study guide wk 2 Flashcards

1
Q

Know the pathological definitions

A

Pathology: study of the essential nature and characteristics of disease, including signs/symptoms,
complications, pathogenesis, and morphologic consequences including structural and functional alterations in cells, tissues, and organs

Disease:An impairment of the normal state of the living animal or plant body or one of its parts that interrupts or modifies the performance of the vital functions, is typically manifested by distinguishing signs and symptoms, and is a response to environmental
factors

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2
Q

On an H&E stain, what structures turn blue, and which red?

A

Hematoxylin and Eosin (H&E)
Eosin stains the cytoplasm, RBC’s and collagen pink to red
• Hematoxylin stains nuclei and bacteria (and some other structures) blue to purple

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3
Q

If proteins in the cytoplasm turn red, how can those normal proteins be differentiated from the protein amyloid, which is found in many diseases?

A

Amyloid - pink to red. Amyloid under polarized light after Congo red staining - apple green

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4
Q

What types of diseases or conditions might amyloidosis be found in? (the last slide of week II)

A
amyloidosis:Idiopathic disease characterized by 
extracellular accumulation of amyloid
pathologic protein: B cell proliferations
• Chronic inflammation
• Chronic renal failure
• Alzheimer disease
• Type II diabetes
• Prion disease
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5
Q

Know what a southern, northern, western and dot blot are used to test for.

A

Southern blot: detection of specific DNA sequence
Northern blot: RNA
Western blot: molecular weight of a protein
Dot blot:biomolecules,identification

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6
Q

Cellular injury can cause necrosis or apoptosis, know the difference between the two.

A

Necrosis: cell injury that results in the premature death. inflammation. messy
Apoptosis: process of programmed cell death

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7
Q

What are common causes of cellular injury?

A
Hypoxia
Infections
Imunological reactions
congential
chemical
physical
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8
Q

What is the difference between Marasmus and Kwashiorkor?

A

Marasmus: (decrease in total caloric intake)
Kwashiorkor:decrease in total protein intake

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9
Q

There will be questions on vitamin deficiency, and which vitamins, should they be lacking, lead to which diseases.

A

Vitamin A  squamous
metaplasia, immune deficiency, night blindness
• Vitamin C  Scurvy
• Vitamin D  Rickets & Osteomalacia
• Vitamin K  Bleeding Diathesis
• Vitamin B12  Megaloblastic anemia, neuropathy, spinal cord degeneration
• Folate  Megaloblastic anemia and Neural TubeDefects (NTD)
• Niacin  Pellagra (diarrhea, dermatitis, and dementia

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10
Q

When does cloudy swelling occur?

A

Injury to cell membrane.appears whenever cells are incapable of maintaining ionic and fluid homeostasis Intracellular proteins accumulate in the serum with cellular degeneration.
in liver and heart injury

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11
Q

Where do free radicals come from?

A

oxygen derived. Redox, xanthine oxidase, free iron, neutrophils, drugs, irradiation

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12
Q

Be able to describe the basic pathway in an injured cell that begins with mitochondrial dysfunction and leads to cellular swelling

A

• Mitochondrial Dysfunction–> Decrease in oxidative
phosphorylation causes a decreased in ATP and makes the mitochondria highly permeable–>Release of cytochrome c is a trigger for apoptosis–>The Na+K+ATPase pumps start to fail–> Influx of Na and H20
–>Efflux of K–>Cellular swelling

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13
Q

What is the most common form of necrosis, and what are the characteristics of the other forms?

A

Coagulative Necrosis (liver, heart, kidney–mosquito)

liquefaction necrosis:Cell destruction by hydrolytic enzymes–> autolysis (brain abscesses, pancreatic)

Caseous Necrosis: Combination of coagulation and
liquefaction necrosis. Cottage cheese–> TB
Fat necrosis (lipase, white)
Fibroid necrosis (fibrin, eosinophils,pink)
gangrenous necrosis

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14
Q

How do the treatments of wet and dry gangrene differ?

A

Dry gangrene micro appearance is Coagulative necrosis

Wet gangrene is liquefactive necrosis

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15
Q

What types of diseases is Caseous necrosis characteristic of?

A

granulomatous diseases like TB

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16
Q

How does gene regulation of apoptosis work?

A

Orderly, NO Inflammation
Cell injury / DNA damage–>Lack of growth factors or hormones–> Receptor-ligand signals–>Fas binding to the Fas ligand–>Tumor necrosis factor TNF binding to TNF receptor 1 (TNFR1)

17
Q

What do caspases do, and why are they important?

A

Execution of apoptosis: Caspases digest nuclear and cytoskeletal proteins
Caspases also activate endonucleases

18
Q

What is steatosis, and what are its two main causes in the western world?

A

Fatty change–> Abnormal accumulation of triglycerides.
• liver,heart, muscle, kidneys, MOs
Usually due to cellular metabolic damage and increased lipids

19
Q

What is the pathological significance and appearance of Lipofuscin?

A

Wear and tear pigment, fine granular brown/yellow, indigestible in lysosomes, lipochrome= lipid peroxidation of subcellular membranes
not patholigical

20
Q

What is hemosiderosis, and why is it seen in venous stasis ulcers of the lower extremity?

A

Hb derived, yellow/gold/brown. major storage of Fe
local or systemic iron overload ferritin–> hemosiderin
bruise evolution to recover iron: heme–> biliverdin–>bilirubin–>iron to ferritin–>hemosiderin

21
Q

What is the difference between dystrophic calcification and metastatic calcification?

A

metastatic: Occurs when there is elevated serum calcium or phosphate (dissolving bone)
dystrophic: local calcification of non-viable tissues (heart)