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RUSVM Path I > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Define acute cell swelling

A

Early, sub-lethal manifestation of cell damage, characterized by increase cell size and volume due to water overload.

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2
Q

Etiology of acute cell swelling

A

-Loss of ionic and fluid homeostasis -Failure of cell energy production -Cell membrane damage -Injury to enzymes regulating ion channels of membranes

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3
Q

Describe the gross appearance of acute cell swelling

A

-Slightly swollen organ with round edges -Pallor when compared to normal -Cut surface: tissue bulges and cannot be easily put in correct apposition

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4
Q

What is this image showing ?

A

Cellular swelling

  • Water uptake dilutes the cytoplasm
  • Cells are enlarged with pale cytoplasm
  • May show increased cytoplasmic eosinophilia
  • Nucleus in normal position, with no morphological changes
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5
Q

Etiology of the image?

A

Swinepox virus

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6
Q

What are the ultrastructural changes of cellular swelling

A
  1. Plasma membrane alterations: blebbing, blunting, and loss of microvilli
  2. Mitochondrial changes: including swelling and the appearance of small amorphous densities
  3. Dilation of ER: with detachment of polysomes, intracytoplasmic myelin figures may be present
  4. Nuclear alterations: with disaggregation of granular and fibtillary elements
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7
Q

Define Fatty change

A
  • sub-lethal cell damage characterized by intracytoplasmic fatty vacuolation
  • May be preceded or accompanied by cell swelling
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8
Q

What is lipidosis

A
  • accumultation of triglycerides and other lipid metabolites within parenchymal cells
  • Heart muscle, skeletal muscle, kidney, liver
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9
Q

What is the etiology of fatty change

A

Main causes: hypoxia, toxicity, metabolic disorders

-Seen in abnormalities of synthesis, utilization and/or mobilization of fat

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10
Q

Pathogenesis of fatty liver

A
  1. Excessive delivery of FFA from fat stores or diet.
  2. Decreased oxidation or use of FFAs
  3. Impaired synthesis of apoprotein
  4. Impaired combination of protein and triglycerides to form lipoproteins
  5. Impaired release of lipoproteins from hepatocytes
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11
Q

Describe the gross appearance of fatty change

A
  • Liver: diffuse yellow (if cells are affected)
  • Enhanced reticular pattern if specific zones of hepatocytes are affected
  • Edges are rounded & will bulge on section
  • Tissue is soft, often friable, cuts easily and has a greasy texture
  • If condition is severe small liver sections may float in fixative or water
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12
Q

What is the image showing? describe it

A

Histologic appearance of fatty change

  • Well delineated, lipid-filled vacuoles in the cytoplasm
  • Vacuoles are single to multiple, either small or large
  • Vacuoles may displace the cell nucleus to the periphery
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13
Q

What is the prognosis of fatty change?

A

-> Initially reversible – can lead to hepatocyte death (irreversible)

Hepatic lipidosis: is seen in cats, ruminants, camelids, and miniature equines, but is rare in dogs and uncommon in other horses. It is seen more often in obese cats, secondary to anorexia of any cause. Mortality is high without treatment.

  • ID and treatment of any predisposing diseases and aggressive nutritional support is required for the therapy of hepatic lipidosis.
  • Oral appetite stimulants can be given but are usually inadequate alone.
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14
Q

Irreversible injury is associated morphologically with?

A

Severe swelling of mitochondria

  • Extensive damage to plasma membranes (giving rise to myelin figures)
  • Swelling of lysosomes
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15
Q

Define Necrosis (irreversible cell injury)

A
  • Cell death after irreversible cell injury by hypoxia, ischemia, and direct cell membrane injury. (Viruses, bacterial, drugs)
  • Morphologic aspect is due to 2 concurrent processes:
  • Denaturation of proteins
  • Enzymatic digestion of the cell
  • by endogenous enzymes derived from the lysosomes of the dying cells= autolysis (self digestion)
  • By release of lysosome’s content from infiltrating WBCs
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16
Q

What is this image showing? Describe it

A

Pale, soft, friable, and sharply demarcated from viable tissue by a zone of inflammation

**Don’t think black**

TURKEY

  • MDx: Hepatitis, multifocal to coalescing, subacute, severe, necrotizing
  • Et: Histomonas Meleagridis (heterakis causes black head)
  • Name = Blackhead
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17
Q

What is the cause of necrotic cells in cytoplasm

A

Denatured proteins: Loss of RNA, Loss of glycogen particles, enzyme-digested cytoplasm organelles.

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18
Q

What is the image showing? Describe the appearance

A

The image is showing changes of necrotic cells in cytoplasm

Appearance:

  • Increase binding of eosin (pink), loosing basophilia, glassy homogeneous, vacuolation and moth eaten appearance, calcification may be seen.
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19
Q

What is a common example of coagulation necrosis

A

infarct

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20
Q

What is the image showing? and what is a common cause?

A

Infarct: localized area of coagulative necrosis

Common cause: Ischemia in all solid organs except the brain

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21
Q

Label 1-4

A
  1. Normal tissue
  2. Congestion and hemorrhage
  3. Leukocyte barrier
  4. Coagulation necrosis
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22
Q

Liquefactive necrosis occurs in:

A
  • Tissue with high neutrophil recruitment and enzymatic release with digestion of tissue
  • Tissues with HIGH LIPID CONTENT
  • Focal bacteria and occasionally, fungal infections
  • Microbes stimulate the accumulation of WBCs and the liberation of enzymes from these cells
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23
Q

What is the image showing ?

A

Liquefactive necrosis - gross

Sheep, brain stem

MDx: Bilateral symmetrical encephalomalacia

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24
Q

What is this image showing?

Pathogenesis?

Species affected?

A

Leukoencephalomalacia = necrosis of the white mater of the brain

Pathogenesis: ingestion of Fusarium moniliforme containing Fumonisin B1 toxin-producing moldy corn > sphingolipid synthesis inhibition > direct cellular toxicity > leukoencephalomalacia

Species affected: Horse, chicken, pig

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25
Q

What is the image showing? Species?

DDx?

A

Horse: multifocal hemorrhagic Polyomyelitis

DDx: Equine herpes vrius 1, Rabies (lyssavirus), West Nile Virus (flavivirus)

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26
Q

What is the image showing?

A

Brain, Polioencephalomalacia

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27
Q

What is the image showing? Species?

A

Gross Liquefactive necrosis

Goat: Pituitary gland abscess

Necrotic material is frequently creamy yellow because of the presence of dead WBC = PUS

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28
Q

Define what an Abscess is

A

A localized collection of pus (liqueified tissue) in a cavity formed by disintegration of tissues surrounded by fibrous CT (not in CNS)

**No CT in the Nervous System**

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29
Q

What are the two types of abscesses

A
  1. Septic: the majority = infection, release of enzymes from WBCs and infectious agent
  2. Sterile: process caused by nonliving irritants such as drugs- likely to turn into firm, solid lumps as they scar, rather than remaining pockets of pus
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30
Q

What is the following image?

A

Histology of liquefactive necrosis - eg. Abscess

  • Loss of cellular detail = main characteristic
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31
Q

What is the following image showing?

A

Gangrenous Necrosis

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32
Q

What is the difference between “Dry” and “Wet” Gangrene

A
  • “Dry” Gangrene no bacterial superinfection; tissue appears dry
  • “Wet” Gangrene- bacterial superinfection has occurred; tissue looks wet and liquefactive
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33
Q

What is Caseous necrosis

A

“Caseous”= cheeselike

-Friable (crumble) white; area of necrosis

Necrotic debris represents dead WBCs

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34
Q

What are the possible causes of Caseous necrosis

A
  • Mycobacterium
  • Corynabacterium
  • Fusobacterium
  • Fungal infections
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35
Q

What is the following image?

A

Corynebacterium pseudotuberculosis

Disease name: Caseous lymphadenitis

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36
Q

What is the following image? Species?

MDx and name of disease

A

Cow

MDx: Multifocal caseous pneumonia

Name of disease: Tuberculosis

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37
Q

What is caseous necrosis often associated with?

A

Poorly degradeable lipids of bacterial origin

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38
Q

What is the following image showing?

A

Histopathology -> necrotic area -> eosinophilic granular cell debris with a rim of inflammatory cells

  • Obliterated tissue architecture
  • Dystrophic calcification (commonly to occur in center of lesion)
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39
Q

What are the three types of Fat Necrosis

A
  1. Enzymatic necrosis
  2. Traumatic Necrosis of fat
  3. Necrosis of abdominal fat
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40
Q

What is the following image?

A

Enzymatic necrosis aka pancreatic necrosis of fat

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41
Q

What is the following image?

A

Enzymatic necrosis of fat, dog with previous bouts of pancreaitis. Necrotic fat often becomes saponified, so grossly the lesion is chalky to gritty white and pale.

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42
Q

What is the following image?

A

Fat necrosis, cow, abdominal cavity

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43
Q

What is the following image? Explain

A

Fibrinoid Necrosis

  • Special form of necrosis usually seen in immune reactions involving blood vessels
  • Occurs when Ag-Ab complexes are deposited in the walls at arteries
  • Deposits of these “immune complexes” together with fibrin that has leaked out of vessels, result in dark pink & amorphous appearance in H&E stains, called “fibrinoid” (fibrin-like) by pathologist.
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44
Q

Define Apoptosis

A
  • A pathway of cell death (others include cell death with autophagy and keratinocyte cornification
  • Induced by a tightly regulated suicide program
  • Cells destined to die activate intrinsic enzymes that degrade the cells’ own nuclear DNA and nuclear and cytoplasmic proteins
  • Apoptotic cells break up into fragments, called apoptotic bodies, which contain portions of the cytoplasm and nucleus.
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45
Q

Is there any inflammation in apoptosis?

A
  • No inflammation
  • It is genetically related -> sometimes referred to as programmed cell death
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46
Q

Describe the morphology of apoptosis

A
  • Cell shrinkage with Increase cytoplasmic density
  • Chromatin condensation (pyknosis)
  • Formation of cytoplasmic blebs and apoptotic bodies (fragmentation)
  • Phagocytosis of apoptotic cells by adjacent healthy cells
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47
Q

What are the mechanisms of apoptosis ?

A

Specific feature: activation of caspases (cysteine proteases family)

  • Initiator caspases: 9 & 8
  • Executioner caspases: 3 & 6
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48
Q

What pathways need to be initated for apoptosis?

A
  • Intrinsic pathway = mitochondrial pathway
  • Extrinsic pathway = death receptor-initiated pathway
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49
Q

How are apoptotic cells removed

A
  • Edible for phagocytes
  • Expressed phospholipids in the outer layer of the membrane (instead inner leaflet) to be ID by MQ receptors
  • May become coated w/ natural Ab & proteins of the complement system (C1q)
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50
Q

What are some disorders associated with dysregulated apoptosis

A

Disorders associated with defective apoptosis and increase cell survival (abnormal cells survive)

  • Cells w/ mutations in p53 are subjected to DNA damage, not only fail to die but are susceptible to the accumulation of mutations because of defective DNA repair, these can give rise to NEOPLASIA
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51
Q

What are some disorders assocaited with increased apoptosis and excessive cell death

A

1. Neurodegenerative dz: manifested by loss of specific sets of neurons (apoptosis caused by mutations and misfolded proteins)

2. Ischemic injury, as in myocardial infarction and stroke

3. Death of virus-infected cells

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52
Q

What is cellular injury

A
  • Damage or pathologic alterations in molecules and/or structure that can occur in cells and extracellular components
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53
Q

What are the classic examples of the cause of cell injury

A
  • Oxygen deficiency
  • Infectious agents
  • Immunologic dysfunction
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54
Q

What causes hypoxia/anoxia?

A
  • Inadequate oxygenation of blood -> heart failure, respiratory failure
  • Reduced transport of oxygen in blood -> anemia, carbon monoxide toxicosis
  • Reduction in blood supply = ischemia -> thrombosis
  • Blockage of cell respiratory enzymes -> cyanide toxicosis
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55
Q

Define hypoxia/anoxia?

A

Hypoxia = partial reduction to oxygen delivery to a tissue

Anoxia = no oxygen delivery to a tissue

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56
Q

What are the 6 major mechanisms of cell injury ?

A
  1. Depletion of ATP
  2. Mitochondrial damage
  3. Loss of Ca homeostasis
  4. Reactive oxygen species
  5. Membrane damage
  6. Protein misfolding, DNA Damage
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57
Q

True or false - ATP is required for almost all synthetic and degradative processes within the cell

A

TRUE

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58
Q

Depletion of ATP is assocaited with ?

Depletion of ATP = Fundamental cause of necrotic cell death

A
  1. Hypoxic injury
  2. Toxic injury -> eg. Cyanide
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59
Q

What happens if the Na/K ATPase pump fails?

A
  • Cell swelling
  • ER swelling
  • Plasma membrane damage
60
Q

When you have ATP depletion what occurs to alter cell metabolism?

A
  • Decrease in Na pump -> increase influx of Ca, water, and Na also increase Efflux of K
  • Increase Anaerobic glycolysis -> decrease glycogen, increase Lactic acid, decrease pH
61
Q

True or False - ATP depletion culminates in the irreversible mitochondrial and lysosomal membrane damage leading to cell necrosis

A

TRUE

62
Q

What are the 3 major consequences of Mitochondrial damage?

A
  1. Formation of the mitochondrial permeability transition pore (MPTP)
  2. Increase production of ROS
  3. Activation of apoptotic pathways
63
Q

What are the 3 sources of accumulation of Ca?

A
  • Extrinsic (cell damage)
  • Intrinsic - release from SER, released from mitochondrion
64
Q

What is the cascade of intracellular events during the loss of calcium homeostasis

A
  1. Opening of MPTP -> decrease ATP
  2. Enzyme activation
    - Phospholipases: membrane damage
    - Proteases: membrane and cytoskeletal proteins
    - endonucleases: DNA and Chromatin fragmentation
    - ATPases: break down ATP, accelerate ATP depletion
65
Q

What are the 3 major forms of damage during loss of calcium homeostasis

A
  1. Membrane damage
  2. Nuclear damage
  3. ATP depletion
66
Q

What are ROS?

A
  • Type of oxygen-derived free radical
  • Well established role in cell injury
  • Normally produced during mitochondrial respiration
  • Degraded and removed by cell scavenging defense systems
67
Q

How do you remove ROS?

A
  • Spontaneous decay
  • Antioxidants; Vit E, , Glutathione
  • Storage and transport proteins
  • Enzymes
68
Q

What are the mechanisms for damaging the plasma membrane

A
  • Reactive Oxygen species (ROS)
  • Decreased phospholipid breakdown
  • Cytoskeleton abnormalities
69
Q

What are the consequences of membrane damage

A
  • Mitochondrial membrane damage -decrease ATP
  • Plasma membrane damage - loss of osmotic balance
  • Injury to lysosomal membranes - leakage of enzymes into the cytoplasm: RNases, DNases, proteases, phosphatases, glucosidases
70
Q

This cow was found recumbent and blind, with dorsomedial strabismus, in tonic-clonic seizures that led to coma and death. On necropsy, lesions shown below light up under UV light. What is the Etiology?

A

-High Sulfur Diet

71
Q

What is the MDx?

A

Enlarged thyroid = thyroid hyperplasia b/c increasing number of cells so increase in SIZE

Goiter-> Iodine deficiency

72
Q

DDx?

A

Enlarge lymph node -> lymph node mesenteric hyperplasia

Lymphoma

73
Q

MDx?

A

Nervous system -> Spinal Cord hypoplasia (neural tube closure)

Hypoplasia (not atrophy b/c didn’t get the chance to grow properly)

74
Q

MDx?

Etiology?

A

5 month old dog -> abnormal teeth should look smooth, white, shiny.

Enamel is gone, destroyed by a virus -> Canine distemper

MDx->Teeth Enamel Hypoplasia

Etiology -> Hyperthermia/viral infection

75
Q

What are we looking at?

A

Muscle Atrophy , diffuse, severe

Causes: Cancer, malnutrition, denervation

76
Q

What is wrong with this chicken?

A

Esophagus -> multifocal convalescing white nodules

Metaplasia -> Changing from one type of tissue to another Know this example for metaplasia -> Vit A deficiency

77
Q

MDx?

A

Stomach increase in size -> hypertrophy

MDx -> Hyperplasia of the gastric glands ->Hypertrophic gastritis

78
Q

What is wrong here?

A

Nasal cavity -> Something missing

Atrophic rhinitis causes by 2 bacteria

79
Q

MDx?

A

Tissue from a dog, organ = uterus

MDx: cystic endometrial hyperplasia

80
Q

What type of necrosis is this?

A

Type of necrosis = Liquefactive

Bovine, type of necrosis?

Possible Etiology? White matter

Lesion in swine? Porcine pulmonary edema

81
Q

What is this image showing ?

A

Bovine, MDx, Possible cause

Grey outside -> Polioencephalomalacia (grey mater) -> disturbance of the CNS. Inflammation -> swelling -> necrosis

82
Q

MDx? Eitology?

A
  • Diffuse congenital Hypoplasia:
  • Etiology: In utero feline panleukopenia vrirus
83
Q

MDx? Etiology?

A

Puppy: MDx, Etiology

Kidney

MDx: Necrosis & hemorrhage

Etiology: canine herpes type 1

84
Q

Tissue from a Kitten. What type of cell adaptation is seen?

MDx? Etiology?

A

Feline, Kitten tissue: heart

MDx: Dilated cardiomyopathy with both atria and ventricle dilatation and hypertrophy

Etiologic Dx: Taurine deficiency cardiomyopathy

85
Q

Define Inflammation

A

Reaction of vascularized living tissues to injury

86
Q

What are the characteristics of inflammation

A
  • Involves changes in vascular bed, blood, CT
  • Intended to eliminate irritant and repair damaged tissue
87
Q

What are the outcomes of inflammation

A

A. Ideal conditions- return to normal

B. Intense inflammatory response- attempt to separate injured tissue

C.Failure to eliminate insult- sequel

88
Q

What is the following image showing?

A

Chronic dermatitis in a cow

89
Q

Define Exudation

A

Escape of fluid, proteins and blood cells from the vascular system into the interstitium or body cavities. Exudation implies alteration of the normal permeability of local blood vessels

90
Q

Define Exudate

A
  • Inflammatory extravascular fluid that has
  • A high protein concentration
  • Much cellular debris
  • Specific gravity above 1.020
91
Q

Define Transudate

A

essentially an ultrafiltrate of blood plasma and results from hydrostatic imbalanes across the vascular endothelium. A transudate is a fluid with: Low protein content, SG of less than 1.020

92
Q

Define Edema

A

denotes an excess of fluid in the interstitial tissue or serous cavities, it can be an exudate (inflammatory edema) or a transudate.

93
Q

Define Pus

A

An inflammatory exudate rich in leucocytes (primarily viable and degenerated neutrophils) and parenchymal cell debris.

94
Q

What are the main characteristics of peracute?

A
  • Usually causes by a potent stimulus
  • Usually the animal has no time to respond
  • Less common than acute disease processes
95
Q

What is the histological image showing?

A

Acute inflammation: migration of neutrophils

96
Q

What is the image showing? Define the term

A
  • Lymphadenitis: Reactive inflammation of lymph node(s) occurs in acute, subacute and chronic inflammation
  • Chronic inflammation of mesenteric lymph nodes in a Llama, due to TB
97
Q

What is the image showing? Define the term

A

Lymphangitis = inflammation of lymphatic vessel(s)

Thickening of serosal lymphatic vessels (chronic lymphangitis) due to Johne’s disease.

98
Q

Define subacute

A
  • Subacute is defined as a gradual change, between acute and chronic
  • This term is used when the inflammatory response does not include reparative responses such as fibroplasia and angiogenesis
99
Q

What is the following image showing?

A

Multifocal ulcerative colitis, chronic. Feline

100
Q

What is the following image showing?

A

Chronic lmymphangitis: Johne’s disease in a goat

101
Q

What is the image showing?

A

Focal lesion in the brain of a deer. Cut surface reveals presence of cloudy, yellowish material (interpreted as pus)

102
Q

What is the image showing?

A

Focal keratitis in a bovine - Which is inflammation of the cornea

103
Q

What is the image showing?

A

multifocal hepatitis in a peacock.

104
Q

What are these two images showing?

A

Locally extensive inflammation

105
Q

Pus: a liquid inflammation product composed of…

A
  • Accumulated dead cells (both tissue cells and inflammatory cells)
  • Variable numbers of viable leucocytes (primarily neutrophils)
  • Fluids added by the inflammatory edema- forming process.
106
Q

Define Suppurative Exudation

A
  • Synonym: Purulent Exudation- consisting of, or containing pus; associated with the formation of pus.
107
Q

What is the image showing?

A

Severe suppurative pyelonephritis in a dog

108
Q

What is the image showing

A
  • Pyometra in a dog: a form of severe suppurative inflammation
109
Q

Define Suppuration

A

Is the process by which pus (suppurative exudation) is formed. The use of the term suppuration implies that neutrophils and proteolytic enzymes are present, and that necrosis of host tissue cells has occurred.

110
Q

Define Abscess

A

Is a circumscribed (partially walled-off) collection of pus. Therefore an abscess is a localized form of suppurative inflammation.

111
Q

What is the image showing?

A
  • Abscess: gross appearance: is yellow-white to gray-white and varies from watery to viscous depending on fluid content.
112
Q

What is the image showing?

A
  • Chronic suppurative osteomyelitis
113
Q

What is this image showing?

A

Fibrinous exudation

114
Q

Define Fibrinous inflammation

A

Gross appearance: yellow-white, or pale tan, stringy, shaggy meshwork (or fibrillary material) which gives a rough irregular appearance to the tissue surface. Casts of this friable material may form in the lumen of tubular organs.

115
Q

What is the image showing?

A

Fibrinous Enteritis

116
Q

What is the following image showing?

A

Fibrous exudate

117
Q

What is the image showing?

A
  • Fibrinopurulent exudate: This term is used to classify an inflammatory process in which neutrophils and fibrin are abundant. Image of fibrinopurulent pericarditis in a foal
118
Q

What is the image showing?

A
  • Diffuse severe fibroinosuppurative pericarditis- porcine
119
Q
  • Presence of a fibrinous exudate involves an ______ process.
  • In contrast, fibrosis is a _______ process.
A

Acute , Chronic

120
Q

What is the images showing ?

A

Fibrinous pleuritis in a horse

  • Left image: pleural surface covered by friable material
  • Right image: Homogenous, eosinophilic material. Bacterial colonies (arrows) are basophilic with HE stain.
121
Q

Define Serous Exudation

A
  • Definition: Inflammatory process in which the exudate occurs in tissues in the absence of a prominent cellular response. May be a dominant pattern of exudation for a wide variety of mild injuries. Example: Traumatic blisters, sunburn.
122
Q

Define granulomatous inflammation

A

Granulomatous refers to an inflammatory response characterized by the presence of lymphocytes, macrophages, and plasma cells with the predominant cell being the macrophage

123
Q

What is this image?

A
  • Diffuse granulomatous inflammation
  • Circle is “cerebroid” appearance of affected intestine
124
Q

What is the etiology of Granulomatous Inflammation

What organisms usually cause this?

A
  • Etiology: usually some non-digestible organism or particle which serves as a chronic inflammatory stimulus, delayed-type hypersensitivity is often required.
  • Organisms: Mycobacterium, actinomyces, Blastomyces, Coccidioides, etc
  • Noninfectious AGENTS: Mineral oil, Complex polysaccharides, foreign bodies
125
Q

What is the image showing

A

Segmental hemorrhagic enteritis

126
Q

What is the image showing

A

Mucopurulent or Catarrhal

  • The inflammatory exudate is composed of mucus and pus (neutrophils and cell debris)
127
Q

What is the image showing

Etiology?

A

Severe multifocal to coalescent dermatitis.

Etiology: Turkey pox virus

128
Q

Why are neutrophils important ?

A
  • Neutrophils constitute the first line of cellular defense (they usually are the first to gather at sites of acute inflammation)
  • They develop in the bone marrow and maturation takes about two weeks
129
Q

The purpose of neutrophils is to eliminate:

A
  • Microorganisms
  • Tumour cells
  • Foreign material
130
Q
A
131
Q

What are the two types of repair?

A
  1. Parenchymal regeneration
  2. Fibrosis
132
Q

What is repair by parenchymal regeneration

A

Of injured tissues by replacement of damaged tissue with cells if identical type, sometimes leaving no residual trace of previous injury.

133
Q

Parenchymal regeneration can only occur if

A
  1. the tissue has the capacity to regenerate
  2. the CT framework of the tissue is maintained, so that regenerating cells have an architectural framework upon which to build
134
Q

What is repair by fibrosis

A

Fibrosis is replacement by fibrous CT or fibroplasia

135
Q

What are some examples of labile cells?

A
  • Surface epithelia: stratified squamous surfaces on skin, oral cavity, vagina and cervix
  • Lining mucosa of all the excretory ducts of the glands of the body (ie. salivary glands, pancreas, biliary tract)
  • Columnar epithelium of the GI tract, uterus and fallopian tubes
  • Transitional epithelium of the Urinary Tract
  • Cells of splenic, lymphoid, and hematopoietic tissue
136
Q

Examples of permanent cells

A

Neurons, Cardiac muscle cells

137
Q

What are some factors favoring fibrosis

A
  • Severe and prolonger tissue injury.
  • Loss of tissue framework (basement membranes)
  • Large amounts of exudate
  • Lack of renewable cell populations
138
Q

What are the consequences of fibrosis

A
  • Loss of functional parenchymal tissue
  • Alteration of physical properities of tissue
139
Q

What is granulation tissue

A

The term granulation tissue derives from its pink. soft, granular apperance on surface wounds. Proliferation of new small blood vessels and fibroblasts are its characteristic features

140
Q

what are the four zones of granulation tissue

A
  1. Zone of necrotic debirs and fibrin
  2. Zone of macrophages (clean-up) and in-growing capillaries (angiogenesis, neovascularization)
  3. Zone of proliferating capillaries and fibroblast
  4. Zone of mature fibrous CT
141
Q

**REMEMER: Granulomas and granulomatous inflammation correspond to chronic inflammation

*Granulation tissue is part of the repair process.

A
142
Q

Define wound healing

A

a process including CT replacement and regeneration by which restoration of tissue continuity is achieved

143
Q

What is healing by first intention?

Healing by secnd intention?

A

First intention: possible when there is little exudate and when tissue elements are closely approximated. i.e surgical wound

Healing by second intention: it occurs when the edges of wounds are widely separated

144
Q

Skin healing steps in general

A
  1. Initial gap (wound) with formation of blood clot.
  2. Epithelial continunity is restored.
  3. Initially the epithelial cells lose contact with one another and the basement membrane -> migration of cells -> mitoses -> gradual covering of epidermal defect
  4. Inflammatory reaction develops in the incised dermis with neutrophil infiltration followed by macrophage infiltration.
  5. Neovascularization occurs with the ingrowth of new capillary buds to bridge the wound
  6. Fibroblast proliferation occurst to provide a sufficient cellular base for the manufacture and laying down of collagen
  7. Devascularization occurs as a consequence of the gradual accumulation of collagen
  8. Egress of inflammatory cells and fibroblast rgression due to absence of a nutrient vasculature
  9. Scar - this acellular and avascular, pale, collagenous tissue is the end product of wound healing
145
Q

Define Neoplasm

A

= “new growth”; irreversible unregulated autonomous proliferation of cells

146
Q

What do neoplasms consist of?

A
  • Neoplastic cells (“parenchyma”)
  • CT and BVs (“stroma”) produced in response to products from the neoplastic cells
147
Q

Parenchymal cells can be what?

A
  • Epithelial cells
  • Mesenchymal cells

RUSVM Path I (2 decks)

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