Cytoplasm Flashcards

Understand staining principles and review organelles (38 cards)

1
Q

Hematoxylin

A

basic (cationic); stain blue-black; stains acidic structures

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2
Q

Eosin

A

stains pink-red; acidic (anionic); stains basic structures

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3
Q

H&E stains: nucleus/cytoplasm/collagen/cartilage/RBCs/adipose

A
blue/dark purple
pink
very pink
dark blue
dark red
white
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4
Q

Mallory’s trichrome stain

RBCs/muscle/collagen

A

orange
red
blue

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5
Q

Masson’s trichrome stain

nucleus/keratin & muscle fibers/collagen & mucin/cytoplasm

A

dark brown/black
red
blue/green
light red/pink

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6
Q

Van Gieson’s strain

collagen/everything else

A

red

yellow

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7
Q

Periodic acid & Shiff’s reagent (PAS)

carb groups color & counterstain method

A

pink/magenta

counterstain w/ hematoxylin

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8
Q

diameter of:
RBC
nucleus

A
RBC = 7 micro
nucleus = 2-9 micro
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9
Q

macromolecule proportions in PM

A

45% lipid
50% protein
5% carb

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10
Q

E-leaflet components & functions

A

phosphatidylcholine (signaling)

sphingomyelinase (myelin sheath)

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11
Q

P-leaflet components & functions

A

phosphotidylethanolamine (nervous tissue, cell division)
phoshpatidylserine (apoptosis, coagulation)
phosphotidylinositol (signaling, membrane trafficking)

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12
Q

Accumulation of sphingomyelin; deficiency in lysosomal enzyme acid sphingomyelinase; neuro damage; what are the types?

A

Niemann-Pick disease
Type A: infants; jaundice, enlarged liver, brain damage
Type B: pre-teens; hepatosplenomegaly

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13
Q

Degradation of myelin sheath; loss of signal transduction capability; upregulation of CSF cytokines that increase sphingomyelinase

A

Multiple sclerosis (MS)

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14
Q

Xs sphingomyelin in RBC membrane; xs lipid accumulation in outer leaflet of RBC PM; acanthocytes

A

Abetalipoproteinemia

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15
Q

Abnormal CFTR Cl- membrane channel proteins; higher viscosity of mucus lining resp tract; blockage of smaller bronchioles; infection; poor lung function; death

A

Cystic fibrosis (CF)

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16
Q

Defective cysteine carrier proteins can’t remove cystine from lumen of proximal renal tubule; high Cys conc –> Cys stones; recurrent kidney stones; pts aged 10-30

17
Q

2 major functions of SER?

A
  1. Fatty acid & phospholipid synthesis

2. Detoxification (P450)

18
Q

3 types of cells where SER most prevalent?

A
  1. Hepatocytes
  2. Adrenocorticoidal cells
  3. Leydig cells
19
Q

Special function of SER in muscle cells?

A

Sequestering/releasing Ca2+ (sarcoplasmic reticulum)

20
Q

What disease:

  • emphysema (COPD)
  • impaired liver function
  • decreased A1AT activity
A

Alpha 1-antitrypsin (A1AT) deficiency

21
Q

What disease:

  • muscle weakness (especially extraocular mm)
  • degenerative CNS due to loss of CN1 fibers
  • abnormally high levels of lactic acid
  • any age group
A

Mitochondrial cytopathy syndromes

22
Q

What disease:

  • muscle weakness
  • ataxia (NS degeneration)
  • seizures
  • cardiac/resp failure
  • aggregates of abnormal mitochondria
A

Myoclonic epilepsy w/ ragged red fibers (MERRF)

23
Q

Cause of MERRF?

A

Mutation of mDNA encoding Lys –> 2 abnormal complexes in ETC of resp enxymes, affecting ATP production

24
Q

Major roles of peroxisomes besides H2O2 decomposition? (2)

A

Lipid catabolism by beta-oxidation of long-chained FA + cholesterol biosynth

25
Function of plasmalogen?
- membrane phospholipid that protects cells against singlet oxygen
26
What disease: - facial, bone, & joint deformities - restricted limb movement - loss of speech & learning ability - intellectual disabilities - freq lung infections & heart disease - hepatosplenomegaly
Lysosomal storage disease
27
What disease: - multisystem lipidosis - organomegaly - bone pains - susceptibility to fractures - common in Asheknazi Jews - hematological changes
Gaucher disease
28
Main cause of Gaucher disease?
- deficient activity of lysosomal hydrolase (glucocerebridase)
29
What disease is this: - children of northeast European Jewish or Cajun ancestry - vegetative state followed by death in Yr3 of life - loss of motor skills - increased startle rxn - macullar pallor & retinal cherry red spot - decreased eye contact - progressive blindness
Tay-Sachs disease
30
Cause of Tay-Sachs disease?
- absence of lysosomal galactosidase (beta-hexosaminidase) | - accumulation of GM2 gangliosides w/i residual bodies of neurons interferes w/ cell function
31
What disease is this: - defective integral protein used for transport of long-chain FA into peroxisome - accumulation of fatty acids (FA) in body fluids can disrupt myelin sheaths in nerve tissue - neuro problems
Adrenoleukodystrophy (peroxisomal disorder)
32
What disease is this: - congenital, incurable, fatal disease in newborns - death after 1yr due to liver/resp failure - dysmorphic faces - progressive degeneration of brain/liver/kidney - hypotonic - seizures - poor feeding - hearing loss - retinal dystrophy
Zellweger syndrome (peroxisomal disorder)
33
Cause of Zellweger syndrome?
- peroxisomal targeting signal receptors missing from peroxisomal membranes - peroxisomes can't perform beta-oxidation of long chain FA for plasmalogen synth - needed for myelin
34
What is lipofuscin & how does it appear?
- rep's an accumulating by-product of lysosomal digestion in long-lived cells - yellow/brown pigment - membrane-bound
35
What is hemosiderin, how does it appear, & where is it found?
- contains ferritin (iron storage) - very electron-dense - brownish, resembles lipofuscin - indigestible remnants of Hb - found in spleen, alveolar macrophages in lung tissue
36
Classification & function of keratin?
- fibrous structural protein | - protects epithelial cells from damage/stress (ie provides mechanical stability)
37
Major factor in establishing electrochemical gradient in ETC?
Proton-translocating activity in inner membrane
38
Function of chaperonins?
- prevent misfolding & aggregation of proteins