Objectives for Exam 1 Flashcards

1
Q

define pathology

A

study of disease

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2
Q

Define disease

A

abnormal body process with or without characteristic sign. It begins at the molecular & cellular level. It can be said that it is any deviation from the normal structure or function of the body.

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3
Q

Define Etiology

A
  • cause of a disease.

- Two major causes: genetic (intrinsic) & acquired (extrinsic)

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4
Q

Define Pathogenesis

A
  • refers to the mechanisms of disease development

- sequence of events from INITIAL stimulus to the ULTIMATE expression of the disease

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5
Q

Define morphologic diagnosis (MDx)

A
  • biochemical & structural alterations induced in the cells and organs of the body.
  • based on the predominant lesion(s) in the tissue(s)
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6
Q

How does one make a Morphologic diagnosis (MDx)?

A

Via Macroscopic & Microscopic evidence found, using the following descriptions:
1) location (organ tissue)
2) Distribution (focal, multifocal, locally extensive, diffuse)
3) Severity (mild, moderate, severe)
4) Duration/time (acute or chronic)
5) Nature of lesion (degenerative, inflammatory, neoplastic)
If inflammatory remember to classify the type of exudate

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7
Q

Define Pathognomonic

A

characteristic or indicative of a specific disease

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8
Q

Define Prognosis

A

refers to the course of the disease= possible outcome

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9
Q

Define clinical diagnosis

A
  • based on case history (Hx), clinical signs, physical exam.
  • may provide differential Dx
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10
Q

Define etiologic diagnosis (Edx)

A

it is a more definitive Dx and names the specific cause(s) of the disease

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11
Q

Define differential diagnosis

A

list of diseases that could account for the evidence or lesions of the case

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12
Q

Define homestasis

A

ability to maintain equilibrium by adjusting its physiological processes

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13
Q

What is somatic death?

A
  • it is due to total diffuse hypoxia

- cells degenerate as described for hypoxic cell injury

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14
Q

What is putrefaction/decomp?

A
  • process by which post mortem bacteria break down tissues

- gives color, texture changes, gas production, & odors

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15
Q

In general, what kind of organs undergo autolysis faster than others? Give examples

A
  • organs that normally contain enzymatic activity or have high bacteria content
  • pancreas, GI tract, & gallbladder
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16
Q

What is the difference between autolysis & decomposition?

A
  • autolysis: self digestion of cells & tissues by OWN hydrolytic enzymes normally found in tissues
  • decomp: post mortem bacteria break down tissues
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17
Q

Herbivore vs. Carnivore. Which will decompose faster?

A

herbivore

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18
Q

When is the onset of Rigor Mortis?

A

begins @ 1-6hrs post death, persistent 1-2 days

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19
Q

How would you test if an animal has anthrax before performing a necropsy?

A

take notch off ear or tail, stain the tissue, see if you have bacillus in blood, if so = anthrax. Normally a freshly dead animal shouldn’t have bacillus in the blood yet.

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20
Q

What are some factors that could make quicken the onset of rigor mortis?

A

high stress, high heat, & high activity before death

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21
Q

What is Algor Mortis?

A

cooling of body post mortem, depends on T of body @ time of death

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22
Q

What are some big indicators that a carcass may be infected with anthrax?

A

absence of rigor mortis, Bleeding from every orifice, bloated

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23
Q

What is Livor Mortis? What is another name for it?

A
  • hypostatic congestion
  • gravity pulls blood post mortem, some areas the tissues will be more red and in other areas pale due to lack of blood. ONLY A POST MORTEM CHANGE!
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24
Q

Describe Post Mortem clotting.

A
  • occurs several hrs post death in heart & vessels.

- usually clots are unattached to vessel walls and are shiny, wet, and are a perfect cast of vessel lumina (like jello!)

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25
Q

Describe Pre Mortem clots.

A

usually attached to vessel walls and are dry & duller in color, “laminated”.

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26
Q

How is clotting affected when it comes to autolysis.

A
  • in moderate–> severe : you will NOT see clotting
  • in light –> moderate : you WILL see clotting
  • usually will see clotting in heart regardless of autolysis.
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27
Q

What is hemoglobin imbibition?

A

red staining of tissue, especially in the heart, arteries & veins. Color may spread to adjacent tissues.

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28
Q

What is bile imbibition?

A

bile in gallbladder starts to penetrate the wall & stain the adjacent tissues yellowish to greenish brown.

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29
Q

What tissues are usually stained with bile imbibition?

A

those in contact with bladder: liver & intestines & feces.

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30
Q

Describe Bloat.

A

results from post mortem bacterial gas formationin the lumen of the GI tract

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31
Q

How does one differentiate bloating from ruminal tympany?

A

if animal died from tympany then the animal would have a bloat line on the esophagus & trachea. This occurs b/c blood gets cut off by the stomach pushing on it and blood starts backing up in that area. You wont see this is bloat was post mortem.

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32
Q

How can you differentiate clouding of the lens due to temperature vs. cataracts?

A

once the carcass goes back to room temp the lens will no longer be clouded if it is just due to being chilled.

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33
Q

What is Pseudomelanosis?

A
  • refers to greenish-black discoloration of tissues post mortem.
  • caused by decomp of bloody by bacterial action forming hydrogen sulfide w/ iron
  • occurs soon after death, closer to the gut the faster it will change color
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34
Q

What is the mnemonic for differential diagnosis?

A
DAMNIT
D = degenerative 
A = Autoimmune 
M = Metabolic 
N = Nutritional, neoplastic 
I = inflammatory, idiopathic, iatrogenic 
T = trauma
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35
Q

Define hypoxia

A

inadequate oxygenation of tissues

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36
Q

Define Ischemia

A

decrease of blood supply in tissues

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37
Q

Define anoxia

A

absence of oxygen in tissues

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38
Q

Define Anemia

A

decrease in number of RBCs, or RBCs are deficient in Hb, or decrease in BV.

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39
Q

What are the general causes of cell injury? (6)

A

1) Oxygen deprivation
2) Physical injury (direct mechanical trauma, Temp extremes)
3) Chemical injury (poisons or toxins)
4) Infectious agents (bacteria, viruses, fungi, parasites)
5) Nutritional imbalances (deficiency (vitamin E/selenium), excess)
6) Genetic (mutations)

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40
Q

Describe irreversible cell injury.

A

“the point of no return” occurs when the injury reaches a certain limit, whereby the cell cannot recover.

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41
Q

What are the 6 intracellular systems vulnerable to injury?

A

1) cell membrane
2) aerobic respiration
3) protein synthesis
4) cytoskeleton
5) genetic apparatus (DNA)

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42
Q

What are the 6 general mechanisms of cell injury?

A

1) ATP depletion
2) Mitochondrial damage
3) Influx of Ca
4) Accumulation of Oxygen-derived free radicals (Oxidative stress)
5) Defects in membrane permebility
6) DNA damage

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43
Q

What is the difference between atrophy & hypertrophy?

A

atrophy is a decrease in size from lack of use & hypertrophy is the cells increase in size in order to increase its function.

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44
Q

What is the difference between hyperplasia, dysplasia, & metaplasia?

A
  • hyperplasia: is the increase of number in cells
  • dysplasia: abnormal development of cells
  • metaplasia: cells changing its phenotype in response to chronic irritation (ex. Smokers lung)
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45
Q

List some stages of cell response to stress or injury.

A

atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia.

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46
Q

List conditions resulting from physiological cell adaptation

A

weightlifting

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47
Q

List some conditions resulting from pathological cell adaptiation

A

thickening of skin, smokers lungs

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48
Q

Describe reversible cell injury

A
  • alteration of homeostasis

- return & recovery to normal when the stress or injurious stimuli are removed

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49
Q

Define Atrophy

A

decrease in size and/or number of cells & their metabolic activity after a normal growth has been reached (note: cells still viable & functional)

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50
Q

Give some examples of physiologic atrophy.

A

muscle disuse in a limb that is in a cast

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51
Q

Give some examples of pathologic atrophy.

A

atrophy in tissues adjacent to a tumor due to pressure & compromised blood supply or serous atrophy of fat

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52
Q

What are some causes of atrophy?

A

decrease workload, blood supply, or oxygen, denervation, inadequate nutrition, loss of endocrine stimulation, aging.

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53
Q

What causes atrophy of the left cricoarytenoideus dorsalis m. in horses & dogs?

A
  • Horses: due to damage to LEFT recurrent laryngeal n. from guttural pouch infection, trauma, tumors, but mostly idiopathic. COMMON secondary to nerve damage.
  • Dogs: inherited in Siberian Husky & Bouvier de Flandres
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54
Q

When does serous atrophy of fat happen?

A

When an animal has a negative energy of fat, in order to compensate body uses stored fat.

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55
Q

Define Hypertophy

A
  • increased size of cells & their functions
  • synthesis of more organelles & structural proteins –> bigger cells
  • more common in stable or permanent cells (cardiomyocytes & neurons)
56
Q

Give an example of Pathologic Hypertropy

A

cardiac hypertrophy from hypertension or aortic valve dz

57
Q

Give 2 examples of Physiologic Hypertrophy

A

weightlifter or pregnant uterus

58
Q

Name the breeds of cats & dogs that are more susceptible to Hypertrophic cardiopathy (HCM)

A
  • Cats:
    1. Main Coon (mutation in MYBPC3 gene)
    2. domestic short haired
  • Dogs: Boxers & Bermese mountain dogs
59
Q

What are the 3 ways we would evaluate a heart for Hypertrophic Cardiomyopathy

A

1) shape of heart (globos, can you see an apex?)
2) ratio of chambers L to R (L should be 3x the thickness of the R)
3) Weight (compare it to the body weight to get ratio. Heart should not be more than 0.03% of body weight)
Note: if cats heart is more than 18g it is suspect of hypertrophy

60
Q

Define Hyperplasia

A

increase in number of cells of an organ, cells that are capable of replication.

61
Q

Define Pathologic hyperplasia

A

commonly caused by excessive hormonla or growth stimulation factor
ex. Epidermal thickening due to repeated irritation

62
Q

Give examples of Physiologic Hyperplasia.

A

hormonal (breast during pregnancy), compensatory (ex. Hepatectomy)

63
Q

Define Metaplasia.

A
  • abnormal change in phenotype of a cell

- it is a normal response to chronic irritation, may cause malignant transformation, reversible if cause is removed.

64
Q

Give some examples of Metaplasia.

A

chronic irritation in lungs, Vit-A deficiency, mammary tumors

65
Q

Define Dysplasia.

A
  • abnormal development

- term mostly used in neoplastic processes

66
Q

Define Hypoplasia

A

underdevelopment of an organ or tissue

67
Q

Define anaplasia

A

condition where cells lose their morphological characteristics

68
Q

Define dysplasia

A

abnormal development

69
Q

Define free radicals

A

chemical species w/ a single unpaired electron in its outer orbit (extremely unstable). They avidly attack & degrade nuclei acids & membrane molecules

70
Q

Define reactive oxygen species

A

Type of oxygen-deprived free radicals which are produced by cell injury. Normally they are removed.

71
Q

Name sources /stimuli for free radicals

A
  • absorption of radiant energy (UV light)
  • redox rxns during normal physiologic processes
  • exposure to toxins (O2, carbon tetrachloride, acetaminophen)
72
Q

Name neutralizers of free radicals

A

Antioxidants (vit A,C,E, B-carotene, Ceroplasmin, Ferritin)

73
Q

List examples of free radical-damage

A

1) Ischemia-reperfusion
2) Chemical & Radiation injury
3) Toxicity from O2 & other gases
4) Cellular aging
5) microbial killing by phagocytic cells
6) tissue injury by inflammatory cells

74
Q

Describe the cell damage induced by free radicals

A

1) Lipid peroxidation of membranes
2) DNA damage leading to mutations & death
3) Cross linking of proteins

75
Q

Describe the pathogenesis of ischemia-reperfusion injury

A

reduction of blood flow leads to hypoxic damage to tissue –>
calcium-activated proteases –> increased xanthine oxidase activity –> generation of more free radicals in the cytosol –>
re-establisment of blood flow bring oxygen & inflammatory cells to hypoxic tissue

76
Q

Define fatty change

A

sub-lethal cell damage characterized by intracytoplasmic fatty vacuolation (may be preceded or accomplanied w/ cell swelling)

77
Q

Define Lipidosis

A

refers to accumulation of triglycerides & other lipid metabolites within the cytosol of PARENCHYMAL cells and are packaged in VLDL’s

78
Q

Define apoptosis

A

programmed cell death

79
Q

Define necrosis

A

irreversible damage to mitochondria & lysosomal membranes

80
Q

Describe the morphologic features of hydropic degeneration

A

affected organs is slightly swollen, paler than normal, bulging tissue, slightly heavy.

81
Q

What is Hydropic degeneration?

A

Cell swelling due to increase uptake of water which causes diffuse disintegration of organelles & cytoplasmic proteins.

82
Q

Describe the pathogenesis of acute cell swelling (hydropic degeneration).

A

hypoxia –> ATP production decreases –> Na & H2O move into cell & K moves out of cell –>
Osmotic pressure increases –> more water moves into cell –> cisternae of ER distend, rupture, form vacuoles –>
extensive vacuolation –> hydropic degeneration.

83
Q

Define Acute cell swelling

A

early, sub-lethal manifestation of cell damage, characterized by increase in cell size & volume

84
Q

Describe the pathogenesis of fatty change

A

impaired metabolism of fatty acids –>
leading to accumulation of triglycerides –>
formation of intracytoplasmic fat vacuoles

85
Q

List the highly vulnerable cells to hypoxia and cell swelling (5)

A

cardiomyocytes, proximal renale tubule epithelium, hepatocytes, endothelium, CNS

86
Q

Name 4 ultrastructural changes seen in reversible cell injury

A

Many organelles are affected:

1) plasma membrane (loss of microvilli, loosening of intercellular attachments.
2) ER (dilation of cisternae (fluid accumulation), detachment & disintegration of polysomes)
3) Mitochondria (swelling, apperance of small densities)
4) Nucles (clumping of chromatin, disintegration of granular & fibrillar components)

87
Q

Name cells susceptible to fatty change

A

hepatocytes, cardiomyocytes & renal tubular epithelium

88
Q

Define necrosis

A

term used to describe the range of morphologic changes that occur following cell death in the living animal

89
Q

Describe clinical differences between necrosis and apoptosis

A

necrosis is a pathologic event, where as apoptosis isnt necessarily a pathologic event.

90
Q

Name the 3 nuclear changes seen in necrosis

A

1) karyolysis (nuclear fading)
2) pyknosis (nuclear shrinkage)
3) karyorrhexis (nuclear fragmentation)

91
Q

Describe the cytoplasmic changes of necrosis seen in routine histology

A

Changes in the nucleus such as:

  • pyknosis
  • karyorrhexis
  • karyolysis
92
Q

Appearance in necrotic cells: Increase binding of eosin (pink). What is the cause?

A

Denatured proteins

93
Q

Appearance in necrotic cells:losing basophilia. What is the cause?

A

loss of RNA

94
Q

Appearance in necrotic cells:glassy homogeneous. What is the cause?

A

Loss of glyocgen particles

95
Q

Appearance in necrotic cells: vacuolation & moth eaten appearance &
calcification may be seen. What is the cause?

A

Enzyme-digested cytoplasm organelles

96
Q

What is coagulative necrosis?

A

ONLY form of necrosis in which the architecture of dead tissues is preserved (days)

97
Q

What is the common cause of necrosis? And where does it normally occur?

A

Ischemia which can occur in all organs except the brain

98
Q

What are the 5 reasions for organs to turn white?

A

1) Ischemia (necrosis)
2) infiltration of WBCs
3) infiltration of fat
4) infiltration of fibrous CT (fibrosis)
5) calcification of tissue ( mineralization)

99
Q

If you suspect a kidney infarction what should you look for?

A

V-shaped lesion usually it is white due to ischemia

100
Q

What happens if you give a horse high doses of NSAID’s or give it to them long term?

A

they get coagulative necrosis

101
Q

Describe the morphologic features of coagulative necrosis

A
  • affected tissues exhibit a firm texture

- eosinophilic, anucleate cells may persist for days

102
Q

Describe the morphologic features of liquefactive necrosis

A
  • necrotic material is frequently creamy yellow

- tissue is liquid and off-white to tan in color

103
Q

List the main causes of liquefactive necrosis

A
  • bacteria & occasionally fungal infections.

- the microbes stimulate the accumulation of WBCs & the liberation of enzymes in these cells

104
Q

Define Abscess

A

site of liquifactive necrosis that is defined by a layer of fibrous connective tissue

105
Q

Define Malacia

A

softening of whatever organ involved

106
Q

Describe the Histology of Liquefactive necrosis

A

1) loss of cellular detail
2) cells are granular
3) eosinophilic and basophilic debris
4) no tissue architecture is preserved

107
Q

If CNS undergoes necrosis, what kind would it most likely be?

A

liquefactive b/c it cant hold its structure

108
Q

What are the 2 types of abscesses?

A

sterile & septic (majority)

109
Q

What is the most common cause of abscesses under the skin?

A

Staphylococcus aureus

110
Q

Describe the morphologic features of caseous necrosis

A
  • “cheeselike”

- friable (crumbly) white

111
Q

List the main causes of caseous necrosis

A

1) mycobacterium
2) corynebacterium
3) fusobacterium
4) fungal infections

112
Q

List the main causes of coagulative necrosis

A

1) ischemia

2) infarction

113
Q

When it comes to abscesses and caseous necrosis, which one is usually chronic?

A

abscesses are usually chronic & caseous necrosis is usually acute

114
Q

define granulomatous (arauz version)

A

has a few MNGC w/ a few macrophages may have a few lymphocytes. Type of inflammation you usually have w/ caseous necrosis.

115
Q

Define gangrene

A

begins as coagulative necrosis and is usually applied to distal extremities (also toes, ear, pinna, udders)

116
Q

Compare and contrast dry and wet gangrene

A
  • Dry: no bacterial superinfection; tissue appears dry

- Wet: bacterial superinfection has occurred; tissue looks wet & liquefactive

117
Q

Describe the pathogenesis of gangrene

A

begins mostly as coagulative necrosis likely due to ischemia then advances and extremities fall off

118
Q

List three types of presentations of fat necrosis

A
  • enzymatic necrosis (aka pancreatic necrosis of fat)
  • traumatic necrosis of fat
  • necrosis of abdominal fat
119
Q

List specific breeds predisposed to fat necrosis

A

Jersey & Guernsey cattle

120
Q

Describe the morphologic features of fibrinoid necrosis

A
  • can ONLY see histologically NOT grossly

- glassy, eosinophilic fibrin-like material is deposited within the vascular walls

121
Q

List examples of physiologic programmed cell death

A

1) hormone-dependent involution of organs in the adult (ex. Thymus)
2) cell deletion in proliferating cell populations (intest. Epith. Turnover)
3) deletion of auto-reactive T-cells in the thymus
4) programmed cell death during embryogenesis

122
Q

List examples of pathologic programmed cell death

A

1) DNA damage
2) TNF induction of apoptosis in many cells
3) accumulation of misfolded proteins
4) cell injury in certain infections: viral
5) pathologic atrophy in parenchymal organs after fuct obstruction

123
Q

What are the initiator caspases for the mechanism of Apoptosis

A

caspases 8 & 9

124
Q

What are the executioner caspases for the mechanism of Apoptosis?

A

caspases 3 & 6

125
Q

Identify cell organelles involved in apoptosis

A

mitochondria, DNA, cytoskeleton

126
Q

Name markers used to identify apoptosis

A

1) Annexin V
2) thrombospodin
3) Caspases
4) C1q

127
Q

What activates the apoptotic intrinsic (mitochondrial) pathway

A
  • withdrawal of growth hormones

- injury (radiation, toxins, free radicals)

128
Q

What activated the apoptotic extrinsic (death receptor-initiated pathway)

A
  • receptor-ligand interactions (Fas & TNF receptor)

- cytotoxic T lymphocytes

129
Q

List disorders associated with defective apoptosis and increased cell survival

A

1) cells w/ mutations in p53 gene are subjected to DNA damage & accumulation of mutations b/c of defective DNA repair, these can give rise to cancer
2) lymphocytes that react against self-Ag
3. ) failure to eliminate dead cells (potential source of self- Ag)
4. ) apoptosis maybe the basis of autoimmune Dz

130
Q

List disorders associated with increase apoptosis & excessive cell death

A

1) neurodegenerative Dz (manifested by loss of specific sets of neurons)
2) ischemic injury (as in myocardial infarction & stroke)
3) death of virus-infected cells

131
Q

Identify the common event in intrinsic and extrinsic pathways

A

membrane blebs (cellular fragmentation) –> apoptotic bodies –> phagocyte phagocytizes

132
Q

Describe the mechanisms of hepatic lipidosis

A

Defects in uptake, catabolism & secretion include:

1) increase synthesis of fatty acid or triglyceride (TG)
2) increase lipolysis & uptake of free fatty acids from TG stores in hepatocytes (aka starvation)
3) decrease in beta-oxidation of fatty acid to ketones & other substances b/c of mitochonrial injury (hypoxia)
4) decrease apolipoprotein synthesis
5) impaired lipoprotein transport out of hepatocytes

133
Q

List types of hepatic lipidosis

A

1) physiologic (happens during late pregnancy aka pregnancy toxemia & heavy early lactation aka ketosis) in ruminants
2) nutritional disorders (obesity, protein-calorie malnutrition)
3) starvation

134
Q

Describe the morphologic features of hepatic lipidosis

A

1) liver itself is diffuse yellow (if all cells infected)
2) enhanced reticular pattern (if only specific zones are infected)
3) edges rounded & bulge on section
4) tissues soft, friable, cuts easily w/ grease texture
5) if severe condition then small liver sections may float in water or fixative

135
Q

“A network of vessels (_____) that parallel the veins also contribute to circulation by draining fluid from the extravascular spaces into the blood vascular system.”

A

lymphatics