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CA1 Extra Qns > Pathology > Flashcards

Pathology Flashcards

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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
Growth factors that stimulate ECM collagen synthesis
Macrophage-derived growth factor Platelet-derived growth factor
26
When can regeneration occur?
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
27
Processes involved in fibrous repair
Granulation tissue formation - Angiogenesis - Fibroblastic proliferation Wound contraction (myofibroblasts) Collagen synthesis and maturation Scar maturation and remodelling
28
Cellular processes involved in healing
Cell proliferation, cell migration, angiogenesis, inflammatory cells to clear out infections, ECM synthesis and remodelling
29
Collagen Synthesis and Maturation
- requires vitamin C - initially type III collagen, later removed and replaced by type I collagen - remodelling occurs -> collagen fibres and bundles are re-organised
30
Scar maturation and remodelling
- Collagen synthesis exceeds degradation - Accumulation of collagen occurs - Tensile strength of collagen increases - Vascular resorption continues -> pale and stable avascular scar
31
Factors affecting wound healing - local
1. Type, size and location of wound 2. Local vascular supply 3. Secondary infection 4. Movement
32
Factors affecting wound healing - systemic
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)
33
Complications of wound healing
Defective scar formation Excessive scar tissue formation (keloid) Excessive contraction
34
Healing by Primary Intention (cutaneous wounds)
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
35
Healing by Secondary Intention (cutaneous wounds)
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
Healing of myocardial infarct
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
Healing of lung
Intact basement membrane: complete resolution Damaged basement membrane: fibrosis
38
Healing of liver
Acute: complete resolution Chronic: combination of fibrosis and regeneration -> liver cirrhosis
39
Healing of kidney
Fibrosis
40
Healing of CNS
Neurons cannot be regenerated -> Gliosis
41
Fracture healing
Haematoma -> granulation tissue -> collagenous fibrous tissue proliferation of osteoblasts -> immature woven bone bone remodelling -> mature lamellar bone
42
Complications of Fracture Healing
Non-union of bone Fibrous union -> false joint Malunion -> angulation Osteomyelitis
42
Active Hyperaemia means...
blood flow TO organ is increased eg blushing, muscles during exercise, acute inflammation
43
Passive Hyperaemia means...
blow flow OUT of organ is decreased (congestion) -> congested organ becomes enlarged, cyanotic, firm and heavy
43
Oedema means...
excessive extravascular accumulation of fluid
44
Primary causes of oedema
1. increased hydrostatic pressure of plasma 2. reduced oncotic pressure of plasma 3. increased endothelial permeability 4. lymphatic obstruction
45
Define shock
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
What are the types of shock?
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
Process of Septic Shock
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
What is Virchow's Triad
Injury to endothelium Alteration to blood flow Alteration to blood coagulability
49
Common clinical state of thrombosis
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
Venous thrombosis
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
Arterial thrombosis
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
What are the fates of a thrombus?
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
White infarct occurs in...
Solid organs
54
Red infarct occurs in...
Spongy organs (lungs) + haemorrhage
55
Effects of Ischaemia
1. Remains viable 2. Infarction 3. Infarction -> heals by fibrosis 4. Ischaemic atrophy (functioning at a reduced size and state)
56
Types of emboli
1. Solid: detached thrombus 2. Liquid: fat globules, amniotic fluid 3. Gaseous: air 4. Septic: infected material -> spread of infection
57
Hypertrophy means...
increase in cell size
58
Hyperplasia means...
increase in cell numbers
59
Cell metaplasia means...
change of one cell type to another cell type (eg, stomach epithelium transforms to intestinal epithelium - presence of goblet cells)
60
Atrophy means...
decrease in cell size
61
Hypoplasia/involution means...
decrease in cell numbers
62
features of reversible cell injury (early cell changes)
1. cytoplasmic vacuolation and swelling 2. mitochondrial and endoplasmic reticulum swelling 3. clumping of nuclear chromatin => CAN RECOVER
63
features of irreversible cell injury (late cell changes)
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
Cell injury changes best seen in...
electron microscopy
65
What is the role of molecular chaperones?
Protect proteins from (further) damage
66
What is the role of ubiquitin?
Removes damaged proteins
67
What inclusion bodies will be seen in alcoholic liver damage?
Mallory's hyaline bodies
68
What inclusion bodies will be see in Parkinson's disease?
Lewy bodies
69
Affected hepatocytes in fatty liver will stain _____ when stained with _______
Affected hepatocytes in fatty liver will stain RED when stained with Oil Red O
70
Difference between apoptosis and necrosis
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
Types of necrosis
- coagulative - caseous - haemorrhagic - suppurative - liquefactive - gangrene - fat - fibrinoid
72
Coagulative Necrosis
- Form of necrosis secondary to hypoxia or loss of blood supply (ischaemia) - Ghost outlines (cell structure present but with loss of nuclei)
73
Caseous Necrosis
- secondary to mycobacterial tuberculosis infection - granulomatous inflammation (special type of chronic inflammation) - "cheesy" necrosis
74
Liquefactive Necrosis
- necrosis in the BRAIN post stroke
75
Haemorrhagic Necrosis
- necrosis in organs with dual blood supply (lungs and liver) - necrosis secondary to venous congestion (deoxygenated blood cannot leave the organ)
76
Suppurative Necrosis
- abscess formation - large collection of neutrophils
77
Microscopic features of Tuberculosis
- granulomatous inflammation - caseous necrosis - langhan's giant cells - positive in giant cell Ziehl-Neelsen stain
78
What stain to use for tuberculosis?
giant cell Ziehl Neelsen stain
79
What is autophagy?
Cell eats its own organelles -> for elimination or recycling -> forms lipofuscin pigments
80
Congenital Rubella
- affects baby's eye, brain, heart - deafness may appear later - due to maternal infection - first trimester -> terminate pregnancy
81
Congenital CMV
- mother may have primary or reactivated CMV infection
82
Congenital Toxoplasmosis
- later pregnancy: transmission high, sequelae low - early pregnancy: transmission low, sequelae high - don't handle contaminated food - risk in newborn kittens
83
Neonatal sepsis and meningitis can be caused by...
1. group B streptococcus 2. E. coli 3. Listeria monocytogenes - treat with ampicillin + gentamicin
84
Routine antenatal screening tests for infections
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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