Class 13: Cholera-kincaid Flashcards

1
Q

How do people get cholera?

A

Contaminated water

Fecal-oral route

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2
Q

Cholera caused by:

A

Vibrio cholerae. Fecal-oral route.

Shellfish are natural reservoirs.

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3
Q

Mechanism of induction:

A

Organisms adhere to intestinal mucosa of small intestine and secrete the toxin choleragen.

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4
Q

Results of cholera:

A

Presence of toxin results in massive loss of water and electrolytes.
-production of rice-water stool.

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5
Q

Choleragen:

A=activity-1 copy
B=binding-5 copies

Oligomeric: AB toxin

Disulfide bonds

A

Cholera toxin

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6
Q

Mechanism of cell entrance:

A

Has to bind to cell and gain entry. It becomes endocytosed. And forms lipid raft. Retrograde to cell golgi. Then goes to the ER. The disulfide bond.

B/c of the disulfide bond the ER chaperons believe the protein is misfolded. Polyubiquitinated to be degraded. Unable to be degraded by proteosome.

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7
Q

CFTR is phosphorylated by:

A

PKA

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8
Q

CFTR is an:

A

Ion channel controlling flow of Cl-

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9
Q

Cholera toxin:

A

(G protein) GTP cant be hydrolyzed - constantly ACTIVATED.

More cAMP-> PKA-> activated CFTR->constant flow of ions out of cell. Water follows the ion flow out of cell.

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10
Q

Main issue w/ cholera:

A

Massive loss of water and electrolytes.
Production of “rice-water stools”
Bluish tinge to skin.

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11
Q

Diagnosis of cholera:

Tx:

A

Culture from feces

Oral Rehydration and antibiotic therapy.

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12
Q

Vaccination for cholera:

A

Not very effective

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13
Q

CFTR:

A

12 Membrane-spanning domain Channel protein that transports Cl- in and out of cells and produce mucus, sweat, digestive enzymes.
Also, regulates function of other channels (NA+)

ABC transporter-essentially facilitated diffusion through a pore. Only use ATP to open the gate

Req’s ATP hydrolysis and phosphorylation.

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14
Q

CFTR mutations:

A

> 1300 categorized into 4 classes:

  • Class I=defective protein product product w/ total loss of function
  • Class 2=defective protein processing leading to CFTR not in the correct location or different from normal CFTR ~70% of CF patients (F508-ERAD)
  • Class 3= defective regulation of channel opening of CFTR.
  • Class 4= defective ion conduction.
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15
Q

Defective protein w/ total loss of function-CFTR

A

Class I mutation

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16
Q

Defective protein processing leading to CFTR not in correct location to different from normal CFTR-most common

A

Class 2 mutation

17
Q

Defective regulation of channel opening-CFTR

A

Class 3 mutation

18
Q

Defective ion conduction-CFTR

A

Class IV mutation

19
Q

Autosomal recessive disorder

> 1300 mutaiton in CF gene

> 10 million white americans are asymptomatic carriers

A

Genetics of Cystic fibrosis

20
Q

Symptoms of CF

A
  • Salty-tasting skin
  • persistent coughing
  • wheezing/shortness of breath-viscous mucous-Prone to bacterial infections
  • excessive appetite, but poor weight gain
  • greasy, bulky stool
21
Q

Connect mutaiton in CFTR and connect to ion flow

A

.

22
Q

Why is incidence of CF in northern europeans and descendants:

A

Decreased risk of obtaining cholera.

Selective advantage over cholera.