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FMS Week 6 > Intracellular Accumulations and Pathologic Calcifications > Flashcards

Intracellular Accumulations and Pathologic Calcifications Flashcards

1
Q

4 Main Pathways of Cellular Accumulation

A
  1. Abnormal Metabolism (Steatosis/Fatty Liver)
  2. Defect in Protein Folding/Transport (Mutated forms of alpha 1 anti trypsin)
  3. Lack of Enzyme (Storage Disorders)
  4. Ingestion of Indigestible Materials (Carbon/Silica)
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2
Q

Steatosis/Fatty Change

A
  • Abnormal accumulation of triglycerides within parenchymal cells
  • Liver (main), heart, muscle, kidneys
  • caused by: toxins, protein malnutrition, diabetes mellitus, obesity, anoxia, alcoholic liver disease
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3
Q
A

Steatosis

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4
Q

Cholesterol and Cholesterol Esters

A
  • metabolism tightle regulated
  • used for synthesis of cell membranes
  • no intracellular communication
  • will see intracytoplasmic vacuoles if accumulated
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5
Q

Atherosclerosis

A
  • Smooth muscle cells and macrophages in surface/wall of arteries filled with lipid vacuoles
    • mostly cholesterol and cholesterol esters
  • Aggregates of foam cell in surface/wall give yellow appearance of atheromas
  • some may rupture releasing lipids into extracellular space
  • will see cholesterol clefts-cholesterol esters crystallized as long needles
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6
Q
A

Atherosclerotic lesion

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7
Q

Xanthomas

A
  • intracellular accumulation of cholesterol
  • Xanthomas=groups of foamy macrophages found in connective tissue of skin and in tendons
  • can be seen in non hyperlipidemic states
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8
Q
A

Gastric Xanthoma

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9
Q
A

Cholesterolosis of Gallbladder

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10
Q

Neimann-Pick Disease, Type C

A
  • lysosomal storage disease
  • mutations in enzyme involved in cholesterol trafficking
  • cholesterol accumulates in multiple organs
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11
Q

Renal Tubule Reabsorption Droplets

A
  • Seen in kidney conditions that have protein loss in the urine
  • increased reabsorption of protein into vessicles
  • protein has a appearance of pink hyaline droplets within cytoplasm of proximal tubular cells
  • reversible
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12
Q
A

Renal tubule reabsorption droplets

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13
Q

Russel bodies

A
  • plasma cells actively synthesizing immunoglobulins may show russel bodies
  • ER becomes hugely distended: large eosinophilic cytoplasmic inclusions
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14
Q
A

Russel bodies

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15
Q

Alpha 1 anti trypsin deficiency

A
  • mutation in protein slows protein folding
  • causes build up of partially folded intermediates that aggregate in liver cells
  • resulting deficiency causes emphysema of the lungs
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16
Q
A

Alpha 1 anti trypsin deficiency

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17
Q

Accumulation of cytoskeletal proteins

A
  • certain injuries cause aggregation of keratin filaments and neurofilaments
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18
Q

Alcoholic Hyaline (Mallory Denk body)

A
  • eosinophilic cytoplasmic inclusion in liver cells
  • composed of keratin intermediate filaments
  • characteristic of alcoholic liver disease
19
Q
A

Mallory Denk Body

20
Q

Neurofibrillary tangle

A
  • Found in alzheimers
  • neurofilaments and other proteins
21
Q
A

Neurofibrillary tangle

22
Q

Hyaline

A
  • descriptive term
  • alteration of cellular or extracellular space that gives homogenous glassy pink appearance on routine H&E
23
Q
A

Arteriolar Hyaline

24
Q

Glycogen

A
  • Stored in cytoplasm
  • excessive deposits with problem in metabolism
  • diabetes is most important disease in glucose metabolism
  • accumulations appear clear
  • Pompe disease, von Gierke disease
25
Q
A
  • normal glycogen on squamous epithelium
26
Q

Carbon (Exoegnous)

A
  • inhaled, picked up by alveolar macrophages, transported through lymphatic channels to regional lymph nodes
  • blackens lungs and node tissues “anthracosis”
  • coal miners may get serious lung disease
27
Q
A

Coal dust/anthracosis

28
Q

Tattoo (Exogenous)

A
  • skin is phagocytosed by dermal macrophages
  • inert, not associated with inflammation
29
Q
A

Bowel tattoo in surgery

30
Q

Lipofuscin

A
  • wear and tear pigment
  • seen in liver and heart of aging or malnutrition cancer cachexia
  • insoluble polymers of lipids and phospholipids in complex with proteins derived from breakdown of subcellular membranes
  • not harmful to cells
  • may indicate cell exposure to free radical injury
31
Q
A
  • Lipofuscin pigment
32
Q

Melanin (Endogenous)

A
  • formed when tyrosinase catalyzes the oxidation of tyrosine to dihydroxyphenylalanine in melanocytes
33
Q
A

Melanin

34
Q

Normal vs excess iron breakdown

A
  • normal: in sites where there is red blood cell breakdown
  • local excess: macrophages breakdown blood. removal of iron–>ferritin–>hemosiderin
    • parallel breakdown of heme moeity: biliverdin–>bilirubin
    • bruising colors
35
Q

Iron metabolism

A
  • Iron is normally carried by transferrin, stored by apoferritin in cells, forms ferritin micelles (normal)
  • excess iron, ferritin forms excess hemosiderin granules (aggregates of ferritin micelles) in cells
36
Q

Hemosiderosis

A
  • systemic overload of iron–>hemosiderin buildup in tissues
  • Causes: increased absorption of dietary iron (hemachromatosis)
    • hemolytic anemias(premature lysis of RBC’s, excess release of iron)
    • repeated blood transfusions (equivalent to exogenous administration of iron)
37
Q
A

Hemosiderosis in liver from hemochromatosis

38
Q

Dystrophic Calcification

A
  • deposits of calcium in dying tissue (necrosis)
  • present in atheromas of advanced atherosclerosis
  • aging, damaged heart valves
  • psammoma bodies, asbestos bodies
39
Q
A

Calcification of cardiac valves

40
Q
A

Psammoma bodies

41
Q
A

Asbestos bodies

42
Q

Metastatic calcification

A
  • Deposition in normal tissues where there is hypercalcemia
    1. Increased secretion of parathyroid hormone (PTH) with subsequent bone resorbtion (e.g. due to parathyroid tumors)
    1. Resorbtion of bone (tumors: myeloma, leukemia, extensive
  • skeletal metastases; accelerated turnover–Paget’s disease; immobilization)
    3. Vitamin D related disorders (Vit D intoxication, sarcoidosis)
    1. Renal failure (Renal failure–>retention of phosphate–>

hyperparathyroidism)

  • Other: mild-alkali syndrome (excessive ingestion of calcium and

absorbable antacids e.g. mild or calcium phosphate)

43
Q

Where does metastatic calcification occur?

A
  • throughout body
  • gastric mucosa, kidneys, lungs
    • these secrete acid –>have alkaline compartment predisposed to calcification
    • usually no clinical dysfunction unless massive deposition in lungs , kidneys

FMS Week 6 (2 decks)

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