49
Q

What are oncogenes? Give an example

A

Abnormally activated versions of proto-oncogenes which enhance neoplastic growth.

Ras, HER-2

50
Q

What does Ras protein do? Therefore what does mutant Ras do?

A

Relays signals into cell that will push cell past cell cycle restriction point

Mutant Ras encodes for a protein that is always active, therefore allows all cells through restriction point

51
Q

What are tumour suppressor genes?

A

Inhibit neoplastic growth

p53 and pRB

52
Q

What is the two hit hypothesis with regards to neoplastic growth?

A

Two mutations needs to occur for cancer to develop.

In inherited cancers, the first hit is an inherited gene mutation

53
Q

What are the 6 hallmark behaviours of cancer mutations?

A
  1. Self-sufficient growth signals
  2. Resistance to growth stop signals
  3. Cell immoirtalisation
  4. Angiogenesis
  5. Resistance to apoptosis
  6. Ability to invade and produce metastases
54
Q

Describe the TNM staging of cancer

A
  • T = Primary tumour size (T1 - T4)
  • N = Extent of regional node metastases (N0 - N3)
  • M = Extent of distance metastases (M0 - M1)

They can then be converted into a stage:

  • Stage I = early local disease
  • Stage 2 = advanced local disease
  • Stage 3 = regional metastases
  • Stage 4 = advanced disease with distant metastases
55
Q

What is the Ann-Arbor staging system used for?

A

Lymphoma

56
Q

Name the common specific tumour markers

A
  • Human gonadotroph = testicular tumours
  • Alpha-fetoprotein = hepatocellular carcinoma
  • PSA = prostate cancer
  • CA-125 = ovarian cancer

PPE Revision (16 decks)

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