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Pathology (shared) > Exam One > Flashcards

Exam One Flashcards

1
Q

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

A

etiology
pathogenesis
molecular and morhologic changes
clinical manifestation

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2
Q

Extrinsic etiology

A

infection, nutritional, chemical, and physical

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3
Q

Intrinsic etiology

A

inhereted, genetic

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4
Q

Pathogenesis

A

Mechanisms of dz development

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

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5
Q

Autolysis

A

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

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6
Q

Somatc Death

A

Cells die due to hypoxia

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7
Q

Putrification

A

Process by which post mortem bacteria break down tissue

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8
Q

Which tissues will undergo autolysis first?

A

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

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9
Q

Rigor Mortis

A

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

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10
Q

Algor Mortis

A

Cooling of the body post mortem, temp is time dependent

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11
Q

Livor Mortis/Hypostatic Congestion

A

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

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12
Q

What are some normal post mortem changes in the eyes?

A

corneal clouding and tache noire

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13
Q

What happens to lips, tounge, scrotum post mortem?

A

Drying and discoloration

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14
Q

How can you differentiate between post and pre mortem clotting?

A

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

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

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15
Q

Hemoglobin imbibition

A

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

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16
Q

What is a chicken clot?

A

sesperation of RBCs and clotted serum

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17
Q

Bile imbibition

A

Bile leaves the gallbladder and stains nearby tissues

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18
Q

Pseudomelanosis

A

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

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19
Q

Corneal opacity/clouding

A

due to cold temperatures

20
Q

Atrophy

A

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

21
Q

Hypertrophy

A

Increased cell size and their functions.

22
Q

Hypertrophic cardiomyopathy in cats

A

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

23
Q

Hyperplasia

A

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

24
Q

Metaplasia

A

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

25
Q

Dysplasia

A

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

26
Q

What can cause a depletion of ATP?

A

Hypoxic injury

Toxic injury

27
Q

What are the 3 major consequences of Mitochondrial Damage

A
  1. Formation of MPTP (loss of membrane proteins)
  2. Production of ROS’s, increase in Ca2+
  3. Activation of apoptotic pathways (cytochrome C)
28
Q

What are some pathological effects of free radicals?

A

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

29
Q

Explain why you might see elevated ALT?

A

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

30
Q

Exudate

A

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

31
Q

Transudate

A

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

32
Q

Edema

A

excess fluid in interstitium, can be exudate or transudate

33
Q

Pus

A

exudate rich in leukocytes and parenchymal cell debri

34
Q

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

A

No

35
Q

What type of inflammation do you see macrophages?

A

Chronic (some in subacute)

36
Q

Exudate

A

escape of fluids, proteins, and blood cells from vascular system into interstitium/body cavaties

high protein conc
much cellular debris
SG>1020

37
Q

Peracute time, vascular involvement, inflammatory cells, clinical signs

A

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

38
Q

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

A

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

39
Q

Lymphadentis

A

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

40
Q

Subacute inflammation time, vascular involvement, inflammatory cells

A

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

41
Q

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

A

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

42
Q

Serous exudate

A

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

43
Q

Granulomatous

A

ALWAYS CHRONIC

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

44
Q

Necrotizing inflammation

A

exudate minimal, process is inflammatory if infectious etiology is suspected

45
Q

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

A

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

46
Q

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

A

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

Pathology (shared) (3 decks)

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