(08) p375 Flashcards
1
Q
(Pathologic Calcification)
- does calcification = minearlization?
2-3. what are the two types?
A
- no
- dystrophic calcification
- metastatic calcification
2
Q
(Pathologic Calcification)
(dystrophic calcification)
- calcification in what tissue? Ca2+ accumulates in what?
- usually what kind of lesion? (harmful?)
- normal or abnormal serum calcium levels?
- rapid process in what two things?
- what two types of granulomas?
A
- necrotic tissue; mitochondria and cytoplasm
- focal to multifocal lesion (harmless)
- normal (normocalcemic)
- cardiomyocytes and muscle cells
- bacterial and parasite granulomas
3
Q
(Pathologic Calcification)
(Metastatic Calcification)
- generalized intra or extracellular calcium salt deposits in what?
- in particular at what and what? cells with acidic of basic cytoplasm?
- do they have hyper or hypo calcemia?
- can cause what in parathryoid? leading to what?
A
- previously undamaged tissue (mainly in mitochondria)
- elastic fibers and basement membranes; acidic
- hypercalcemia (eg hyperacalcemia of malignancy, iatrogenic hypervitaminosis D, consuption of vitamin D and/or calcium accumulating plants such as cestrum diurnum
- hyperparathyroidism (primary, secondary renal or secondary nutritional form); leading to hypercalcemia due to hyperplasia of chief cells - get calcium from bones
4
Q
(Pathologic Calcification)
Dystophic vs. metastatic
- happens in what kind of tissue
- blood calcium?
A
- necrotic tissue vs. begins in healthy tissue
- normocalcemic vs. hypercalcemic
5
Q
(Pigments)
1-2 what are the two types?
A
- exogenous pigments
- endogenous pigments
6
Q
(exogenous pigments)
- what is carbon deposition (black pigment) called?
- what is usual route of entry?
- where are carbon particles found?
(…)
4-5. what are two more examples
A
- anthracosis
- usually inhaled into lung and lung lymph nodes “smoker or living with smoker”
- peribronchial, peribronchioloar, or alveolar macrophages
- dusts (silica; silicosis; birefriengent under polarized light)
- tattoos
7
Q
(Exogenous pigments)
(carotenoids)
- fat soluble pigments of what origin? including precursors of what?
- are they detectable in standard histo-sections? why?
(tetracyclins)
- treatment of pregnant/gravid mother or neonatal (developing) animal –> ?
A
- plant origin; vitamin A (beta carotene)
- no - washed out during embedding process
- discolorization of bones and teeth
8
Q
(Endogenous Pigments)
- melanin can cause what?
- ones that contain lipids and proteins
- what’s the third kind of pigment?
A
- melanosis
2 lipofuscin-ceroid
- hemtagenous pigments
9
Q
(Melanin)
- what kind of pigment?
- produced by what?
- cause what of skin? if focal? if generalized?
(depigmentation)
- focal: destruction of melanocytes with release of what?
- generealized: what metal deficency?
- what is inherited defect of enzyme secretion for melanin production?
A
- black intracellular pigment
- melanoblasts/melanocytes (neuroectodermal)
- hyperpigmentation; moles and freckles; increased secretion of melanotropin in some cases of Cushing’s disease
- melanin (is phagocytozeid and removed)
- copper deficiency (decreased melanin sytnehsis due to enzyme deficiency)
- albinism
10
Q
(Lipofuscin)
- what color and where?
- composed of what?
- autofluroscent: weakly luxol fast blue positive, PAS positive AFB stain positive
- may cause what discolorization of tissues?
- accumulates to degree of visibility in what kind of cells in light microscopy?
- enon-degradable end product of autophagocytosis of damaged/senescent organelles in “residual bodies”
- Usually harmless to cell unless what?
A
- yellow brown intracellular “aging wear and tear pigment”
- protien and lipids
- brown
- post-mitotic cells (old) - so permanent (neurons, cardiomyocyes, and myocytes) but also in slowly dividing (hepatocytes)
- storage disease (Batten disease) (this is what you think if you see this pigment in young animals - will get neurologic disease)
11
Q
(Hemoglobin)
- what pigment?
- hemoglobin degradation in macrophages of what three things?
- broken down to what and what?
- heme –> bile acids and iron binds to what?
- acute severe hemolysis leads to what and what? What is this indistinguishable from?
A
- red
- liver, spleen, and bone marrow
- heme (with iron) and globin (–> AA)
- protein (apoferritin and siderin)
- hemoglobinemia and hemoglobinuria; myoglobinemia and myoglobinuria due to severe acute muscle damage
12
Q
(Hemosiderin)
- what color?
- Reserve iron is bound to protein - what two?
- siderin stored in what?
- stainable with what stain?
A
- brown pigment
- ferritin (readily available) or siderin (not readily available)
- siderosomes (granules)
- Prussian blue stain
13
Q
(Hemosiderin cont)
(Generalized hemosiderosis - bone marrow, spleen, liver)
- usually due to what?
- first detectable in when and where?
(Localized hemosiderosis)
- in areas of what?
(Hemochromatosis)
- increased resorption of what with massive storage in what?
A
- hemolysis
- in macrophages appr 3 days after hemorrhage
- hemorrhages (including in body cavity after intracavitary hemmorhage)
- increased enteric iron resorbption with massive storage in hepatocytes
14
Q
(Hematin)
- what is a waste product of certain parasites? which ones?
- what is melena?
- what is annoying microscopic formalin artifact when pH of fixative < pH6 (–> use buffered formalin!)
A
- parasite hematin; liver flukes and plasmodium sp.
- acid hematin - blood exposed to HCl in stomach
- formalin pigment
15
Q
(Hematoidin)
- produced from what in tissue after hemorrhage?
- first detectable about how many days after hemorrhage?
- free of what?
- birefringent (something with polarized light)
- resembles what?
A
- hemoglobin
- 9 days
- iron
- bilirubin
18
Q
(Icterus - hyperbilirubinemia)
- what is the end product of hemoglobin metabolism during erythrocyte degradation in cells of mononuclear macrophage system (
A
- bilirubin
fuck it - just read this slide
