Basic Pathology Exam 1 Flashcards
Thanatology
Study of death
Signs of death
unequivocal and equivocal
Agony
life to death, loss of function of all systems leading to organ dysfunction. Can be short or long depending on the trauma
Cause of Death
disease or injury that is responsible for the death, root cause or immediate cause
Mechanism of Death
physiologic derangement initiated by the cause of death and resulting in death
Ex: brain death leading to subsequent respiratory arrest
Manner of Death
natural vs. non-natural
rigor mortis
once ATP runs out in the muscles and have a myosin-actin binding rigidity. (ATP reserves depleted and cannot detach)
pallor mortis
pale skin due to lack of circulation in peripherals
Livor Mortis
dark spots appear in the skin in the lower portion of the body (gravitational pooling of blood)
Algor Mortis
Body temperature reduces to environmental temperature. Speed of cool down inversely proportional to rate of decomposition
Postmortem Autolysis/ Decomposition
this begins by progressive release of endogenous enzymes and then action of saprophytic bacteria (escaping from the gut)
Postmortem Clotting
in the heart and vessels and is diffusely red and elastic, does not adhere to vessels and the plasma may separate from the RBC
Chicken Fat Clots
the plasma that separates from the RBC resulting more yellowish
imbibition
the absorption of one substance by another
Hemoglobin imbibition
HgB released by the RBC breakdown (after death) leading to staining in the tissues (endocardium, blood vessels, aborted fetuses and frozen tissues)
Bile Imbibition
bile leaking from the gallbladder staining the surrounding tissues green and yellow
Pseudomelanosis
artificial black discoloration of tissues due to the saprophytic bacteria production of hydrogen sulfide and iron (iron sulfide)
Putrefaction
enzymatic decomposition of organic material and foul smelling compounds
postmortem Emphysema
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
euthanasia artifacts
deposition of formalin- soluble precipitates of barbiturates on serosal surfaces or endocardium
Etiology
manner of causation of death (endogenous or intrinsic: genetic) (Exogenous or acquired: infectious, nutritional etc.)
pathogenesis
events of the body cells and tissues to the etiological agent from that initial interaction to the expression of the disease.
Clinical diagnosis
estimated identification of the underlying disease based on diagnostics and history
morphological diagnosis
short phrase to sum up the important aspects of the lesion
etiologic diagnosis
defining the agent that has caused the disease
disease diagnosis
naming the disease
Blood loss anemia
hypovolemic shock and loss of 33% of BV during acute blood loss is lethal
wound shock
loss of fluid due to histamine release in damaged tissues
hyperkalemia
higher potassium level in blood than normal due to release of the K from large number of lethally injured cells
Crush Kidneys
reduced blood supply to kidneys and increased myoglobin from damaged muscle cells
Trauma 6
Blood loss anemia, wound shock, hyperkalemia, crush kidneys, bone marrow emboli to lungs after bone fractures, generalized infections
embolus
object carried from sight of issue to lodge in a blood vessel
Temperature 6
hyperthermia, Hypothermia combustio, congelatio, actinic stimuli, electricity, Atmospheric pressure changes
hyperthermia
dehydration with vasodilation in the skin and vasoconstriction in the organs, heat shock leads to liver necrosis which leads to DIC
heat shock proteins
proteins produced that protect the secondary and tertiary structures of proteins (prevent denaturation and remove damaged proteins
malignant hyperthermia
mutation in the ryanodine receptor altering Ca channels and increasing their release Ca from the Sarcoplasmic reticulum under bodily stress
insolation/sunstroke
local hyperthermia in the brain and may lead to cerebral edema or death before you see a body temp increase
Combustio
Burns: 1 - C. erythematosa (redness)
2 - C. Bullosa (blister)
3- escharotica (dead skin)
4- carbonisata (carbonized)
Hypothermia
dangerously low body temperature
Congelatio
frost bite: 1-3 same as burns - erythematosa, bullosa, escharotica,
4) gangraenosa (complete freezing)
actinic stimuli
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
Primary Photosensitivity
uptake of photodynamic compounds
(plants, cancer drugs, etc.) with food → deposition in skin,
absorption of UV light → free radicals
Secondary Photosensitivity
impairment of porphyrin metabolism during heme synthesis (rare)
Hepatogenic Photosensitivity
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.
UV light
sunburn leading to cancers
ionizing radiation
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
Central Nervous Syndrome (Radiation)
high doses, death within minutes to hours (vomiting, cramping, somnolence, marked lymphopenia, coma)
Gastrointestinal Syndrome
death within two weeks (therapyresistant vomiting, diarrhea, gastrointestinal infections,
lymphopenia / neutropenia / thrombocytopenia with hemorrhages,
hair loss, oral inflammation, fever, nausea)
hematopoietic syndrome
intermittent nausea, vomiting,
diarrhea, lymphopenia / neutropenia / thrombocytopenia with
petechiae; infections or hemorrhagic diathesis may necessitate
bone marrow transplantation.
Subclinical or Prodromal Syndrome
low dose, nausea,
vomiting, and lymphopenia; patient can recover
Epilation - skin reaction to radiation
first degree - loss of keratin and depigmentation of skin and hair
Erythema- skin reaction to radiation
second degree - dermatitis, hair loss, depigmentation of re-growing hair
exudative- skin reaction to radiation
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
Electricity (Temperature)
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
atmospheric pressure changes
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
chemicals and drugs (causes of disease)
Exogenous toxins – environmental
o Endogenous toxins – byproduct of metabolism
o Some toxins have characteristic (“pathognomonic”) lesions but many have no or only
unspecific findings
Nutritional factors (cause of disease)
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
iatrogenic
caused by the veterinarian
Infectious agents
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
immune responses (causes of disease)
Cells damaged as innocent bystanders to immune response (release of reactive
oxygen species)
Hypersensitivity
Autoimmune diseases
workload imbalances (causes of disease)
overwork - adapt to demand or exhaustion and death
underwork - muscle atrophy
Aging (causes of disease)
culmination of injuries in life, default cause of injury in elderly animals
hypoxia (cell injury)
body or region of the body is deprived of adequate oxygen supply at the tissue level
Nature and severity of injurious stimulus
Chart on screenshot 14
Reversible cell injury
(“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
irreversible injury and cell death
continued injury, cell cannot recover even when the
injurious stimulus is removed. Plasma membrane damage, hemolysins of bacterial origin and MAC
intracellular systems most vulnerable to injury 5
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
Injurious stimulus picture
Flow chart on notes
hydropic degeneration (reversible cell injury)
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
mechanisms for acute swelling
damage to cell membranes, failure of cellular energy production, injury to enzymes regulating ion channels of membranes
ischemia
reduced blood flow due to mechanical obstruction
in the arterial system, catastrophic fall in blood pressure, or
significant blood loss
infarction
due to thrombosis of arterial vessels =
localized area of ischemic (or hemorrhagic) necrosis
anemia hypoxia
reduction in numbers or volume of
erythrocytes or quality of hemoglobin
histotoxic hypoxia
interfere with respiratory chain, oxidative phosphorylation (CN poisoning)
Cell demand for O2
Neurons – high demand, irreversible injury in 3-5 minutes
o Fibrocytes, myocytes – low demand, several hours until
irreversible injury
events of reversible ischemic injury
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
Hydropic degeneration (irreversible)
(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)
Pyknosis
irreversible condensation of chromatin.
shrunken densly basophilic nuclei
karyorrhexia
destructive fragmentation of the nucleus.
nuclear fragmentation
karyolysis
dissolution of a cell nucleus.
dissolution of the nucleus
fate of acute cell swelling
depends on the type of cell and its current status, the injury and its duration and severity, sensitivity to hypoxia
changes associated with irreversible cell injury
extensive damage to all cellular membranes, swelling of lysosomes, vacuolization of mitochondria with reduced ATP generation capacity
Events following functional changes of irreversible cell injury
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
normal to irreversible cell injury picture
on notes!
cell death
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
necrosis
dissolution and cell death
oncosis
usually consequence of degenerative cellular changes, also caused
directly by massive lethal injury. lysosomal leakage and spread of inflammation to adjacent cells
reperfusion injury
cells under ischemia get a sudden increase in Ca and O2 leading to overload of the cell and deteriorates more
Apoptosis
induced by some noxious stimuli, especially those that damage DNA
Ca role in cell injury
increased intracellular Ca leads to increased activity of enzymes that break down structural components leading to death
Free radical injuries
oxidative modifications of proteins lesions on DNA, lipid peroxidation
oxidative stress
imbalance of free radicals generating and free radical
scavenging systems of the cell
Pathogenesis of cell death in cell that lost blood supply
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
Coagulative necrosis
MOST COMMON MANIFESTATION OF CELL DEATH.
hypoxic/ischemic characteristics in all tissues (besides brain) protein denaturation
Coagulation gross features
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)
nuclear hyperchomasia
accumulation of chromatin in the nuclear membrane
White infarctions (anemic/arterial)
affects solid organs and intestinal segments lacking
arterial collateral blood supply, leads to lack of blood in
affected tissue
red infarctions (hemorrhagic/venous)
occlusion of veins where blood enters but does not drain
Lytic necrosis
liquefactive oncotic necrosis (make liquid and lyse everything instead of denaturing (common in bacteria, also hypoxic damage of brain and spinal cord)
Appears liquified
caseous oncotic necrosis
cheese like appearance and many lesions (TB)
Gangrene
ischemic necrosis of extremities
Dry gangrene
– coagulation necrosis of an extremity without secondary
bacterial infection; essentially mummification of a body part in a living
organism
Wet gangrene
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
Gas (emphysematous) gangrene
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
Fat oncotic necrosis
due to inflammation, Vit. E deficiency and Trauma, and is distinguished by the location of fat storage (firm hard and chalky adipose tissue)
Fibrinoid vascular necrosis
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
Apoptosis features
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
initiation phase (apoptosis)
stimulate targets on surface or in the cell
execution phase (apoptosis)
actual death program accomplished by proteases
caspase
family of protease enzymes playing essential roles in programmed cell death
Apoptosis too little
increased survival of abnormal cells
apoptosis too much
loss of cells in neurodegenerative diseases, ischemic injured cells or cells with viral infections
Differentiation between apoptosis and necrosis
Electron microscopy, immunohostochemistry (antigen of caspase), TUNEL method (DNA fragments), DNA laddering assay (gel electrophoresis)
Comparing oncosis and apoptosis
Chart in notes
atrophy
shrinkage in organ due to simple or numeric atrophy
Simple atrophy
shrinkage of the parenchymal cells due
to loss of cell substance
Numeric atrophy
loss of cells
senile atrophy
aging shrinkage
hypertrophy
increased size of the cells (increased size of organ)
increased demand or higher DNA content, more synthesis of structural components, hemodynamic overload to heart
Hyperplasia
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
Metaplasia
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
autophagy
removal of damaged organelles during cell injury and the
cellular remodeling or differentiation; lysosomal digestion of the cell’s own
cytosolic components
heterophagy
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
Dystrophy
lesion of deranged metabolism / disorder in which an organ or tissue
of the body wastes away
steatosis
abnormal accumulations of triglycerides within parenchymal
cells, often seen in the liver because it is the major organ involved in fat
metabolism
Fatty Change
accumulation of lipid within the cytoplasm
most likely hepatocytes and can be reversible
Fatty liver
due to excessive FFA to the liver, blockage of FA oxidation to ketones or others, impaired synthesis of apoproteins
cholesterol
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”)
chart of diseases and Fat
on the notes
glycogen infiltration
lacking the ability to process glycogen and utilize it or to make it. it is reversible
hyaline change
protein causing pink homogenous staining of the tissue (accumulation of proteins in the tissues)
Gout
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
pseudogout
deposition of salts other than urate salts like in joints
dystrophic calcification
calcification of injured cells: cannot regulate Ca in the dying cells and spreads causing calcification
metastatic calcification
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
hemoglobin
red iron containing pigment- red to brown to black discoloration of the tissue during hemorrhage
methemoglobin
inactive form of hemoglobin with wrong Fe3+ more bluish chocolate color and nitrate toxicity
Hemosiderin
Brown, granular, iron containing pigment found in macrophages of some
organs and sites of old hemorrhage
▪ Degradation product of hemoglobin
hematin
▪ 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
hematoidin
breakdown product of hemoglobin not containing iron (breaks down after iron is dissociated from it) occurs extracellularly during hemorrhage
red brown to orange
bilirubin
yellow brown breakdown of heme (macrophages of spleen, liver, bone marrow, and sites of hemorrhage)
in the live can see it
RBC breakdown
chart in notes
icterus
hyperbilirubinemia
prehepatic icterus
– due to hemolysis leading to a flooding of the
liver with unconjugated bilirubin
hepatic icterus
due to damage of hepatocytes or biliary cells
leading to impaired uptake, metabolism, secretion and transport of
bile pigments within the liver
Post hepatic icterus
occurs when there is an outflow obstruction
of bile
Hyperkeratosis
increased cornification of the epidermis with thickening of the
str. spinosum and str. corneum
Parakeratosis
faulty maturation of the str. corneum so that the cornified cells still contain nuclei. greasy skin,
Zn deficiency
concentrations
Hard masses that occur in cavities of secreting or excreting glands / organs or in
the alimentary tract. Can be sediment or appear as stones
true concentrations
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
pseudoconcentratons
stony conglomerations of inspissated exudates
teratology
study of malformations
agenesis
complete lack of the anlage (earliest developmental stage) for an organ
hypoplasia
limited development of an organ
hetertrophy
entire organ tissues in other organ (hair on tongue)
hamartoma
neoplasia arising from faulty developed tissue
endogenous abnormality causes
mutation and morph in chromosomes, may not be spontaneous
exogenous abnormaliites
physical, chemical, viral
