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Exam 1

Total questions: 75

Worksheet time: 2hrs 58mins

Name
Class
Date
1.

  1. Selenium is a component of the ____ a free radical scavenging system that limits the damage free radicals cause

a)

  1. Glutathione peroxidase

b)

  1. Selenium peroxidase

c)

  1. Cytosolic phospholipidase

d)

  1. Enzymatic redoxase

2.

  1. How is cell injury different from cell death?



4 lines
3.

  1. Select all of the key mechanisms of cell injury or death

    2. Decreased intracellular calcium

    3. Permeabilization of cell membranes

a)

  1. Damage to DNA and proteins

b)

  1. Permeabilization of cell membranes

c)

  1. Disruption of biochemical pathways

d)

  1. Decreased intracellular calcium

e)

  1. ATP depletion

4.

  1. The major causes of ATP depletion are…

a)

  1. Hypoglycemia

b)

  1. Free radical damage

c)

  1. Hypoxia

d)

  1. Mitochondrial damage

e)

  1. Necrosis

5.

  1. Which of these are the correct sequence of events leading to cell injury or death due to ATP depletion?

a)

  1. Switch to anerobic glycolysis→Decrease O2→ Results in decreased ATP production→ Decreased function of Na+/K+ pumps → Increased influx of Ca2+, H20 and Na+ → Cellular swelling

b)

  1. Decreased function of Na+/K+ pumps→ Increased influx of Ca2+, H20 and Na+ → Cellular swelling→ Decrease O2→ switch to anerobic glycolysis→ Results in decreased ATP production

c)

  1. Cellular swelling→Increased influx of Ca2+, H20 and Na+ → Decrease O2→ Decreased function of Na+/K+ pumps→Switch to anerobic glycolysis→ Results in decreased ATP production

d)

  1. Decrease O2→ Switch to anerobic glycolysis→ Results in decreased ATP production→ Decreased function of Na+/K+ pumps→ Increased influx of Ca2+, H20 and Na+ → Cellular swelling

6.

Which of these does mitochondrial damage NOT lead to?

a)

Formation of mitochondrial permeability transition pore

b)

Abnormal oxidative phosphorylation leading to the formation of ROS

c)

Phospholipase activation

d)

Leakage of pro-apoptotic proteins from the mitochondiral membrane leading ot cellular death by apoptosis

7.

Increased Cytosolic Ca2+ activates what?

4 lines
8.

Select all the ways there can be an increase in cytosolic Ca2+ as a response to ischemia and toxins

a)

Release from intracellular stores in mitochondrial and ER membranes

b)

Anerobic glycolysis causing the release of Ca2+ intracellularly

c)

Formation of the mitochondrial permeability transition pore

d)

Increased influx of Ca2+ across the plasma membrane late in cell injury

9.

What are free radicals?

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10.

Which of these are not sources of free radicals?

a)

Redox reactions that occur during ATP production

b)

Bursts produced in activated leukocytes during inflammation

c)

Nitric Oxide

d)

Glutathione peroxidase

11.

DNA damage, Protein modification and lipid peroxidation all occur as a result of what?

(a)  

12.

What is the most common cause of cell swelling?

a)

Decreased oxidation and use of FFAs

b)

Hypoxia

c)

Excess deposition of glycogen

13.

What is the pathogenesis of cell swelling?

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14.

What changes can you observe in this histologic slide? What changes do you expect to see in the gross organ?

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15.

Select the main categories of the morphological manifestations of injury

a)

Degeneration

b)

Intracellular accumulation

c)

Necrosis

d)

Extracellular Alterations

e)

Hyaline changes

16.

Is cell swelling a reversible or irreversible morphological alteration during cell injury?

a)

Reversible

b)

Irreversible

17.

What are some other names for acute cell swelling?

a)

Hydropic degeneration

b)

Cellular hypertrophy

c)

Ballooning degeneration

18.

What is a possible sequelae if there was hepatocellular hydropic degeneration occuring?

a)

Obstruction of a bile duct

b)

Hepatocellular necrosis

c)

Increased bile flow

19.

Given these gross and histological images what type of cellular injury is occurring? Why is this occurring?

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20.

What are three conditions that there is a pathologic alteration in glucose metabolism leading to glycogen accumulation?

a)

Diabetes Insipidus

b)

Diabetes Mellitus

c)

Steroid hepatopathy

d)

Glycogen storage disease

21.

You have two slides. You stain one slide with PAS stain and it turns pink. Is it glycogen?

4 lines
22.

Describe the pathogenesis of glycogen accumulation starting with diabetes mellitus or steroid hepatopathy.

4 lines
23.

Is glycogen accumulation able to be seen grossly?

a)

Yes

b)

No

24.

Which of the following are intracellular hyaline changes?

a)

Hyaline droplets

b)

Amyloid

c)

Fibrinoid change

d)

Deposition of collagen

25.

What is hyaline?

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26.

Is glycogen accumulation reversible?

a)

Yes

b)

No

27.

In what types of cells are hyaline droplets more prominent?

a)

renal tubular epithelium

b)

Liver

c)

Brain

d)

Enterocytes

e)

epithelium

28.

What is the pathogenesis of hyaline droplets?

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29.

What inclusions may look similar to hyaline droplets?

a)

Viral inclusions

b)

Acidophilic crystalline intranuclear inclusions

c)

glycogen accumulation

d)

Lead inclusions

e)

Bacterial endotoxins

30.

What stain causes amyloid to glow apple green under polarized light? What stain turns the amyloid deposits blue?

a)

Hematoxylin and eosin (H&E) staining/Lugols iodine

b)

Lugols iodine/PAS

c)

Congo red/PAS

d)

Lugols iodine/Wrights stain

e)

Condo red/Lugols iodine

31.

What is the pathogenesis of amyloid deposition through reactive systemic amyloidosis?

4 lines
32.

What is the difference between systemic familial amyloidosis and reactive systemic amyloidosis?

a)

If there was an inciting cause vs genetic predisposition

b)

If there was inflammation vs individual mutation

33.

What are the two more common location for localized amyloidosis?

4 lines
34.

What sequelae can occur due to amyloidosis?

a)

Pressure atrophy of cells

b)

Proteinuria leading to kidney failure

c)

Diabetes mellitus

d)

Hepatic failure

e)

Clotting disorders

35.

What is fibrinoid change?

a)

Deposition of fibrin in any tissue

b)

Fibrous changes in a tissue

c)

Necrosis of a blood vessel

36.

What is the pathogenesis of fibrinoid change?

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37.

What are some components of fibrinoid change?

a)

fibrin

b)

immunoglobulins

c)

epithelium

d)

Platelets

e)

complement

38.

What are causes of extracellular hyaline deposition? What would it look like grossly (just think about this one, no answer in the choices)

a)

Aging change

b)

Acute injury

c)

Ischemia

d)

Chronic injury

39.

What is fatty infiltration

a)

Accumulation of fat in extracellular stromal tissue

b)

Accumulation of fat in tissues that dont normally have adipocytes

c)

Intracellular accumulation of fat droplets

d)

hypertrophy of adipocytes

40.

What is the difference between dystrophic and metastatic mineralization?

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41.

What are some examples of diseases that lead to metastatic calcification

a)

Humoral hypercalcemia of malignancy

b)

Secondary renal hyperparathyroidism

c)

Chronic granulomatous disease

d)

Vitamin D toxicosis

e)

Necrosis of myocardium

42.

What is coagulative necrosis?

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43.

Which of the following pathogenesis could occur and result in coagulative necrosis?

a)

Fumonisin B1 ingested-->inhibits sphingosine N-acetyltransferase-->inhibits production of sphingolipids which are important in protecting the cell surface

b)

Downer cow-->weight of body occludes vessels -->ischemia-->necrosis of thigh muscle

c)

Diets high in fat-->Increase in ROS-->Free radical damage can lead to fat necrosis

d)

  1. Anemia-->hypoxia--> central lobular hepatic necrosis

44.

What microscopic changes will you see with coagulative necrosis?

a)

Nuclear pyknosis

b)

inflammation at the center of the lesion

c)

Increased basophilia

d)

Karyorrhexis or karrylolysis

45.

What is a cause of coagulative necrosis?

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46.

What is an infarct?

4 lines
47.

What is liquefactive necrosis?

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48.

What does liquefactive necrosis look like?

a)

Abscesses

b)

dry crumbly and gritty lesion

c)

ischemic necrosis in the CNS

49.

What is the cause of leukoencephalomalacia? What species is affected? What is the pathogenesis?

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50.

What is the suspected cause of polioencephalomalacia? What species is affected? What is the pathogenesis?

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51.

What lesions would you not see grossly if there is polioencephalomalacia?

a)

Swelling of the brains gyri

b)

necrosis of the white matter

c)

cerebral laminar necrosis

d)

Florescence under UV light

52.

What are some causes of gas gangrene?

a)

Aspiration pneumonia

b)

ischemia

c)

Viruses

d)

Bacterial toxins

53.

Is this wet or dry gangrene?

Dark red to black tissue

Soft moist and friable tissue

Foul odor with a line of demarcation where the necrosis is occurring

a)

Wet gangrene

b)

Dry gangrene

54.

Is this wet or dry gangrene?

Dry shriveled leathery tissue

Cold tissue

Not smell or gas present

a)

Wet gangrene

b)

Dry gangrene

55.

Whats the difference between wet and dry gangrene?

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56.

What is the pathogenesis of ergot poisoning resulting in wet gangrene?

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57.

What are some causes of caseous necrosis?

a)

Corynebacterium pseudotuberculosis

b)

Salmonella

c)

Mycobacterium bovis

d)

Ecoli

58.

What is fat necrosis and what are some causes?

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59.

What is the term for death of a cell at the end of its normal lifespan as seen in embryonic cells
that are no longer needed in development

(a)  

60.

What is the term for the death of a cell before the end of its normal life span, result of irreversible cell injury

(a)  

61.

What is the morphologic changes that follow cell death in a living animal, resulting from progressive, degradative action of enzymes on the cell

(a)  

62.

What is cell death directed by cellular signaling cascades and typically affects individual cells. Could be physiologic or pathologic

(a)  

63.

What is the term for the degradative changes in a cell due to action of endogenous enzymes, primarily from lysosomes. See in postmortem decomposition

(a)  

64.

What is it called when post mortem bacterial metablism and dissolution of host tissues result in the production of color and texture changes, gas production and odors?

(a)  

65.

From left to right what nuclear patterns are being shown? What process are these cells going through?

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66.

List three potential sequelae to necrosis

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67.

What are some characteristic of apoptotic cells?

a)

Cell swelling

b)

cell shrinkage

c)

Cytoplasmic blebs

d)

Phagocytosis of apoptotic bodies

e)

Inflammation

68.

What are the two mechanisms of apoptosis?

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69.

Describe the mitochondrial pathway of apoptosis.

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70.

Describe the death receptor pathway of apoptosis

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71.

What post mortem change is present?

(a)  

72.

The cooling of the body after death

(a)  

73.

The stiffening of muscles after death

(a)  

74.

What postmortem change occured in the top section of a vessel compared to the bottom section

(a)  

75.

What postmortem change is occurring here

(a)  

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