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

Mechanisms of Disease Flashcards

1
Q

Name 8 causes of cell injury.

A 
Hypoxia
Toxins
Heat
Cold
Trauma
Radiation
Microorganisms
Immune mechanisms
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2
Q

What is hypoxia and what is a common cause?

A

Reduced O2 often caused by ischaemia

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3
Q

What are the reversible changes in hypoxia?

A

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

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4
Q

What are the irreversible changes in hypoxia?

A

Massive accumulation of intracellular Ca2+ resulting in mass enzyme activation

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5
Q

What are the reversible structural changes in cell injury?

A 
Swelling
Chromatin clumping
Autophagy - cell self destruction
Ribosome dispersal
Blebbing
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6
Q

What are the irreversible structural changes in cell injury?

A

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

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7
Q

Define necrosis and apoptosis.

A

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

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8
Q

Name 4 types of necrosis.

A

Coagulative
Liquefactive
Caseous
Fat

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9
Q

Explain coagulative necrosis.

A

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

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10
Q

Explain liquefactive necrosis.

A

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

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11
Q

Explain caseous necrosis.

A

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

NEVER MENTION CASEOUS NECROSIS UNLESS TB

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12
Q

Explain fat necrosis.

A

Cell death in adipose tissue

Dead fat can break off in blood and cause embolism

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13
Q

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

A

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

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14
Q

What is infarct and how can it be classified?

A

Necrosis due to ischaemia.

Can be white or red depending on amount of haemorrhage.

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15
Q

Explain the differences between white and red infarct.

A

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.

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16
Q

Describe what you would see in apoptosis.

A

Cells appear shrunken and very eosinophilic (pink)

Chromatin condensation, pyknosis, nuclear fragmentation

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17
Q

Name the three stages of apoptosis.

A

Initiation
Execution
Degradation/phagocytosis

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18
Q

Describe the intrinsic and extrinsic pathways in apoptosis.

A

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)

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19
Q

What can you see during degradation in apoptosis?

A

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

20
Q

Name 7 important mediators of apoptosis and their general function.

A 
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
Q

Name and describe two reactions which produce free radicals.

A

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

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

22
Q

Name 5 causes of acute inflammation. Bitch.

A 
Microbial infections
Hypersensitivity reactions
Physical agents
Chemicals
Tissue necrosis
23
Q

List the cardinal signs of acute inflammation.

A

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

Also loss of function.

24
Q

Outline the steps causing acute inflammation.

A
  1. Vasodilation
  2. Gaps form in endothelium
  3. Exudation
  4. Margination and emigration of neutrophils
  5. Migration and emigration of macrophages and lymphocytes
25
Q

What are the chemical mediators of vasodilation in acute inflammation?

A

Histamine
Prostaglandins
C3a, C5a

26
Q

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

A

Histamine
Prostaglandins
Kinins

27
Q

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

A

Leukotrines
IL-8
C5a

28
Q

Describe the action of neutrophils in acute inflammation.

A

Phagocytosis of microorganisms

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

29
Q

Name some chemical mediators for chemotaxis of neutrophils.

A

C5a
Cytokines

Bacterial peptides and LTB4 too

30
Q

What are the symptoms of the acute phase response?

A

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

31
Q

What are the causes of fever in acute inflammation?

A

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

32
Q

What are the causes of leukocytosis in acute inflammation?

A

IL-1 and TNF-α produce accelerated release from marrow.

Macrophages and T lymphocytes produce colony stimulating factors (causes proliferation and differentiation)

33
Q

What are the possible outcomes of acute inflammation?

A
  1. Complete resolution
  2. Continued acute inflammation with chronic inflammation
  3. Chronic inflammation and fibrous repair, with probable tissue damage
  4. Death
34
Q

What factors help stop acute inflammation?

A

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

35
Q

Describe the changes that occur during resolution in acute inflammation.

A 
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
Q

When is resolution during acute inflammation possible?

A

If tissue architecture is intact, regeneration is possible.

37
Q

What are some possible complications of acute inflammation?

A 
Swelling - can block tubes/compress vital structures
Shock (loss of fluid)
Pain and loss of function
Chronic inflammation
Tissue damage
38
Q

Describe what happens in blistering.

A

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
Q

Describe what happens in an abscess.

A

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

40
Q

Describe what happens in pericarditis.

A

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

41
Q

Describe hereditary angio-oedema.

A

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

42
Q

Describe α1-antitrypsin deficiency.

A

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

43
Q

Describe chronic granulomatous disease.

A

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

44
Q

What is the difference between exudate and transudate?

A

Exudate - fluid loss in inflammation - high protein

Transudate - fluid loss due to hydrostatic pressure

45
Q

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

A

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

Corticosteroids - immunosupressants decrease inflammation

ESA 2 - Jake and Ron (3 decks)

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