Exam One

Question 1

What are the four aspects of a dz process that form the core of pathology?

Answer 1

etiology
pathogenesis
molecular and morhologic changes
clinical manifestation

Question 2

Extrinsic etiology

Answer 2

infection, nutritional, chemical, and physical

Question 3

Intrinsic etiology

Answer 3

inhereted, genetic

Question 4

Pathogenesis

Answer 4

Mechanisms of dz development

Sequence of events from initial stimulus to the ultimate expression of dz

Question 5

Autolysis

Answer 5

self digestion or degradation of cells and tissues by the hydrolytic enzymes normally present in tissue. Occurs after somatic death.

Question 6

Somatc Death

Answer 6

Cells die due to hypoxia

Question 7

Putrification

Answer 7

Process by which post mortem bacteria break down tissue

Question 8

Which tissues will undergo autolysis first?

Answer 8

Those with a greater concentration of proteolytic enzymes, GI tract, pancreas, gall bladder, liver, kidney

Question 9

Rigor Mortis

Answer 9

Contraction of muscles after death, 1-6 hours post death, persistant: 1-2 days. High heat and activity accelerate Rigor mortis.

Question 10

Algor Mortis

Answer 10

Cooling of the body post mortem, temp is time dependent

Question 11

Livor Mortis/Hypostatic Congestion

Answer 11

gravity pulls the blood after death, results in variation of color in tissues

Question 12

What are some normal post mortem changes in the eyes?

Answer 12

corneal clouding and tache noire

Question 13

What happens to lips, tounge, scrotum post mortem?

Answer 13

Drying and discoloration

Question 14

How can you differentiate between post and pre mortem clotting?

Answer 14

Pre mortem: attached to walls, dry and dull, friable

Post mortem: unattached to vessel walls, shiny and wet, elastic

Question 15

Hemoglobin imbibition

Answer 15

Red staining of tissue, especially in heart, arteries and veins. Hg released by lysed RBCs and penetrates the vessel wall.

Question 16

What is a chicken clot?

Answer 16

sesperation of RBCs and clotted serum

Question 17

Bile imbibition

Answer 17

Bile leaves the gallbladder and stains nearby tissues

Question 18

Pseudomelanosis

Answer 18

greenish-black discoloration of tissue post mortem. Decomposition of blood by bacterial action forming hydrogen sulfide with iron. Occurs soon after death, like in the gut and tissues surrounding the gut

Question 19

Corneal opacity/clouding

Answer 19

due to cold temperatures

Question 20

Atrophy

Answer 20

Decrease in cell size. Cells are not dead. Could be due to decrease in protein synthesis or increase in protein degredation

Question 21

Hypertrophy

Answer 21

Increased cell size and their functions.

Question 22

Hypertrophic cardiomyopathy in cats

Answer 22

Common in main coons, mutations in MYBPC3 gene (inherited autosomal dominant)

Question 23

Hyperplasia

Answer 23

Increase in number of cells of an organ. Pathologically commonly caused by factor stimulation (repeated stimulation)

Question 24

Metaplasia

Answer 24

Change in phenotype of a differentiated cell. May result in decreased functions or increase malignant transformation. Most often in epithelial cells.

Question 25

Dysplasia

Answer 25

abnormal development, mostly of epithelial cells. "One step before neoplasia"

Question 26

What can cause a depletion of ATP?

Answer 26

Hypoxic injury | Toxic injury

Question 27

What are the 3 major consequences of Mitochondrial Damage

Answer 27

1. Formation of MPTP (loss of membrane proteins) 2. Production of ROS's, increase in Ca2+ 3. Activation of apoptotic pathways (cytochrome C)

Question 28

What are some pathological effects of free radicals?

Answer 28

lipid peroxidation in membranes ( membrane damage) oxidative modification of proteins (breakdown, misfolding) Lesions in DNA (mutations)

Question 29

Explain why you might see elevated ALT?

Answer 29

Damaged hepatocyte releases ALT, ALT is needed in hepatocytes to convert alanine to pyruvate.

Question 30

Exudate

Answer 30

escape of fluids, proteins, and blood cells from the vascular system into the interstitium or body cavities

Question 31

Transudate

Answer 31

ultrafiltrate of blood plasma and results from hydrostatic imbalances across vascular endothelium (low protein conc)

Question 32

Edema

Answer 32

excess fluid in interstitium, can be exudate or transudate

Question 33

Pus

Answer 33

exudate rich in leukocytes and parenchymal cell debri

Question 34

Would you see fibrosis and neovascularization/angiogenesis in subacute inflammation?

Answer 34

No

Question 35

What type of inflammation do you see macrophages?

Answer 35

Chronic (some in subacute)

Question 36

Exudate

Answer 36

escape of fluids, proteins, and blood cells from vascular system into interstitium/body cavaties high protein conc much cellular debris SG>1020

Question 37

Peracute time, vascular involvement, inflammatory cells, clinical signs

Answer 37

0-4 hrs hyperemia, slight edema, hemorrhage not usually numerous cells, few leukocytes shock, sudden death

Question 38

Acute inflammation time, vascular involvement, Inflammatory cells, Clinical signs

Answer 38

4-6 hrs active hyperemia, edema, lymphatics and small blood vessels Neutrophils predominate Clincial signs- warm red swollen painful loss of function

Question 39

Lymphadentis

Answer 39

reactive inflammation of lymph nodes. Occurs in acute, subacute, and chronic inflammation.

Question 40

Subacute inflammation time, vascular involvement, inflammatory cells

Answer 40

days-weeks not as much vascular involvement as acute Primarily neutrophils, some macrophages and plasma cells Increased lymphatic drainage

Question 41

Chronic inflammation time, vascular involvement, host involvement, inflammatory cells, lymphatics, clinical signs

Answer 41

time variable Vascular involvment- angiogenesis/neovascularization resulting in hemorrhage and congestion Host involvment- parenchymal regeneration or repair via fibrosis Cells- Macrophages, lymphocytes, plasma cells, fibroblasts Lymphatics- variable Clin signs- prolonged duration of inflammatory lesion

Question 42

Serous exudate

Answer 42

fluid rich in protein derived from blood and locally injured cells exudate is in tissues because there is no cellular response

Question 43

Granulomatous

Answer 43

ALWAYS CHRONIC | Presence of macrophages (epitheloid cells, Giant cells), lymphocytes and plasma cells

Question 44

Necrotizing inflammation

Answer 44

exudate minimal, process is inflammatory if infectious etiology is suspected

Question 45

How do you differentiate a Simple Granuloma from a Complex granuloma?

Answer 45

Simple: organized accumulation of macrophages and epithelial cells often rimmed by lymphocytes Complex: central area of necrosis + above

Question 46

What 2 gross pattens are possible in macroscopic characteristics of chronic inflammation

Answer 46

diffuse- thickening of affected tissue solid, firm, nodular lesion- may compress adjacent tissue (may contain organized granulomas w/ necrotic or suppurative centers).