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123 Cards in this Set

  • Front
  • Back
What are the 4 main tissue types?
epithelia, CT, muscle, nervous
What do epithelial tissues arise from?
3 primary germ layers of the embryo: mesoderm, ectoderm, endoderm
Skin epithelium derived from what germ layer?
Digestive tract epithelium derived from what germ layer?
Epithelium? Mesothelium? Endothelium?
epi: skin, digestive tract
mesothelium: peritoneal cavity
endothelium: blood vessels, lymph vessels, heart
What are the morphological characteristics of epithelium?
cells in close apposition (sheets of cells)
cells rest on BM
cells are adhesive (intercellular jxns)
tissue is avascular
If tissue is avascular, how does it receive nutrition?
there are capillaries underneath the cells
-overlie vascular CT
What is on the apical surface of epithelial cells?
microvilli, cilia, sterocilia
What is on the basal surface of epithial cells?
BM, hemi-desmosomes, plasma membrane interdigitations
What is on the lateral surface of epithelial cells?
intercellular jxns (tight, adherent, desmo, gap)
What are the 5 functions of epithelia?
1. protection (keratin and mucus prevent drying)
2.absorption (microvilli in kidney and intestine)
3.surface transport (cilia)
4.secretion (secretory glands)
5.sensory reception
What are the clinical correlations of CF?
sputum culture grows Pseudomonas aeruginosa
sweat test reveals high Na and Cl
bronchiectasis (toothpaste lines)
Prevalence of CF?
How does CF affect functioning of several organs?
ducts or other tubes become clogged, usually by thick, sticky mucus or other secretions
Malfxn of CFTR in sweat gland prevents what?
Na and Cl reabsorption therefore preventing water influx as well
sweat contains lots of NaCl
What is CFTR?
voltage gated Cl channel on apical membranes of epithelial cells (lung, pancreas, sweat glands)
-glycosylated extracellular domain
-12 membrane spanning domain
-2 ATP nucleotide binding domains
-R domain dependent on PKA
What regulates CFTR?
PKA dependent phosphorylation
What needs to be bound to CFTR for fxn?
ATP binding, but ATP hydrolysis indpendent
Describe structure of CFTR?
2 sets of 2 transmembrane domains
2 ATP binding cassettes: ABC transporters
R domain
How is CFTR involved w/ binding actin?
through ESP50/Ezrin Adapter protein that links actin cytoskeleton
What is relationship w/ PKA and cholera toxin?
constant p-lation by PKA
Na out, water out therefore diarrhea
In lung epithelia, what is associated w/ CFTR?
beta adrenergic R b/c when bound leads to increase cAMP activating PKA which then regulates CFTR
In CFTR, what counterion does Na flux require?
Cl is counter ion that flows when Na channels open
-water then flows around cells maintaining osmotic pressure
-result: isotonic NaCl soln flows from blood to lumen
Most common mutation of CF (channelopathy)?
deltaF508 causes 2/3 of cases
no frameshift b/c deletes 3 nucleotides 2 from Phe 1 from isoleucine
What does deltaF508 mutation result in?
prevents proper folding of protein fails to become fully glycosylated and is quickly degraded by proteosome
What effect does temp have on misfolding of CFTR?
at normal temps (37c) degraded
at 23-30 R's will get to cell surface and work even though missing Phe
Describe intracellular trafficking of CFTR.
Normally leaves rER for golgi where it is not glycosylated to mature protein then leaves golgi for apical membrane or recycling endosome
Where does CFTR eventually end up?
late endosome to lysosome pathway for degradation
What are the 5 CF class mutations?
1. defect in protein production
2. defect in processing (ER-deltaF508)
3.defect in regulation (PKA can't p-late properly)
4.defect in Cl condxn
5. mutations causing decreasing synthesis (mutator in promoter)
Action of CFTR in lung epithelia?
transports Cl out, Na and H20 follow therefore when no CFTR = thick mucus build up
S. aureus P. aeruginosa adheres to mucus
What 3 symptoms do CF patients exhibit?
-male infertility due to vas deferens blockage
-obliteration of pancreatic excrine fxn
-progressive tissue deterioration in lung
-viscous mucus
-recurrent infxns
-establishment of Ab resistant strains
What is almost always the cause of death in CF?
loss of lung fxn
Where is CF incidence high?
most common inherited disease of Caucasian pop (1 in ever 29) demonstrating heterozygote by providing protection against loss of intestinal fluid during cholera, typhoid fever and tuberculosis b/c bad CFTRs decrease levels of water and Cl secretion in small intestines (2% selective advantage)
Describe gene therapy for CF?
deliver normal copy of CFTR gene to site of action by modified & synthetic vectors
-gene transfer to CF airway via nose drops or aerosol is possible but limited efficiency of transfer
-risk of serum immunological rxns is primary factor b/c vectors associated w/ acute inflam rxns
Continual pressure in bone leads to what?
tension/stress in bone leads to what?
strengthening and new bone formation
Describe the inorganic structure of bone matrix
primarily hydroxyapatite (calcium phosphate) also contains bicarb, citrate, magnesium, potassium, and Na
What is the inorganic bone matrix good at?
compression, a crystal!
Describe the organic structure of bone matrix.
mostly Type I collagen
ground substance, proteoglycans
keratin and chondroitin sulphates
glycoproteins: osteocalcin & sialoprotein
What is the organic bone matrix good at?
What is the fxn of osteocalcin and sialoprotein as components of organic matrix of bone?
improve adherence of the varous constituents
What do mesenchymal stem cells differentiate into
osteoprogenitor cells
What do osteoprogenitor cells diff. into?
What is the seq of bone cell diff?
What do osteoclasts arise from?
blood borne monocytes
Which of the bone cells doesn't originate from mesenchymal stem cells?
What is the name of bone-lining cells on external bone surfaces?
periosteal cells
What is the name of bone-lining cells on internal bone surfaces?
endosteal cells
Describe the coverings of bone.
outer covering-periosteum
inner marrow cavities-endosteum
What attaches periosteum to bone?
sharpey's fibers of Type I collagen
Where do Sharpey's fibers extend from?
periosteum to bone matrix
Fxn of periosteum?
supplies blood vssls to bone
Fxn of osteoblasts?
secrete the organic matrix (collagen I) of bone (osteoid) and control mineralization
What is osteoid?
Type I collagen and varous proteoglycans (organic matrix of bone)
Fxn of alkaline phosphatase?
cell surface enzyme that hydrolyzes phosphate esters at high pH thus increases phosphate concentrations--crystallization
Fxn of osteocalcin?
provides nucleation sites for crystal formation
When do osteoblasts(young) diff into osteocytes (mature)?
when they become trapped in lacuna thus triggering diff.
Compare osteoblast and osteocytes
osteocytes have more heterochromatin, less rER, less golgi relative to blast
How do osteocytes talk and transfer nutrients?
via cell processes in canaliculi across gap jns
Fxn of osteocyts?
bone turnover and maintenance
Where are the cell processes of osteocytes located?
embedded w/n canaliculi, spaces surrounded by mineralized bone
Nucleation of osteoclasts?
mutlinucleated via fusion of monocytes
Fxn of osteoclasts?
resorbs (eats) bone
secretes acid to dissolve crystal (pH 4.5)
secretes enzymes to hydrolyze collagen
What hormone inhibits osteoclast?
calcitonin (tones down ECF Ca)
Describe components of osteoclast.
Howships's lacuna or subosteoclastic compartment
-big adherens jxn of actin
-bicarb/Cl exchanger to ensure cytoplasmic pH neutrality
-Cl channel to prevent excessive rise in intracellular pH
-carbonic anhydrase II generates H to create acidic environment
-ATP dependent pump
in osteoclasts, what follows Cl that is removed by Cl channel?
H by V-type ATPase to Howships lacuna
Explain action of carbonic anhydrase in osteoclasts?
Co2 + water -H2CO3-H + HCO3-
How do osteoblasts and osteoclasts interact?
via paracrine agents to control Ca
Action of MMPs in bone.
proteases break down collagen in acidic environment created by H pump
-they are released by lysosomes
What gland is calcitonin secreted from?
thyroid gland "C cells"
What do calcitonin and PTH act on?
bone, kidney, intestines
Compare calcitonin w/ PTH
calcitonin decreasing Ca in ECF
PTH increasing Ca in ECF
Where in bone is compact bone? spongy?
compact: surface
spongy: ends of bone
Where is yellow marrow? red?
yellow: compact bone
red: spongy
What is the organization center of compact bone?
osteon or Haversion system w/ central core canal that carries nutrients
What 2 canals are found in compact bone?
Volkmann's canal
Haversian canal
What is another name for spongy bone?
trabecullar bone
Is spongy bone haversion?
no, lamellar
Flat bones are mostly what type of bone?
Where are osteocytes found?
concentrically arrayed b/n lamellae
osteocytes in adjacent lamella are interconnected by cell processes lodged in canaliculi that are linked by gap jxns
What type of ossification for long bones? flat bones?
long bones and vertebral column: endochondral ossif.
flat: mesenchymal ossif.
What is the term for a newly synthesized bone ECM?
osteoid, deposited in forms of bands or lamella
osteoclasts are trapped w/n osteoid and become osteocytes when the matrix is calcified
What is the process of making spongy bone?
intramembranous ossification
What 3 things do intramembranous ossification require?
1. well-vascularized primitive CT
2. bone formation is not preceded by the formation of a cartilage
3. an aggregate of mesenchymal cells differentiates directly into osteoi-producing osteoblasts
What is endochondral ossfication?
replacement of hyaline cartilage by bone
Explain the process of endochondral ossification.
periosteal collar forms
chondrocyte hypertrophy
secretion of angiogenic factors
blood brings calcium
calcified cartilage
apoptosis of chondrocytes
blood vssls bring in osteoclasts, osteoblasts
What initiates the formation of the primary ossification center?
prolif of chondrocytes followed by their hypertrophy at the midpoint of the shaft
What do hypertrophic chondrocytes secrete?
vascular endothelial cell growth factor to induce sprouting of blood vessels from the perichondrium (periosteal bud)
What is happening in the secondary ossification center?
cartilage at ends replaced w/ spongy bone but some articular cartilage left
Why doesn't cartilage regrow?
b/c it doesn't have blood supply
What do osteoprogenitor cells do in the primary ossfication center?
they are derived from the perivascular mesenchyme and when they reach the primary ossification center they generate osteoblasts
What are the 3 zones of bone replacement?
proliferation zone
hypertrophic zone
vascular invasion zone
explain what you see in proliferation zone of bone.
flattenend chondrocytes in columns or clusters parallel to the growth axis
cluster of cells in this zone: chondrion
What is the functional unit of growth in the proliferative zone of bone?
chondron: a cluster of cells
What is happening in the hypertrophic zone?
apoptosis of chondrocytes and calcification of the territorial matrix
What happpens in the vascular invasion zone?
blood vessels penetrate the transverse calcified septa, and carry osteoprogenitor cells with them
Where is the epiphyseal plate?
b/n the metaphysis and the epiphysis
Explain the epiphyseal plate.
cartilaginous growth plate where bone is dense and is recognized as an epiphyseal line
Where is the periosteal collar?
it extends along the diaphysis
when is a secondary ossification center established?
when blood vessels infiltrate the epiphysis
when is the epiphyseal plate replaced with epiphyseal line?
occurs gradually from puberty to maturity
all the epiphyseal cartilage is replaced by bone except where?
the articular surface
What is Indian Hedgehog?
stimulates chondrocyte proliferation in the growth plate and prevents chondrocyte hypertrophy
What characterizes osteoporosis?
low bone mass and deterioration of bone tissue that leads to increased bone fragility and risk of fracture particulary of the hip, spine and wrist
*silent killer b/c occurs w/o symptoms
explain steps of bone repair
1. thrombus/hematoma forms
2. WBC's remove debris
3. death of osteocytes
4. osteoprogenitor cells of the periosteum proliferate
5. fibrous and cartilagionus callus forms on inside and outside surface of bone
6. endochondral and intramembraneous ossificatoin occurs, forming a bony callus
7.remodeling occurs as the fracture continues to heal and new bone responds to stresses
what happens with too little GH? too much?
too little: pituitary dwarfism
too much: acromegaly
What disease is the most common of a group of growth defects characterized by abnormal body proportions?
achondroplasia: arms and legs too short but torso is more nearly normal size. they do have cartilage but the rate at which cartilage cells in the growth plates of the long bones turn into bone is slow leading to short bones and reduced ht
explain symptoms in muscular dystrophies
muscle weakness and deterioration usually occuring in proximal to distal direction due to muscle protein abnormality
facts on DMD
X linked
severe degenerative disorder of skeletal and cardiac mm
1 in 3500 male births
onset: early childhood
leg weakness, increasing convex curvature of spine and waddle like gait
wheelchair bound by 11 or 12
What do DMD patients die of?
respiratory or cardiac failure
common signs and symptoms of DMD
difficulty taking first steps
gower sign: diffiiculty getting up from sitting or supine position
walk on toes or balls of feet
belly pushed out and shoulders back
what techinique is used to determine DMD?
western blot of dystrphen
explain dystrophin gene
giant gene spanning 2.4Mbp
99% introns (accounts for high mutation rate)
14kb dystrophin mRNA that enocodes 3,685 aa
7 different dystrophin transcripts with cell type specificities: determined by promotors
common mutation in DMD?
96% with framshift mutation, 30% with new mutation
what determines the cell type specificity of dystrophin?
expressed primarily in skeletal, cardiac and smooth muscle and retina
action of dystrophin in muscle?
links actin-cytoskeleton to membrane glycoprotein complex that interacts with ECM
where is dystrophin localized?
to inner surface of plasma membrane where Z lines contact membrane linking muscle cell to ECM and providing structural support for PM of muscle fiber during repeated contraction cycles
what is dystrophin a member of ?
spectrin superfamily based on structure..related to alpha actinin
close cousins of dystrophin?
utropin, DRP2 (dystrophin related protein-2), dystrobrevin
Mucle fibers that are lacking dystrophin increase expression of what?
explain dystrophin associated glycoprotein complex
3 subcomplexes: alpha, beta dystroglycan complex; sarcoglycan complex; cytosolic adaptor subcomplex
all work as organizer and adaptor for signalling
components of cytosolic adaptor subcomplex?
alpha actinin syntrophins, Grb-2, nitric oxide synthase, caveolin-3 and NOS
explain dystroglycan complex.
dystroglycan is proteolytically cleaved into 2 subunits
alpha: bind to laminin, percalan, and agrin
beta: binds dystrophin
*complex confers structural stability during contraction