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ESA 2 - Recap > MOD > Flashcards

MOD Flashcards

1
Q

What is healing by primary and secondary intention?

A

Primary - Minimal scarring, epidermis regenerates

Secondary - Scab form, more scarring,

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2
Q

What are the 5 signs of acute inflammation?

A

Redness, swelling, heat, pain, loss of function

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3
Q

What is reperfusion injury?

A

Ischaemia followed by return of blood results in inflammation and oxidative damage.

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4
Q

What structural changes occur during reversible and irreversible hypoxia?

A

Reversible - Chromatin clumping, swelling, detachment of ribosomes from RER, cytoplasmic blebs

Irreversible - lysosome lysis, ER lysis, membrane defects, shrinkage chromatin, fragmentation chromatin, dissolution chromatin,

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5
Q

What are the 4 types of necrosis

A

Coagulative - Protein denaturation dominates. Leaves ghost outlines.

Liquifactive - Enzyme degradation dominates. Infection

Fat necrosis

Caseous necrosis - TB

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6
Q

Difference between dystrophic and metastatic calcification?

A

Both deposition of calcium in tissues

Metastatic - due to elevated serum calcium

Dystrophic - due to abnormalities of tissue

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7
Q

What is hereditary angio-edema? How is it treated?

A

Disorder of C1 inhibitor, results in excess bradykinin release and edema.

Treat with C1 inhibitor infusion.

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8
Q

List 5 cells involved in chronic inflammation

A

Macrophages, lymphocytes, plasma cells, eosinophils, giant cells

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9
Q

Main cell involved in acute inflammation?

A

Neutrophils

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10
Q

Describe the process of fibrous repair

A
  1. Clot formed and Inflammatory cells invade.
  2. Clot replaced with granulation tissue. Fibroblasts migrate and produce ECM
  3. Fibroblasts contract to reduce volume. Scar occurs.
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11
Q

What are 2 methods through which growth factors can reach a cell?

A
  1. Extracellular signals via hormones etc.
  2. Loss of contact between adjacent cells and basement membrane
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12
Q

What is virchow’s triad?

A

Factors that influence thrombosis formation.

  1. Abnormalities in blood vessel wall
  2. Abnormalities of blood flow
  3. Abnormalities of blood components
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13
Q

How would you treat a DVT?

A

Prevention - stockings, leg compression, heparin IV.

Treated - IV heparin, warfarin.

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14
Q

What is an atheroma, arteriosclerosis and atherosclerosis?

A

Atheroma - Lipid accumulation in tunica intima of arteries

Arteriosclerosis - Hardening of arteries due to atheroma

Atherosclerosis - Hardening of arteries due to DM or hyeprtension

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15
Q

Describe how atheromas occur

A
  1. Cholosterol accumulates in endothelium due to endothelial damage e.g. smoking.
  2. Macrophages enter wall and attempt to digest cholesterol and become foam cells
  3. Foam cells die and release contents
  4. Calcium salts and fibrous tissue accumulates and forms hard plaque.
  5. Endothelium over plaque ruptures and exposes collagen, recruiting platelets and forming platelet plug.
  6. Plug causes blood clot which can break off or result in ischaemia.
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16
Q

How would you differentiate a benign from malignant neoplasm?

A

Benign - round outer margin

Malignant - Irregular outer margin, may show necrosis

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17
Q

What needs to occur to a cell for it to form a tumour?

A

Tumour suppressor genes turned off and proto-oncogenes need to be turned on

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18
Q

How would you differentiate a benign and malignant neoplasm histologically?

A

Bengin - well differentiated, nuclei same size.

Malignant - well to poorly differentiated, nuclei different size

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19
Q

What alterations does invasion require?

A
  1. No adhesion between adjacent cells – reduction in E-cadherin
  2. No adhesion to basement membrane – reduction in integrin.
  3. Degradation of the basement membrane – Expression of proteases
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20
Q

What is xeroderma pigmentosa? Pattern of inheritance?

A

Autosomal recessive.

Cannot DNA nucleotide excision repair. Sensitive to UV –> mutations.

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21
Q

What is ataxia telangiectasia?

A

Cannot repair radiation damage. Lymphoid malignances.

22
Q

What is hereditary non polyposis colon cancer syndrome?

A

Mutation in DNA mismatch repair genes.

Colon carcinomas.

23
Q

What genes are associated with:

  1. Familial Adenomatous Polyposis
  2. Breast cancer
  3. Retinoblastoma
A
  1. APC
  2. BRCA1/2
  3. RB
24
Q

What is TNM staging? How is it used?

A 
T = Size of primary tumour, T1 --\> T4
N = Extent of regional node metastasis, N0 (no lymph node involvement) --\> N3 (involvement of an increasing number of nodes)
M = Extent of distant metastatic spread, M0 (none) --\> M1 (blood borne metastases)
25
Explain Dukes staging for colorectal carcinomas
Stage A – Invasion into but not through the bowel Stage B – Invasion through Bowel wall Stage C – Involvement of lymph nodes Stage D – Distant metastases
26
What is grading of a cancer?
Level of differentiation of cancer. Less differentiated = more aggressive.
27
How does radiotherapy kill a cancer?
Triggers apoptosis by direct or ROS DNA damage that is detected by cell checkpoints.
28
How does chemotherapy kill cancers?
Alkylating drugs - Cross links DNA helix and promotes apoptosis. Antimetabolites - Attach to DNA and prevents further replication occurring.
29
Give the tumour markers found in: a) colon, pancreas, lung, stomach, heart b) testicles c) liver
a) carcinoembryonic antigen b) HCG c) alpha fetoprotein
30
what is metaplasia
reversible change of 1 differentiated cell to another
31
appearance of arterial and venous thrombi
aterial - lines of zahn, pale, granular, low cell count venous - high cell count, deep red, soft
32
collagen structure
left handed helix, 3 alpha chains
33
process of neutrophil invasion
margination (neutrophils line up at edge of BVs), rolling, adhesion, emigration
34
process of fibrous repair
inflammatory cells invade bloot clot and digest. then angiogenesis and ECM and collagen lay down by fibroblasts then collagen pulled together
35
artery and vein histology
endothelium, CT, internal elastic lamina, muscular media, external elastic lamina, adventitia veins have valves and thin muscular media
36
substance promotes angiogenesis
VEGF
37
blood flow during acute inflammation
1) transient vasoconstriction 2) vasodilation 3) increase permeability
38
explain collagen biosynthesis
CHADPOGRL Cleavage of signal peptide, hydroxylation of proline and lysine, addition of N-linked oligosaccs, disulphide bond formed, procollagen and formation of triple helix, o-linked glycosylation, golgi then exocytosis, reomval of terminal peptides, lateral aggregation to form fibrils
39
OD symptoms of aspirin
hyperventiliation then metabolic acidosis
40
intrinsic and extrinsic mechanisms of apoptosis
intrinsic - DNA damage sensed by p53 and cause smitochondria to release cytochrome c which activates caspases extrinsic - external TRAIL or Fas ligand binds to death receptors and activates caspases
41
results of acute and chronic inflammation
acute - pain, loss of function, redness, swelling, heat chronic - fibrosis, decrease function, atrophy, immune response
42
what is abscess, ulcer, cyst?
abscess - pus, infection ulcer - break in epithelium cyst - closed sac with fluid inside
43
acute and chronic inflammation cells
acute - neutrophils (primarily), basophils, and eosinophils , macrophages and monocytes chronic - microphages, fibroblasts, lymphocytes, monocytes, plasma cells
44
what is labile, stable, and permanent cells. give eg,
labile - high proliferation e.g. epithelial stable - proliferative when needed e.g. hepatocytes permanent - e.g. cardiac
45
what causes red and white infarcts
whitte - end artery red - anastamoses
46
give feature of TB granuloma
central caseous necrosis
47
give cell cycle
G0 - arrested G1 - cell contents doubled S - chromosomes doubled G2 - double checks chromosomes Mitosis
48
function of pRB and p53
pRB - stops G1 to S and is inhibited when cell is ready p53 - prevents G1 to S and initiates apoptosis if damage to DNA is irreparable
49
what is wallerian degeneration
degeneration of axon distal to injury
50
signs of apoptosis
shirnkage, chomatin condense, nuclear fragmentation. NO INFLAMMATION
51
cofactors of prolyl hydroxylase
vit c and Fe
52
give 2 example pyrogens
TNFalpha and IL-1

ESA 2 - Recap (4 decks)

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