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Phase 2 Medicine > Pathology > Flashcards

Pathology Flashcards

Intro to Clinical Sciences pathology

1
Q

What is inflammation?

A

Inflammation is the response of living tissues to cellular injury. It involves both innate and adaptive immune mechanisms

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2
Q

What are the 3 purposes of inflammation?

A
  1. localise and eliminate causative agent
  2. limit tissue injury
  3. restore tissue to normality
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3
Q

What are the 2 types of inflammation?

What are the differences between them?

A
  1. Acute
  2. Chronic

Acute inflammation has a sudden onset and has a short duration. Acute Inflammation usually resolves.
Chronic inflammation has a slow onset, or can be a sequel to acute. Usually has a long duration and may never resolve.
Chronic inflammation can start without an acute phase.

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4
Q

List 5 causes of acute inflammation.

A
  1. physical agents (trauma, heat, cold, UV-light, radiation)
  2. corrosive/irritant substances (acids/alkalis)
  3. microbial infection (pyogenic bacteria)
  4. immune-mediated hypersensitivity reactions (hay-fever, vasculitis)
  5. tissue necrosis (ischaemia resulting in MI)
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5
Q

List 4 causes of chronic inflammation.

A
  1. micro-organisms resistant to phagocytosis and intracellular killing mechanisms (TB or leprosy)
  2. foreign bodies (endogenous (uric acid crystals or adipose tissue) or exogenous (suture materials, silica, implanted prosthetics))
  3. some autoimmune diseases (Hashimoto’s thyroidosis, rheumatoid arthritis, contact hypersensitivity)
  4. primary granulomatous diseases (Crohn’s disease, sarcoidosis)
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6
Q

What is contact hypersensitivity? Give an example

A

Secondary immune response to a small, chemically reactive molecule that has bound to self proteins in the uppermost layers of the skin. This produces an antigen. An example - reaction to poison ivy.

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7
Q

What makes inflammation chronic? (2)

A

1, Inflammation occurs over a period of time where there is simultaneous tissue destruction and attempted repair.
2. Chronic inflammation can occur secondary to acute inflammation if the causative agent persists.

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8
Q

What are the 5 signs of acute inflammation?

A
  1. Rubor
  2. Calor
  3. Dolor
  4. Tumor
  5. Functio Laesa
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9
Q

What is the vascular response in acute inflammation?

A
  1. vasodilation
  2. increased vascular permeability?
  3. increased endothelial contraction
  4. inflammatory oedema
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10
Q

How does vasodilation occur in acute inflammation?

A

Precapillary sphincters relax and smooth muscle in arterioles relax to increase blood flow to injured area.

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11
Q

How does vascular permeability increase in acute inflammation?

A

Chemical inflammatory mediators such as bradykinin, histamine, and leukotriene B4 cause endothelial cell proteins to contract.

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12
Q

What does endothelial cell contraction do?

A

Contraction of endothelial cells increases fenestrations between endothelial cells
This increases permeability of vessels to plasma proteins.

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13
Q

What is the effect of increasing permeability of vessels to plasma proteins?

A

Proteins leak out of plasma into interstitial spaces. This decreases oncotic pressure of plasma.
Increase in hydrostatic pressure and decrease in oncotic pressure causes net fluid movement from the plasma into the interstitial spaces. This is inflammatory oedema.

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14
Q

List 5 advantages of inflammatory oedema.

A
  1. fluid increase in tissue neutralises toxins and modifies actions of toxins.
  2. protein levels increase in tissue - more protective antibodies and more fibrin
  3. fibrin net/mesh provides scaffold for inflammatory cells. this prevents spread of microorganisms
  4. Non-specific antibodies act as opsonins for neutrophil-mediated phagocytosis and can function to neutralise toxins
  5. circulation of exudate through lymph system assists in antigen presentation and helps mount a specific immune response.
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15
Q

What are the characteristics of a neutrophil?

A
  1. short-lived
  2. no memory
  3. mostly cytoplasmic granules that contain enzymes that kill bacteria
  4. called neutrophil polymorphs bc their nuclei are poly-lobated
  5. Eat material with antibodies on them
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16
Q

What is the role of neutrophils in inflammation?

A
  1. First on the scene in acute inflammation
  2. Release chemicals that attract other inflammatory cells
  3. Eat foreign material
  4. Usually die at the scene of inflammation
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17
Q

What are the 4 characteristics of macrophages?

A
  1. Long-lived (months)
  2. Eat foreign material but don’t die as fast as neutrophils
  3. May carry debris away from site of inflammation
  4. Can present antigens to lymphocytes
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18
Q

What are the 3 characteristics of lymphocytes?

A
  1. Long-lived (years)
  2. Produce chemicals that attract other inflammatory cells
  3. Possess immunological memory for past infections and antigens. Secondary immune response activated rapidly by lymphocytes.
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19
Q

What are humans born with?

A

Born with wide variety of lymphocytes which proliferate specific to current infection.

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20
Q

What are endothelial cells?

A
  1. Line capillaries
  2. Become sticky in areas of inflammation so inflammatory cells stick to them.
  3. Become porous to allow the inflammatory cells to pass into tissues
  4. Grow into areas of damage to become new capillary vessels
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21
Q

What are fibroblasts? What do they form?

A

Long-lived cells that form collagen in areas of chronic inflammation and repair.

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22
Q

What are the possible outcomes of acute inflammation?

A
  1. Resolution
  2. Suppuration - pus discharged
  3. Repair and organisation - can result in fibrosis
  4. Fibrosis
  5. Chronic inflammation - can result in fibrosis
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23
Q

Give an example of acute inflammation. What causes this?

A

Acute appendicitis. Unknown precipitating factor.

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24
Q

How is appendicitis characteristic of acute inflammation?

A
  1. Neutrophils appear
  2. Blood vessels dilate
  3. Inflammation of serosal surface
  4. Pain is felt
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25
Q

How is appendicitis treated?

A

Appendicitis can resolve on its own. If not, appendix should be surgically removed; if it’s not removed, it may burst, resulting in generalised peritonitis and sometimes death.

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26
Q

Give an example of chronic inflammation.

A

Tuberculosis

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27
Q

How is TB an example of chronic inflammation? How does TB progress?

A

No initial acute inflammation

  1. Mycobacteria are ingested by macrophages
  2. Macrophages fail to kill mycobacteria
  3. Lymphocytes appear
  4. Macrophages appear
  5. Fibrosis occurs
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28
Q

What are granulomas? What are epithelioid histiocytes?

A

Collections of macrophages surrounded by lymphocytes. The macrophages are activated and are called epithelioid histiocytes.

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29
Q

What does the presence of granulomas suggest?

A
  • TB
  • Leprosy
  • Foreign material (silica, adipose tissue, bone, uric acid)
  • Sarcoidosis
  • Crohn’s disease
  • Wegener’s granulomatosis
  • Drugs such as allopurinol and sulphonamides
30
Q

What is granulation tissue? (Very brief)

A

Combination of capillary loops and myofibroblasts. It is a wound-healing phenomenon.

31
Q

How is inflammation treated?

A

Aspirin
Ibuprofen and other NSAIDs
Steroids

32
Q

How does Ibuprofen reduce inflammation?

A

Inhibits prostaglandin synthetase

Prostaglandins act as chemical mediators of inflammation.

33
Q

Define cirrhosis. What causes cirrhosis?

A

Irreversible architectural disturbance characterised by nodules of hepatocytes with intervening fibrosis.
Occurs as a consequence of many forms of chronic liver injury.

34
Q

Why do abrasion wounds heal quickly?

A

Only epidermis is removed. The remaining layers of skin remain and so can regenerate epidermis quickly.

35
Q

Describe the process of healing by first intention.

A

Apposed wound margins are joined by fibrin deposition. Fibrin is subsequently replaced by collagen and is covered by epidermal growth.

36
Q

Describe the process of healing by second intention.

A
  1. Wound margins are unapposed due to extensive tissue damage
  2. Tissue defect fills with granulation tissue.
  3. Epithelial regeneration to cover surface of the wound
  4. Granulation tissue eventually contracts, resulting in scar formation.
37
Q

What is granulation tissue?

A

Newly formed connective tissue usually found at the edge/base of ulcers and wounds. Comprises:

  • capillaries
  • fibroblasts
  • myofibroblasts
  • inflammatory cells

Embedded in mucin-rich ground substance.

38
Q

Define repair.

A

Healing by replacement of lost tissue, but not necessarily by similar tissue.
Usually replaced by fibrous tissue.

39
Q

What causes repair and not resolution?

A
  • Initiating factor still present.

- Tissue damaged and unable to regenerate (eg neurones cannot regenerate)

40
Q

Give examples of repair occurring in the body.

A
  • Heart post-MI
  • Spinal cord post-trauma
  • Brain post-cerebral infarct (gliosis)
41
Q

Give 2 reasons why blood clots don’t form all the time.

A
  1. Laminar flow

2. Endothelial cells lining the vessels are not sticky when healthy.

42
Q

Define thrombosis

A

Thrombosis the formation of a solid mass from the blood constituents in an intact vessel in a living person.

43
Q

What is the difference between a clot and a thrombus?

A

Thrombi are solid masses of coagulated blood formed within the cardiovascular system.
Clots are blood coagulated outside the cardiovascular system or after death.

44
Q

What is the first stage in thrombosis?

A

Platelet aggregation

45
Q

What happens in platelet aggregation?

A

When platelets aggregate, they release chemicals which attract other platelets to stick to them. These chemicals also trigger the coagulation cascade.

46
Q

Why is it difficult to stop platelet aggregation?

A

Both platelet aggregation and the coagulation cascade have positive feedback loops so once they have started it is difficult to stop.

47
Q

What happens when the coagulation cascade starts?

A

Fibrin is formed and this makes a mesh for the entrapment of RBCs and more platelets.

48
Q

What are the three factors in Virchow’s triad?

A
  1. Change in vessel wall
  2. Change in blood constituents
  3. Change in blood flow
49
Q

Give an example of how thrombosis forms

A

Smoking cigarettes causes damage to the endothelial cells and the CO in smoke causes formation of more RBCs so the blood is more turgid. The damage to endothelial wall also causes change in blood flow so thrombosis occurs. Thrombosis is more likely due to the higher turgidity of the blood (due to the presence of more RBCs)

50
Q

Define embolus

A

An embolus is a solid mass of material in the blood that is able to become lodged within a vessel and block it.

51
Q

Give examples of emboli

A
  • parts of thrombus that have broken off
  • talcum powder from IV drug use
  • gases (injection of air into a vessel can block that vessel)
52
Q

What happens to the embolus if it enters into a venous system?

A

Emboli in the venous system reach the vena cava and go through the heart into the pulmonary arteries and lodge somewhere inside them.

53
Q

What happens to the embolus if it enters into an arterial system?

A

Travels anywhere downstream of its entry point.

54
Q

What is ischaemia? What does its severity depend on?

A

Reduction in blood flow. Severity depends on how much blood flow is reduced.

55
Q

What is infarction?

A

Severe ischaemia resulting in cell death.

56
Q

What causes infarction (usually)

A

Thrombosis of an artery

57
Q

What is end-arterial supply?

A

An organ only has one artery supplying it. If this single supply is interrupted, organs are very susceptible to infarction.

58
Q

List 3 organs which have a dual blood supply.

A
  1. Liver (hepatic artery and portal vein)
  2. Lungs (bronchial arteries and pulmonary veins)
  3. Brain (circle of Willis)
59
Q

What does atherosclerosis begin as, and what age does this occur?

A

Begins as a fatty streak from approx. 20 years old then gradually develops into atherosclerosis when it is noticed at age of 50-60.

60
Q

Which type of circulation does atherosclerosis occur in?

A

High pressure arteries such as aorta and coronary arteries on the left side of the heart. The pulmonary artery is a low pressure artery and therefore is not usually affected by atherosclerosis.

61
Q

List 6 things that cause atherosclerosis

A
  1. Free radicals in cigarette smoke damage endothelial cells.
  2. Nicotine in cigarette smoke damages endothelial cells.
  3. CO in cigarette smoke damages endothelial cells.
  4. Hypertension - shearing forces.
  5. Poorly controlled diabetes - superoxide anions and glycosylation products damage endothelial cells.
  6. Hyperlipidaemia - lipids damage the endothelial cells.
62
Q

What are the risk factors for atherosclerosis?

A
  1. Increasing age
  2. Male gender
  3. Smoking
  4. Diabetes
  5. Hypercholesterolaemia
  6. Hypertension
  7. Sedentary lifestyle
  8. Obesity
  9. Race (uncommon in China, Japan, and Africa)
63
Q

How does atherosclerosis develop?

A
  1. Chronic endothelial injury results in endothelial dysfunction. This causes an increased permeability of the vessel wall. Receptors for leucocytes are expressed on the surface of the endothelial cells.
  2. Plasma proteins (inc. LDL) diffuse into the arterial intima.
  3. Monocytes bind to the exposed receptors and migrate into the intima. They differentiate into macrophages and take up the LDL to form foam cells.
  4. Foam cells die and their contents become an extracellular lipid pool.
  5. Cytokines and growth factors are released by platelets and macrophages.
  6. The cytokines and growth factor attract smooth muscle cells from the media to the intima.
  7. The smooth muscle cells stop being contractile and express a repair phenotype in which they produce collagen in an attempt to stabilise the lesion.
64
Q

What can be found in a plaque?

A
  1. Lymphocytes
  2. Smooth muscle cells
  3. Macrophages
  4. Lipid deposits
  5. Cholesterol
  6. Fibrous tissue
65
Q

What is apoptosis?

A

Apoptosis is an energy dependent mechanism of programmed cell death for the deletion of individual cells. Apoptosis does not result in an inflammatory response.

66
Q

Where does apoptosis take place naturally?

A
  • In the gut
  • In the skin
  • In an embryo - death of cells between individual fingers and toes to prevent webbed hands and feet
67
Q

How does apoptosis occur?

A
  1. Cell is triggered to apoptose.
  2. Nuclear membrane fragments
  3. Nucleus fragments.
  4. Cell compartments are packaged into blebs, which fall off the cell.
  5. Macrophages eat the blebs.
68
Q

What triggers a cell to apoptose? How is this detected.

A

DNA damage triggers apoptosis before cell division can occur. DNA damage is detected by p53, which checks for any damage. If the DNA has not been significantly damaged, cell division can commence.
If the DNA has been significantly damaged, the cell will apoptose.

69
Q

What are caspases, and what can trigger them?

A

Caspases are enzymes that carry out apoptosis. They can be switched on by proteins in the Bcl2 family. They can also be switched on by the binding of the Fas ligand to the Fas receptor on cells.

70
Q

What is the link between apoptosis and cancer?

A

In cancer, there is a lack of apoptosis. The p53 gene is mutated, so DNA damage is not detected.
Cancer cells continue to grow and divide, but do not die.

71
Q

What is the link between apoptosis and HIV?

A

In AIDS, there is too much apoptosis. HIV triggers apoptosis in CD4 lymphocytes causing immunodepletion.

72
Q

Which of necrosis and apoptosis is energy-dependent?

A

Apoptosis is energy dependent. Necrosis occurs as a consequence of sudden changes in the microenvironment abolishing cell function.

Phase 2 Medicine (10 decks)

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