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Inflammation and Neoplasia Flashcards

1
Q

What is rubor?

A

visible redness in skin

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2
Q

What in calor?

A

heat emanating from skin

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3
Q

What is dolor?

A

Pain in area

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4
Q

What tumour?

A

Swelling

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5
Q

What can cause acute inflammation?

A 
Injury
Infection
Trauma
Immune reaction
Foreign bodies
Necrosis for any reason
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6
Q

How does the body respond to injury? (inflammation)

A

Vascular changes
Cellular changes

brought about by chemical mediators and showing morphologic patterns

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7
Q

What are the vascular changes which occur?

A

Changes in blood flow and vessel caliber

ie. Vasodilation - arterioles then capillary beds

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8
Q

What mediates the vascular changes?

A

Histamine and nitric oxide

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9
Q

What visible sign is the result of vascular changes?

A

Calor - increased heat

Rubor / erythema - redness

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10
Q

What can cause necrosis?

A

Trauma, hypoxia, toxins

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11
Q

What are the cellular changes which occur?

A 
Stasis
White cell margination
Rolling
Adhesions
Migration
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12
Q

Where does blood normally flow in a vessel?

A

Down centre of lumen

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13
Q

What happens to blood flow when vessel dilates?

A

Flow slows, larger cells drift to edges of vessel

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14
Q

What is white cell margination?

A

When white cells drift to the edge of the lumen

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15
Q

What changes in the blood vessel wall when dilated?

A

Cells in wall express proteins on lumenal surface which correspond to proteins on white cell surface

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16
Q

What two types of protein are expressed by white cells on their surface?

A

Glycoproteins

Integrins

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17
Q

What does VCAM stand for?

A

vascular cell adhesion molecule

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18
Q

What does ICAM stand for?

A

Intercellular adhesion molecule

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19
Q

Why do white blood cells roll along lumenal surface?

A

They quickly form and break low affinity interactions with proteins on lumenal surface

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20
Q

What do histamine and thrombin promote in cells?

A

Expression of selectin

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21
Q

What do tumour necrosis factor (TNF) and interleukin-1 (IL-1) promote in epithelial cells?

A

VCAM and ICAM expression

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22
Q

What do chemokines do?

A

Bind to proteoglycans on lumenal endothelial cells

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23
Q

What do proteoglycans do when chemokines bind?

A

Increase affinity of VCAMS and ICAMS for integrins

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24
Q

What happens to vascular permeability during inflammation?

A

Increases so vessels become leaky

  • lose proteins
  • osmotic pressure changes
  • fluid leaks into tissues (swelling/tumour)
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25
Why do blood vessels become leaky
Endothelial contraction - gaps appear between cells Direct injury to blood vessel wall (burns) Damage from own white cells Transcytosis New vessels - delicate
26
What can intiate endothelial contraction?
Histamine Bradykinin Substance P leukotrienes
27
What does VEGF do?
Mediate transcytosis | Stimulate growth of new blood vessels
28
What is chemotaxis?
When a motile cell follows a gradient of a particular chemical/signal
29
What kind of signal can a white cell follow?
Bacterial components Complement Leukotrienes Cytokines - interleukins
30
What is diapedesis?
When a white cell flattens against the lumenal surface due to protein binding and moves out of the blood vessel into the tissues
31
What two types of protein are expressed by endothelial cells in the lumen to 'catch' white blood cells?
Selectin | ICAM
32
What are the three phases of phagocytosis?
Recognition and attachment Engulfment Degradation
33
How do white cells recognise substances for phagocytosis?
TBH dont understand need to look into it Using Mannose receptors Bacterial surface glycoproteins and glycolipids which contain mannose residues do not contain sialic acid or N-acetylgalactosamine Scavenger receptors Opsonins
34
What are the four characteristics of inflammation?
``` Calor Rubor Tumor Dolor Loss of function ```
35
What is dolor mediated by?
Prostaglandins and bradykinin
36
Which type of leukocyte is particularly involved in acute inflammation?
Neutrophil
37
What could be targeted with drugs to affect inflammation?
Chemical signals
38
What is hyperplasia?
When cells multiply but remain the same size External stimulus needed Reverses when signal removed Can increase size of organ Can be both pathological or physiological
39
What is hypertrophy?
When cells increase in size Can be physiological or pathological
40
What is atrophy?
When cells decrease in size Can be pathological or physiological
41
What is metaplasia?
When cells adapt and take on new functions
42
What happens when cells are subjected to higher levels of stress?
Hyperplasia or hypertrophy
43
What happens when cells are subjected to lower levels of stress?
Atrophy
44
What happens when the kind of stress put on cells changes?
Metaplasia
45
What are the two ways in which cells can grow?
Get bigger - hypertrophy | Multiply - hyperplasia
46
What stimulates cells to divide?
Growth factors
47
How can more cell division be stimulated?
Increase production of growth factors | Increase production of growth factor receptors
48
What are the three types of growth factor receptor?
Receptors linked to intrinsic tyrosine kinases Receptors not linked to intrinsic tyrosine kinases G-protein coupled receptors
49
What are the four main steps in the cell cycle?
G1 (G0) S G2 M
50
What controls progression through the cell cycle?
CDKs and Cyclins
51
What activates a CDK?
a specific cyclin
52
What four letters represent the 4 types of cyclin?
D E A B
53
What four letters represent the 4 types of cyclin?
D E A B
54
What happens during G1?
Proteins made and cell increases in size CDK4 activated by D CDK4 activates retinoblastoma protein so cycle can continue
55
What is Rb? And what is it normally bound to?
Retinoblastoma protein Bound to E2F Dissociated E2F starts S phase
56
What happens during S?
``` DNA replication (stimulated by E2F) E2F increases levels of cyclin A which activates CDK2 which promotes DNA replication ``` Cell now has 2 copies of DNA
57
What happens during G2?
Cell grows even more - more proteins | p53 checks DNA replication completed successfully
58
What does p53 do?
``` Many roles In cell cycle, checks DNA for mistakes If mistake found, cycle stopped while it attempts to fix it If fixed - cycle continues If not fixed - p53 initiates apoptosis ``` Mutations in p53 can cause cancer
59
What is replicative senescence?
Inability to divide indefinitely
60
What are telomeres?
Tip of chromosomes Made of TTAGGG repeat sequences Every time the cell divides, repeats can be lost
61
Why are telomeres important?
Ensure important genetic information isn't degraded from the end of the chromosome
62
What are physiological reasons for hyperplasia?
Puberty - breast tissue | Pregnancy - endometrial lining
63
When does hyperplasia occur to compensate for damage?
After loss of tissue eg Liver Bone marrow - when not enough leukocytes present
64
What are some examples of pathological hyperplasia?
Endometrial hyperplasia after menopause (because of oestrogen) - abnormal bleeding Hyperplasia in prostate due to hormones released by testes Both conditions will reverse if hormones are no longer produced Also lymph nodes undergo hyperplasia when reacting to an infection
65
What is hyperplastic tissue at risk of?
Cancer developing
66
Why would someone experience hypertrophy in their cardiac muscle?
Heart under stress eg from lots of exercise from hypertension
67
When is cardiac hypertrophy pathologic?
When heart cannot function correctly and has cannot be sustained by the blood supply it receives Leads to heart failure
68
When is atrophy physiological?
During embryonic development | In uterus after childbirth
69
What can cause pathological atrophy?
``` Immobilisation Loss of nerves or nerve function Loss of blood supply (brain) Lack of nutrition Due to pressure ie tissue next to tumour ```
70
Which hormones promote atrophy?
Glucocorticoids and thyroid
71
Which hormone promotes growth?
Insulin
72
What happens to cell during atrophy?
Cellular components reduced | Proteins digested by lysosomes and ubiquitin proteasome pathway

Principles (21 decks)

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