PPE Revision > MoD > Flashcards

MoD Flashcards

(56 cards)

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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?

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A

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

24
Q

What are the stages of fibrous repair?

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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
Describe the difference in content of thrombi arising from arteries and those arising from veins?
Arteries = paler, granular structure, lines of Zahn, fewer red cells Veins = soft, gelatinous, deep red, higher cell content
26
What can happen to a thrombus?
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
What is disseminated intravascular coagulation?
Pathological activation of coagulation mechanisms resulting in blood clots throughout circulation. * Thromboemboli causing compromised blood supply to organs * Uses up all clotting factors
28
What is the difference between atherosclerosis and arteriosclerosis?
Atherosclerosis = thickening and hardening of arterial walls Arteriosclerosis = arterial and arterioles (usually as a result of HTN and DM)
29
Define hyperplasia. Give an example
Increase in tissue or organ size due to increase in number of cells Endometrium, eczema
30
Define hypertrophy. Give an example
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
Define atrophy. Give an example
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
Define metaplasia. Give an example
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
Define dysplasia. Give an example
A reversible, pre-neoplastic alteration in which cells show disordered tissue organisation.
34
Define benign neoplasm
Abnormal growth of cells that persists after the initial stimulus is removed
35
Define malignant neoplasm
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
Describe appearance of a benign neoplasm
* Remain confined to site of origin * Pushing outer margin * Cells closely resemble parent tissue - well differentiated
37
Describe appearance of malignant neoplasm
* Potential to metastasise * Irregular outer margin and shape - may show areas of necrosis and ulceration * Range from well to poorly differentiated
38
What are the features of poorly differentiated cells?
* 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
What does the grade of a tumour signify?
Differentiation of cells * G1 = well differentiated * G2 = moderately differentiated * G3 = poorly differentiated * G4 = Undifferentiated/aplastic
40
What are the general names for: * Benign epithelial neoplasm * Malignant neoplasm * Other benign * Other malignant of connective tissue or non-epithelial tissue
* Benign epithelial neoplasm = -papilloma * Malignant neoplasm = -carcinoma * Other benign = -oma * Other malignant of connective tissue or non-epithelial tissue = -sarcoma
41
What changes occur for a neoplasm to grow and invade at primary site? What are these changes referred to as?
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
What does the site of a secontary tumour depend on?
* Regional drainage of blood, lymoh or coelemic fluid * Seed and soil phenomenon
43
Explain the seed and soil phenomenom
Explains the unpredictable distribution of blood-borne metastases - due to interaction between malignant cells and local environment at secondary site
44
What are the common site for metastases?
Lung, bone, liver, brain
45
What are common neoplasms that spread to the bone?
Bronchus, thyroid, kidney, prostate, breast
46
What are pro-carcinogens?
Substances that are converted into carcinogens by CYP450 system in liver
47
What are complete carcinogens?
Carcinogens that act as both intiators and promoters
48
Explain initation and promotion with regards to chemical carcinogens
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
What are oncogenes? Give an example
Abnormally activated versions of proto-oncogenes which enhance neoplastic growth. Ras, HER-2
50
What does Ras protein do? Therefore what does mutant Ras do?
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
What are tumour suppressor genes?
Inhibit neoplastic growth p53 and pRB
52
What is the two hit hypothesis with regards to neoplastic growth?
Two mutations needs to occur for cancer to develop. In inherited cancers, the first hit is an inherited gene mutation
53
What are the 6 hallmark behaviours of cancer mutations?
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
Describe the TNM staging of cancer
* 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
What is the Ann-Arbor staging system used for?
Lymphoma
56
Name the common specific tumour markers
* Human gonadotroph = testicular tumours * Alpha-fetoprotein = hepatocellular carcinoma * PSA = prostate cancer * CA-125 = ovarian cancer
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