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CA1 Extra Qns > Pathology > Flashcards

Pathology Flashcards

1
Q

What are the causes of inflammation?

A
  1. Infection
  2. Tissue necrosis
  3. Foreign body
  4. Immune reactions
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2
Q

Histamines are released from _______ and causes ________

A

Histamines are released from mast cells and causes vasodilation

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3
Q

Cytokines are released from _______ and causes ________

A

Cytokines are released from macrophages and causes systemic effects (fever)

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4
Q

Chemokines are released from _______ and causes ________

A

Chemokines are released from macrophages and causes chemotaxis

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5
Q

Prostaglandins are released from _______ and causes ________

A

Prostaglandins are released from mast cells and causes vasodilation, pain, fever

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6
Q

Bradykinins are released from _______ and causes ________

A

Bradykinins are released from plasma (produced in liver) and causes pain

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7
Q

Signs of Acute Inflammation

A

pain (stimulation of nerve endings)
redness (vasodilation)
swelling (exudate)
heat (vasodilation)
loss of function (damaged tissue/voluntary)

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8
Q

Differences between acute and chronic inflammation.

A

Acute:
1. Fast onset
2. Mediated by neutrophils
3. Mild and self-limited tissue injury
4. Prominent signs
5. Can have pus formation

Chronic:
1. Slow onset
2. Mediated by macrophages/monocytes & lymphocytes
3. Severe and progressive tissue injury
4. Less prominent signs
5. No pus formation

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9
Q

What is exudate?

A

Exudate is the product of acute inflammation.
(note: transudate is NOT due to inflammation, more like due to increase of blood pressure -> edema)

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10
Q

Features of Exudate

A
  • high protein content (proteins and fluid leaks out)
  • high specific gravity
  • coagulates easily
  • “yellowish” pus -> not clear in colour
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11
Q

Features of Transudate

A
  • low protein content (only fluid leaks out)
  • low specific gravity
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12
Q

What is the role of lymphatics in acute inflammation?

A

Lymphatics help to carry away the exudate and drains into lymph nodes for further deactivation by immune system.

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13
Q

Special patterns of acute inflammation

A

Serous, Fibrinous, Suppurative, Ulcer

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14
Q

Serous

A

When the exudate is cell poor and typically does not involve an infection eg. blister

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15
Q

Fibrinous

A

When there is increased fibrinogen in the exudate, leading to threads of fibrins being formed eg. pericarditis

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16
Q

Suppurative

A

When there is pus - neutrophils, necrotic debris, bacteria
When it is localised, it’s called an abscess

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17
Q

Ulcer

A

When there is a defect in the epithelial surface eg. gastric ulcer

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18
Q

Causes of chronic inflammation

A

Persistent infections
Hypersensitivity diseases
Atherosclerosis from cholesterol (endogenous)
Silicosis from silica (exogenous)

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19
Q

Special type of chronic inflammation

A

Granulomatous inflammation

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20
Q

Features of granulomatous inflammation

A
  1. Epithelioid histiocytes (aka macrophages that come out from the bloodstream and into the tissue)
  2. Multinucleated giant cells
  3. T lymphocytes (forms a rim around histiocytes)
  4. Central necrosis
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21
Q

Causes of granulomatous inflammation

A
  1. Tuberculosis
  2. Leprosy
  3. Syphilis
  4. Cat scratch disease
  5. Fungi
  6. Parasite
  7. Sarcoidosis
  8. Crohn disease
  9. Foreign body
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22
Q

Outcomes of acute inflammation

A

Resolution, Pus formation -> Fibrosis, Fibrosis, Can lead to chronic inflammation

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23
Q

Cell tissue regeneration means…

A

Restoration of original tissues, no loss of function (occurs simultaneously with fibrosis)

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24
Q

Fibrous tissue repair means…

A

Fibrous scar, loss of function (occurs simultaneously with regeneration)

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25
Q

Growth factors that stimulate ECM collagen synthesis

A

Macrophage-derived growth factor
Platelet-derived growth factor

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26
Q

When can regeneration occur?

A

The tissue must contain pluripotent stem cells that are capable of dividing.
The more specialised the cell, the less likely that it can be replaced eg. neurons, cardiac muscle
Only labile and stable cells can regenerate

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27
Q

Processes involved in fibrous repair

A

Granulation tissue formation
- Angiogenesis
- Fibroblastic proliferation
Wound contraction (myofibroblasts)
Collagen synthesis and maturation
Scar maturation and remodelling

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28
Q

Cellular processes involved in healing

A

Cell proliferation, cell migration, angiogenesis, inflammatory cells to clear out infections, ECM synthesis and remodelling

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29
Q

Collagen Synthesis and Maturation

A
  • requires vitamin C
  • initially type III collagen, later removed and replaced by type I collagen
  • remodelling occurs -> collagen fibres and bundles are re-organised
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30
Q

Scar maturation and remodelling

A
  • Collagen synthesis exceeds degradation
  • Accumulation of collagen occurs
  • Tensile strength of collagen increases
  • Vascular resorption continues -> pale and stable avascular scar
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31
Q

Factors affecting wound healing - local

A
  1. Type, size and location of wound
  2. Local vascular supply
  3. Secondary infection
  4. Movement
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32
Q

Factors affecting wound healing - systemic

A
  1. Age (young heal better)
  2. Circulatory status (blood supply to injured area)
  3. Nutrition (malnutrition -> poor healing)
  4. Metabolic status
  5. Hormones (increased corticosteroids -> inhibit collagen synthesis)
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33
Q

Complications of wound healing

A

Defective scar formation
Excessive scar tissue formation (keloid)
Excessive contraction

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34
Q

Healing by Primary Intention (cutaneous wounds)

A

Wound with closely apposed edge
Minimal hematoma
- Re-epithelialization of epidermis
- Well formed granulation tissue (angiogenesis)
- Mature collagenization with good tensile strength
Minimal wound contraction
- Complete wound healing with minimal scar formation

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35
Q

Healing by Secondary Intention (cutaneous wounds)

A

Large gaping wound with skin edges not apposed
Much more inflammation and granulation tissue
Longer time to achieve epidermal cover
More tissue fibrosis and wound contraction
Larger deforming scar

36
Q

Healing of myocardial infarct

A

Cardiomyocytes are permanent specialised cells that cannot regenerate
Healing is by fibrous repair
Hypertrophy of surviving cardiomyocytes to compensate for loss of cells to infarct
Large infarct will lead to heart failure

37
Q

Healing of lung

A

Intact basement membrane: complete resolution
Damaged basement membrane: fibrosis

38
Q

Healing of liver

A

Acute: complete resolution
Chronic: combination of fibrosis and regeneration -> liver cirrhosis

39
Q

Healing of kidney

A

Fibrosis

40
Q

Healing of CNS

A

Neurons cannot be regenerated -> Gliosis

41
Q

Fracture healing

A

Haematoma -> granulation tissue -> collagenous fibrous tissue
proliferation of osteoblasts -> immature woven bone
bone remodelling -> mature lamellar bone

42
Q

Complications of Fracture Healing

A

Non-union of bone
Fibrous union -> false joint
Malunion -> angulation
Osteomyelitis

42
Q

Active Hyperaemia means…

A

blood flow TO organ is increased eg blushing, muscles during exercise, acute inflammation

43
Q

Passive Hyperaemia means…

A

blow flow OUT of organ is decreased (congestion) -> congested organ becomes enlarged, cyanotic, firm and heavy

43
Q

Oedema means…

A

excessive extravascular accumulation of fluid

44
Q

Primary causes of oedema

A
  1. increased hydrostatic pressure of plasma
  2. reduced oncotic pressure of plasma
  3. increased endothelial permeability
  4. lymphatic obstruction
45
Q

Define shock

A

Shock is a state of inadequate perfusion of cells and tissues which leads to reversible hypoxic injury and, if severe and prolonged enough, can lead to irreversible cell and organ injury and death

46
Q

What are the types of shock?

A

Hypovolemic shock
- loss of blood/bodily fluids
Cardiogenic shock
- due to myocardial infarction
Distributive shock
- septic shock (infection), anaphylactic shock (allergy), neurogenic shock -> leads to a drop of blood pressure
Obstructive shock
- eg pulmonary embolism

47
Q

Process of Septic Shock

A

Microbial antigens eg endotoxins will bind to endotoxin receptors on macrophages -> release cytokines (initially protective) but will lead to:
- vasodilation
- decrease cardiac contractility
- endothelial injury
- promotes blood coagulation
-> disseminated intravascular coagulation

48
Q

What is Virchow’s Triad

A

Injury to endothelium
Alteration to blood flow
Alteration to blood coagulability

49
Q

Common clinical state of thrombosis

A
  1. Atrial fibrillation -> thrombus in atria
  2. Prosthetic cardiac valve -> thrombus develop on valves
  3. Post surgery or post partum
  4. Prolonged bed rest / immobilisation
  5. Disseminated cancer
  6. Oral contraceptives
50
Q

Venous thrombosis

A

Stasis -> increase clotting factors, platelet aggregation -> deep vein thrombosis -> embolism -> vascular occlusion of distant organ (most likely thrombus travels to pulmonary artery) -> congestion (arterial blood can flow in but venous blood cannot flow out)

51
Q

Arterial thrombosis

A

thrombus in artery -> arterial occlusion (cerebral artery / renal artery / coronary artery) -> ischaemia due to loss of blood supply -> necrosis in the brain / kidney / heart

52
Q

What are the fates of a thrombus?

A
  1. Resolution -> dissolves the clot
  2. Propagation -> partial occlusion becomes complete occlusion
  3. Organisation (thrombus replaced by granulation tissue) and Recanalization (new red blood cells start to form)
  4. Embolism -> detach of clot
53
Q

White infarct occurs in…

A

Solid organs

54
Q

Red infarct occurs in…

A

Spongy organs (lungs) + haemorrhage

55
Q

Effects of Ischaemia

A
  1. Remains viable
  2. Infarction
  3. Infarction -> heals by fibrosis
  4. Ischaemic atrophy (functioning at a reduced size and state)
56
Q

Types of emboli

A
  1. Solid: detached thrombus
  2. Liquid: fat globules, amniotic fluid
  3. Gaseous: air
  4. Septic: infected material -> spread of infection
57
Q

Hypertrophy means…

A

increase in cell size

58
Q

Hyperplasia means…

A

increase in cell numbers

59
Q

Cell metaplasia means…

A

change of one cell type to another cell type (eg, stomach epithelium transforms to intestinal epithelium - presence of goblet cells)

60
Q

Atrophy means…

A

decrease in cell size

61
Q

Hypoplasia/involution means…

A

decrease in cell numbers

62
Q

features of reversible cell injury (early cell changes)

A
  1. cytoplasmic vacuolation and swelling
  2. mitochondrial and endoplasmic reticulum swelling
  3. clumping of nuclear chromatin
    => CAN RECOVER
63
Q

features of irreversible cell injury (late cell changes)

A
  1. densities in mitochondrial matrix
  2. cell membrane disruption
  3. nuclear shrinkage (pyknosis)
  4. nuclear dissolution (karyolysis)
  5. nuclear break up (karyorrhexis)
  6. lysosome rupture
    => CANNOT RECOVER -> DEATH
64
Q

Cell injury changes best seen in…

A

electron microscopy

65
Q

What is the role of molecular chaperones?

A

Protect proteins from (further) damage

66
Q

What is the role of ubiquitin?

A

Removes damaged proteins

67
Q

What inclusion bodies will be seen in alcoholic liver damage?

A

Mallory’s hyaline bodies

68
Q

What inclusion bodies will be see in Parkinson’s disease?

A

Lewy bodies

69
Q

Affected hepatocytes in fatty liver will stain _____ when stained with _______

A

Affected hepatocytes in fatty liver will stain RED when stained with Oil Red O

70
Q

Difference between apoptosis and necrosis

A

Apoptosis:
1. Membrane not breached
2. No inflammation response
3. Single cells
4. Active process (requires protein synthesis and consumes ATP)
5. Can be pathological or physiological

Necrosis:
1. Membrane breached
2. Inflammation response
3. Contiguous cells
4. Passive process
5. Always pathological

71
Q

Types of necrosis

A
  • coagulative
  • caseous
  • haemorrhagic
  • suppurative
  • liquefactive
  • gangrene
  • fat
  • fibrinoid
72
Q

Coagulative Necrosis

A
  • Form of necrosis secondary to hypoxia or loss of blood supply (ischaemia)
  • Ghost outlines (cell structure present but with loss of nuclei)
73
Q

Caseous Necrosis

A
  • secondary to mycobacterial tuberculosis infection
  • granulomatous inflammation (special type of chronic inflammation)
  • “cheesy” necrosis
74
Q

Liquefactive Necrosis

A
  • necrosis in the BRAIN post stroke
75
Q

Haemorrhagic Necrosis

A
  • necrosis in organs with dual blood supply (lungs and liver)
  • necrosis secondary to venous congestion (deoxygenated blood cannot leave the organ)
76
Q

Suppurative Necrosis

A
  • abscess formation
  • large collection of neutrophils
77
Q

Microscopic features of Tuberculosis

A
  • granulomatous inflammation
  • caseous necrosis
  • langhan’s giant cells
  • positive in giant cell Ziehl-Neelsen stain
78
Q

What stain to use for tuberculosis?

A

giant cell Ziehl Neelsen stain

79
Q

What is autophagy?

A

Cell eats its own organelles -> for elimination or recycling
-> forms lipofuscin pigments

80
Q

Congenital Rubella

A
  • affects baby’s eye, brain, heart
  • deafness may appear later
  • due to maternal infection
  • first trimester -> terminate pregnancy
81
Q

Congenital CMV

A
  • mother may have primary or reactivated CMV infection
82
Q

Congenital Toxoplasmosis

A
  • later pregnancy: transmission high, sequelae low
  • early pregnancy: transmission low, sequelae high
  • don’t handle contaminated food
  • risk in newborn kittens
83
Q

Neonatal sepsis and meningitis can be caused by…

A
  1. group B streptococcus
  2. E. coli
  3. Listeria monocytogenes
  • treat with ampicillin + gentamicin
84
Q

Routine antenatal screening tests for infections

A

Blood test for:
- Hep B virus
- syphilis
- rubella
- HIV

Vaginal swab
- group B streptococcus @ 35 weeks

No need do test for:
- toxoplasma
- HSV (examine for vesicles at delivery)
- CMV

CA1 Extra Qns (5 decks)

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