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Mechanisms of disease Flashcards

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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?

Study These Flashcards
A

When cells bear no resemblance to any tissue type

25
What is classified as a poorly differentiated growth?
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
What is meant by 'progression' in terms of neoplasia?
When cells emerge from monoclonal population formed by initators and promoters, with different characterisitics
27
What are the steps a cancer cell must go through to metastasise?
``` Growth and invasion at primary site Enter a transport system Embolise Arrest Exit Grow at secondary site ```
28
What must cancer cells change in order to invade surrounding tissues?
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
Why might a cancer cell not succeed at metastasis?
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
How does HPV cause cancer?
Release E6 which inhibits p53 and E7, which inhibits retinoblastoma protein
31
What are some common proto-oncogenes?
RAS which pushes cell through restriction point of cell cycle C-myc - stimulates trancription of immunoglobulin so is lymphoproliferative
32
What are the 6 main hallmarks of cancer?
``` 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
In what cancers is grading of a cancer more important than staging?
``` Breast Lymphoma Soft tissue sarcoma Primary brain tumour Prostate ```
34
What is the difference between adjuvant and neoadjuvant therapy?
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
How does radiation act to kill cancer cells?
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
What are some disadvantages of screening for cancer?
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
What are the main cell types found in chronic inflammation?
``` Macrophages Lymphocytes Plasma cells Fibroblasts Eosinophils Giant cells (langhans, touton, foreign body type) ```
38
In what inflammation are touton giant cells commonly found?
In fat necrosis and in xanthoma
39
When do granulomas form?
In hypersensitivity reactions and in persistent, low grade antigenic stimulation
40
What situations stimulate need for fibrous repair?
Necrosis of permanent cells | Necrosis of stable or labile cells when collagen framework is destroyed so can't regenerate
41
How does angiogenesis occur?
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
What are the main cell types involved in fibrous repair?
``` Macrophages Lymphocytes (myo) Fibroblasts Endothelial cells Neutrophils ```
43
What is regenerate controlled by?
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
What is the process behind fibrous repair?
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
How do peripheral nerves regenerate?
By Wallerian degeneration. There's break down of myelin and schwann cell proliferation
46
What is the process behind scurvy?
Vitamin C deficiency means there's decreased hydroxylation of procollagen so collagen is then vulnerable to enzymatic degradation.
47
What does haemostasis depend on?
Vessel wall Platelets Coagulation Fibrinolysis
48
What three factors promote thrombus formation?
Abnormal vessel wall Abnormal blood flow Abnormal blood contents
49
What is thrombosis?
The formation of a solid mass of blood in the circulation, during life
50
What are the possible outcomes of thrombosis?
``` Lysis Propagation Organisation Recanalisation Embolism ```
51
How do venous and arterial thrombi differ in appearance?
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
What's the difference between atherosclerosis and arteriosclerosis?
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
What is the unifying hypothesis of atheroma formation?
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
What cells are involved in atheroma formation?
``` Endothelial cells Platelets Neutrophils Lymphocytes Macrophages Smooth muscle cells ```
55
How is the main restriction point of the cell cycle regulated?
By cyclin and cyclin dependent kinases which phoshporylate cell cycle transition proteins, eg retinoblastoma susceptibility protein, to push cell through cycle
56
What are the different outcomes of cell signalling by hormones/growth factors?
Divide Die Resist apoptosis Differentiate
57
What are the main 3 growth factors and what do they do?
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
What is aplasia?
The complete failure of tissue or organ to develop, embryonically
59
What is hypoplasia?
Under development of incomplete development of a tissue or organ at the embryonic stage

ESA 2 (4 decks)

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