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Y1 > Foundation - General Pathology > Flashcards

Foundation - General Pathology Flashcards

1
Q

Define hyperplasia

A

Increased number of cells due to increased functional demand

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2
Q

Define hypertrophy

A

Increased size of cells due to increased functional demand

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3
Q

Define hypoplasia

A

Decreased number of cells (involution) due to decreased functional demand

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4
Q

Define atrophy

A

Decreased size of cells due to decreased functional demand

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5
Q

Explain how atrophy could arise

A
  1. Lysosome autophagy of worn out organelles
  2. Ubiquitin-proteosome degradation of cytoskeleton
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6
Q

Explain what happens during autophagy

A
  1. Lysosome eats its own worn-out organelles
  2. Formation of residual bodies
  3. Residual bodies may accumulate as lipofuscin (wear and tear pigments)
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7
Q

Explain the importance of autophagy

A
  1. Eliminate abnormal molecules that may be toxic
  2. Recycling of components for survival
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8
Q

Define metaplasia

A

Change in cell type due to change in stress (via reprogramming of stem cells)

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9
Q

Describe the reversible, early stage changes when a cell undergoes stress

A

Stress = swell
1. Swelling of cytoplasm
2. Fatty changes
3. Nuclear chromatin clumping
4. Mitochondrial and ER swelling
Protein-related
5. Increased expression of protective proteins (e.g. molecular chaperons that protect cell from further damage, ubiquitin that tag damaged proteins for proteolysis)
6. Formation of aggregates of ubiquitin and damaged proteins aka inclusion bodies

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10
Q

Describe the irreversible, late stage changes when a cell is about to undergo apoptosis

A
  1. Nuclear condensation/shrinkage → pyknosis
  2. Nuclear break up → karyorrhexis (karyotype + ex)
  3. Nuclear dissolution → karyolysis (karyotype + lyse)
  4. Lysosome rupture
  5. Amorphous densities in mitochondrial matrix (mitochondria messy and dense)
  6. Disruption of cell membrane
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11
Q

Describe the main mechanisms of cellular injury/stress

A
  1. Cell membrane damage
  2. Mitochondrial damage
  3. Ribosomal damage
  4. Nuclear damage
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12
Q

The consequences of cell injury depend on:

A
  1. Time of exposure
  2. Severity of injury
  3. Type of injury
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13
Q

State the types of cell death

A
  1. Autophagy
  2. Autolysis
  3. Necrosis
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14
Q

Define autolysis

A

Death of cells and tissues after death of whole organism by post-mortem release of digestive enzymes from lysosomes

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15
Q

Define necrosis

A

Death of body tissues when there is inadequate perfusion/too little blood flowing through it (due to pathological reasons)

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16
Q

Distinguish between apoptosis and necrosis

A
  1. Apoptosis involves fewer cells; necrosis involves more cells
  2. Membrane intact for apoptosis but completely disrupted for necrosis
  3. Apoptosis is active process; necrosis is passive
  4. Apoptosis is never with inflammation but necrosis is usually
  5. Apoptosis is mostly physiological but necrosis is always pathological
  6. Apoptosis involves controlled dissolution of nucleus; necrosis involves fragmentation of nuclear DNA into nucleosomes
  7. During apoptosis, cell contents are released in apoptotic bodies within cell but during necrosis, cell contents freely leak out of the cell
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17
Q

State the physiological functions of apoptosis

A
  1. Regulating the number of cells in a tissue/organ
  2. Deletion of self-reactive cells (e.g. lymphocytes) to prevent autoimmunity
  3. Shedding of endometrial cells in menstrual cycle
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18
Q

Describe the morphological features of cells undergoing apoptosis

A

Mid-stage: highly eosinophilic due to denatured proteins
Late-stage: very pink, condensed nucleus

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19
Q

Briefly describe the process of necrosis

A
  1. Release of hydrolytic enzymes from damaged lysosomes
  2. Digestion and denaturation of cellular proteins
  3. Breakdown of cell membrane
  4. Contents like intracellular enzymes leak freely out of the cell
  5. Cessation of cell function
  6. Initiation of inflammatory response
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20
Q

Define anoikisis

A

When epithelial cells detach from neighbouring cells and ECM during apoptosis/programmed cell death

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21
Q

Define granuloma and its contents

A

Core of necrosis
1. Epithelioid macrophages (formed when macrophages from tissue stroma fail to engulf the offending agent)
2. Lymphocytes, neutrophil infiltration
3. Multinucleated Langhans giant cells (formed by fused epithelioid macrophages)

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22
Q

Classify the types of necrosis

A
  1. Coagulative necrosis
  2. Haemorrhagic necrosis
  3. Caseous necrosis
  4. Suppurative necrosis
  5. Liquefactive necrosis
  6. Fat necrosis
  7. Gangrenous necrosis
  8. Fibrinoid necrosis
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23
Q

Describe the pathogenesis of coagulative necrosis

A

Some occlusion → ischaemia → infarction → coagulative necrosis

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24
Q

List the classical presentations of coagulative necrosis

A
  1. Affects cell far from blood vessels or solid organs, usually occurs in heart, lungs, liver
  2. Appears white coz no blood
  3. GHOST CELLS (intact cytoplasm but no nucleus)
  4. Cell retains its architecture even with necrosis
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25
Q

Describe the pathogenesis of haemorrhagic necrosis

A

ENDPOINT: leakage of blood into surrounding tissues

E.g. 1 Occlusion of one blood supply → ischaemia → infarction including endothelium lining vessels of 2nd blood supply → loss of endothelial integrity of 2nd blood vessel → extravascular leakage into surrounding tissues

E.g. 2 Venous congestion → increased pressure → rupture of blood vessels → extravascular leakage

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26
Q

List the classical presentations of haemorrhagic necrosis

A
  1. Appears red coz blood flow out
  2. Affects organs with dual perfusion (e.g. liver, lungs)
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27
Q

Describe reperfusion injury

A

Reperfusion of ischaemic tissue worsens tissue hypoxic injury due to persisting endothelial defects

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28
Q

Describe the pathogenesis of liquefactive necrosis

A

Injury/infection/stroke → cell death of glial cells and neurons → myelin sheath breakdown → gelatinous, viscous liquid rich in fats → abscess formation → impaired blood flow

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29
Q

List the classical presentations of liquefactive necrosis

A
  1. Affects brain and other soft organs
  2. Cystic “liquefied” appearance
  3. Abscess formation
  4. Cell does not retain its architecture
30
Q

List the classical presentations of caseous necrosis

A
  1. Associated with TB
  2. Friable/crumbly appearance
  3. Occurs at the core of granuloma
  4. Acid fast bacilli in giant cell in Ziehl-Neelsen stain
31
Q

Describe the pathogenesis and list the classical presentations of suppurative necrosis

A

Infection → tissue injury and inflammation → cell death → abscess formation → impaired blood flow

  1. Pus-filled exudate
  2. Abscess formation
  3. Neutrophil infiltration
32
Q

Describe the pathogenesis and list the classical presentations of fat necrosis

A

Trauma/mechanical injury → ischaemia + impaired blood flow

  1. Affects areas with high subcutaneous fat content (e.g. buttock, breast)
  2. Chalky-white appearance as fatty acids bind with calcium
33
Q

Classify the types of gangrenous necrosis

A

DRY GANGRENE = coagulative necrosis
WET GANGRENE = liquefactive necrosis
GAS GANGRENE = bacterial fermentation of tissue carbohydrates by Clostridium perfringens

34
Q

Describe the pathogenesis of dry gangrene

A

Ischaemic insult (e.g. arterial occlusion, diabetes mellitus) → infarction → gas gangrene

35
Q

Describe the pathogenesis of wet gangrene

A

Ischaemia → infarction → secondary infection and inflammation → pus accumulation → wet gangrene

36
Q

Describe the pathogenesis of gas gangrene

A

Bacterial infection (particularly by anaerobic bacteria) → ischaemia → cell death → anaerobic environment promotes further growth of bacteria → release toxins and enzymes that further damage the tissue → impaired blood flow

37
Q

Describe the pathogenesis of fibrinoid necrosis

A

Immune complexes or antibodies deposit within vessel walls → inflammation → endothelial injury → trigger agglutination of fibrin → further weakening of vessel wall → extravascular leakage

38
Q

Define inflammation

A

The response of vascularised tissue that brings cells and molecules of host defence from circulation to sites where they are needed to eliminate offending agents

39
Q

List the cardinal signs of acute inflammation

A
  1. Pain
  2. Oedema
  3. Warmth
  4. Redness
  5. Loss of function
40
Q

Outline the steps of acute inflammation

A
  1. Mast cells/resident macrophages detect offending agent
  2. Mast cell degranulation, releasing inflammatory mediators
  3. Local vasodilation → redness, warmth
  4. Increased vascular permeability → extravasation of plasma proteins and cells through fenestrations between endothelial cells
  5. Kinins that leak out activated to form bradykinins → bradykinins and prostaglandins irritate local nerve endings and send impulses to brain → perception of pain
  6. Margination of neutrophils on endothelial lining (selectins slow neutrophils down → rolling → integrins force to complete stop → adhesion)
  7. Chemokines released by inflammatory cells mediate transmigration of neutrophils through fenestrations
  8. Neutrophils attracted by leukotrienes and complement system to actual infection site → inflammatory exudate
  9. Infiltration, swelling or offending agent itself impairs tissue function
41
Q

Fever is caused by

A

Cytokines IL-1, TNF and prostaglandins

42
Q

Inflammatory mediators released by mast cell degranulation include

A
  1. Histamine (pre-formed in granules)
  2. Eicosanoids aka thromboxane, leukotriene and prostaglandins (non-protein molecules synthesised in cytoplasm)
  3. Cytokines (not immediate as transcription and translation takes time)
43
Q

Describe the roles of M1 macrophages in inflammation

A
  1. Secrete pro-inflammatory cytokines (TNF-alpha, IL-1)
  2. Increase expression of selectins and integrins
  3. Boost phagocytic killing by neutrophils
  4. Fever response
  5. Phagocytic killing of foreign agents
44
Q

Distinguish between exudate and transudate

A
  1. Exudate indicates inflammation; transudate indicates haemodynamic disorder
  2. Exudate has high protein content; transudate has low protein content
  3. Exudate may contain some white/red cells and neutrophils; transudate has few ells
45
Q

Describe the role of lymphatics in inflammation

A

Lymphatics help to carry away the exudate and injurious stimuli and drain into lymph nodes for further deactivation by immune system

46
Q

Describe the outcomes of acute inflammation and how they are determined

A

Outcomes:
1. Resolution
2. Progression to chronic inflammation
3. Pus formation → abscess (if localised), empyema (if contained in body cavity)
4. Healing to fibrosis (loss of function + scarring)

Determined by:
1. Extent of death and damage
2. Tissue’s regenerative capacity
3. Speed of destruction of causal agent
4. Speed of removal of fluid and debris

47
Q

Describe the special patterns of acute inflammation

A
  1. Serous: special cell-poor exudate, does not involve infection
  2. Fibrinous: exudate has fibrinogen which is converted to fibrin (e.g. pericarditis)
  3. Suppurative: pus-filled exudate
  4. Ulcer: defective epithelial surface
48
Q

List the systemic signs of inflammation

A
  1. Fever
  2. Constitutional symptoms: malaise, anorexia, nausea
  3. Anaemia: shunting to make WBCs, not enough resources to make RBCs
  4. Leukocytosis: elevated WBCs
  5. Increased erythrocyte sedimentation rate: more fibrinogen → blood cells stick together → settle faster
  6. Reactive hyperplasia: swelling of lymph nodes
  7. Amyloidosis: shunting to make WBCs → bone marrow cannot manufacture correctly folded proteins → misfolded proteins deposit around body esp heart
  8. Loss of appetite and weight
49
Q

Describe the full blood count abnormalities that point towards inflammation

A
  1. Increased erythrocyte sedimentation rate
  2. Increased C reactive protein count (acute phase reactant made in liver to enhance effect of leukocytes)
  3. Increased white cell count
50
Q

List the benefits and harms of inflammation

A

Benefits
1. Dilution of toxins
2. Facilitate leukocyte migration
3. Transport drugs
4. Fibrin formation → blood clot
5. Delivery of nutrients, O2 and antigens
6. Stimulate immune response
7. Delivery of vital plasma proteins (e.g. fibrinogen, antibodies, complement)

Harms
1. Digestion of normal tissue
2. Swelling
3. Inappropriate inflammatory response (e.g. autoimmunity/ allergies)

51
Q

Define chronic inflammation

A

A response of prolonged duration (weeks to months) in which inflammation, tissue injury and attempts at repair co-exist in varying combinations

52
Q

Distinguish between acute and chronic inflammation

A
  1. Acute inflammation involves mostly neutrophils; chronic inflammation involves mostly macrophages and lymphocytes
  2. Fast onset vs slow onset
  3. Exudation faster vs slower/absent exudate
  4. Mild tissue damage (self-limited) VS severe, more progressive tissue damage
  5. More prominent signs and symptoms vs less prominent
53
Q

Define granulomatous inflammation

A

A special type of chronic inflammation comprising granulomas

Granulomas are made up of
1. Epithelioid histiocytes
2. Lymphocytes/neutrophil infiltration
3. Multinucleated Langhans giant cells

54
Q

Define the following terms
(i) Endemic rate
(ii) Epidemic
(iii) Outbreak
(iv) Pandemic

A

(i) Expected rate of infection in a population/geographic area
(ii) Cases occurring above normal rates
(iii) Cases occurring above normal rates + within a small geographical area and more sudden
(iv) Cases occurring over wide geographical area and affecting exceptionally high proportion of population

55
Q

Define the following terms related to bloodstream infections:
(i) Bacteremia
(ii) Septicemia
(iii) Sepsis

A

(i) Presence of bacteria within bloodstream
(ii) Infection due to bacteria within bloodstream
(iii) Result of septicaemia

56
Q

Describe the symptoms of sepsis

A
  1. Fever
  2. Increased HR
  3. Increased RR
  4. Macrophage encounter endotoxin → produce vasodilating cytokines → decrease BP → shock
  5. Organ failure
57
Q

Name the patterns of infectious diseases for the following:
(i) Necrosis
(ii) Abscess
(iii) Granulomatous inflammation
(iv) Increased eosinophil count
(v) Individual cell dysfunction

A

(i) Exotoxin-mediated
(ii) Pus-forming bacteria
(iii) Mycobacteria, fungal infection → tough cell wall so can survive in host for long periods of time
(iv) Helminth infection
(v) Viral cytopathic effect

58
Q

Define the following terms
(i) Healing
(ii) Regeneration
(iii) Resolution
(iv) Organisation/Repair
(v) Fibrosis

A

(i) Regeneration + organisation
(ii) Restoration of normal architecture, with no loss of function
(iii) No more exudate
(iv) Healing by fibrosis/scarring, with some loss of function
(v) Accumulation of excessive amounts of fibrous tissue

59
Q

The criteria for regeneration is that

A
  1. The tissue must contain pluripotent stem cells that are capable of dividing
  2. Less specialised cells have higher likelihood
  3. Underlying connective tissue scaffold must remain intact
60
Q

Explain how cells are classified based on their regenerative ability

A
  1. Labile: always regenerating/in the cell cycle (e.g. bone marrow, skin, hair follicles, mucosa)
  2. Stable: can regenerate when appropriate signals are present (e.g. pancreas, liver, kidney)
  3. Permanent: never regenerates (e.g. neurons, cardiac/skeletal muscles)
61
Q

Explain what myofibroblasts are and their role in healing and repair

A

Myofibroblasts are differentiated/ activated fibroblasts + transformed immature epithelial and endothelial cells

They are used for
1. ECM and collagen secretion
2. Bring edges of wound closer together for contraction

62
Q

Name the components of fibrous scar tissue

A

Fibroblasts
Endothelial cells
Stromal stem cells

63
Q

Outline the steps of healing and repair

A
  1. Haemostasis, blood clotting
  2. Granulation tissue formation consisting of blood vessels, myofibroblasts, fibroblasts and a mixture of inflammatory cells + angiogenesis
  3. Myofibroblasts contract and bring edges of wound closer together
  4. Following stimulation by growth factors like macrophage-derived growth factor, fibroblasts and myofibroblasts produce collagen
  5. Collagen form cross-linkages which increase tensile strength and stability of the extracellular matrix
  6. Scar remodelling, mature fibrous scar become more stable
  7. Precursors to collagen synthesis decrease, blood vessels undergo resorption
  8. Pale fibrous scar remains
64
Q

Describe the role of M2 macrophages in healing and repair

A
  1. Debridement: getting rid of debris/exudate/neutrophils/necrotic tissue to promote wound healing
  2. Secrete anti-inflammatory cytokines and growth factors for ECM deposition
65
Q

Outline the process of angiogenesis that starts 48-72 hours after haemostasis

A
  1. Endothelial cells divide to form solid sprouts
  2. Sprouts develop a lumen by fusion of intracytoplasmic vacuoles containing RBCs
  3. Formation of capillaries
  4. Capillaries join to form an arbourising vascular network
  5. Vascular network brings nutrients, oxygen and inflammatory cells to infection site
66
Q

Discuss the factors affecting wound healing

A

Local factors
1. Size, location of wound
2. Movement → tear immature collagen fibres
3. Nearby infection → prolong inflammation
4. Local vascular supply
5. Radiation, medications (e.g. steroid use) → deplete actively dividing cells

Systemic factors
1. Endocrinopathies
2. Metabolic status (e.g. diabetes → sugar-based complexes build up in vessel walls → impaired blood flow)
3. Systemic circulation
4. Nutrition deficiency (e.g. Vit C deficiency → weak cross-linking of collagen → weak vessels → spontaneous haemorrhage)
5. Age

67
Q

Discuss the complications of wound healing

A
  1. Defective scar formation
  2. Excessive scar tissue
  3. Contraction (usually following burns and chemical injury)
68
Q

Distinguish between healing by first and second intention

A
  1. 1st intention has smaller wounds vs 2nd intention has larger wounds/lacerations
  2. No need for contraction by myofibroblasts in 1st intention but need for 2nd intention
  3. Low angiogenesis and inflammation in 1st intention but high in 2nd intention
  4. Small/no scar vs large, deforming scar
  5. Approx 12 weeks healing vs >12 weeks healing
  6. Wound has closely apposed edges vs wound is gaping/not apposed
69
Q

Outline the timeline for healing by 1st intention

A

2 days: re-epithelialisation
6 days: formation of granulation tissue
4 weeks: mature collagenisation with good tensile strength in wound
12 weeks: complete healing and repair, with small scar formation

70
Q

Describe the healing process of a fracture

A
  1. Blood vessels supplying bone and periosteum damaged
  2. Haematoma formed at fracture site
  3. Platelets and inflammatory cells recruited to fracture site
  4. Formation of granulation tissue + angiogenesis
  5. Newly formed blood vessels allow further migration of mesenchymal stem cells
  6. Hard callus of immature bone formed
  7. Resorption by osteoclasts and new bone formation by osteoblasts
  8. Regeneration of normal bone structure
71
Q

Discuss the complications of fracture healing

A
  1. Non-union of bone
  2. Fibrous union → pseudoarthrosis (fake joint)
  3. Malunion (with angulation/ abnormal bend)
  4. Infection/osteomyelitis (esp when bone exposed during open fracture)
72
Q

Describe the levels of prevention for pathologies

A

Primary: pre-disease
- Eliminate causes/risk factors

Secondary: latent/asymptomatic
- Early detection and intervention
- Aka screening

Tertiary: symptomatic
- Limit physical and social disability due to disease
- Before progression, complications and death

Y1 (14 decks)

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