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Basic Pathology > Basic Pathology Exam 1 > Flashcards

Basic Pathology Exam 1 Flashcards

1
Q

Thanatology

A

Study of death

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2
Q

Signs of death

A

unequivocal and equivocal

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3
Q

Agony

A

life to death, loss of function of all systems leading to organ dysfunction. Can be short or long depending on the trauma

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4
Q

Cause of Death

A

disease or injury that is responsible for the death, root cause or immediate cause

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5
Q

Mechanism of Death

A

physiologic derangement initiated by the cause of death and resulting in death
Ex: brain death leading to subsequent respiratory arrest

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6
Q

Manner of Death

A

natural vs. non-natural

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7
Q

rigor mortis

A

once ATP runs out in the muscles and have a myosin-actin binding rigidity. (ATP reserves depleted and cannot detach)

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8
Q

pallor mortis

A

pale skin due to lack of circulation in peripherals

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9
Q

Livor Mortis

A

dark spots appear in the skin in the lower portion of the body (gravitational pooling of blood)

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10
Q

Algor Mortis

A

Body temperature reduces to environmental temperature. Speed of cool down inversely proportional to rate of decomposition

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11
Q

Postmortem Autolysis/ Decomposition

A

this begins by progressive release of endogenous enzymes and then action of saprophytic bacteria (escaping from the gut)

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12
Q

Postmortem Clotting

A

in the heart and vessels and is diffusely red and elastic, does not adhere to vessels and the plasma may separate from the RBC

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13
Q

Chicken Fat Clots

A

the plasma that separates from the RBC resulting more yellowish

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14
Q

imbibition

A

the absorption of one substance by another

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15
Q

Hemoglobin imbibition

A

HgB released by the RBC breakdown (after death) leading to staining in the tissues (endocardium, blood vessels, aborted fetuses and frozen tissues)

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16
Q

Bile Imbibition

A

bile leaking from the gallbladder staining the surrounding tissues green and yellow

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17
Q

Pseudomelanosis

A

artificial black discoloration of tissues due to the saprophytic bacteria production of hydrogen sulfide and iron (iron sulfide)

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18
Q

Putrefaction

A

enzymatic decomposition of organic material and foul smelling compounds

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19
Q

postmortem Emphysema

A

Saprophytic bacteria produce gas, distend the GI tract and organs and body cavities (bloating). May cause rectal/vaginal prolapse. gas bubbles form in liver and brain and displacing the organs

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20
Q

euthanasia artifacts

A

deposition of formalin- soluble precipitates of barbiturates on serosal surfaces or endocardium

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21
Q

Etiology

A

manner of causation of death (endogenous or intrinsic: genetic) (Exogenous or acquired: infectious, nutritional etc.)

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22
Q

pathogenesis

A

events of the body cells and tissues to the etiological agent from that initial interaction to the expression of the disease.

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23
Q

Clinical diagnosis

A

estimated identification of the underlying disease based on diagnostics and history

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24
Q

morphological diagnosis

A

short phrase to sum up the important aspects of the lesion

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25
Q

etiologic diagnosis

A

defining the agent that has caused the disease

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26
Q

disease diagnosis

A

naming the disease

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27
Q

Blood loss anemia

A

hypovolemic shock and loss of 33% of BV during acute blood loss is lethal

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28
Q

wound shock

A

loss of fluid due to histamine release in damaged tissues

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29
Q

hyperkalemia

A

higher potassium level in blood than normal due to release of the K from large number of lethally injured cells

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30
Q

Crush Kidneys

A

reduced blood supply to kidneys and increased myoglobin from damaged muscle cells

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31
Q

Trauma 6

A

Blood loss anemia, wound shock, hyperkalemia, crush kidneys, bone marrow emboli to lungs after bone fractures, generalized infections

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32
Q

embolus

A

object carried from sight of issue to lodge in a blood vessel

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33
Q

Temperature 6

A

hyperthermia, Hypothermia combustio, congelatio, actinic stimuli, electricity, Atmospheric pressure changes

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34
Q

hyperthermia

A

dehydration with vasodilation in the skin and vasoconstriction in the organs, heat shock leads to liver necrosis which leads to DIC

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35
Q

heat shock proteins

A

proteins produced that protect the secondary and tertiary structures of proteins (prevent denaturation and remove damaged proteins

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36
Q

malignant hyperthermia

A

mutation in the ryanodine receptor altering Ca channels and increasing their release Ca from the Sarcoplasmic reticulum under bodily stress

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37
Q

insolation/sunstroke

A

local hyperthermia in the brain and may lead to cerebral edema or death before you see a body temp increase

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38
Q

Combustio

A

Burns: 1 - C. erythematosa (redness)
2 - C. Bullosa (blister)
3- escharotica (dead skin)
4- carbonisata (carbonized)

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39
Q

Hypothermia

A

dangerously low body temperature

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40
Q

Congelatio

A

frost bite: 1-3 same as burns - erythematosa, bullosa, escharotica,
4) gangraenosa (complete freezing)

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41
Q

actinic stimuli

A

from the photosensitization in the photo compounds of the skin forming radicals that leads to damage of the non-hair non pigmented skin regions (photodermatitis)
primary, secondary, hepatogenic

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42
Q

Primary Photosensitivity

A

uptake of photodynamic compounds
(plants, cancer drugs, etc.) with food → deposition in skin,
absorption of UV light → free radicals

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43
Q

Secondary Photosensitivity

A

impairment of porphyrin metabolism during heme synthesis (rare)

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44
Q

Hepatogenic Photosensitivity

A

mostly ruminants but also horses and llamas: chlorophyll is metabolized to
phylloerythrin by bacteria in rumen and/or colon; phylloerythrin
(from plants) is usually metabolized in healthy livers and excreted
via bile but persists in circulation in animals with liver disease and
is being deposited in skin. The chronically damaged livers are
unable to eliminate phylloerythrin. Photosensitivity occurs weeks
after the intake of the hepatotoxic plants.

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45
Q

UV light

A

sunburn leading to cancers

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46
Q

ionizing radiation

A

ionization of water with radical formation. X ray and gamma rays and normally form in mitotic active cells or water containing tissues. Repair mechanism works for mild issues, chronic leads to cancer and fibrosis

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47
Q

Central Nervous Syndrome (Radiation)

A 
high doses, death within minutes
to hours (vomiting, cramping, somnolence, marked lymphopenia,
coma)
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48
Q

Gastrointestinal Syndrome

A

death within two weeks (therapyresistant vomiting, diarrhea, gastrointestinal infections,
lymphopenia / neutropenia / thrombocytopenia with hemorrhages,
hair loss, oral inflammation, fever, nausea)

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49
Q

hematopoietic syndrome

A

intermittent nausea, vomiting,
diarrhea, lymphopenia / neutropenia / thrombocytopenia with
petechiae; infections or hemorrhagic diathesis may necessitate
bone marrow transplantation.

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50
Q

Subclinical or Prodromal Syndrome

A

low dose, nausea,

vomiting, and lymphopenia; patient can recover

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51
Q

Epilation - skin reaction to radiation

A

first degree - loss of keratin and depigmentation of skin and hair

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52
Q

Erythema- skin reaction to radiation

A

second degree - dermatitis, hair loss, depigmentation of re-growing hair

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53
Q

exudative- skin reaction to radiation

A

third degree - exudative dermatitis with blisters and
crusts and permanent alopecia (due to hair follicle damage)
o Necrosis and ulcers (“radiation dermatitis”); poor wound healing;
may result in squamous carcinoma or basal cell tumors

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54
Q

Electricity (Temperature)

A

household issues lead to burns and necrotic skin and muscle tissues.
lighting strikes lead to markings normally and typically also in the coronary band of hoof. (messes with the neurological function of respiration and fibrillations.
power line electrocution in birds

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55
Q

atmospheric pressure changes

A

Slow decrease in atmospheric pressure and oxygen concentration (“high
altitude disease” = “brisket disease”)
▪ Sudden decrease of atm. pressure: diver disease
▪ Sudden increase in atm. pressure (explosions): e.g. pulmonary hemorrhages

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56
Q

chemicals and drugs (causes of disease)

A

Exogenous toxins – environmental
o Endogenous toxins – byproduct of metabolism
o Some toxins have characteristic (“pathognomonic”) lesions but many have no or only
unspecific findings

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57
Q

Nutritional factors (cause of disease)

A

quantitative: undernourished emaciation/cachexia - see atrophy of adipose in the bone tissues
qualitative: mineral deficiencies, vitamin imbalance, dehydration, Na loss (hypotonic) kidney failure, water loss (hypertonic), hyperhydration

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58
Q

iatrogenic

A

caused by the veterinarian

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59
Q

Infectious agents

A

cause invasion and colonization within the body and activate.

local: stays at portal of entry and doesn’t spread
systemic: spread, sepsis, virus-induced tumor diseases

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60
Q

immune responses (causes of disease)

A

Cells damaged as innocent bystanders to immune response (release of reactive
oxygen species)
Hypersensitivity
Autoimmune diseases

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61
Q

workload imbalances (causes of disease)

A

overwork - adapt to demand or exhaustion and death

underwork - muscle atrophy

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62
Q

Aging (causes of disease)

A

culmination of injuries in life, default cause of injury in elderly animals

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63
Q

hypoxia (cell injury)

A

body or region of the body is deprived of adequate oxygen supply at the tissue level

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64
Q

Nature and severity of injurious stimulus

A

Chart on screenshot 14

65
Q

Reversible cell injury

A

(“cellular degeneration”) - functional and morphologic changes
that are reversible if the damaging stimulus is removed
o reduced oxidative phosphorylation, adenosine triphosphate (ATP) depletion, and
cellular swelling caused by changes in ion concentrations and water influx

66
Q

irreversible injury and cell death

A

continued injury, cell cannot recover even when the

injurious stimulus is removed. Plasma membrane damage, hemolysins of bacterial origin and MAC

67
Q

intracellular systems most vulnerable to injury 5

A

Cell membranes - ionic and osmotic homeostasis of the cell
o Aerobic respiration (mitochondria) - Oxidative phosphorylation, production of ATP
o Protein synthesis - ribosomes detach, cell has reduced protein synthesis, and can’t
move lipid due to lack of lipoproteins
o Genetic apparatus
o Cytoskeleton

68
Q

Injurious stimulus picture

A

Flow chart on notes

69
Q

hydropic degeneration (reversible cell injury)

A

no longer maintaining fluid homeostasis with functional issues of energy dependent ion pumps.
sensu lato: water intake or intracellular accumulation of material (ballooning)
Sensu stricto: water intake
gross lesion: degenerative organ changes if enough cells are affected

70
Q

mechanisms for acute swelling

A

damage to cell membranes, failure of cellular energy production, injury to enzymes regulating ion channels of membranes

71
Q

ischemia

A

reduced blood flow due to mechanical obstruction
in the arterial system, catastrophic fall in blood pressure, or
significant blood loss

72
Q

infarction

A

due to thrombosis of arterial vessels =

localized area of ischemic (or hemorrhagic) necrosis

73
Q

anemia hypoxia

A

reduction in numbers or volume of

erythrocytes or quality of hemoglobin

74
Q

histotoxic hypoxia

A

interfere with respiratory chain, oxidative phosphorylation (CN poisoning)

75
Q

Cell demand for O2

A

Neurons – high demand, irreversible injury in 3-5 minutes
o Fibrocytes, myocytes – low demand, several hours until
irreversible injury

76
Q

events of reversible ischemic injury

A

Deficiency of oxygen delivery, cell oxygen depleted within
seconds → oxidative phosphorylation halts and ATP
decreases → fermentation (anaerobic glycolysis does not
occur in neurons – especially vulnerable to hypoxia)
Reduced activity of ATP-dependent Na+ pump
Altered cellular energy metabolism
Detachment of ribosomes from RER → reduced protein
synthesis
Morphological changes
functional impairment

77
Q

Hydropic degeneration (irreversible)

A

(irreversible) – disintegration of membrane
system, marked swelling do to coalescing vacuoles with
displacement of nucleus to side and pyknosis (irreversible
condensation of chromatin), karyorrhexia (destructive fragmentation
of the nucleus), and karyolysis (dissolution of a cell nucleus)

78
Q

Pyknosis

A

irreversible condensation of chromatin.

shrunken densly basophilic nuclei

79
Q

karyorrhexia

A

destructive fragmentation of the nucleus.

nuclear fragmentation

80
Q

karyolysis

A

dissolution of a cell nucleus.

dissolution of the nucleus

81
Q

fate of acute cell swelling

A

depends on the type of cell and its current status, the injury and its duration and severity, sensitivity to hypoxia

82
Q

changes associated with irreversible cell injury

A

extensive damage to all cellular membranes, swelling of lysosomes, vacuolization of mitochondria with reduced ATP generation capacity

83
Q

Events following functional changes of irreversible cell injury

A

Entry of extracellular calcium into the cell
o Release of any intracellular calcium stores
o Activation of enzymes that can catabolize membranes, proteins, ATP, and nucleic
acids
o Continued loss of proteins, essential coenzymes, and ribonucleic acids from the
hyperpermeable plasma membrane
o Leakage of metabolites vital for the reconstitution of ATP from the cell
o Further depletion of intracellular high-energy phosphates

84
Q

normal to irreversible cell injury picture

A

on notes!

85
Q

cell death

A

Unable to reverse mitochondrial dysfunction (lack of oxidative phosphorylation and ATP
generation) even after resolution of the original injury
• Develop profound disturbances in membrane function

lysosomal secretion of enzymes

86
Q

necrosis

A

dissolution and cell death

87
Q

oncosis

A

usually consequence of degenerative cellular changes, also caused
directly by massive lethal injury. lysosomal leakage and spread of inflammation to adjacent cells

88
Q

reperfusion injury

A

cells under ischemia get a sudden increase in Ca and O2 leading to overload of the cell and deteriorates more

89
Q

Apoptosis

A

induced by some noxious stimuli, especially those that damage DNA

90
Q

Ca role in cell injury

A

increased intracellular Ca leads to increased activity of enzymes that break down structural components leading to death

91
Q

Free radical injuries

A

oxidative modifications of proteins lesions on DNA, lipid peroxidation

92
Q

oxidative stress

A

imbalance of free radicals generating and free radical

scavenging systems of the cell

93
Q

Pathogenesis of cell death in cell that lost blood supply

A

Ischemia → decreased ATP synthesis → plasma membrane Na+ / K+ ATPase
pump fails and Na+ enters the cell with excess water, leading to cell swelling and
dilation of the RER
Ca2+ pump fails and causes excess calcium to enter the cell, activating destructive
enzymes → cell death

94
Q

Coagulative necrosis

A

MOST COMMON MANIFESTATION OF CELL DEATH.

hypoxic/ischemic characteristics in all tissues (besides brain) protein denaturation

95
Q

Coagulation gross features

A

Lighter in color due to coagulation of cytoplasmic proteins and
decreased blood flow
• Firm texture
• Usually dry
• May be swollen or shrunken
• Local reaction to necrotic tissue (surrounding red zone of congestion
or white layer of inflammatory cells)

96
Q

nuclear hyperchomasia

A

accumulation of chromatin in the nuclear membrane

97
Q

White infarctions (anemic/arterial)

A

affects solid organs and intestinal segments lacking
arterial collateral blood supply, leads to lack of blood in
affected tissue

98
Q

red infarctions (hemorrhagic/venous)

A

occlusion of veins where blood enters but does not drain

99
Q

Lytic necrosis

A

liquefactive oncotic necrosis (make liquid and lyse everything instead of denaturing (common in bacteria, also hypoxic damage of brain and spinal cord)
Appears liquified

100
Q

caseous oncotic necrosis

A

cheese like appearance and many lesions (TB)

101
Q

Gangrene

A

ischemic necrosis of extremities

102
Q

Dry gangrene

A

– coagulation necrosis of an extremity without secondary
bacterial infection; essentially mummification of a body part in a living
organism

103
Q

Wet gangrene

A

coagulative necrosis of dry gangrene is modified by the
liquefactive action of saprophytic (live in dead organic matter) / putrefactive
bacteria; colonize area of necrosis and cause putrefaction

104
Q

Gas (emphysematous) gangrene

A

clostridial infection with gas
production; requires a) clostridial organisms inoculated into tissues, and b)
oxygen tension must be low enough for the clostridial organisms to
proliferate and they produce gas from digestion by bacterial enzymes

105
Q

Fat oncotic necrosis

A

due to inflammation, Vit. E deficiency and Trauma, and is distinguished by the location of fat storage (firm hard and chalky adipose tissue)

106
Q

Fibrinoid vascular necrosis

A

Due to deposition of antigen-antibody complexes in walls of small arteries
leading via complement activation to necrosis of vessel wall
▪ not caused by a primary degeneration and necrosis of smooth muscle cells
but rather due to deposition of fibrin, complement, etc. in the smooth
muscle layer of vessels

107
Q

Apoptosis features

A

Rapid, may occur in tissues before evident in histology
• Cell shrinkage
• Chromatin condensation
• Formation of cytoplasmic blebs then apoptotic bodies
• Phagocytosis of apoptotic cells / cell bodies

108
Q

initiation phase (apoptosis)

A

stimulate targets on surface or in the cell

109
Q

execution phase (apoptosis)

A

actual death program accomplished by proteases

110
Q

caspase

A

family of protease enzymes playing essential roles in programmed cell death

111
Q

Apoptosis too little

A

increased survival of abnormal cells

112
Q

apoptosis too much

A

loss of cells in neurodegenerative diseases, ischemic injured cells or cells with viral infections

113
Q

Differentiation between apoptosis and necrosis

A

Electron microscopy, immunohostochemistry (antigen of caspase), TUNEL method (DNA fragments), DNA laddering assay (gel electrophoresis)

114
Q

Comparing oncosis and apoptosis

A

Chart in notes

115
Q

atrophy

A

shrinkage in organ due to simple or numeric atrophy

116
Q

Simple atrophy

A

shrinkage of the parenchymal cells due

to loss of cell substance

117
Q

Numeric atrophy

A

loss of cells

118
Q

senile atrophy

A

aging shrinkage

119
Q

hypertrophy

A

increased size of the cells (increased size of organ)

increased demand or higher DNA content, more synthesis of structural components, hemodynamic overload to heart

120
Q

Hyperplasia

A

increase number of cells in an organ or tissue. if cells can synthesize DNA, increased growth factors
may be hormonal or compensatory (after damage or cellular demand)q

121
Q

Metaplasia

A

reversible change in which one adult cell type is replaced by another cell type more able to withstand an adverse environment (adaptation)
changing of ciliated cell type to squamous for less irritation with chronic issues, CT in areas it would not normally grow

stem cell reprogramming

122
Q

autophagy

A

removal of damaged organelles during cell injury and the
cellular remodeling or differentiation; lysosomal digestion of the cell’s own
cytosolic components

123
Q

heterophagy

A

initiated by the cell to digest materials ingested
from the extracellular environment; for example, after the uptake and
digestion of bacteria by neutrophils and the removal of apoptotic cells by
macrophages

124
Q

Dystrophy

A

lesion of deranged metabolism / disorder in which an organ or tissue
of the body wastes away

125
Q

steatosis

A

abnormal accumulations of triglycerides within parenchymal
cells, often seen in the liver because it is the major organ involved in fat
metabolism

126
Q

Fatty Change

A

accumulation of lipid within the cytoplasm

most likely hepatocytes and can be reversible

127
Q

Fatty liver

A

due to excessive FFA to the liver, blockage of FA oxidation to ketones or others, impaired synthesis of apoproteins

128
Q

cholesterol

A

Accumulation of lipid and cholesterol in arterial intima due to
deranged lipid metabolism is common in humans and results in
atherosclerosis
• Tend to accumulate in areas of cell necrosis and inflammation
(“resorptive lipidosis”)

129
Q

chart of diseases and Fat

A

on the notes

130
Q

glycogen infiltration

A

lacking the ability to process glycogen and utilize it or to make it. it is reversible

131
Q

hyaline change

A

protein causing pink homogenous staining of the tissue (accumulation of proteins in the tissues)

132
Q

Gout

A

Derangement of nucleic acid metabolism – urates are deposited in kidney or on
serosal surfaces / joints
o Urate concentration increased when diet is too rich in purine bases or renal
secretion of uric acid is decreased
o Uric acids form insoluble urate salts that are deposited extracellularly and elicit
granulomatous “foreign body” inflammatory reaction

133
Q

pseudogout

A

deposition of salts other than urate salts like in joints

134
Q

dystrophic calcification

A

calcification of injured cells: cannot regulate Ca in the dying cells and spreads causing calcification

135
Q

metastatic calcification

A

deposition of Ca salts in normal tissues beginning extracellularly but can also happen within the cell and occurs with imbalance of Ca and P.
Hypervitaminosis D, renal disease

136
Q

hemoglobin

A

red iron containing pigment- red to brown to black discoloration of the tissue during hemorrhage

137
Q

methemoglobin

A

inactive form of hemoglobin with wrong Fe3+ more bluish chocolate color and nitrate toxicity

138
Q

Hemosiderin

A

Brown, granular, iron containing pigment found in macrophages of some
organs and sites of old hemorrhage
▪ Degradation product of hemoglobin

139
Q

hematin

A

▪ Degeneration product of hemoglobin
▪ Main pigment in melena, generated when hemoglobin is exposed to the
hydrochloric acid during episodes of intraluminal gastric hemorrhage
▪ Acid hematin – annoying histologic artifact of formalin fixation
▪ Parasite hematin – waste product of certain parasites

140
Q

hematoidin

A

breakdown product of hemoglobin not containing iron (breaks down after iron is dissociated from it) occurs extracellularly during hemorrhage
red brown to orange

141
Q

bilirubin

A

yellow brown breakdown of heme (macrophages of spleen, liver, bone marrow, and sites of hemorrhage)
in the live can see it

142
Q

RBC breakdown

A

chart in notes

143
Q

icterus

A

hyperbilirubinemia

144
Q

prehepatic icterus

A

– due to hemolysis leading to a flooding of the

liver with unconjugated bilirubin

145
Q

hepatic icterus

A

due to damage of hepatocytes or biliary cells
leading to impaired uptake, metabolism, secretion and transport of
bile pigments within the liver

146
Q

Post hepatic icterus

A

occurs when there is an outflow obstruction

of bile

147
Q

Hyperkeratosis

A

increased cornification of the epidermis with thickening of the
str. spinosum and str. corneum

148
Q

Parakeratosis

A

faulty maturation of the str. corneum so that the cornified cells still contain nuclei. greasy skin,
Zn deficiency

149
Q

concentrations

A

Hard masses that occur in cavities of secreting or excreting glands / organs or in
the alimentary tract. Can be sediment or appear as stones

150
Q

true concentrations

A

Precipitation of organic material and calcium or other minerals frequently around a
crystallization point (stone, etc.)
o Occurs mainly in alimentary tract and urinary tract

151
Q

pseudoconcentratons

A

stony conglomerations of inspissated exudates

152
Q

teratology

A

study of malformations

153
Q

agenesis

A

complete lack of the anlage (earliest developmental stage) for an organ

154
Q

hypoplasia

A

limited development of an organ

155
Q

hetertrophy

A

entire organ tissues in other organ (hair on tongue)

156
Q

hamartoma

A

neoplasia arising from faulty developed tissue

157
Q

endogenous abnormality causes

A

mutation and morph in chromosomes, may not be spontaneous

158
Q

exogenous abnormaliites

A

physical, chemical, viral

Basic Pathology (4 decks)

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