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Physiology 1 > Week 2 > Flashcards

Week 2 Flashcards

1
Q

What are the types of intercellular communication (5)

A

Autocrine
Paracrine
Contact-mediated
Synaptic
Endocrine

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2
Q

What is Kd

A

Binding affinity of a receptor
When binding saturation is 50%
(The lower the higher affinity, cause less dose is needed for action)

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3
Q

What is Ec50

A

Characterizes potency of a drug
When bio response is 50%
Lower Ec50 is more potent
(Effective conc. 50)

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4
Q

Biological response of Agonist, Partial Agonist, and Antagonist.

A

Agonist: 1 (100%)
P.Agonist: 0.5 (50%)
Antagonist: 0 (0%)

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5
Q

Antagonists can be

A

Neutral Antagonists
Inverse Agonists

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6
Q

Cariprazine

A

Stimulates / Inhibits D3/D2
Agonist / Antagonist
Works like dopamine but only 40-60%
Depression and Schizophrenia

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7
Q

What are the Vasopressin Receptors

A

V1- Smooth Muscles
V2- Kidney

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8
Q

Why do we administer Desmopressin if Antidiuretic Hormone is Low

A

Because administering Vasopressin directly would mean that both V1 and V2 receptors would be affected.
So smooth muscles and the kidneys would be affected.

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9
Q

Desmopressin

A

V2 Receptor Agonist

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10
Q

GPCR Steps

A

1) Agonist Binds R —-> R*
2) Receptor / G-protein Interaction a-GDP to a-GTP.
3) G-protein dissociates from Receptor.
4) a and by subunits dissociate.
5) Subunits interact with effectors.
6) Termination and subunits bind again.

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11
Q

What converts GDP to GTP

A

GEF
Guanine exchange factor
e.g: Active G-prot coupled Receptor

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12
Q

What inactivates GTP to GDP

A

GAP
GTPase Activating Protein

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13
Q

What types of receptors are Adrenergic R

A

All G Protein coupled receptors

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14
Q

Gs Proteins Examples

A

B - Adrenergic R
ACTH R
Glucagon R

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15
Q

What does PDE do? What can inhibit it>

A

Metabolizes cAMP to AMP
Caffeine, leads to more alertness.

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16
Q

G i/o Protein Examples

A

a2 - Adrenergic R
Opiate R
Cannabinoid R
Somatostatin R

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17
Q

Effects of G i/o Proteins

A

Inhibition of Adenylyl Cyclase (no cAMP)
Activation of K Channels
Inhibition of Ca Channels
Phospholipase A2 Activation

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18
Q

3 Paths of Arachidonic acid Signaling

A

Cyclooxygenase
Lipoxygenase
Epoxygenase

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19
Q

What does Arachidonic acid in cyclooxygenase path produce?

A

Prostaglandins
Therefore, blocking COX helps with fever inflamation and pain.

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20
Q

What Mediates Transducin and Gustducin actions?

A

cGMP —> GMP

21
Q

G q/11 Protein Examples

A

a1 R
Angiotensin R

22
Q

Events after Gq/11 activation

A

1) a subunit activates Phospholipase C.
2) PLC acts on PIP2
3) DAG+ IP3
4) DAG activates PKC
5) IP3 –> R –> Opens Ca flux from ER to cytoplasm.

23
Q

What does Capacitive Ca entry do?

A

Ensures that Ca stores in cell (ER) do not get depleted

24
Q

Capacitive Ca mechanism / SOC

A

STIM-1 Ca Sensor
Orai-1 Ca Channel

25
Q

What happens in response to increased Ca (Signal)

A

Ca binds Calmodulin, forms complx
Ca-Calmodulin activate CAM Kinases
CAMK phosphorylate target proteins

26
Q

Ga 12/13 Protein examples

A

Thrombin R
Angiotensin R

27
Q

G 12/13 Protein mech

A

1) a 12/13 - GTP activates GEF (Rho)
2) Rho - GTP
3) Rho Kinases

28
Q

Actions of Gt (Transducin) and Gg (Gustducin) Protein

A

1) at/g - GTP Activate PDE
2) PDE metabolizes cGMP to GMP

29
Q

What is Desensitization

A

The deactivation of a G-protein coupled receptor

30
Q

2 Methods of desensitization

A

Agonist dissociation
B-Arrestin Binding

31
Q

Types of Cholinergic receptors

A

Nicotinic / Ion channels
Muscarinic / GPCRs

32
Q

Receptor Tyrosine Kinases Ligands

A

Growth Hormone
Insulin

33
Q

Activation mech of Tyrosine Kinase receptors

A

1) Agonist Binding
2) Receptor dimerization
3) Autophosphorylation of Tyr

34
Q

RAS Pathway

A

1) Ligand binds to RTK
2) RTK autophosphorylation
3) SH2 binds phosphotyrosine
4) SOS binds (GEF)
5) RAS (GDP to GTP)
6) MAPK Phosphorylates cytosolic proteins and nucleus.

35
Q

What inhibits apoptosis and keeps cell survival

A

PI 3 Kinase

36
Q

What type of R is ANP-receptor

A

Guanylyl cyclase R

37
Q

Guanylyl Cyclase / ANP Receptor mech

A

1) ANP (Agonist) binds GC.
2) GC makes cGMP
3) PKg —-> Smooth m relaxation

38
Q

What is JAK

A

Tyrosine Kinase
(Janus Faced Kinase)

39
Q

Cytokine receptor examples

A

Growth Hormone R
Prolactin R

40
Q

JAK can phosphorylate

A

Receptors
Other JAK
STAT proteins

41
Q

What does phosphorylation of STAT proteins lead to?

A

This effects the nucleus
Leads to up/down reg. of gene expression (Slow)

42
Q

What type of Agonists are used for Intracellular R

A

Lipid permeable agonists

43
Q

Types of Intracellular Receptors

A

Cytosol (Type-I) / Glucocorticoid R
Nucleus (Type-II) / Thyroid HR R

44
Q

Can lipid permeable Agonists be used other than Intracellular receptors

A

Yes, in Plasma m. R (Faster)
in Cannabinoid R and Prostaglandin R

45
Q

NO Signaling

A

1) NO made by NOS
2) NO binds Guanylyl Cyclase
3) GTP —> cGMP
(Leads to vasodilation)

46
Q

2 Examples of Gene regulation

A

cAMP
JAK - STAT Pathway

47
Q

5 mechanisms of Intracellular Ca homeostasis

A

1) Gq
2) PLC
3) Voltage gated channel
4) Ligand-Gated channels
5) CICR
6) RYR (Ryanodine R)

48
Q

OFF mechanism of Ca signaling

A

1) SERCA (Sar/endo Ca ATPase)
2) PMCA (P.m. Ca ATPase)
3) NCX (Na/Ca exchanger)

49
Q

What activates the endocytosis of a GPCR

A

Arrestin Binding

Physiology 1 (12 decks)

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