Cytoplasm Flashcards

Understand staining principles and review organelles

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

A

Cystinuria

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
Q

Function of plasmalogen?

A
  • membrane phospholipid that protects cells against singlet oxygen
26
Q

What disease:

  • facial, bone, & joint deformities
  • restricted limb movement
  • loss of speech & learning ability
  • intellectual disabilities
  • freq lung infections & heart disease
  • hepatosplenomegaly
A

Lysosomal storage disease

27
Q

What disease:

  • multisystem lipidosis
  • organomegaly
  • bone pains
  • susceptibility to fractures
  • common in Asheknazi Jews
  • hematological changes
A

Gaucher disease

28
Q

Main cause of Gaucher disease?

A
  • deficient activity of lysosomal hydrolase (glucocerebridase)
29
Q

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
A

Tay-Sachs disease

30
Q

Cause of Tay-Sachs disease?

A
  • absence of lysosomal galactosidase (beta-hexosaminidase)

- accumulation of GM2 gangliosides w/i residual bodies of neurons interferes w/ cell function

31
Q

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
A

Adrenoleukodystrophy (peroxisomal disorder)

32
Q

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
A

Zellweger syndrome (peroxisomal disorder)

33
Q

Cause of Zellweger syndrome?

A
  • 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
Q

What is lipofuscin & how does it appear?

A
  • rep’s an accumulating by-product of lysosomal digestion in long-lived cells
  • yellow/brown pigment
  • membrane-bound
35
Q

What is hemosiderin, how does it appear, & where is it found?

A
  • contains ferritin (iron storage)
  • very electron-dense
  • brownish, resembles lipofuscin
  • indigestible remnants of Hb
  • found in spleen, alveolar macrophages in lung tissue
36
Q

Classification & function of keratin?

A
  • fibrous structural protein

- protects epithelial cells from damage/stress (ie provides mechanical stability)

37
Q

Major factor in establishing electrochemical gradient in ETC?

A

Proton-translocating activity in inner membrane

38
Q

Function of chaperonins?

A
  • prevent misfolding & aggregation of proteins