Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 5 signs of acute inflammation?

A

Redness, swelling, heat, pain, loss of function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is reperfusion injury?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

List 5 cells involved in chronic inflammation

A

Macrophages, lymphocytes, plasma cells, eosinophils, giant cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Main cell involved in acute inflammation?

A

Neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How would you treat a DVT?

A

Prevention - stockings, leg compression, heparin IV.

Treated - IV heparin, warfarin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How would you differentiate a benign from malignant neoplasm?

A

Benign - round outer margin

Malignant - Irregular outer margin, may show necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is xeroderma pigmentosa? Pattern of inheritance?

A

Autosomal recessive.

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

Explain Dukes staging for colorectal carcinomas

A

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
Q

What is grading of a cancer?

A

Level of differentiation of cancer. Less differentiated = more aggressive.

27
Q

How does radiotherapy kill a cancer?

A

Triggers apoptosis by direct or ROS DNA damage that is detected by cell checkpoints.

28
Q

How does chemotherapy kill cancers?

A

Alkylating drugs - Cross links DNA helix and promotes apoptosis.

Antimetabolites - Attach to DNA and prevents further replication occurring.

29
Q

Give the tumour markers found in:

a) colon, pancreas, lung, stomach, heart
b) testicles
c) liver

A

a) carcinoembryonic antigen
b) HCG
c) alpha fetoprotein

30
Q

what is metaplasia

A

reversible change of 1 differentiated cell to another

31
Q

appearance of arterial and venous thrombi

A

aterial - lines of zahn, pale, granular, low cell count

venous - high cell count, deep red, soft

32
Q

collagen structure

A

left handed helix, 3 alpha chains

33
Q

process of neutrophil invasion

A

margination (neutrophils line up at edge of BVs), rolling, adhesion, emigration

34
Q

process of fibrous repair

A

inflammatory cells invade bloot clot and digest. then angiogenesis and ECM and collagen lay down by fibroblasts then collagen pulled together

35
Q

artery and vein histology

A

endothelium, CT, internal elastic lamina, muscular media, external elastic lamina, adventitia

veins have valves and thin muscular media

36
Q

substance promotes angiogenesis

A

VEGF

37
Q

blood flow during acute inflammation

A

1) transient vasoconstriction
2) vasodilation
3) increase permeability

38
Q

explain collagen biosynthesis

A

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
Q

OD symptoms of aspirin

A

hyperventiliation then metabolic acidosis

40
Q

intrinsic and extrinsic mechanisms of apoptosis

A

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
Q

results of acute and chronic inflammation

A

acute - pain, loss of function, redness, swelling, heat

chronic - fibrosis, decrease function, atrophy, immune response

42
Q

what is abscess, ulcer, cyst?

A

abscess - pus, infection

ulcer - break in epithelium

cyst - closed sac with fluid inside

43
Q

acute and chronic inflammation cells

A

acute - neutrophils (primarily), basophils, and eosinophils , macrophages and monocytes

chronic - microphages, fibroblasts, lymphocytes, monocytes, plasma cells

44
Q

what is labile, stable, and permanent cells. give eg,

A

labile - high proliferation e.g. epithelial

stable - proliferative when needed e.g. hepatocytes

permanent - e.g. cardiac

45
Q

what causes red and white infarcts

A

whitte - end artery

red - anastamoses

46
Q

give feature of TB granuloma

A

central caseous necrosis

47
Q

give cell cycle

A

G0 - arrested

G1 - cell contents doubled

S - chromosomes doubled

G2 - double checks chromosomes

Mitosis

48
Q

function of pRB and p53

A

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
Q

what is wallerian degeneration

A

degeneration of axon distal to injury

50
Q

signs of apoptosis

A

shirnkage, chomatin condense, nuclear fragmentation. NO INFLAMMATION

51
Q

cofactors of prolyl hydroxylase

A

vit c and Fe

52
Q

give 2 example pyrogens

A

TNFalpha and IL-1

ESA 2 - Recap (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions