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(MUL) Pathomorphology > Chap 1 Cell Injury & Necrosis > Flashcards

Chap 1 Cell Injury & Necrosis Flashcards

1
Q

hypertrophy

A
  • an increase in the size of cells, no new cells

- resulting in increase in size of an organ

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2
Q

hyperplasia

A

-an increase in their number of cells or tissue, usually resulting in increased mass of the organ or tissue. -

  • Hyperplasia takes place if the cell population is capable of dividing, and thus increasing the number of cells.
  • Hyperplasia can be physiologic or pathologic.
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3
Q

atrophy

A

-decrease in the size and metabolic activity of cells
Reduced functional demand, reduction in trophic stimuli, or reduction in nutrients are the usual stimuli which cause involution or cell atrophy
-atrophy is also accompanied by increased autophagy ( self eating)
-structural proteins and organelles of a cell are destroyed

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4
Q

metaplasia

A
  • a change in the phenotype of cells
  • Metaplasia is a reversible change in which one differentiated cell type (epithelial or mesenchymal) is replaced by another cell type.
  • note: Metaplasia is NOT a normal physiologic process and may be the first step toward neoplasia
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5
Q

In many tissues that have undergone cellular atrophy, a brown pigment is formed called?

A

( Lipofuscin )

  • which accumulates in a shrunken cells
  • This pigment composed of a degenerate lipid material in secondary lysosomes is produced by breakdown of the cell membranes and organelles through autophagy
  • lipofuscin in the atrophic myocardial fibres of eldery people
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6
Q

Atrophy can affect cell mass physiologically:

Ex:

A
  1. Thymus gland
  2. Myometrium ( smooth muscle tissue of the uterus)
  3. skeletal muscle fibres decrease in size
  4. parathyroid gland, hormone-secreting cells diminish in number
  5. The testis undergoes atrophy as a result of reduced gonadotrophic stimulation
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7
Q

Involution

A

Shrinking of an organ due to age or inactivity

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8
Q

Caspases

A

family of protease enzymes playing essential roles in programmed cell death (including apoptosis, pyroptosis and necroptosis) and inflammation.

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9
Q

ischaemic atrophy

A

restriction in blood supply to tissues, causing a shortage of oxygen that is needed for cellular metabolism (to keep tissue alive

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10
Q

denervation atrophy

A
  • Loss of innervation : damage of axons supplying muscle causes atrophy of affected muscle fibres
  • Diseases that affect the lower motor neuron at any point cause myofiber atrophy. The motor neuron exerts a trophic influence on muscle. This influence is mediated by induced contractions and by chemical substances (trophic factors) released at the synapse, which influence protein synthesis in muscle
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11
Q

Ablation

A

the surgical removal of body tissue

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12
Q

reduction in cell mass may be pathological:

Name pathological reasons:

A
  1. decreased work load
  2. lack or diminished blood supply
  3. Loss of innervation
  4. loss of endocrine stimulation
  5. inadequate nutrition
  6. tissue compression = pressure
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13
Q

hypertrophy can be caused by several factors
name the factors:
ex:

A

Can be Physiologic or Pathologic
caused by increased functional demand or by stimulation by hormones and growth factors.
ex: Cardiac hypertrophy

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14
Q

PHYSIOLOGIC hyperplasia can be divided into:

A
  1. Hormonal hyperplasia-increases the functional capacity of a tissue when needed
    ex: female breast & prominent folds of endometrium
  2. Compensatory hyperplasia- which increases tissue mass after damage or partial resection
    ex: regeneration of the liver
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15
Q

PATHOLOGIC hyperplasia is usually caused by what & provide ex:

A

Caused by: excesses of hormones or growth factors acting on target cells
ex: Abnormal endometrial hyperplasia (hormonal deregulation : estrogen)
: Prostatic hyperplasia (The pattern of increase is not uniform, but nodular)

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16
Q

neoplasia

A

the formation or presence of a new, abnormal growth of tissue

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17
Q

Ex of Metaplasia

A
  1. Metaplasia of laryngeal respiratory epithelium in smoker’s lungs. The chronic irritation has led to an exchanging of one type of epithelium (the normal columnar respiratory epithelium) for another (the more resilient squamous epithelium)
  2. Barrett esophagus : the esophageal squamous epithelium is replaced by intestinal-like columnar cells under the influence of refluxed gastric acid
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18
Q

Cell injury results from different biochemical mechanisms acting on several essential cellular components-
Name cellular components that are most frequently damaged by injurious stimuli :

A
  • Cell membranes
  • Mitochondria
  • Cytoskeleton
  • Cellular DNA
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19
Q

Primary impairment of mitochondrial energy production is due mainly to

A

lack of oxygen and glucose, but may also be caused by toxins (cyanide).

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20
Q

Mecanism of cell injury

A
  1. ATP depletion and decreased ATP synthesis
  2. Mitochondrial dammage
  3. Entry of Ca2+ (because of a loss of ATP-dependant calcium pumps which remove the calcium outside the cell)
  4. Protein mis-folding DNA damage : activation of pro-apoptotic proteins
  5. increase of ROS : damage to lipid, proteins, DNA
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21
Q

ATP depletion and decreased ATP synthesis causes what?

A

(leads to reduction of the activity of the sodium pump (Na+/K+ ATPase) which is accompanied by an ismotic gain of water and so a swelling of the cell)

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22
Q

Mitochondrial dammage :

A

o Decreased ATP synthesis

o Leakage of pro-apoptotic proteins

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23
Q

Entry of Ca2+ (because of a loss of ATP-dependant calcium pumps which remove the calcium outside the cell) :

A

o Increase of mitochondrial permibility

o Activation of multiple cellular enzymes

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24
Q

Protein misfolding DNA damage :

A

activation of pro-apoptotic proteins

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25
Q

Increase of ROS (Reactive Oxygen Species):

A

damage to lipid, proteins, DNA

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26
Q

Examples of reactive oxygen metabolites :

A 
o Free iron
o Xanthine, which accumulates in hypoxic tissues as a metabolite of ATP. In hypoxic conditions, accumulated xantine can be oxydized by the enzyme xantine oxidase
o Redox Reactions o Irradiation
o Neutrophils
o Drugs, toxin
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27
Q

ischemia-reperfusion injury

A
  • Ischemic injury occurs when the blood supply to an area of tissue is cut off.
  • The incidence of ischemic injury is vast: myocardial infarction, stroke, and other thrombotic events
  • Ischemic injury also occurs during surgery when blood vessels are cross-clamped, and in organs for transplant.
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28
Q

Hydropic

degeneration

A
  • is a severe form of cloudy swelling.

- It occurs with hypokalemia due to vomiting or diarrhea.

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29
Q

hypokalemia

A

deficiency of potassium in the bloodstream

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30
Q

What are the reasons of Fatty change

A

• Increased peripherial mobilization of free fatty acids and uptake into cells : diabetes mellitus or nutritional deprivation
• Increased convertion of fatty acids to triglicerydes : alcohol
• Reduced oxidation of triglicerides to acetyl-CoA : hypoxia ant toxins including ethanol
• Deficiency of lipid acceptor proteins, preventing export or formed triglicerides : carbon tetrachloride and
protein malnutrition

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31
Q

Hemosiderosis

A
  • is a form of iron overload disorder resulting in the accumulation of hemosiderin.
    Types include: Transfusion hemosiderosis. Idiopathic pulmonary hemosiderosis.
    “hemosiderosis” is used to denote a relatively benign accumulation of iron.
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32
Q

Example of Sublethal damage

The term “hemochromatosis” is used when

A
  • organ dysfunction occurs.
  • Hemochromatosis is a hereditary disorder that causes the body to absorb too much iron, causing iron to build up in the body and damage organs
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33
Q

Transferrins are what

A

-specific transport proteins that carry Iron

in cells it is stored with association with a protein (apoferritin) to form a ferritin micelles.

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34
Q

What is the difference between ferritin and hemosiderin?

A

Iron is stored, mostly in the liver, as ferritin or hemosiderin. Ferritin is a protein with a capacity of about 4500 iron (III) ions per protein molecule. This is the major form of iron storage. … As the body burden of iron increases beyond normal levels, excess hemosiderin is deposited in the liver and heart.

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35
Q

Explain Hemosiderin

A

Hemosiderin is a hemoglobin- derived, yellow to brown granular or crystaline pigment.
This pigment is lying within the cells cytoplasm and is easily seen with a light microscope.

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36
Q

Ferrin forms what

A

Hemosiderin granules

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37
Q

Transfusion ; transfused red cells constitute an exogenous LOAD OF WHAT ?

A

load of iron

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38
Q

Pneumoconiosis

A
  • a disease of the lungs caused by the habitual inhalation of irritants (as mineral or metallic particles)
  • called also miner’s asthma, miner’s consumption, pneumonoconiosis-caused by inhalation of dust
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39
Q

Lung damage occurs when: name steps

A
  1. the dust interacts with defence mechanisms in the lung.
  2. If dust is toxic to macrophages
  3. there is local inflammation,
  4. secretion of cytokines
  5. stimulation of fibrosis.
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40
Q

Provide ex of materials causing lung damage

A
  1. silicates
  2. iron oxid
  3. coal.
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41
Q

The anthracosis of the lung :

A
  • The black streaks seen between lobules of lung beneath the pleural surface are due to accumulation of anthracotic pigment.
  • accumulation of carbon pigment from breathing dirty air
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42
Q

COALWORKERS PNEUMOCONIOSIS is diagnosed by:

A

-is diagnosed by the presenc of small nodules, in the lung fields on chest radiograph
• The pattern of disease is not associated with any clinically significant impairment of respiratory
function
• Histologically there is:
• Acumulation of anthrosilicotic dust in macrophages at the center of acinus
• Emphysema of local dust type

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43
Q

Coalworkers pneumoconiosis can lead to

A

progressive massive fibrosis (PMF) :
• This disease is characterized by large nodules in the lungs, greater than 10 mm in diameter, they are most
common in the upper lobes. They become so extensive as to occupy 30% of the lung fields
• The nodules are usually surrounding irregular emphysema

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44
Q

Silicosis

A

-caused by inhalation of silicon dioxide (quartz).
-occupational exposure: slate mining, metal foundaries, stone masonry, tunneling, granite quarying, coal mining through granit rocks.
 Short heavy doses produce acute silicosis with pulmonary oedema and alveolar exudation.
 Prolonged exposure leads to formation of multiple fibrous nodules composed with collagen

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45
Q

What is a common complication of silicosis:

Increases the risk of what?

A
  • Development of tuberculosis

- It increases the risk of lung carcinoma.

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46
Q

Asbestosis

Name 2 forms:

A
  • caused by heavy exposure to asbestos,
  • usually with a latent period of 25 years before clinical symptoms become evident.
  • Fibres longer then 8 μm are very pathogenic
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47
Q

Name 2 forms of Asbestosis

A
  1. Serpentine asbestos (including white asbestos) : most common form, the fibres persist in lung for a
    limited time
  2. Amphibole asbestos (including blue and brown asbestos) : main cause of malignant mesothelioma
48
Q

Farmer’s lung

ex:

A
  • One form of (hypersensitivity pneumonitis) is known as farmer’s lung because the farmer inhales thermophilic actinomycetes in moldy hay that set off the reaction.
  • Bird dust (bird fancier’s disease) and molds in air conditioners may produce similar problems.
49
Q

thermophilic actinomycetes

A
  • are ubiquitous organisms usually found in contaminated ventilation systems and in decaying compost, hay, and sugar cane (bagasse).
  • Exposure to large quantities of contaminated hay is the most common source of inhalational exposure for farmers who develop farmer’s lung
50
Q

What is an example of Hypersensitivity pneumonitis

A 
( farmer's lung ) because the farmer inhales thermophilic actinomycetes in moldy hay that set off the reaction.
Bird dust (bird fancier's disease) and molds in air conditioners may produce similar problems.
51
Q

Hypersensitivity pneumonitis

A
  • is a disease of the lungs in which your lungs become inflamed as an allergic reaction to inhaled dust, fungus, molds or chemicals
52
Q

what causes Pathologic calcification:

Name two forms of Pathologic Calcification:

A

It is due to an abnormal deposition of calcium salts, together with small amounts of iron, magnesium and other mineral salts.
There are two forms of pathologic calcification:
1. Dystrophic calcification
2. Metastatic calcification

53
Q
  1. Dystrophic calcification
A
  • Dystrophic calcification (DC) is the calcification occurring in degenerated or necrotic tissue, as in hyalinized scars, degenerated foci in leiomyomas, and caseous nodules.
  • This occurs as a reaction to tissue damage, including as a consequence of medical device implantation.
54
Q

leiomyomas

A
  • A leiomyoma, also known as fibroids
  • is a benign smooth muscle tumor that very rarely becomes cancer (0.1%).
  • They can occur in any organ, but the most common forms occur in the uterus, small bowel, and the esophagus.
55
Q

too much of PO4 (phosphate) can cause

A

Too much phosphate can cause health problems, such as kidney damage and osteoporosis.

56
Q

the formation of crystalline calcium phosphate minerals causes what type of calcification?

A

Dystrophic calcification

57
Q

Dystrophic calcification happens through the formation of _____ _____ ______ _____. The process has two phases :

A

-crystalline calcium phosphate mineral
-the process has two phases :
1. Inhitiation :
a. Intracellular initiation : occurs in mitochondria of dead or dying cells
b. Extracellular initiation : include phospholipids found in membrane vesicles which are derived from
degenerating or ageing cells

  1. Propagation
    Propagation of crystal formation depends of the concentration of Ca +2 and PO 4 and the presence of inhibitors
58
Q

dystrophic calcification can be found where?

A

In areas of necrosis, whether they are of coagulative, caseous or liquefactive type and in foci of enzymatic
necrosis of fat
• In atheromas of advanced atherosclerosis
• In ageing or damaged heart valves

59
Q

atheromas

A
  • atheromatous plaque (“plaque”), is an abnormal accumulation of material in the inner layer of the wall of an artery
  • it is present in the arteries of most adults.
  • The material consists of mostly macrophage cells, or debris, containing lipids, calcium and a variable amount of fibrous connective tissue.
60
Q

dystrophic calcification can be observed microscopically as :

A

Macroscopically, we can observe white granules or clumps, offen felt as gritty deposites. Sometimes, tuberculous lymph node is virtually converted to stone through calcification.

61
Q

Metastatic calcification occurs in what type of tissue in presence of what ?

A

It may occur in normal tissue whenever there is hypercalcemia

62
Q

Metastatic calcification, may occur in normal tissue whenever there is hypercalcemia as well as: name 4 situations

A
  1. Increased secretion of parathyroid hormone (parathyroid tumors or ectopic secretion of PTH)
  2. Destruction of bone tissue (primary tumors or metastasis, immobilization)
  3. Vitamine D related disorders
  4. Renal failure (retention of phosphate leading to secondary hyperparathyroidism)
63
Q

Metastatic calcification mainly affects tissues of what type of organs?

A
  • It mainly affects the interstitial tissues of the gastric mucosa, kidneys, lungs, systemic arteries, pulmonary veins
  • All of these tissues lose acid and therefore have an internal alkaline compartment that predisposes them to metastatic calcification.
64
Q

Apoptosis=

A

It is a programed and energy depend process designed specyficaly to switch cells off and eliminate them and it is very different from that witch occurs as a direct result of a damaging stimulus to cell.

65
Q

Oncosis =

A

prelethal changes preceding necrotic cell death, they are characterized by cell swelling and can be distinguished from the prelethal changes in apoptosis, associated largely with cell shrinkage.

66
Q

Apoptosis is responsible for numerous :

A

Physiologic, adaptive events
&
Pathologic events

67
Q

Describe Physiologic: adaptive events of apoptosis

A
  1. The programmed destruction of cells during embryogenesis
  2. Hormone- dependent involution in the adult
  3. Cell deletion in proliferating cell population
68
Q

Describe Pathologic events :

A
  1. Cell death in tumor
  2. Death of neutrophils
  3. Cell death inducted by cytotoxic T-cells
  4. Pathologic atrophy in parenchymal organs after duct obstruction
  5. Cell injury in certain viral diseases
  6. Cell death produced by a variety of injurious stimuli- which are given in low doses- large dose of
    the same stimuli result in necrotic cell death (heat, radiation, cytotoxic anticancer drugs, hypoxia)
69
Q

How does Apoptosis happens ?

A

It is an energy dependent cascade of molecular events depending on signaling pathways (transmembrane signals may be negative or positive determinants of apoptosis) and a control/integration state (specific proteins that connect death signals to the execution program).
There are two ways :

  1. Direct transmission of signals by specific adapter proteins (Fas-Fas ligand model)
  2. Regulating mitochondrial functions (Bcl-2 family of proteins)
70
Q

What are the different phases of Apoptosis:

A

First phase- priming
Second phase- cell executioner pathway:
Third phase- degradation:
Fourth phase- phagocytosis:

71
Q

describe First phase- priming of apoptosis

A

First phase- priming
• Normall cells are aranged in close contact with each other and are united by cell junctions
• There is syntesis of enzymes needed to cause cell dissolution, not associated with structural changes
• In development many cells are primed for apoptosis and survive only if rescuded by a specific trophic
factor

72
Q

describe Second phase- cell executioner pathway of apoptosis

A

Second phase- cell executioner pathway:
• Apoptotic cells lose surface specializations and junctions, shrinking in size, nuclear chromatin condenses, but cell organels remain normal
• Endonuclease enzymes cleave chromosomes into individual nucleosome fragments

73
Q

describe Third phase- degradation: of apoptosis

A

Third phase- degradation:
• Splinting off the cell into several fragments = apoptotic bodies
• Occurs nuclear fragmentation
• Each fragment contains viable mitochondria and intact organelles
This phase takes a few minutes. Caspases (specyfic proteases) are the main enzymes in this process.

74
Q

describe Fourth phase- phagocytosis: of apoptosis

A

Fourth phase- phagocytosis:
• Apoptotic fragments are recognized by adjacent cells, which ingest them by phagocytosis for destruction
• Some fragments degenerate extracellulary, while others are ingested by local phagocytic cells

75
Q

Necrosis

A

Necrosis is caused by factors external to the cell or tissue, such as infection, toxins, or trauma which result in the unregulated digestion of cell components

76
Q

What are the cellular events in Necrosis ?

A
  1. Many of the changes seen in necrosis are caused by the action of lysosomal hydrolases, which are released into the cell when cell membrane integrity is lost.
  2. Intense eosinophilia of the dead cell is due to loss of RNA and coagulation of proteins.
  3. The nucleus of necrotic cell first become small, condensed, and intensely stained with
    haematoxylin. This appearance is termed pyknosis.
  4. Next, pyknotic nuclei become fragmented into several particles, a change known as karyorrhesis. Complete breakdown or karyolysis of the nucleus then takes place.
77
Q

pyknosis

A

karyopyknosis, is the irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis

78
Q

karyorrhesis

A

pyknotic nuclei become fragmented into several particles

79
Q

Ex’s of Necrosis

A
  1. Coagulative necrosis
  2. Colliquative Necrosis
  3. Caseosus Necrosis
  4. Fat Necrosis
80
Q

Coagulative necrosis

A
  • Gross Appearance: characterised by dead tissue that appears firm and pale, as if cooked.
  • Microscopic: Preserved cell outlines without nucleiI areas of coagulative necrosis, much of the cellular outline and tissue architecture can still be discerned histologically, even though the cells are dead (cells have relatively few lysosomes to bring about complete breakdown of cellular proteins).
  • The most common cause of this pattern of necrosis is occlussion of the arterial suply to a tissue. Proteins liberated from dead cell can enter the blood.
81
Q

Colliquative Necrosis

A

Colliquative Necrosis
- Dead tissue appears semi-liquid as a result of dissolution of tissue by the action of hydrolytic enzymes.
-The most common types of damage leading to the liquefactive pattern are necrosis of the brain because of arterial occlusion, and necrosis caused by bacterial infections.
In brain the huge lysosomal content in neurons, together in the relative lack of extracellular proteins leads to rapid loss of tissue architecture and activating lysosomal enzymes. In bacterial infection, mico-organisms attract neutrophils into the area, which then release neutrophil hydrolases.

82
Q

Caseosus Necrosis

A

Caseosus Necrosis

  • Dead tissue is soft and white, resembling creme cheese.
  • Dead cells form an amorphus proteinaceous mass, but in contrast to coagulative necrosis, no original architecture can be seen histologically. This pattern is associated with tuberculosis.
83
Q

Fat Necrosis

A

Fat Necrosis
Foci of hard, yellow material seen in dead adipose tissue. The reaction can occur after liberation of pancreatic enzymes into the peritoneal cavity, following inflammation of the pancreas. It may also be seen after trauma to fat, for example in the breast.

84
Q

Acute Myocardial Infarction

A

myocardial necrosis resulting from acute obstruction of a coronary artery

85
Q

Provide 2 examples of Acute myocardial Infarction

A
  1. Regional myocardial infarction

2. Circumferential subendocardial infarction

86
Q

Explain: Regional myocardial infarction

A

(90% of cases) involves one segment of ventricular wall

1) Cause : thrombus formation on a complicated atheromatosus plaque
2) If the occlusion is complete : the infarct is full thicknes ;
3) if there is lysis of the thrombus or a collateral supply to the myocardium : the infarct will be limited to the subendocardial zone

87
Q

atheromatosus plaque

A

An atheroma, or atheromatous plaque (“plaque”), is an abnormal accumulation of material in the inner layer of the wall of an artery; it is present in the arteries of most adults. The material consists of mostly macrophage cells, or debris, containing lipids, calcium and a variable amount of fibrous connective tissue.

88
Q

subendocardial zone

A

situated or occurring beneath the endocardium or between the endocardium and myocardium

89
Q

Explain: Subendocardial infarction

A

Circumferential subendocardial infarction (10% of cases) involves the subendocardial zone of the ventricule
1. Cause : hypoperfusion of the main coronary arteries (high grade atherosclerotic stenoses)

90
Q

Appearance of myocardial infarct involves 5 ackinoledgements

A
  1. Between 0-12 hours :
  2. Between 12 and 24 hours :
  3. Between 24 and 72 hours :
  4. Between 3 and 10 days :
    5 .After weeks or month : the infarct is replaced by collagenous scar
91
Q

Between 0-12 hours : MCI appearance

A
  • An infarct is not macroscopically visible (the infarcted area appears uncoloured)
  • The ischaemic muscle can be detected by showing loss of oxidative enzymes (NBT)
92
Q

Between 12 and 24 hours : MCI appearance

A
  • The infarcted area is macroscopically pale

* Histologically infarcted muscle is brightly eosinophilic with intercellular oedema

93
Q

Between 24 and 72 hours : MCI appearance

A

• The infarcted area excites in acute inflammatory response : macro- soft and pale with a slight
yellow colour
• Histologically neutrophils infiltrate between dead cardiac muscule fibres

94
Q

Between 3 and 10 days : MCI appearance

A

• We have an organisation of the infarcted area : macro- hyperaemic border developes around the
yellow dead muscule
• Histologically : vascular granulation tissue

95
Q

After weeks or month : MCI appearance

A
  • the infarct is replaced by collagenous scar
96
Q

The earliest change histologically seen with acute myocardial infarction in how many days & explain

A

The earliest change histologically seen with acute myocardial infarction in the first day is contraction band necrosis. The myocardial fibers are beginning to lose cross striations and the nuclei are not clearly visible in most of the cells seen here. Many irregular darker pink wavy contraction bands are extending across the fibers.

97
Q

What are some Complications of myocardial infarction:

A
  1. Cardiac arrhythias (75 – 95% of complicated cases)
  2. Left ventricular congestive failure (60%)
  3. Pulmonary oedema (60%)
  4. Cardiogenic shock (10-15%)
  5. Rupture of free wall, septum, or papillary muscle (1 – 5%)
  6. Thromboembolism
  7. Aneurysms of the heart
  8. Epicarditis
  9. Death of the patient
98
Q

oedematous

A
  • characterized by an excessive accumulation of serous fluid in the intercellular spaces of tissue.
99
Q

Acute pancreatitis:

A

The first type of necrosis is autodigestive in nature and is typical of the most common forms of acute pancreatitis,

Associated with:
alcohol,
bile duct disease,
metabolic conditions,

100
Q

Acinar cells:

A

Are the exocrine (exo=outward) cells of the pancreas that produce and transport enzymes that are passed into the duodenum where they assist in the digestion of food. Islets of Langerhans

101
Q

What enzymes do acinar cells secrete?

A

Pancreatic Secretion:

  • There are two types of exocrine secretions produced by the pancreas.
  • Acinar cells produce digestive enzymes: amylase, lipase, and peptidases.
  • Pancreatic peptidases: are produced as inactive zymogens that are only activated after they reach the duodenum (see webpage on Zymogens).
102
Q

What organs are in the retroperitoneal?

A 
Abdominopelvic organs are retroperitoneal 
"SAD PUCKER"
S = Suprarenal (adrenal) glands.
A = Aorta/Inferior Vena Cava.
D = Duodenum (second and third segments)
P = Pancreas.
U = Ureters.
C = Colon (ascending and descending only)
K = Kidneys.
E = Esophagus.
103
Q

Describe Acute pancreatitis

A
  1. In acute pancreatitis the pancreas appears oedematous and is commonly haemorrhage
  2. Pancreatic tissue becomes necrotic and sometimes semi- liquid
  3. Lipase realised from the pancreatic acini causes the development of foci of fat necrosis (white spots in
    mesenteric and retroperitoneal fat) with adjacent retroperitoneal inflammation
104
Q

Predisposing factors due to acute pancreatitis:

A
  1. Mechanical obstruction of pancreatic ducts (gallstones, trauma, post-operative)
  2. Metabolic, toxic causes (alcohol, drugs, hypercalcemia, hyperlipoproteinaemia)
  3. Vascular : poor perfusion (atherosclerosis, hypothermia)
  4. Infections (mumps)
105
Q

Necrosis of the brain is know as What?

Describe:

A

Encephalomalacia:

  • “Stoke” is the clinical term thar refers to the sudden development of a neurologic deficit caused by abnormalities of the blood supply.
  • The clinical manifestation is up to the localization, size and shape of the necrotic changes within the brain.
106
Q

What causes encephalomalacia

A
  1. Not sufficient blood supply is caused by thrombosis or embolisation of brain arteries
  2. Atherosclerosis is responsible for the most cases of encephalomalacia (stenosis af the arteries)
107
Q

Morphology of encephalomalacia

A

Morphology :
1. 6 – 48 hours : the tissue is pale, swollen, soft and the corticomedullary junction becomes indistinct
2. 2 – 10 days : brain becomes gelatinous and friable, the border between necrotic and healthy tissue is more
distinct; oedema in the adjacent tissue is resolved
3. 10 days – 3 weeks : the tissue liquefies and eventually is removed, leaving a fluid – filled cavity lined by
dark grey tissue

108
Q

Microscopic examination of encephalomalacia

A

Microscopic examination :

  1. After 12 hours ishemic neuronal changes and oedema predominate
  2. Endothelial and glial cells swell and myelinated fibers begin to disintegrate
  3. Activation of microglial cells, histiocytes and macrophages from circulation come near the necrotic place
  4. The basic cells that take part in ”cleaning” process are astrocytes
  5. After several months we can see a cavity with astrocytes at the cavity wall
109
Q

Gangrenous necrosis

A

Gangrenous necrosis is not a specific pattern of cell death, but the term is commonly used in clinical practice.

  • t is usually applied to a limb, generally the lower leg, that has lost its blood supply and has undergone necrosis (typically coagulative necrosis) involving multiple tissue planes.
  • When bacterial infection is superimposed there is more liquefactive necrosis because of the actions of degradative enzymes in the bacteria and the attracted leukocytes (giving rise to so-called wet gangrene).
110
Q

Fibrinoïd necrosis

A

Fibrinoid necrosis is a special form of necrosis usually seen in immune reactions involving blood vessels.

  • This pattern of necrosis typically occurs when complexes of antigens and antibodies are deposited in the walls of arteries.
  • Deposits of these “immune complexes,” together with fibrin that has leaked out of vessels, result in a bright pink and amorphous appearance in H&E stains, called “fibrinoid” (fibrin-like) by pathologists.
111
Q

Muscle hypertrophy:

myofibrillar hypertrophy

A
  • involves an increase in size of skeletal muscle through a growth in size of its component cells.
  • actin and myosin contractile proteins increase in number and add to muscular strength
  • Two factors contribute to hypertrophy:
    1. sarcoplasmic hypertrophy, which focuses more on increased muscle glycogen storage
    2. myofibrillar hypertrophy, which focuses more on increased myofibril size.
112
Q

sarcoplasmic hypertrophy

A

sarcoplasmic hypertrophy, the volume of sarcoplasmic fluid in the muscle cell increases with no accompanying increase in muscular strength

-NOTE: whereas during myofibrillar hypertrophy, actin and myosin contractile proteins increase in number and add to muscular strength as well as a …

113
Q

Trophic hormone

A

Trophic hormone is a hormone that has a growth effect, hyperplasia or hypertrophy, on the tissue it is stimulating

114
Q

Neoplasia

A

the formation or presence of a new, abnormal growth of tissue

115
Q

Secondary Lysosomes

A

Compared to primary lysosomes, secondary are larger in size and capable of releasing their content (enzymes) outside the cells where they degrade foreign material.

(MUL) Pathomorphology (57 decks)

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