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HYMS Block 9 > Cellular Pathology > Flashcards

Cellular Pathology Flashcards

1
Q

Define the following:

  1. risk factor
  2. predisposition
  3. pathogenesis
  4. premalignant
  5. aetiology
  6. disease
  7. disease mechanism
A
  1. something, either intrinsic or extrinsic which confers an increased risk of developing disease
  2. increased susceptibility to develop disease, which is usually inherited
  3. pathological mechanisms resulting in clinical disease
  4. lesion or process that will probably transform into invasive malignancy
  5. cause of the disease
  6. consequences of a failure of homeostasis
  7. the way that homeostasis is impaired
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2
Q

H&E stain

  1. what does eosin stain? What colour?
  2. what does hematoxylin stain? What colour?
A
  1. acidic dye that stains basic structures pink/red. commonly stains cytoplasm.
  2. basic dye that stains acidic structures purple/blue. Commonly stains DNA/RNA
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3
Q
  1. Describe the 4 processes that occur during apoptosis
  2. describe the intrinsic pathway of apoptosis
  3. describe the extrinsic pathway of apoptosis
  4. what do both the intrinsic and extrinsic pathways converge on?
A
  1. cytoskeleton collapses, nuclear envelope disassembles. nuclear DNA breaks up unto fragments. Cell surface displays markers that cause the cell to be phagocytosed
  2. activated by cell stress. Mediated by mitochondria
  3. activated by extracellular ligands binding to cell surface death receptors
  4. both converge on capsases (proteases) which produce budding apoptotic bodies
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4
Q
  1. what is autophagy?
  2. what is the purpose of autophagy?
  3. what is macroautophagy?
  4. What are the implications of autophagy in disease?
A
  1. autophagocytosis/self eating. regulated mechanism
  2. disassembly of unnecessary or dysfunctional cellular components
  3. targeted cytoplasmic constituents are isolated from the rest of the cell in a double membraned vesicle (autophagosome), which fuses with lysosomes.
  4. adaptive response to stress, which can promote survival. n other cases, it appears to promote cell death and morbidity
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5
Q

Necrosis

  1. What is coagulative necrosis? When is it typically seen?
  2. What is colliquitive necrosis? When is it typically seen?
  3. What is caseating necrosis? When is it typically seen?
A
  1. formation of gelatinous subsrance in dead tissues in which the architecture of the tissue is maintained. Hypoxic environments
  2. digestion of dead cells to form a viscous liquid mass (due to release of hydrolytic enzymes from dead cells). Typical of bacterial infections and cerebral infarcts
  3. combination of coagulative and colliquitive necrosis. Caused by mycobacteria (TB) and some foreign substances
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6
Q

Complete the VITAMIN A&C mnemonic of the surgical sieve

A 
V - vascular
I - infection
T - trauma
A - autoimmune
M - metabolic
I - iatrogenic
N - neoplastic
A - acquired
C - congenital
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7
Q
  1. What is hyperplasia?
  2. What is hypertrophy?
  3. What is atrophy?
A
  1. increase in cell number
  2. increase in cell size
  3. decrease in cell size and number
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8
Q

Describe 7 mechanisms that infectious agents use that underly disease pathogenesis

A
  1. impairing capacity, mechanical interferences, competition for nutrients
  2. tissue destruction
  3. toxins
  4. virulence factors
  5. proteases
  6. deplete host immune response
  7. self damage (host immune response causes tissue damage)
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9
Q

Describe the following types of hypersensitivity reactions

A

Type 1 - IgE mediated; mast cell activation
Type 2 - IgG or IgM mediated; cause tissue cytotoxicity or modification of receptors
Type 3 - IgG immune complexes; tissue deposition; tissue damage caused by continuous complement activation
Type 4 - T cell mediated; delayed response

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10
Q

a. name 3 things that fluid homeostasis requires

b. name 2 things that can occur following changes in the above factors

A

a1. vessel wall integrity
2. blood osmolarity
3. maintenance of intravascular pressure

b1. extravasation - movement of water or blood across the vascular wall
reduction in blood fluidity > blockage

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11
Q

describe the three layers of the vessel wall

A
  1. tunica intima - consists of endothelial cells and a basement membrane
  2. tunica media - consists of muscle and connective tissue. acts to regulate the diameter of the lumen
  3. tunica adventitia - elastic and collagen fibres. contains nerves and vasa vasorum.
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12
Q
  1. describe the two forces that maintain fluid balance
  2. What is transudation?
  3. what is oedema?
  4. name 6 general causes of oedema
A
  1. HYDROSTATIC PRESSURE - drives fluid out of the tissues. higest on the arterial side
    OSMOTIC COLLOID PRESSURE - fluid absorption driven by the osmolarity of proteins in the blood. Highest on venous side
  2. movement of fluid/solute through a membrane by a hydrostatic or osmotic pressure gradient
  3. abnormal increased fluid in the interstitial space
  4. increase in vascular pressure/volume (generalised as in heart failure or localised due to DVT)
    decreases in plasma protein content (liver failure. malnutrition)
    changes in endothelial cell function
    lymphatic obstruction
    sodium retention
    inflammation (septic shock)
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13
Q
  1. what is haemorrhage?
  2. what is a consequence of blood loss >20%
  3. what can recurrent blood loss lead to?
  4. Describe the following haemorrhages:
    a) petechiae
    b) purpura
    c) eccymosis
A
  1. extravasation of blood due to vessel rupture
  2. hypovolaemic shock
  3. iron deficiency/anaemia
    4a) minute haemorrhage of the skin and mucosa. Purple/red spots. Caused by clotting deficiency
    4b) small haemorrhage due to trauma or vasculitis
    4c) bruises. Subcutaneous haematoma. Change in colour due to metabolims of Hb to billirubun and haemosiderin.
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14
Q
  1. What is thrombosis?
  2. name 3 factors that cause embolism
  3. what is a thrombus composed of?
  4. name 2 types of arterial thrombi
  5. what are the characteristics of arterial thrombi?
  6. what are the characteristics of venous thrombi?
  7. name 3 clinical consequences of thrombi
A
  1. formation of blood clot within a vessel which is attached to a vessel
  2. endothelial injury; abnormal blood flow; hyper-coagulability
  3. platelets, RBCs, trapped neutrophils and lymphocytes
  4. mural - those that do not occlude the vessel (responsible for transient clinical events)
    occlusive - those that occlude the vessel
  5. formed under high shear flow; platelet rich; occur around ruptured atheroscleroitc plaques and or/damaged endothelium
  6. driven by hypercoagulation. formed under low shear flow. fibrin and erythrocyte rich
  7. starvation of oxygen and nutrients > necrois
    occlusion of coronary vessels > mI
    occlusion of carotid arteries > stroke
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15
Q
  1. What is an embolism?
  2. what are most emboli the result of?
  3. what is the clinical significance of an embolism related to?
A
  1. a solid, liquid or gaseous mass carried in the blood to a site distant from the point of origin.
  2. dislodged thrombus
  3. related to where they lodge rather than its origin
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16
Q
  1. what is hyperaemia?
  2. is hyperaemia physiological or pathological?
  3. what is reactive hyperaemia?
  4. what is active hyperaemia?
A
  1. local increase in blood volume in tissues in response to a change in the environment
  2. physiological
  3. local vasodilation in response to O2 debt or accumulation of metabolic waste
  4. increased blood glow in response to period of activation
17
Q
  1. what is congestion?
  2. what is it caused by?
  3. what does it result in?
A
  1. impaired venous return from an affected area
  2. physical obstruction of veins or failure of heart to pump blood (siphon) away from the affected area
  3. increased venous pressure
18
Q
  1. What is circulatory shock?
  2. what is it caused by? (2)
  3. what is it associated with? (consequences)

describe the following:

  1. cardiogenic shock
  2. hypovolaemic shock
  3. septic shock
  4. neurogenic shock
  5. anaphylactic shock
A
  1. systemic hypoperfusion leading to reduced delivery of oxygen and nutrients > cellular injury and inadequate tissue function
  2. reduced cardiac output or ineffective circulation
  3. hypotension, hypoperfusion and cellular hypoxia
  4. failure of heart to pump sufficient blood
  5. loss of blood or plasma
  6. systemic infection > bacteraemia > systemic vasodilation and hypotension > vascular leakage and oedema
  7. loss of systemic stimulatuon to blood vessels by severe CNS damage leading to widespread vasodilation
  8. severe allergic reaction causes the release of inflammatory mediators which triggers widespread vasodilation and hypoperfusion
19
Q
  1. what is atherosclerosis?
  2. which vessels are usually affected?
  3. which vessel layers are usually implocated
  4. name 5 causes of enothelial damage
  5. what is an atheromatous plaque formed of (2 basic components)
  6. describe the formation of an atheromatous plaque
A
  1. hardening of the arteries due to the formation of atheromatous plaques
  2. large to medium sized arteries
  3. tunica intima
  4. LDL; smoking; hypertension; diabetic vascular changes; inflammation
  5. fibrous cap and fatty streak
  6. endothelilal damage enables LDLs to enter the vessel wall
    monocytes enter the vessel wall and break down LDL via oxidation
    monocytes engulf oxLDL leading to the accumulation of cytoplasmic lipid in monocytes
    monocytes die and become deposited under the damaged endothelium - FOAM CELLS
    monocytes, foam cells and endothelium release cytokines > further monocyte recruitment
    [fatty streak has been formed]
    fatty streak is thrombogenic - activates platelets
    PDGF is released from activated platelets, which encourages smooth muscle growth of the media
    connective tissue is secreted which forms a wall around the fatty streak - Fibrous cap
20
Q

Describe the characteristics of the following leucocytes:

  1. neutrophils
  2. eosinophils
  3. basophils
  4. monocytes
  5. NK cells
  6. mast cells
A
  1. phagocyte; multilobed nucleus; initiates inflammatory response
  2. phagocyte; protection against parasites; bilobed nucleus and red granules
  3. allergic reactions and protection against parasites; bilobed nuclues and dark granules
  4. phagocytic. Differentiate into tissue macrophages or dendritic cells. Horseshow nucleus
  5. kill virally infected cells
  6. found in tissues. Histologically similar to basophils
21
Q

define the following:

  1. microvascular change in inflammation
  2. exudate
  3. oedema
  4. pus
  5. suppuration
  6. what do exudates contain; what is the relevance of this?
A
  1. increased permeability of local blood vessels
  2. fluid rick in protein an/or cells
  3. excess fluid in extravascular space and body cavities
  4. a purulent exudate with dying leucocytes and bacteria
  5. pus forming
  6. fibrinogen; converted into a fibrin mesh which acts as a scaffold for healing and repair
22
Q
  1. describe the acute inflammatory response

2. describe the complement cascade

A
  1. pathogen binds to complement C3 > activation of complement cascade > release of histamine and chemoattractants > increased vascular permeability leads to fluid exudation > altered adhesiveness of endothelium allows for cellular migration > phagocyte recognition and destruction of C3b opsonised pathogen
  2. C3 > C3a & C3b
    C3b = opsonin; C3a is a chemoattractant
    C3b splits C5 into C5a and C5b
    C5b binds with other components to form membrane attack complex
    C3a and C5a cause mast cell degranulation
23
Q
  1. what are atachidonic acid derivatives derived from?
  2. how are prostaglandins produced by arachidonic acid?
  3. How are leukotrienes produced?
  4. what is the role of PGE2
  5. What is the role of PGF?
  6. What is the role of TXA2?
  7. describe general roles of leukotrienes
A
  1. membrane phospholipids - converted by phospholipase A2
  2. COX enzymes
  3. lipo-oxygenase pathway
  4. vasodilation
  5. vasoconstriction
  6. Vascular permeability, vasoconstriction, chemotaxis, neutrophil adhesion
24
Q

Define the following:

  1. congestion
  2. consolidation
  3. grey hepatisation
  4. resolution
  5. organisation
  6. absess
A
  1. outpouring of protein rich fluid into alveolus. Caused by bacteria
  2. entry of red cells and neutrophils into the alveolus. Fluid and cells spread into adjacent alveoli leading to solidification
  3. recruitment of macrophages, which phagocytose dead neutrophils
  4. restoration of normal tissue when architecture is intact
  5. scar formation due to loss of structural integrity
  6. accumulation of neutrophils walled off by fibrin and often surrounded by chronic inflammatory cells
25
Q
  1. name 3 mediators of inflammatory resolution
  2. how can chronic inflammation occur? (2 mechanisms)
  3. which cells are a hallmark of acute inflammation
  4. which cells are implicated in chronic inflammation
A
  1. lipoxins. resolvins. protectins.
  2. failure to initiate resolution or failure to clear stimulus
  3. neutrophils
  4. lymphocyte, plasma cells and macrophages
26
Q
  1. describe chronic suppurative inflammation
  2. what can granulomatous infection be a result of?
  3. name the 2 macrophage types in granulomatous inflammation
  4. name a parasite that can cause granulomatous inflammation
A
  1. absess. continuing stimulus to neutrophil production. Walled off by fibrous tissue
  2. agents that are difficult to cleare
  3. epithelioid cell
    langhan cell (multinucleate; nuclei arranged in horseshoe shape around periphery)
  4. schistosoma

HYMS Block 9 (9 decks)

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