pathology Flashcards
etiology
cause of disease
intrinsic predisposing factors
species, breed, age, sex, color
intrinsic predisposing factors
species, breed, age, sex, color
extrinisic predisposing factors
temp, nutrition
intrinsic determinate factors
genetic abnormalities
extrinsic determinate factors
biologic
* bacteria, prions, viruses, fungi, parasites, etc
chemical
* exogenous (toxins, drugs, poison)
* endogenous (metabolites, free radicals)
physical
* mechanic (injury)
* thermal
* atmospheric pressure
* actinic (radiation)
order of fat accumulation
- bone marrow
- pericardia groove
- perirenal area
- abdomen (mesentary)
- subcutis
abrasion
skin damage with loss of epidermis and portion of the dermis
laceration
deep cut or tear in skin or flesh
puncture
penetrating wound caused by sharp object
incision
Wound created by a sharp tool
perforation
hole that develops through the wall of a body organ
rupture
a break or tear in any organ or soft tissue
fracture
fracture or breaking of hard object or material, typically a bone.
actinic
radiation
extrinsic determinant factor
4 “what” of submitting lab samples
What do you see? (gross description, exact location)
What did you do?
What do you think? (differential diagnoses)
What do you want? (neoplasm, inflammation, surgical margins)
multifocal
multiple seperate lesions across organ
multifocal
multiple seperate lesions across organ
likely coming from somewhere else
multifocal to coalescing
multifocal lesions that bump into each other on organ
diffuse lesion
covers entire organ
focal lesion
in one spot
triangular shaped lesion
usually has vascular organ
tip of triangle at occluded vessel
rhomboidal lesion
vascular origin
lesion
abnormal tissue
cell injury
when a cell fails to maintain homeostasis
can be reversible or irreversible
cell/tissue general response to injury
- adaptation
- degeneration
- death (apoptosis, necrosis)
hypertrophy
- increase in cell size (but not number)
- cells synthesize more organelles to enlarge
- most common in striated muscle (increased workload)
- reversible (can atrophy)
can be:
* physologic
* pathologic: pulmonic stenosis causing R ventricular mycardial hypertrophy, hypertrophic cardiomyopathy in cats
hyperplasia
- increase in cell number (usually concurrent with hypertrophy)
- some cells can undergo hyperplasia, some can’t (labile cells can replicate- epithelial, bone marrow, permanent cannot- neurons, cardiac/skel musc)
- physiologic: hormonal (mammary gland prolif, enlargement of uterus) and compensatory (partial hepatectomy)
- pathologic: excessive hormonal stim, irritation (goiter- thyroid hyperplasia, benign prostatic hyperplasia)
hyperplasia
- increase in cell number (usually concurrent with hypertrophy)
- some cells can undergo hyperplasia, some can’t (labile cells can replicate- epithelial, bone marrow, permanent cannot- neurons, cardiac/skel musc)
- physiologic: hormonal (mammary gland prolif, enlargement of uterus) and compensatory (partial hepatectomy)
- pathologic: excessive hormonal stim, irritation (goiter- thyroid hyperplasia, benign prostatic hyperplasia)
hyperplasia vs neoplasia
Hyperplasia
* Increase in cell number in response to known stimulus
* Stimulus stops = hyperplasia stops
Neoplasia
* Uncontrolled cellular replication
* Cell proliferation is autonomous = does not respond to external stimuli
what processes can increase the size of an organ/tissue?
inflammation
hypertrophy
hyperplasia
neoplasia
metaplasia
One differentiated cell type replaced by another
* NOT transformation of one differentiated cell type to another differentiated cell type
* Stem cell differentiates along a different line
Adaptive change to withstand adverse environmental conditions
Potentially reversible (up to a point)
ex: mucosal epithelium to stratified squamous epithelium in resp tract from chronic irritation due to smoking
atrophy
decrese in size of cell, tissue, or organ after normal growth has been reached
decreased cell number and/or size
physiologic: involution of thymus, postpartum uterus (apoptosis)
pathologic:
* inadequate nutriative supply (starvation, dimished blood supply)
* decreased workload (muscle atrophy)
* denervation
* pressure (benign neoplasma)
* loss of endocrine stim
mechanisms of cell injury main categories
ATP depletion
Membrane damage
Metabolic disturbance
Genetic damage
etiology
cause of disease
hypoxia vs ischemia
hypoxia: not enough O2
ischemia: impaired blood flow to tissue (no O2 and other problems)
infarct
tissue death due to ischemia
segmental lesion
a segment of a tubular organ
hydropic degeneration
increased cell size/volume
cytoplasmic vacuolation (swollen mitochondria, ER. golgi)
mechanism
1. hypoxia
2. ATP production decreases
3. Na+/water move into cell, K+ out
4. osmotic pressure increases and more water moves into cell
5. cisternae of ER distend, rupture, form vacuoles
6. extensive vacuolation
7. necrosis
necrosis causes
Cell death after injury by hypoxia, ischemia, cell membrane damage
Acute cell swelling can lead to necrosis – point of no return unclear
Cell membrane damage due to chemical injury
Cell membrane damage due to free radical injury
* Anti-oxidant protective mechanisms to avoid free radical injury
–Superoxide dismutase (SOD)
–Glutathione peroxidase
–Vitamins E, C
Ischemia-reperfusion injury
* Follows restoration of blood supply to ischemic tissue
* Generation of ROS following restored oxygen supply
* Ca2+ influx – impaired ion pumps
cytoplasmic hypereosiniphilia
cytoplasmic necrosis change
eosin stain is pink
cell appears more red by uptake of more eosin stain
pyknosis
necrosis nuclear change
shrunken, dark, round
karyorrhexis
necrosis nuclear change
nuclear fragments
karyolysis
necrosis nucleus change
pale nucleus (dissolution of chromatin)
necrosis nuclear changes
Pyknosis – shrunken, dark, round
Karyorrhexis – nuclear fragments
Karyolysis – pale nucleus (dissolution of chromatin)
morphological (gross appearance) types of necrosis
Coagulation necrosis
Caseous necrosis
Liquefactive necrosis
Gangrenous necrosis
Fat necrosis
coagulation necrosis
from stopping of blood flow
infarcts
caseous necrosis
cheese like
lots of dying leukocytes (white)
liquefactive necrosis
tissue liquefies
tissue dissolves and falls apart
gangrenous necrosis
usually forms in extremities
lack of blood flow or bacterial infection
Ischemia-reperfusion injury
- Follows restoration of blood supply to ischemic tissue
- Generation of ROS following restored oxygen supply
- Ca2+ influx – impaired ion pumps
apoptosis
‘cellular suicide’
Physiologic
* Involution after hormone withdrawal
* Elimination of self-reactive lymphocytes
* Age-related thymic involution
Pathologic
* Viral infections
* Gland involution following duct blockage
* Accumulation of misfolded protreins
* Immune mediated
extrinsic pathway of apoptosis
Binding of cell surface death receptors
TNF family receptors – FAS
Both extrinsic and intrinsic pathways lead to activation of the caspase cascade: Culminates in DNA degradation and apoptosis
intrinsic pathway of apoptosis
Increased mitochondrial permeability
Release of pro-apoptotic molecules into cytoplasm
Cytochrome c
Both extrinsic and intrinsic pathways lead to activation of the caspase cascade: Culminates in DNA degradation and apoptosis
morphologic features of apoptosis vs necrosis
- Cell shrinkage (cell swelling for necrosis)
- apotosis: Condensed chromatin
- apoptosis: Cytoplasmic buds (Phagocytosis of apoptotic bodies)
- apoptosis: NO inflammation (vs yes inflammation for necrosis)
dystrophic calcification
Areas of necrosis
(caused by necrosis when dying cells release Ca2+)
Calcium accumulation in mitochondria
Metastatic calcification
Occurs in normal tissue secondary to hypercalcemia
(caused by increased Ca2+)
Examples
* Renal failure
* Vitamin D toxicosis
* Elevated PTH or PTHrp (Primary hyperparathyroidism = rare)
* Neoplastic bone destruction
cellular aging
Decline in cell function/viability
* Progressive exposure to exogenous influences & accumulation of cellular damage
* Reduced oxidative phosphorylation
* Reduced protein/nucleic acid synthesis
Decreased cellular replication
* Multiple mechanisms
* Progressive telomere shortening
* Telomerase activity in somatic cells = neoplasia
intracellular accumulations from dysregulated cellular metabolism
Normal product but inadequate removal
* Fatty change in the liver
Normal product but defective enzymatic removal
* Lysosomal storage diseases
Abnormal product due to gene mutation
Abnormal exogenous substances
* ie. carbon (tattoos), silicon
intracellular accumulation of lipids
Hepatic lipidosis (steatosis)
* Accumulation of intracellular triglycerides due to increased supply of FFA, or decreased metabolism/excretion of lipoproteins
Examples:
* Early lactation dairy cows
* Obese animals suddenly off feed (feline fatty liver syndrome)
Morphologic features
Gross: pale tan, friable/greasy
Histo: distinct, clear, smooth walled cytoplasmic vacuoles
glycogen intracellular accumulation
- Corticosteroids
- Diabetes mellitus
- Glycogen storage diseases
