Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Biochem Winter 2012 > Biochem Hormone Action 3 > Flashcards

Biochem Hormone Action 3 Flashcards

1
Q

What is the growth hormone pathway

A

Protein Tyrosine Kinase

Kinase on a separate protein and signals thorugh JAK-STAT pathway

Growth hormone is released form teh pituitary and is important for growth periods of mammals, sucha s puberty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe how receptors with tyrosine kinase activity have oncogenic potential

A

Many tumors and tumor cell lines coexpress GF and their recpetors in incresednubers

PDGF and paltelet dreived growth factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is Her 2/neu

A

oncogene, correlation between extend of oer-expressino and prognioss for five year survival

an EGF receptor-like molecula

It is a funcitonal tyrosine kinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What forms NO

A

arginine, oxygen, and NADPH by enzye NO synthase (NOS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is NO used for?

A

NS, SM, Macrophage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What ar eth three type sof NOS that are known

A

nNOS- neuronal

eNOS-endothlial

iNOS-macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is nNOS?

A

In postynaptic regions of the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is nNOS activated by?

A

Ca2+ /Calmodulin in response to NMDA oepnign o postynatpic Ca cahnnels

nM levels of NO increse as the level of cGMP (through guanyl cyclase) and also diffuse back to presynaptic neuron and are invovled in long term potentiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is eNOS?

A

in endothelial vascular membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What activates nNOS

A

ca/calmodulin in response to Ach or Bradykinin activatin of Ca channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what does nM eNOS cause (2 things)

A
  1. NO diffuses into the lumen to prevent platelet aggregation and thus reduce clotting
  2. NO diffuses back to teh vascular SM to increase cGMP which lowers Ca2+ levels that then causes dilation of the vessel and ultimately lowers BP.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

WHat is iNOS

A

expression of NOS in macrophaages (and also in SM. Inducible in response to cytoking stimulation but this NOS is NOT activated by Ca/Calmodulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what happens if NO is at high uM concencrations gnerated by Macropahgs

A

NO is a free radical and can oxidize the metal centers of various metalloenzymes

used by macrophage to attack foreign material sor cells, including tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Hormones that use cyclic AMP as a 2nd messenge

A 
Calcitonin 
-chorionic gonadotropin
-ACTH
-epinephrine (adrenaline, beta adrenergic receptor)
-Follicle-stimulating hromeone
-Glucagon 
-Lipotropin 
-LH
-MSH
-Noreprinephrine (NE)
-PTH
-TSH
-Vasopressin
-muscuranic Ach
-calcitonin
-Somatostatin
-Beta-adrenergic catecholamines
CRH
-alpha-2 catecholamines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Hormones that use Ca or Phosphatdidylinositides (or both)

A 
alpha-1 adrenergic catecholamines
Cholecystokinin
Gastrin
TRH
Vasopressin
Ach (muscrarinic)
Antiotenssein II
GnRH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Efects mediated by phosphoionisitde cascade

A

Glycogenolysis in liver cells
Histamine secretion by mast cells
Serotonin release by blood paltelets
Aggregation of blod plaetlets
Insulin secretion by pancreatic islet cells
Epinephrine secretion by adrenal chormaffin cells
SMooth muscle contraction
Visual transcdciton in invertebrea phoreceptors

17
Q

Wha is spinocerebellar Ataxia 14

A

Ataxia-inabilityt o coordinate muscular movement

A disease of Protein Kinase C-gamma

16 of 22 cases have a mutation in teh C1 domain that prevents the enzyme tfrom binding to the membrane

PKC can no longer phospphorylate one of its substrates, TRP Ca2+ channel

Neurons can no longer regulate Ca2+ concentration

18
Q

How are anabolic steroids mediated?

A

Anabolic effect of AASs is mediated mprimarily by androgen receptors (ARs) in skeletal muscle.

ARs regulate transpcriton of target genes that control expression required for muscle growth

19
Q

Why does cholear toxin lead to dairrhea

A

stimulates salt and water secretion into the GI tract, leading to diarrhea

20
Q

Why does treating cholera toxin with saline not work?

A

massive loss of ECF can lead to death.

Administration of saline solution orally doesn’t replace the salt lost as a result of toxin. The salt is not absorbed rapidly without glucose as a co-transporter

Electrolyte balance is maintained by oral administration of a salt plust glucose solution (99 mM Na+, 74 mM Cl-, 29 mM HCO3=, 4 mM K+)

21
Q

Hormones that use cyclic AMP as a 2nd messenge

A

Calcitonin

  • chorionic gonadotropin
  • ACTH
  • epinephrine (adrenaline, beta adrenergic receptor)
  • Follicle-stimulating hromeone
  • Glucagon
  • Lipotropin
  • LH
  • MSH
  • Noreprinephrine (NE)
  • PTH
  • TSH
  • Vasopressin
  • muscuranic Ach
22
Q

Hormones that use Ca or Phosphatdidylinositides (or both)

A 
alpha-1 adrenergic catecholamines
Cholecystokinin
Gastrin
TRH
Vasopressin
Ach (muscrarinic)
Antiotenssein II
GnRH
23
Q

Efects mediated by phosphoionisitde cascade

A

Glycogenolysis in liver cells
Histamine secretion by mast cells
Serotonin release by blood paltelets
Aggregation of blod plaetlets
Insulin secretion by pancreatic islet cells
Epinephrine secretion by adrenal chormaffin cells
SMooth muscle contraction
Visual transcdciton in invertebrea phoreceptors

24
Q

Wha is spinocerebellar Ataxia 14

A

Ataxia-inabilityt o coordinate muscular movement

A disease of Protein Kinase C-gamma

16 of 22 cases have a mutation in teh C1 domain that prevents the enzyme tfrom binding to the membrane

PKC can no longer phospphorylate one of its substrates, TRP Ca2+ channel

Neurons can no longer regulate Ca2+ concentration

25
Q

Whaat is the insulin, GH, and IGF-1 connection?

A

Direction action of GH on lipid, carbohydrate, and protein metabolism–anabolic

IN hypoglycemia, GH stimulates lipolysis, and induces peripheral resistane t insulin, tehreby stimulating use of FA and sparing glucose for the brain.

26
Q

Why weren’t serum levels of GH measured direction?

A

Human pituitary coantians about 10mg of GH

5% is released each day in bursts over 3-4 hours. 100x hnage in serum concentration. Highest release is during sleep. Therefore, tehre is no constant measurable GH level.

GHRH and somatostatin form teh hypothalamus control GH release, as well as the IGF-1 inhibitory feedback loop

27
Q

what does GH stmulate during hypoglycemia

A

GH stimulates lipolysis and induces preipheral resistance ot insulin, thereby stimulating use of FA andsparing glucose for brain.

Biochem Winter 2012 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions