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Principles > Inflammation and Neoplasia > Flashcards

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
Q

Why do blood vessels become leaky

A

Endothelial contraction - gaps appear between cells
Direct injury to blood vessel wall (burns)
Damage from own white cells
Transcytosis
New vessels - delicate

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26
Q

What can intiate endothelial contraction?

A

Histamine
Bradykinin
Substance P
leukotrienes

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27
Q

What does VEGF do?

A

Mediate transcytosis

Stimulate growth of new blood vessels

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28
Q

What is chemotaxis?

A

When a motile cell follows a gradient of a particular chemical/signal

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29
Q

What kind of signal can a white cell follow?

A

Bacterial components
Complement
Leukotrienes
Cytokines - interleukins

30
Q

What is diapedesis?

A

When a white cell flattens against the lumenal surface due to protein binding and moves out of the blood vessel into the tissues

31
Q

What two types of protein are expressed by endothelial cells in the lumen to ‘catch’ white blood cells?

A

Selectin

ICAM

32
Q

What are the three phases of phagocytosis?

A

Recognition and attachment
Engulfment
Degradation

33
Q

How do white cells recognise substances for phagocytosis?

A

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
Q

What are the four characteristics of inflammation?

A 
Calor
Rubor
Tumor
Dolor
Loss of function
35
Q

What is dolor mediated by?

A

Prostaglandins and bradykinin

36
Q

Which type of leukocyte is particularly involved in acute inflammation?

A

Neutrophil

37
Q

What could be targeted with drugs to affect inflammation?

A

Chemical signals

38
Q

What is hyperplasia?

A

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
Q

What is hypertrophy?

A

When cells increase in size

Can be physiological or pathological

40
Q

What is atrophy?

A

When cells decrease in size

Can be pathological or physiological

41
Q

What is metaplasia?

A

When cells adapt and take on new functions

42
Q

What happens when cells are subjected to higher levels of stress?

A

Hyperplasia or hypertrophy

43
Q

What happens when cells are subjected to lower levels of stress?

A

Atrophy

44
Q

What happens when the kind of stress put on cells changes?

A

Metaplasia

45
Q

What are the two ways in which cells can grow?

A

Get bigger - hypertrophy

Multiply - hyperplasia

46
Q

What stimulates cells to divide?

A

Growth factors

47
Q

How can more cell division be stimulated?

A

Increase production of growth factors

Increase production of growth factor receptors

48
Q

What are the three types of growth factor receptor?

A

Receptors linked to intrinsic tyrosine kinases
Receptors not linked to intrinsic tyrosine kinases
G-protein coupled receptors

49
Q

What are the four main steps in the cell cycle?

A

G1 (G0)
S
G2
M

50
Q

What controls progression through the cell cycle?

A

CDKs and Cyclins

51
Q

What activates a CDK?

A

a specific cyclin

52
Q

What four letters represent the 4 types of cyclin?

A

D
E
A
B

53
Q

What four letters represent the 4 types of cyclin?

A

D
E
A
B

54
Q

What happens during G1?

A

Proteins made and cell increases in size
CDK4 activated by D
CDK4 activates retinoblastoma protein so cycle can continue

55
Q

What is Rb? And what is it normally bound to?

A

Retinoblastoma protein
Bound to E2F

Dissociated E2F starts S phase

56
Q

What happens during S?

A 
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
Q

What happens during G2?

A

Cell grows even more - more proteins

p53 checks DNA replication completed successfully

58
Q

What does p53 do?

A 
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
Q

What is replicative senescence?

A

Inability to divide indefinitely

60
Q

What are telomeres?

A

Tip of chromosomes
Made of TTAGGG repeat sequences
Every time the cell divides, repeats can be lost

61
Q

Why are telomeres important?

A

Ensure important genetic information isn’t degraded from the end of the chromosome

62
Q

What are physiological reasons for hyperplasia?

A

Puberty - breast tissue

Pregnancy - endometrial lining

63
Q

When does hyperplasia occur to compensate for damage?

A

After loss of tissue
eg Liver

Bone marrow - when not enough leukocytes present

64
Q

What are some examples of pathological hyperplasia?

A

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
Q

What is hyperplastic tissue at risk of?

A

Cancer developing

66
Q

Why would someone experience hypertrophy in their cardiac muscle?

A

Heart under stress
eg from lots of exercise
from hypertension

67
Q

When is cardiac hypertrophy pathologic?

A

When heart cannot function correctly and has cannot be sustained by the blood supply it receives

Leads to heart failure

68
Q

When is atrophy physiological?

A

During embryonic development

In uterus after childbirth

69
Q

What can cause pathological atrophy?

A 
Immobilisation
Loss of nerves or nerve function
Loss of blood supply (brain)
Lack of nutrition
Due to pressure ie tissue next to tumour
70
Q

Which hormones promote atrophy?

A

Glucocorticoids and thyroid

71
Q

Which hormone promotes growth?

A

Insulin

72
Q

What happens to cell during atrophy?

A

Cellular components reduced

Proteins digested by lysosomes and ubiquitin proteasome pathway

Principles (21 decks)

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