pathology Flashcards
1
Q
etiology
A
cause of disease
2
Q
intrinsic predisposing factors
A
species, breed, age, sex, color
2
Q
intrinsic predisposing factors
A
species, breed, age, sex, color
3
Q
extrinisic predisposing factors
A
temp, nutrition
4
Q
intrinsic determinate factors
A
genetic abnormalities
5
Q
extrinsic determinate factors
A
biologic
* bacteria, prions, viruses, fungi, parasites, etc
chemical
* exogenous (toxins, drugs, poison)
* endogenous (metabolites, free radicals)
physical
* mechanic (injury)
* thermal
* atmospheric pressure
* actinic (radiation)
6
Q
order of fat accumulation
A
- bone marrow
- pericardia groove
- perirenal area
- abdomen (mesentary)
- subcutis
7
Q
abrasion
A
skin damage with loss of epidermis and portion of the dermis
8
Q
laceration
A
deep cut or tear in skin or flesh
9
Q
puncture
A
penetrating wound caused by sharp object
10
Q
incision
A
Wound created by a sharp tool
11
Q
perforation
A
hole that develops through the wall of a body organ
12
Q
rupture
A
a break or tear in any organ or soft tissue
13
Q
fracture
A
fracture or breaking of hard object or material, typically a bone.
14
Q
actinic
A
radiation
extrinsic determinant factor
15
Q
4 “what” of submitting lab samples
A
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)
16
Q
multifocal
A
multiple seperate lesions across organ
17
Q
multifocal
A
multiple seperate lesions across organ
likely coming from somewhere else
18
Q
multifocal to coalescing
A
multifocal lesions that bump into each other on organ
19
Q
diffuse lesion
A
covers entire organ
20
Q
focal lesion
A
in one spot
21
Q
triangular shaped lesion
A
usually has vascular organ
tip of triangle at occluded vessel
22
Q
rhomboidal lesion
A
vascular origin
23
Q
lesion
A
abnormal tissue
24
cell injury
when a cell fails to maintain homeostasis
can be reversible or irreversible
25
cell/tissue general response to injury
* adaptation
* degeneration
* death (apoptosis, necrosis)
26
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
27
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)
28
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)
29
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
30
what processes can increase the size of an organ/tissue?
inflammation
hypertrophy
hyperplasia
neoplasia
31
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
32
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
33
mechanisms of cell injury main categories
ATP depletion
Membrane damage
Metabolic disturbance
Genetic damage
34
etiology
cause of disease
35
hypoxia vs ischemia
hypoxia: not enough O2
ischemia: impaired blood flow to tissue (no O2 and other problems)
36
infarct
tissue death due to ischemia
37
segmental lesion
a segment of a tubular organ
38
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
39
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
40
cytoplasmic hypereosiniphilia
cytoplasmic necrosis change
eosin stain is pink
cell appears more red by uptake of more eosin stain
41
pyknosis
necrosis nuclear change
shrunken, dark, round
42
karyorrhexis
necrosis nuclear change
nuclear fragments
43
karyolysis
necrosis nucleus change
pale nucleus (dissolution of chromatin)
44
necrosis nuclear changes
Pyknosis – shrunken, dark, round
Karyorrhexis – nuclear fragments
Karyolysis – pale nucleus (dissolution of chromatin)
45
morphological (gross appearance) types of necrosis
Coagulation necrosis
Caseous necrosis
Liquefactive necrosis
Gangrenous necrosis
Fat necrosis
46
coagulation necrosis
from stopping of blood flow
infarcts
47
caseous necrosis
cheese like
lots of dying leukocytes (white)
48
liquefactive necrosis
tissue liquefies
tissue dissolves and falls apart
49
gangrenous necrosis
usually forms in extremities
lack of blood flow or bacterial infection
50
Ischemia-reperfusion injury
* Follows restoration of blood supply to ischemic tissue
* Generation of ROS following restored oxygen supply
* Ca2+ influx – impaired ion pumps
51
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
52
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**
53
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**
54
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)
55
dystrophic calcification
Areas of **necrosis**
(caused by necrosis when dying cells release Ca2+)
Calcium accumulation in **mitochondria**
56
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
57
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
58
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
59
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**
60
glycogen intracellular accumulation
* Corticosteroids
* Diabetes mellitus
* Glycogen storage diseases
