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52 Cards in this Set
- Front
- Back
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Hematoxylin -what color does it stain -what is it made of |
Stains Purply-blue
Made of nucleic acid, and calcium salts |
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Eosin -what is it made of -what color does it stain |
Arginine and lysine
Stains Pink-Red |
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Periodic acid- Schiff -what are they -what do they stain -where are the found |
Made of cis-diols and are extreme hot pink
found in glycogen, epithelial mucin, cartilage, fungus wall, basement membrane, reticulin, and alpha-1-antitrypsin |
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What is PAS+ or Diastase PAS- (dPAS-) |
Diastase (which is found in saliva) is used to remove glycogen from slides to be PAS stained.
PAS+ and dPAS- means there is glycogen. (liver biopsy reports) |
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Reticulin stain -what color -where is it found |
Stains black
they support liver, spleen, LN, and BM |
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Prussian blue -what does it stain for |
storage iron
Bright midnight blue.
(same reaction for blueprints) |
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Mucicarmine stains
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It stains epithelial mucins bright pink and everything else brown-green.
It also lights up cryptococcus yeasts. |
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Alcian blue |
it used to stain mesenchymal mucin and distinguish subtypes of epithelial mucin in stomach biopsies.
(not used anymore) |
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What does trichrome stain? what color? |
Stains dense type 1 collagen blue
(connective tissue and scar) |
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Argentaffin and argyrophil stains |
use silver stain for serotonin-rich granules of carcinoids. |
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Methenamine silver |
Lights up fungi including pneumocystis.
Nephropathologists call it jones silver stain. (traces the nephron with black) |
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Metachromasia |
Most blood smears use this principle for staining.
It stains various cell components different colors. |
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Papanicolaou's stain |
used for pap smears Light green= RNA Orange = cysteine disulfide bonds |
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When do we use nucleic acid probes as stains?
When do we use gene probes? |
HPV- research tool
Expensive way to spot a virus before they show classic histopathology |
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What is fatty change? What are 6 different mechanisms which produce it in the liver? |
Extra neutral fat in vacuoles in non-adipocytes 1. too much free fat coming in to liver 2. too much fatty acid synthesis in liver 3. impaired fatty acid oxidation by liver 4. Excess esterification of fatty acid to triglycerides by the liver. 5. too little apoprotein synthesis by liver 6. failure of lipoprotein secretion by liver |
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Alcohol fatty liver vs non-alcoholic fatty liver |
Alcohol abuse (even over a few days) can cause the 6 mechanisms of fatty change to occur.
Non-alcholic fatty liver is very common because of metabolic syndrome |
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Fatty Liver under the microscope |
Lipid drops have sharp edges. (trichrome)
Heart has tiger stripes/thrush-breast |
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Causes of Fatty Liver |
ETOH abuse Metabolic syndrome (some AIDS meds) Protein Malnutrition/kwashiorkor/AIDS wasting Hep C Reye's syndrome Poisoning by phosphorus, CCl4, outdated tetracycline. Pregnancy bad galactosemia inborn errors of metabolism (check ammonia levels) |
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Diphtheria heart |
Uniform fatty change.
The heart poison produced by microbes interferes with burning of lips no matter what the oxygen levels. |
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Atherosclerosis under the microscope |
Cholesterol needles Lipid build up from MQ eating fats which then accumulate in artery wall. |
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Xanthelasma of eye and gallbladder |
clusters of lipid-laden macrophages on insides of eye. Lipid in quasineoplastic macrophages.
"strawberry" gallbladder. Little xanthomas look like strawberry seeds. (usually with cholesterol gallstones too)
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Tendon xanthomas are seen in
Palmar xanthomas are seen in |
Tendon: familial hypercholesterolemia
Palmar: primary biliary cirrhosis |
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Death by aspirated mineral oil |
He always mentions this...
Old person, takes mineral oil to poop. They accidentally aspirate on it and it gets into lung and they die.
Look for lipid droplets in a lung biopsy. |
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Abetalipoproteinemia |
Lack of apolipoproteins B48 and B100.
Patient can't absorb fat so it accumulates in intestinal lining cells.
They also have deformed RBC membranes ACANTHOCYTES. |
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Fatty ingrowth |
It is NOT fatty change
It is the appearance of extra mature fat cells in unusual places like pancreas, and lymph node. |
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Glycogen in hepatic nuclei |
Can suggest hyperglycemia
but is unreliable. |
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Hurler's -what accumulates -why does it happen? -what does it lead to? |
Mucopolysaccharosis 1 Lacks enzyme which causes accumulation of sulfate and dermatan sulfate in lysosomes.
Leads to progressive brain damage/mental and motor deterioration, enlarged liver and spleen, short stature, and "gargoyle" appearance. |
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Hurler's and Hunters under the microscope |
Storage product accumulation in lysosome creates ZEBRA BODIES
Aortic and mitral valve can be involved causing stenosis from lysosome accumulation.
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Hunters -what is accumulated -inheritance |
Mucopolysaccharosis 2 X-linked accumulation of heparan sulfate and dermatan sulfate.
Gargoyle appearance |
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Sanfilippo -what is accumulated? -why doe it happen? -what results |
Mucopolysaccharidosis 3 Defect in any 4 enzymes leading to accumulation of heparan sulfate. Problems mostly involve brain causing progressive metal deterioration. |
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Brain accumulation of mucopolysaccharidoses (especial sanfilippo) |
The neurons are enlarged and get damaged. They are full of pink stuff. |
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Morquio -what builds up -what is deficient -what happens |
Mucopolysaccharidosis 4 Low of 2 enzymes which leads to the build up of keratan sulfate.
They are mentally normal, but are short and develop corneal clouding. |
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Fabry's Disease -deficiency of? -what builds up? -what does it lead to? |
X-linked Deficiency of alpha-galactosidase Ceramide trihexoside accumulates in lysosomes.
Pain is a problem because of peripheral nerve involvement and creates an intractable burning pain in palms and soles.
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Fabry's under the microscope |
Inclusions in endothelium of capillaries
Angiokeratomas (little clusters of blood vessels)
Artery deposits are purple
Pale zebra bodies |
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Heart and Brain in fabry's |
Brain is not likely to have deposits and any problems are from vascular issues.
Heart is prone to cardiomyopathy with rhythm problems. Septum may be thick which looks like hypertropic cardiomyopathy. |
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Fabry's in the kidney |
Only major storage disease which affects the glomeruli.
You can see deposits in the vessel intima and media |
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Gaucher's Disease -what is deficient -what is accumulated -what structures are involved |
Glucocerebrosidase deficiency leading to accumulation of gulcocerebroside inside cells especially in mixed monocyte phagocytes.
Hepatosplenomegally is seen SPLEEN IS HUGE Also involves bone and brain There are different degrees of severity |
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Gaucher's Disease under the microscope |
Watered silk moire (crumpled kleenex) Gaucher cells light up with toluidine blue |
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Gaucher XRay |
H-shaped gaucher vertebral bodies
Gaucher cells in marrow weaken the bone causing deformity. |
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Niemann-Pick Disease -Mutation of? -Accumulation of? -what do the storage cells look like? -what does it lead to? |
Mutations at any 3 loci with accumulation of sphingomyelin.
Storage cells look more spotty thank crinkly
usually causes death as child or teen. |
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Brain involvement in Niemann-Pick's disease |
brain involvement is severe. Neurons are filled with spotty/bubbly storage product.
"childhood alzheimers" |
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Tay-Sach's Disease -what does it lack? -what builds up? |
GM2 gangliosidosis Lack of hexosaminidase A (gene HEXA) with accumulation of ganglioside, mostly in brain.
Enlargement of neurons results in enlargement of entire head. Cherry red spot |
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Cholesterol Ester Storage Disease -what does it lack -what does it cause -what structures does it effect |
There is no normal acid lipase in lysosomes which makes it impossible to break down cholesterol esters.
It primarily effects the liver and causes precocious atherosclerosis |
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Von-Gierke's Glycogen storage disease type 1 -what is deficient? -what occurs? |
There is a deficiency of glucose-6-phosphatase.
Patients have difficulty breaking down glycogen especially in liver and it becomes overloaded with time. "kewpie doll faces" if accumulates in heart can cause problem. causes uric acid and gout |
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Von-Gierke's glycogen storage disease under the microscope |
glycogen is in the cytoplasm (Not lysosomes) large liver
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Treatment of von-gierke's glycogen storage disease |
continuous ingestion of carbohydrates (cornstarch) to avoid the fasting state and dangerous hypoglycemia. |
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Pompe's Disease -deficiency of? -build up of? -which organs are involved? |
Deficiency of acid alpha-glycosidase ONLY glycogen storage disease where glycogen is actually in the lysosomes . It involves the heart, skeletal muscle, and liver. BRAIN IS NOT INVOLVED. |
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Progression of pompe's disease |
It ranges from killing young children (floppy baby)
To a mild disease in older adults (scapular winging) |
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Galactosemia -deficiency of? -what does it cause? |
Deficiency of any 3 enzymes which metabolize galactose from milk.
If galactose is not metabolized it becomes galactitol or galactose1phosphate which can cause cellular edema.
cataracts can be seen in mild version (reversible) water-bloated hepatocytes and cerebral edema |
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Before screening for galactosemia what was a diagnostic finding? |
Kids with reducing sugar in urine |
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Treatment for galactosemia? what can still occur despite treatment? |
No lactose and galactose in diet.
but severely-affected children can still suffer brain damage.
especially swapping consonants (verbal dyspraxia) |
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I-Cell disease -what is deficient -what occurs? |
mucolipidosis 2 Lack of N-acetylglucosamine-1-phosphate transferase, which is needed to tag proteins which need to be discarded via golgi.
Accumulations in MQ |
