Midterm Flashcards
Huntingtons diseas
30-35 y/o
Striatal nuclei, loss of motion
Chorea (jerking movements)
Dementia
Toxoplasmosis
Toxoplasma gondi
Ghandi was the shit
Thalidomide
Pfizer drug given to pregnant women
Babies born with 1 eye no extremities
Parameningeal infection
Brain abscess due to improper treatment of pimples
Staphylococcus aureus
Streptococcus pyogenes
Sjogrën’s syndrome
Autoimmune
Females over 35
Total dryness of mucous membranes
Bilateral parotitis: inflamed parotid glands, look like hamsters
Local disease
Confined to one organ/region of the bady
Ex: stomach cancer
Focal damage
Limited to one or more distant sites within a diseased organ
Ex: one tumor in stomach
Diffuse damage
Uniformly distributed damage within a diseased organ
ENTIRE ORGAN IS AFFECTED
Ex: entire stomach is cancerous
Alkaptonuria
Oxidanormally phenylalanine is converted to tyrosine
However if oxidase is not produced, homogentistic acid (an intermediate), aka alkapton, is not converted
Homogentistic acid accumulates and is excreted in The urine causing urine to appear black
Homogentistic acid
Can accumulate in specific tissues causing ONCHRONOSIS
Cartilage is site of accumulation
Leads to osteoarthritis and sever degeneration
Calcifies IVDs
Alkapton deposits in ears
Ears look blue
Accumulation of normal metabolite
Alkaptonuria
Homogentistic acid
Activation of an alternative pathway
Phenylketonuria
Phenylketonuria
50% of phenylalanine is used
50% is converted to tyrosine
Non-production of the enzyme hydroxylase results in a switch to an alternative pathway
—> production of phenylpyruvic acid, phenyllactic acid and phenylacetic acid
Accumulation of metabolic byproducts
Gout
Gout
Metabolic disorder
3 factors:
1) gouty arthritis
2) deposition of uric acid salts in joints/ tissues
3) deposition of salts in kidneys–> renal failure
Impaired purine metabolism
Asymmetrical presentation
Tophus
Deposition in tissue
Tropism
Attraction
Malaria
Plasmodium (protozoa) in RBCs
Echinococcus
Meat with worms egg
Balloon shaped bodies
Hydropic changes
Aka cloudy swelling, hydropic degeneration
Nephron tubule cells
Steatosis
Residual bodies
Intracellular accumulation (inside cell)
Possibly due to damaged organelles
Remains of injury left inside the cell
Liver, kidney, nervous tissues
Hyalinization
Reversible change
protein accumulation
Intra (inside) or Inter cellular (in between)
Looks like hyaline cartilage under microscope but is not,
it is protein
Intracellular deposition
Reabsorption droplets Mallory alcoholic hyaline (mallory bodies) Russell bodies Dutcher bodies Waldenström macroglobulinemia Residual bodies
Reabsorption droplets
Aka minimal change disease
Renal proximal convoluted tubule cells
Abnormal protein loss in urine
Cells try to prevent loss and become filled with protein droplets
When no more protein is excreted in urine protein droplets are released back into urine and cells return to normal