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ESA 2 - Jake and Ron > Mechanisms of Disease > Flashcards

Flashcards in Mechanisms of Disease Deck (45):
1

Name 8 causes of cell injury.

Hypoxia
Toxins
Heat
Cold
Trauma
Radiation
Microorganisms
Immune mechanisms

2

What is hypoxia and what is a common cause?

Reduced O2 often caused by ischaemia

3

What are the reversible changes in hypoxia?

Decreased oxidative phosphorylation and ATP production
Increased anaerobic glycolysis
Decreased pH
Accumulation of Na+
Cell swelling via osmosis
Detachment of ribosomes leads to decreased protein synthesis

4

What are the irreversible changes in hypoxia?

Massive accumulation of intracellular Ca2+ resulting in mass enzyme activation

5

What are the reversible structural changes in cell injury?

Swelling
Chromatin clumping
Autophagy - cell self destruction
Ribosome dispersal
Blebbing

6

What are the irreversible structural changes in cell injury?

Nuclear changes - eg. pyknosis, karyorrhexis, and karyolysis
Lysosome rupture
Membrane defects
ER lysis

7

Define necrosis and apoptosis.

Necrosis - changes that occur after cell death in living tissue
Apoptosis - programmed cell death

8

Name 4 types of necrosis.

Coagulative
Liquefactive
Caseous
Fat

9

Explain coagulative necrosis.

More protein denaturation than enzyme release
Cellular architecture preserved creating ghost outline of cells - only lasts a few days before phagocytosis
Often caused by infarct in solid organs - eg. liver

10

Explain liquefactive necrosis.

More enzyme release than protein denaturation
Tissue is lysed and disappears
Often caused by infection
Occurs more commonly in loose tissue - eg. lungs

11

Explain caseous necrosis.

Tissue appears amorphous
Halfway between coagulative and liquefactive
If in the lung, likely to be TB

NEVER MENTION CASEOUS NECROSIS UNLESS TB

12

Explain fat necrosis.

Cell death in adipose tissue
Dead fat can break off in blood and cause embolism

13

What is gangrene? Explain the difference between wet and dry gangrene.

Clinical term for grossly visible necrosis.
Dry = coagulative
Wet = liquefactive

14

What is infarct and how can it be classified?

Necrosis due to ischaemia.
Can be white or red depending on amount of haemorrhage.

15

Explain the differences between white and red infarct.

White infarct - occlusion of an end artery, leaving the area completely devoid of blood, much like Voldemort's soul.
Red infarct - there some collateral supply, which leads to congestion of blood in the damaged tissue.

16

Describe what you would see in apoptosis.

Cells appear shrunken and very eosinophilic (pink)
Chromatin condensation, pyknosis, nuclear fragmentation

17

Name the three stages of apoptosis.

Initiation
Execution
Degradation/phagocytosis

18

Describe the intrinsic and extrinsic pathways in apoptosis.

Intrinsic - all apoptotic machinery within cell. Caused by DNA damage, lack of growth factors/hormones etc.

Extrinsic - TRAIL and Fas bind to death receptors

Both lead to capsase activations (proteases which mediate apoptosis)

19

What can you see during degradation in apoptosis?

Cell breaks into membrane bound fragments called apoptotic bodies. These are phagocytosed.

20

Name 7 important mediators of apoptosis and their general function.

p53 - Guardian of the Genome - acts in response to DNA damage
TRAIL - death ligand
TRAIL-R - death receptor
BcI-2 - inhibits cytochrome c release
Caspase - effector molecule of apoptosis

Cytochrome C (from mitochondria), APAF 1 and caspase 9 form the apoptosome (protein which causes apoptosis)

21

Name and describe two reactions which produce free radicals.

Fenton rection - Fe2+ + H2O2 -> Fe3+ + OH- + *OH

Haber-Weiss reaction - O2- + H+ + H2O2 -> O2 + H2O + *OH

22

Name 5 causes of acute inflammation. Bitch.

Microbial infections
Hypersensitivity reactions
Physical agents
Chemicals
Tissue necrosis

23

List the cardinal signs of acute inflammation.

Calor - heat
Rubor - redness
Tumor - swelling
Dolor - pain

Also loss of function.

24

Outline the steps causing acute inflammation.

1. Vasodilation
2. Gaps form in endothelium
3. Exudation
4. Margination and emigration of neutrophils
5. Migration and emigration of macrophages and lymphocytes

25

What are the chemical mediators of vasodilation in acute inflammation?

Histamine
Prostaglandins
C3a, C5a

26

What are the chemical mediators of increased vascular permeability in acute inflammation?

Histamine
Prostaglandins
Kinins

27

What are the chemical mediators of emigration of leukocytes in acute inflammation?

Leukotrines
IL-8
C5a

28

Describe the action of neutrophils in acute inflammation.

Phagocytosis of microorganisms
Release toxic enzymes and metabolites causing damage to host tissue - eg. ROS

29

Name some chemical mediators for chemotaxis of neutrophils.

C5a
Cytokines

Bacterial peptides and LTB4 too

30

What are the symptoms of the acute phase response?

Decreased apetite
Raised HR
Altered sleep patterns
Changes in plasma conc. of acute phase proteins - eg. CRP, fibrinogen, α1-antitrypsin

31

What are the causes of fever in acute inflammation?

Endogenous pyrogens - IL-1, TNF-α, prostoglandins

32

What are the causes of leukocytosis in acute inflammation?

IL-1 and TNF-α produce accelerated release from marrow.
Macrophages and T lymphocytes produce colony stimulating factors (causes proliferation and differentiation)

33

What are the possible outcomes of acute inflammation?

1. Complete resolution
2. Continued acute inflammation with chronic inflammation
3. Chronic inflammation and fibrous repair, with probable tissue damage
4. Death

34

What factors help stop acute inflammation?

Mediators have short half-lifes and may be inactivated by degradation, dilution in exudate or inhibition.

35

Describe the changes that occur during resolution in acute inflammation.

Vascular changes stop
Neutrophils no longer marginate
Vessel permeability and calibre return to normal
Exudate drains via lymphatic system
Fibrin is lysed by plasmin
Neutrophils die

36

When is resolution during acute inflammation possible?

If tissue architecture is intact, regeneration is possible.

37

What are some possible complications of acute inflammation?

Swelling - can block tubes/compress vital structures
Shock (loss of fluid)
Pain and loss of function
Chronic inflammation
Tissue damage

38

Describe what happens in blistering.

Caused by heat, sunlight, chemicals, etc.
Symptoms are pain and profuse exudate.
Collection of fluid strips off overlying epithelium.
Clear exudate (few cells).
Normally leads to resolution/scarring.

39

Describe what happens in an abscess.

Happens in solid tissue where inflammatory exudate forces tissue apart.
Liquefactive necrosis in center
Can cause high pressure, pain, and tissue damage.

40

Describe what happens in pericarditis.

Inflammation of the serous cavity of the pericardium
Increased pressure on heart
Can lead to cardiac tamponade.

41

Describe hereditary angio-oedema.

Deficiency of C1 inhibitor which inhibits bradykinin
Uninhibited bradykinin caused increased vascular permeability leading to oedema
Treat with C1 inhibitor

42

Describe α1-antitrypsin deficiency.

α1-antitrypsin inhibits elastase
Uninhibited elastase breaks down elastic tissue in lungs and liver
Causes emphysema and liver sclerosis

43

Describe chronic granulomatous disease.

Recessive sex linked
Immune phagocytes unable to form ROS, so some bacteria can't be killed
Leads to excessive granuloma formation.

44

What is the difference between exudate and transudate?

Exudate - fluid loss in inflammation - high protein

Transudate - fluid loss due to hydrostatic pressure

45

Explain the action of some drugs used to treat acute inflammation.

NSAIDs (eg. aspirin and ibuprofen) - inhibit prostaglandin formation

Corticosteroids - immunosupressants decrease inflammation