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DWT exam 1 > pathology > Flashcards

pathology Flashcards

1
Q

etiology

A

cause of disease

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2
Q

intrinsic predisposing factors

A

species, breed, age, sex, color

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2
Q

intrinsic predisposing factors

A

species, breed, age, sex, color

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3
Q

extrinisic predisposing factors

A

temp, nutrition

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4
Q

intrinsic determinate factors

A

genetic abnormalities

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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)

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6
Q

order of fat accumulation

A
  1. bone marrow
  2. pericardia groove
  3. perirenal area
  4. abdomen (mesentary)
  5. subcutis
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7
Q

abrasion

A

skin damage with loss of epidermis and portion of the dermis

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8
Q

laceration

A

deep cut or tear in skin or flesh

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9
Q

puncture

A

penetrating wound caused by sharp object

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10
Q

incision

A

Wound created by a sharp tool

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11
Q

perforation

A

hole that develops through the wall of a body organ

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12
Q

rupture

A

a break or tear in any organ or soft tissue

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13
Q

fracture

A

fracture or breaking of hard object or material, typically a bone.

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14
Q

actinic

A

radiation
extrinsic determinant factor

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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)

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16
Q

multifocal

A

multiple seperate lesions across organ

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17
Q

multifocal

A

multiple seperate lesions across organ
likely coming from somewhere else

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18
Q

multifocal to coalescing

A

multifocal lesions that bump into each other on organ

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19
Q

diffuse lesion

A

covers entire organ

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20
Q

focal lesion

A

in one spot

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21
Q

triangular shaped lesion

A

usually has vascular organ
tip of triangle at occluded vessel

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22
Q

rhomboidal lesion

A

vascular origin

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23
Q

lesion

A

abnormal tissue

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24
Q

cell injury

A

when a cell fails to maintain homeostasis
can be reversible or irreversible

25
Q

cell/tissue general response to injury

A
  • adaptation
  • degeneration
  • death (apoptosis, necrosis)
26
Q

hypertrophy

A
  • 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
Q

hyperplasia

A
  • 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
Q

hyperplasia

A
  • 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
Q

hyperplasia vs neoplasia

A

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
Q

what processes can increase the size of an organ/tissue?

A

inflammation
hypertrophy
hyperplasia
neoplasia

31
Q

metaplasia

A

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
Q

atrophy

A

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
Q

mechanisms of cell injury main categories

A

ATP depletion
Membrane damage
Metabolic disturbance
Genetic damage

34
Q

etiology

A

cause of disease

35
Q

hypoxia vs ischemia

A

hypoxia: not enough O2
ischemia: impaired blood flow to tissue (no O2 and other problems)

36
Q

infarct

A

tissue death due to ischemia

37
Q

segmental lesion

A

a segment of a tubular organ

38
Q

hydropic degeneration

A

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
Q

necrosis causes

A

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
Q

cytoplasmic hypereosiniphilia

A

cytoplasmic necrosis change
eosin stain is pink
cell appears more red by uptake of more eosin stain

41
Q

pyknosis

A

necrosis nuclear change
shrunken, dark, round

42
Q

karyorrhexis

A

necrosis nuclear change
nuclear fragments

43
Q

karyolysis

A

necrosis nucleus change
pale nucleus (dissolution of chromatin)

44
Q

necrosis nuclear changes

A

Pyknosis – shrunken, dark, round
Karyorrhexis – nuclear fragments
Karyolysis – pale nucleus (dissolution of chromatin)

45
Q

morphological (gross appearance) types of necrosis

A

Coagulation necrosis
Caseous necrosis
Liquefactive necrosis
Gangrenous necrosis
Fat necrosis

46
Q

coagulation necrosis

A

from stopping of blood flow
infarcts

47
Q

caseous necrosis

A

cheese like
lots of dying leukocytes (white)

48
Q

liquefactive necrosis

A

tissue liquefies
tissue dissolves and falls apart

49
Q

gangrenous necrosis

A

usually forms in extremities
lack of blood flow or bacterial infection

50
Q

Ischemia-reperfusion injury

A
  • Follows restoration of blood supply to ischemic tissue
  • Generation of ROS following restored oxygen supply
  • Ca2+ influx – impaired ion pumps
51
Q

apoptosis

A

‘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
Q

extrinsic pathway of apoptosis

A

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
Q

intrinsic pathway of apoptosis

A

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
Q

morphologic features of apoptosis vs necrosis

A
  • 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
Q

dystrophic calcification

A

Areas of necrosis
(caused by necrosis when dying cells release Ca2+)
Calcium accumulation in mitochondria

56
Q

Metastatic calcification

A

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
Q

cellular aging

A

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
Q

intracellular accumulations from dysregulated cellular metabolism

A

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
Q

intracellular accumulation of lipids

A

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
Q

glycogen intracellular accumulation

A
  • Corticosteroids
  • Diabetes mellitus
  • Glycogen storage diseases

DWT exam 1 (13 decks)

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