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ESA 2 > Mechanisms of disease > Flashcards

Mechanisms of disease Flashcards

1
Q

Define disease

A

A consequence of the failure of homeostasis with consequent morphological and functional disturbances

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2
Q

What does the degree of cell injury depend on?

A

Type of injury, severity of injury and type of tissue affected

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3
Q

What are some of the main causes of cell injury and death?

A

Hypoxia, toxins, immune mechanisms, physical agents eg trauma. radiation, microorganisms and dietary insufficiencies

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4
Q

How can the immune system cause cell injury?

A

Through hypersensitivity reactions so tissue is injured, secondary to overly vigorous immune reaction or by Autoimmune reaction where system faiols to distinguish self from non-self

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5
Q

What are the main structural targets for cell damage?

A

Cell membrane, nucleus, proteins and mitochondria

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6
Q

What are the different types of hypoxia?

A

Anaemic, hypoxaemic, ischaemic and histiocytic

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7
Q

When are free radicals produced?

A

In chemical and radiation injury, in ischaemia-reperfusion injury, cellular aging and in high oxygen concentrations, also by leukocytes for bacteria killing,

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8
Q

What are the 3 main free radicals?

A

OH. hydroxylH202 hydrogen peroxide02- superoxide

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9
Q

What are the main causes of acute inflammation?

A 
Microbial infections
Physical agents
Chemicals
Hypersensitivity reactions
Tissue necrosis
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10
Q

What are the sequelae of acute inflammation?

A

Resolution
Acute inflammation alongside chronic inflammation, forms abscess
Chronic inflammation with fibrous repair
Death

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11
Q

What is the purpose of vasodilatation in acute inflammation?

A

To increase delivery of plasma proteins

To increase systemic temperature to attack microorganisms

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12
Q

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

A

Histamine and leukotrienes
IL-1 and TNF
VEGF

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13
Q

What is the purpose of increased vascular permeability in acute inflammation?

A

Dilution of toxins
Increased delivery of plasma proteins to injury site
Increased lymphatic drainage

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14
Q

What are the steps of neutrophil migration?

A

Stasis then margination where they line up along walls of vessels. Neutrophils roll along wall and then adhere to it. They then eventually migrate through wall with help of chemotoxins C5a and LTB4 and cytoskeletal rearrangement

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15
Q

What are the systemic consequences of acute inflammation?

A

Fever caused by endogenous pyrogens
Leukocytosis caused by IL-1 and TNF
Acute phase response

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16
Q

What is the process behind skin blisters?

A

Due to heat, sunlight or chemicals.

There is profuse exudate and fluid strips of overlying epithelium

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17
Q

What is hereditary angioedema?

A

An autosomal dominant mutation where there’s overactivation of the complement system and high bradykinin leading to frequent, spontaneous oedema. Due to a defect in C1 inhibitor. If there’s intestinal oedema, causes abdominal pain. Can cause death if laryngeal oedema.

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18
Q

How does aspirin work?

A

Irreversibly inhibits the COX 1 and 2 enzymes which are normally involved in homeostasis and released by inflammatory cells. This decreases prostaglandin formation and inhibits the transcription of genes for inflammatory mediators

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19
Q

What are some macroscopic features of acute appendicitis?

A

Discolouration
Swelling
Less defined structure
Fibropirulent exudate (neutrophils+fibrin)

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20
Q

What are the possible sequelae of acute appendicitis?

A

Perforation causing peritonitis, fistulae or abscesses
Chronic inflammation. Becomes obstructed, forming a mucocele which can then perforate releasing mucus secreting cells into peritoneum
Resolution with fibrous scarring of tip

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21
Q

What is chronic granulomatous disease?

A

A defect in NADPH so respiratory oxidative bust is defective. Causes frequent deep set infections. DUe to an x-linked recessive disorder

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22
Q

What are some consequences of liver abscesses?

A

Breakdown of liver tissue so liver enzymes enter blood stream
Fever caused by inflammatory cells
Low perfusion of kidneys - kidney failure
Decreased brain function - inefficient breathing

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23
Q

How do the appearances of benign and malignant neoplasms differ?

A

Benign tend to have an irregular outline with a ‘pushing border’
Malignant tumours tend to have an irregular outline, possible with necrosis or ulceration at surface

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24
Q

What is anaplasia?

A

When cells bear no resemblance to any tissue type

25
Q

What is classified as a poorly differentiated growth?

A

Increased nuclear size and increased nucleus to cytoplasm ratio
Increase in number of mitotic bodies
Increased variation in the size and shape of cells nd their nuclei

26
Q

What is meant by ‘progression’ in terms of neoplasia?

A

When cells emerge from monoclonal population formed by initators and promoters, with different characterisitics

27
Q

What are the steps a cancer cell must go through to metastasise?

A 
Growth and invasion at primary site
Enter a transport system
Embolise
Arrest
Exit
Grow at secondary site
28
Q

What must cancer cells change in order to invade surrounding tissues?

A

Adhesion between cells by decreased E-cadherin expression
Interaction between stroma and the cell by using proteases such as MMPs to break down basement membrane
Motility by changing the actin cytoskeleton

29
Q

Why might a cancer cell not succeed at metastasis?

A

May undergo embolic trauma and be fragmented or sheared by vessel wall.
May be damaged by free radicals
May be destroyed by immune response

30
Q

How does HPV cause cancer?

A

Release E6 which inhibits p53 and E7, which inhibits retinoblastoma protein

31
Q

What are some common proto-oncogenes?

A

RAS which pushes cell through restriction point of cell cycle
C-myc - stimulates trancription of immunoglobulin so is lymphoproliferative

32
Q

What are the 6 main hallmarks of cancer?

A 
Self sufficiency to grow without growth signals
Resistance to stop-growth signals
Sustained angiogenesis ability
Limitless ability to divide
Resistance to apoptosis
Ability to invade and metastasise
33
Q

In what cancers is grading of a cancer more important than staging?

A 
Breast
Lymphoma
Soft tissue sarcoma
Primary brain tumour
Prostate
34
Q

What is the difference between adjuvant and neoadjuvant therapy?

A

Adjuvant is treatment that takes place after surgery to resect tumour, Acts to decrease risk of micrometastases
Neo-adjuvant is where treatment is given prior to surgery, in order to shrink the tumour

35
Q

How does radiation act to kill cancer cells?

A

Can stimulate apoptosis by causing DNA damage so can’t pass through cell cycle checkpoint and apoptosis is triggered.
Also causes chromosomal damage so can’t complete mitosis

36
Q

What are some disadvantages of screening for cancer?

A

Lead time bias so because cancer was caught earlier, appears that survival time is longer
Length bias - long screening intervals will mean that mostly slow growing and less aggressive tumours will be detected
Overdiagnosis - false positives may cause psychological harm

37
Q

What are the main cell types found in chronic inflammation?

A 
Macrophages
Lymphocytes
Plasma cells
Fibroblasts
Eosinophils
Giant cells (langhans, touton, foreign body type)
38
Q

In what inflammation are touton giant cells commonly found?

A

In fat necrosis and in xanthoma

39
Q

When do granulomas form?

A

In hypersensitivity reactions and in persistent, low grade antigenic stimulation

40
Q

What situations stimulate need for fibrous repair?

A

Necrosis of permanent cells

Necrosis of stable or labile cells when collagen framework is destroyed so can’t regenerate

41
Q

How does angiogenesis occur?

A

Stimulated by pro-angiogenic growth factors eg VEGF. Hypoxia stimulate endothelium and there’s proteolysis of basement membrane so endothelial cells migrate and proliferate at new sites and primitive blood vessels are formed. There’s then maturation of endothelium and there’s tubular remodelling.

42
Q

What are the main cell types involved in fibrous repair?

A 
Macrophages
Lymphocytes
(myo) Fibroblasts
Endothelial cells
Neutrophils
43
Q

What is regenerate controlled by?

A

Proliferative growth factors eg PDGF, oestrogen etc. Bind to tyrosine kinase receptors to affect transcription.
Basement membrane and adjacent cell contact, via e-cadherin. When cells are in contact, it’s antiproliferative. If there’s loss of contact, there’s proliferation. This is defective in cancer.

44
Q

What is the process behind fibrous repair?

A

A blood clot forms and there’s acute inflammation at the edges so there’s inflammatory cell infiltration and angiogenesis is stimulated, Myofibroblasts migrate and differentiate. Extracellular matrix develops and there’s maturation and remodelling of collagen. Myofibroblasts contract to reduce the defect volume, vessels regress and you’re left with a fibrous scar

45
Q

How do peripheral nerves regenerate?

A

By Wallerian degeneration. There’s break down of myelin and schwann cell proliferation

46
Q

What is the process behind scurvy?

A

Vitamin C deficiency means there’s decreased hydroxylation of procollagen so collagen is then vulnerable to enzymatic degradation.

47
Q

What does haemostasis depend on?

A

Vessel wall
Platelets
Coagulation
Fibrinolysis

48
Q

What three factors promote thrombus formation?

A

Abnormal vessel wall
Abnormal blood flow
Abnormal blood contents

49
Q

What is thrombosis?

A

The formation of a solid mass of blood in the circulation, during life

50
Q

What are the possible outcomes of thrombosis?

A 
Lysis
Propagation
Organisation
Recanalisation
Embolism
51
Q

How do venous and arterial thrombi differ in appearance?

A

Arterial thrombi are pale and granular due to high levels of platelets and fibrin but low cell content. They also show distinctive lines of Zahn
Venous thrombi are gelatinous and have a deep red colour due to high cell content

52
Q

What’s the difference between atherosclerosis and arteriosclerosis?

A

Atherosclerosis is the thickening and hardening of artery walls due to atheroma and arteriosclerosis is the thickening of artery and arteriole walls due to hypertension/ diabetes mellitus

53
Q

What is the unifying hypothesis of atheroma formation?

A

Endothelium gets damaged by hypertension, haemodynamic stress, toxins or high LDLs. This causes Platelet adhesion, smooth muscle cell proliferation, lipid deposits in intima and media and monocyte migration. There’s also foam cell formation which secrete cytokines to stimulate more inflammatory cells and smooth muscle cells

54
Q

What cells are involved in atheroma formation?

A 
Endothelial cells
Platelets
Neutrophils
Lymphocytes
Macrophages
Smooth muscle cells
55
Q

How is the main restriction point of the cell cycle regulated?

A

By cyclin and cyclin dependent kinases which phoshporylate cell cycle transition proteins, eg retinoblastoma susceptibility protein, to push cell through cycle

56
Q

What are the different outcomes of cell signalling by hormones/growth factors?

A

Divide
Die
Resist apoptosis
Differentiate

57
Q

What are the main 3 growth factors and what do they do?

A

Epidermal growth factor, increases mitosis of epithelial cells, hepatocytes and fibroblasts
Vascular endothelial growth factor - stimulates angiogenesis and vasculogenesis
Platelet derived growth factor - causes migration and proliferation of smooth muscle cells, firboblasts and monocytes

58
Q

What is aplasia?

A

The complete failure of tissue or organ to develop, embryonically

59
Q

What is hypoplasia?

A

Under development of incomplete development of a tissue or organ at the embryonic stage

ESA 2 (4 decks)

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