Chap 1 Cell Injury & Necrosis

Question 1

hypertrophy

Answer 1

• an increase in the size of cells, no new cells
• resulting in increase in size of an organ

Question 2

hyperplasia

Answer 2

-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.

Question 3

atrophy

Answer 3

-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

Question 4

metaplasia

Answer 4

• 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

Question 5

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

Answer 5

( 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

Question 6

Atrophy can affect cell mass physiologically:
Ex:

Answer 6

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

Question 7

Involution

Answer 7

Shrinking of an organ due to age or inactivity

Question 8

Caspases

Answer 8

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

Question 9

ischaemic atrophy

Answer 9

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

Question 10

denervation atrophy

Answer 10

-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

Question 11

Ablation

Answer 11

the surgical removal of body tissue

Question 12

reduction in cell mass may be pathological:
Name pathological reasons:

Answer 12

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

Question 13

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

Answer 13

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

Question 14

PHYSIOLOGIC hyperplasia can be divided into:

Answer 14

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

Question 15

PATHOLOGIC hyperplasia is usually caused by what & provide ex:

Answer 15

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)

Question 16

neoplasia

Answer 16

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

Question 17

Ex of Metaplasia

Answer 17

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

Question 18

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

Answer 18

• Cell membranes
• Mitochondria
• Cytoskeleton
• Cellular DNA

Question 19

Primary impairment of mitochondrial energy production is due mainly to

Answer 19

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

Question 20

Mecanism of cell injury

Answer 20

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

Question 21

ATP depletion and decreased ATP synthesis causes what?

Answer 21

(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)

Question 22

Mitochondrial dammage :

Answer 22

o Decreased ATP synthesis
o Leakage of pro-apoptotic proteins

Question 23

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

Answer 23

o Increase of mitochondrial permibility
o Activation of multiple cellular enzymes

Question 24

Protein misfolding DNA damage :

Answer 24

activation of pro-apoptotic proteins

Question 25

Increase of ROS (Reactive Oxygen Species):

Answer 25

damage to lipid, proteins, DNA

Question 26

Examples of reactive oxygen metabolites :

Answer 26

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

Question 27

ischemia-reperfusion injury

Answer 27

-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.

Question 28

Hydropic
degeneration

Answer 28

-is a severe form of cloudy swelling.
-It occurs with hypokalemia due to vomiting or diarrhea.

Question 29

hypokalemia

Answer 29

deficiency of potassium in the bloodstream

Question 30

What are the reasons of Fatty change

Answer 30

• 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

Question 31

Hemosiderosis

Answer 31

• 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.

Question 32

Example of Sublethal damage
The term “hemochromatosis” is used when

Answer 32

-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

Question 33

Transferrins are what

Answer 33

-specific transport proteins that carry Iron
in cells it is stored with association with a protein (apoferritin) to form a ferritin micelles.

Question 34

What is the difference between ferritin and hemosiderin?

Answer 34

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.

Question 35

Explain Hemosiderin

Answer 35

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.

Question 36

Ferrin forms what

Answer 36

Hemosiderin granules

Question 37

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

Answer 37

load of iron

Question 38

Pneumoconiosis

Answer 38

• 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

Question 39

Lung damage occurs when: name steps

Answer 39

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.

Question 40

Provide ex of materials causing lung damage

Answer 40

1. silicates
2. iron oxid
3. coal.

Question 41

The anthracosis of the lung :

Answer 41

-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

Question 42

COALWORKERS PNEUMOCONIOSIS is diagnosed by:

Answer 42

-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

Question 43

Coalworkers pneumoconiosis can lead to

Answer 43

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

Question 44

Silicosis

Answer 44

-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

Question 45

What is a common complication of silicosis:
Increases the risk of what?

Answer 45

-Development of tuberculosis
- It increases the risk of lung carcinoma.

Question 46

Asbestosis
Name 2 forms:

Answer 46

-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

Question 47

Name 2 forms of Asbestosis

Answer 47

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

Question 48

Farmer’s lung
ex:

Answer 48

-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.

Question 49

thermophilic actinomycetes

Answer 49

-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

Question 50

What is an example of Hypersensitivity pneumonitis

Answer 50

( 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.

Question 51

Hypersensitivity pneumonitis

Answer 51

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

Question 52

what causes Pathologic calcification:
Name two forms of Pathologic Calcification:

Answer 52

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

Question 53

1. Dystrophic calcification

Answer 53

-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.

Question 54

leiomyomas

Answer 54

-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.

Question 55

too much of PO4 (phosphate) can cause

Answer 55

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

Question 56

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

Answer 56

Dystrophic calcification

Question 57

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

Answer 57

-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

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

Question 58

dystrophic calcification can be found where?

Answer 58

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

Question 59

atheromas

Answer 59

-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.

Question 60

dystrophic calcification can be observed microscopically as :

Answer 60

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

Question 61

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

Answer 61

It may occur in normal tissue whenever there is hypercalcemia

Question 62

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

Answer 62

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)

Question 63

Metastatic calcification mainly affects tissues of what type of organs?

Answer 63

• 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.

Question 64

Apoptosis=

Answer 64

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.

Question 65

Oncosis =

Answer 65

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.

Question 66

Apoptosis is responsible for numerous :

Answer 66

Physiologic, adaptive events
&
Pathologic events

Question 67

Describe Physiologic: adaptive events of apoptosis

Answer 67

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

Question 68

Describe Pathologic events :

Answer 68

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)

Question 69

How does Apoptosis happens ?

Answer 69

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)

Question 70

What are the different phases of Apoptosis:

Answer 70

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

Question 71

describe First phase- priming of apoptosis

Answer 71

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

Question 72

describe Second phase- cell executioner pathway of apoptosis

Answer 72

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

Question 73

describe Third phase- degradation: of apoptosis

Answer 73

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.

Question 74

describe Fourth phase- phagocytosis: of apoptosis

Answer 74

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

Question 75

Necrosis

Answer 75

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

Question 76

What are the cellular events in Necrosis ?

Answer 76

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.

Question 77

pyknosis

Answer 77

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

Question 78

karyorrhesis

Answer 78

pyknotic nuclei become fragmented into several particles

Question 79

Ex’s of Necrosis

Answer 79

1. Coagulative necrosis
   2.Colliquative Necrosis
   3.Caseosus Necrosis
2. Fat Necrosis

Question 80

Coagulative necrosis

Answer 80

-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.

Question 81

Colliquative Necrosis

Answer 81

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.

Question 82

Caseosus Necrosis

Answer 82

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.

Question 83

Fat Necrosis

Answer 83

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.

Question 84

Acute Myocardial Infarction

Answer 84

myocardial necrosis resulting from acute obstruction of a coronary artery

Question 85

Provide 2 examples of Acute myocardial Infarction

Answer 85

1. Regional myocardial infarction
   2.Circumferential subendocardial infarction

Question 86

Explain: Regional myocardial infarction

Answer 86

(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

Question 87

atheromatosus plaque

Answer 87

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.

Question 88

subendocardial zone

Answer 88

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

Question 89

Explain: Subendocardial infarction

Answer 89

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)

Question 90

Appearance of myocardial infarct involves 5 ackinoledgements

Answer 90

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

Question 91

Between 0-12 hours : MCI appearance

Answer 91

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

Question 92

Between 12 and 24 hours : MCI appearance

Answer 92

• The infarcted area is macroscopically pale
• Histologically infarcted muscle is brightly eosinophilic with intercellular oedema

Question 93

Between 24 and 72 hours : MCI appearance

Answer 93

• 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

Question 94

Between 3 and 10 days : MCI appearance

Answer 94

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

Question 95

After weeks or month : MCI appearance

Answer 95

• the infarct is replaced by collagenous scar

Question 96

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

Answer 96

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.

Question 97

What are some Complications of myocardial infarction:

Answer 97

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

Question 98

oedematous

Answer 98

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

Question 99

Acute pancreatitis:

Answer 99

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,

Question 100

Acinar cells:

Answer 100

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

Question 101

What enzymes do acinar cells secrete?

Answer 101

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).

Question 102

What organs are in the retroperitoneal?

Answer 102

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.

Question 103

Describe Acute pancreatitis

Answer 103

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

Question 104

Predisposing factors due to acute pancreatitis:

Answer 104

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)

Question 105

Necrosis of the brain is know as What?
Describe:

Answer 105

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.

Question 106

What causes encephalomalacia

Answer 106

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)

Question 107

Morphology of encephalomalacia

Answer 107

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

Question 108

Microscopic examination of encephalomalacia

Answer 108

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

Question 109

Gangrenous necrosis

Answer 109

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).

Question 110

Fibrinoïd necrosis

Answer 110

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.

Question 111

Muscle hypertrophy:
(myofibrillar hypertrophy)

Answer 111

• 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.

Question 112

sarcoplasmic hypertrophy

Answer 112

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 …

Question 113

Trophic hormone

Answer 113

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

Question 114

Neoplasia

Answer 114

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

Question 115

Secondary Lysosomes

Answer 115

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