Brainscape's Knowledge GenomeTM

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


See full index

Phase 2 Medicine > Immunology and Cancer > Flashcards

Immunology and Cancer Flashcards

1
Q

Describe acute inflammation

A
  • sudden onset, short, usually resolves

* neutrophil reaction

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

Describe chronic inflammation

A
  • slow onset (may follow acute inflammation), long, may never resolve
  • lymphocyte and macrophage reaction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

3 main cells from the inflammatory response

A
  • neutrophils - pus cells
  • macrophages - phagocytic
  • lymphocytes - immunological memory
  • (endothelial cells)
  • (fibroblasts)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe neutrophils

A
  • short lived
  • first response for acute inflammation
  • granular cytoplasm - contain lysosomes (enzymes) that digest bacteria
  • usually does at the scene - become yellow
  • release chemicals that attract other inflammatory cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe macrophages

A
  • live weeks to months
  • phagocytic
  • May present antigen to lymphocytes
  • a few die at the scene
  • (many types of macrophage, this is the generic name)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe lymphocytes

A
  • live for years
  • control inflammation - produce chemicals that attract other inflammatory cells
  • immunological memory for past infections/antigens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe endothelial cells

A
  • become sticky during inflammation so inflammatory cells stick to them
  • become porous so inflammatory cells can pass into tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe fibroblasts

A
  • long lived
  • particularly present in chronic inflammation
  • responsible for scarring (form collagen)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Define:
• B lymphocytes
• T lymphocytes

A

B lymphocytes - produce antibodies

T lymphocytes - memory cells that produce chemicals to draw other inflammatory cells in

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Define
• regeneration
• repair

A

Regeneration - initiating factor removed OR damaged tissue can regenerate

Repair - initiating factor still present OR damaged tissue is unable to repair
(Tissue replaced with fibrous tissue and scarring)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

2 types of skin wound healing

A

Healing by 1st intention - best possibility
• incision fills with fibrin and blood
• fibroblasts make collagen
• repair + scar

Healing by 2nd intention
• if can’t suture smoothly
• can grow across eventually, but repair is not upwards
• larger scar, paler tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Define:
• thrombosis
• embolus

A

Thrombosis - solid mass of blood constituents formed within intact vascular system during life

Embolus - mass of material in vascular system able to become lodged within a vessel and block it

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

Describe thrombus formation

A
  • damaged endothelium of artery
  • collagen underneath exposed
  • positive feedback loop - placement activation factor makes more platelets stock
  • disruption of laminar flow - RBCs may stick too
  • fibrin deposited (positive feedback loop of fibrin from fibrinogen)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

3 parts of Virchow’s triad

Any 1 or combination increases risk of thrombosis

A

Changes to:
• vessel wall
• blood flow
• blood constituents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

4 potential outcomes if thrombus is not treated?

A
  • lysis and resolution - thrombus breaks down, but still need to consider what that vessel was supplying
  • organisation - repair and scar tissue (vessel becomes stuck to itself)
  • recanalisation - return of blood flow after previous occlusion (scar and residual thrombus at site)
  • embolism - usually if part of the thrombus breaks off and spreads to other places
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

3 ways to prevent thrombus formation

A
  • exercise
  • elastic circulation stockings - squeezes blood out of leg veins
  • aspirin - inhibits platelet aggregation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Causes of embolus

A
  • atheroma with thrombus
  • atrial thrombus
  • valve vegetation - growth of bacteria on a heart valve causing infection
  • thrombus from old/recent myocardial infarct
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Define:
• ischaemia
• infarction

A

Ischaemia
• reduction in blood flow

Infarction
• reduction in blood flow that causes cell death (subset of ischaemia)

19
Q

What is reperfusion injury?

Ischaemia-reperfusion injury, IRI

A
  • when tissue is damaged by return of blood supply after a period of ischaemia or lack of oxygen
  • induces comas can help prevent this
20
Q

Define
• end artery supply
• dual supply

A

End artery supply
• only one way in
• e.g. the heart is mainly end arteries (not watershed though)

Dual supply
• if one is blocked, blood can still get to the organ
• few organs have this
• (e.g. lungs and liver, therefore rarely get infarction in these organs)

21
Q

Describe watershed areas/territories

A
  • region of the body that receives dual blood supply from the most distal branches of 2 large arteries
  • if blood supply is decreased in either vessel, this can be problematic (despite being dual supply)
  • can cause watershed strokes in the brain
22
Q

Define and describe atherosclerosis

A
  • buildup of plaque on artery walls which can restrict blood flow - also comes with inflammation and fibrosis
  • can be fats, cholesterols and other substances
  • the plaque can burst, leading to thromboses
  • almost all >70s will have it
23
Q

Describe the distribution of atherosclerosis in the body

A
  • very prevalent in systemic arteries (i.e. derive from aorta)
  • often occurs at bifurcation of arteries

• does not occur in veins or pulmonary arteries - low pressure so thrombus forms rather than plaque

24
Q

Risk factors for atherosclerosis

A
  • smoking
  • hypertension
  • diabetes mellitus - only if poorly controlled
  • hyperlipidaemia - high cholesterol
  • more prevalent in more deprived, industrial areas
  • more prevalent in men with ischaemic heart disease
25
Q

Atherosclerosis formation theory

A

Endothelial damage theory
• based on risk factors also damaging endothelial cells
• endothelial cells are delicate and very metabolically active
• recurrent endothelial cell injury - microthrombi formation, healing and haemorrhaging over years to form atherosclerosis

(Note, lipid insudation theory is incorrect)

26
Q

Treatment of atherosclerosis

A
  • lower risk factors

* aspirin - antiplatelet

27
Q

Complications of atherosclerosis

A
  • blocked arteries
  • infarctions
  • weakened aorta - aneurism (excessive, localised swelling of an artery wall)
28
Q

2 types of cell death

A
  • apoptosis - falling off, one cell at a time

* necrosis - killing, traumatic cell death in large areas of cells

29
Q

Describe apoptosis

A
  • programmed cell death
  • something, usually DNA damage, indicates to resting cell that it’s time to die
  • cell releases enzymes that cause it to shrink, nucleus shrivels too
  • organelles go into membrane bound vesicles
  • macrophages eventually digest fragments
30
Q

Gatekeeper of genome

Effectors of apoptosis

A

P53 protein - detects DNA damage and produces other chemicals which cause apoptosis

Caspases
• internal (within cell) - apoptosis inhibited by Bcl-2 proteins
• internal (within cell) - apoptosis stimulated by BAX proteins
• external - Fas receptor on surface of cells. It switches on caspases if Fas ligand binds

31
Q

Use of apoptosis

A
  • stop damaged cells from reproducing in disease
  • development - e.g. unwebbing fingers
  • normal function - tissue with high cell turnover need to remove cells at end of useful life
  • lack of apoptosis in cancer (i.e. cancer isn’t too much growth, but too little cell death)
  • too much apoptosis in HIV
32
Q

4 clinical examples of necrosis

A
  • frostbite
  • cerebral infarction
  • avascular necrosis of bone - many bones have poor blood supply, e.g. scaphoid
  • pancreatitis
33
Q

Word roots

  • hyper-
  • meta-
  • dys-
  • a-
  • -trophy
  • -plasia
A
  • hyper- = excess
  • meta- = change
  • dys- = bad, not right
  • a- = without
  • -trophy = nourishment
  • -plasia = formation
34
Q

Names for tissues getting bigger

A
  • hypertrophy - increase in size of cells (usually in cells that can’t divide, e.g. muscle)
  • hyperplasia - increase in the number of constituent cells (cells stay the same size, e.g. smooth muscle)

• can have a mixture of hypertrophy and hyperplasia - occurs in pregnant uterus smooth muscle

35
Q

Name for tissues getting smaller

A
  • atrophy - decrease in size of cells OR decrease in number of constituent cells
  • e.g. muscular atrophy - muscles become smaller when not used, but number of cells is constant
  • a term for both of what could be called ‘hypotrophy’ or ‘hypoplasia’…but aren’t
36
Q

Define metaplasia

A

change in differentiation of a cell from one fully differentiated type to another fully differentiated type

37
Q

2 examples of metaplasia

A
  • bronchus - ciliated columnar epithelium becomes squamous when exposed to cigarette smoke. Consider chronic bronchitis and smokers’ cough
  • Barret’s oesophagus - stratified squamous epithelium to simple columnar with goblet cells due to GORD
38
Q

Define dysplasia

A

imprecise term for morphological changes seen in cells in the progression to becoming cancer (i.e. not yet cancer)

39
Q

What is spina bifida?

A
  • formation of tube but failure to close

* exposed spinal cord

40
Q

3 main types of spina bifida

A
  • spina bifida oculta - missing spinus process, asymptomatic
  • meningocele - meninges bulge out and may be repaired and function normally
  • myelomeningocele - parts of spinal cord and cauda equina comes out, often paralysis of lower limbs
41
Q

Types of genetic abnormality

A
  • chromosome - autosomal/sex chromosome
  • single gene inheritance - Mendelian
  • polygenetic (most common)
42
Q

Define:
• inherited
• acquired

A

Inherited
• due to genetic abnormality, which may or may not be present at birth

Acquired
• caused by non-genetic (environmental) factors, may be congenital, e.g. foetal alcohol syndrome

43
Q

Why don’t adult cells divide as much?

A

Telomeres
• are at end of chromosome to allow replication of DNA for cell division
• telomere becomes shorter after each division
• eventually it can’t replicate anymore
• paternally inherited

Phase 2 Medicine (1 decks)

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