Physio Test 3 - Ans And Cardiac

Front 1

Dopamine, NE and E are derivatives of

Back 1

phenylethylamine

Front 2

catecholamine synthesis

Back 2

Made in dopaminergic/noradrenergic neurons in brain, postgang sympathetic nerve variscosities, adrenal medulla

Front 3

NE synthesis pathway

Back 3

Tyrosine >> Dopa (Tyrosine hydroxylase) >> dopamine (L-aromatic amino acid decarboxylase >> NE (dopamine beta hydroxylase in vesicle)

Front 4

Rate limiting enzyme in catecholamine synth

Back 4

tyrosine hydroxylase

Front 5

TH regulated by

Back 5

phosphorylation and feedback inhibition

Front 6

conversion of NE to E

Back 6

by Phenylethanolamine-N-methyltransferase in adrenal medulla and some neurons

Front 7

catecholamine storage/release in adrenal medulla

Back 7

Nicotinic cholinergic receptor on chromaffin cells is activated and causes Ca-dependent release into bloodstream. Mostly E stored here.

Front 8

catecholamine release from symp nerve terminals

Back 8

Ca-dependent; exocytosis

Front 9

Termination of catecholamine action occurs due to...

Back 9

#1 reuptake of NT into sympathetic nerve ending (most important!) #2 diffusion away from site of action; #3 metabolism (important for E, not NE)

Front 10

COMT

Back 10

terminates physiological effects of E by converting it to metanephrine. Found in kidneys, liver

Front 11

COMT inhibitors

Back 11

used in conjunction w/ L-Dopa to treat Parkinson's. Reduces side effects from L-Dopa in periphery but doesn't interfere in brain b/c it can't cross BBB

Front 12

Monoamine Oxidase

Back 12

mitochondrial enzyme that converts catecholamines to aldehydes. Found in liver, intestines. Metabolizes phenylethylamines from diet and regulates cytoplasmic catechol levels in symp nerve endings.

Front 13

MAO inhibitors

Back 13

elevate NE and serotonin in brain. 1st antidepressants

Front 14

Neuronal uptake of NE

Back 14

active transport across plasma membrane; repackaged into vesicles.

Front 15

Cocaine and TCA's

Back 15

Block reuptake of NE, potentiating sympathetic neurotransmission. Not taken up themselves.

Front 16

Vesicular uptake

Back 16

Dopamine or NE can be actively transported into vesicles.

Front 17

Reserpine

Back 17

Inhibits NE transport into vesicles, rapidly depleting intraneuronal levels b/c they are inactivated by MAO. Rapid depletion in brain/periph.

Front 18

Regulation of NE release

Back 18

alpha 2 adrenergic receptor is activated by NE to inhibit further NE release. This "autoreceptor" allows NT to regulate its own release.

Front 19

alpha 2 agonists

Back 19

decrease NE release

Front 20

alpha 2 antagonists

Back 20

increase NE release

Front 21

Indirect activation of phenylethylamines

Back 21

tyramine, amphetamine, ephedrine can be taken up into vesicles, displacing NE and leading to its nonexocytotic release. Acute sympathomimetric effects (massive vasoconstriction).

Front 22

Indirect sympathomimetics

Back 22

all action due to release of NE; tyramine, amphetamine

Front 23

Direct

Back 23

only activates adrenergic receptors

Front 24

Mixed

Back 24

direct and indirect effects

Front 25

alpha 1 receptors

Back 25

mediate blood vessel constriction in response to catecholamines

Front 26

alpha 2 receptors

Back 26

mediate inhibition of NE on sympathetic nerve endings

Front 27

alpha receptor affinity

Back 27

E > NE >> ISO

Front 28

alpha 1 receptor mechanism

Back 28

GPCR alpha Q >> PLC >> DAG >> PKC >> Ca influx
and PLC >> IP3 >> Ca release from SR

Front 29

alpha 2 receptor mechanism

Back 29

GPCR alpha-I; inhibit adenyl cyclase, activate K channels

Front 30

beta 1 receptor affinity

Back 30

ISO > E = NE

Front 31

beta 1 found on

Back 31

heart

Front 32

beta 2 affinity

Back 32

ISO > E >> NE

Front 33

beta 2 found on

Back 33

vascular, bronchial smooth muscle

Front 34

beta receptor mechanisms

Back 34

GPCR alpha-S; activate adenyl cyclase, CAMP

Front 35

inhibition of beta receptor mechanism

Back 35

phosphodiesterases break down CAMP; caffeine and methyl xanthines inhibit this process, potentiate sympathetic effects

Front 36

receptor distribution on heart

Back 36

mainly beta-1; increase cardiac output and O2 consumption

Front 37

long-term activation of beta-1 AR on heart

Back 37

can be toxic, because heart must work harder. Beta blockers target these receptors.

Front 38

receptor distribution on arteries, arterioles

Back 38

alpha-1 predominate in skin, mucosa and mediate constriction; beta-2 predominate in liver, skeletal muscle and mediate dilation

Front 39

receptor distribution on veins

Back 39

alpha 1 and 2; constrict when activated to increase venous return to heart, increase CO

Front 40

Iso is what type of agonist

Back 40

beta 1 and 2

Front 41

effects of Iso

Back 41

acts on beta-1 to increase contractility of heart and raise systolic blood pressure; acts on beta-2 on vessels to decrease peripheral resistance, lower diastolic pressure.
**net effect may cancel out.
**Does raise HR

Front 42

NE is what type of agonist

Back 42

alpha 1, beta 1

Front 43

Effects of NE

Back 43

alpha-1: contracts vasculature, increasing peripheral resistance and diastolic pressure.
beta-1: same as Iso, BUT...
big increase in BP leads to vagal reflex slowing of HR, overcoming its actions on beta-1

Front 44

effects of NE in presence of muscarinic Ach receptor antagonist

Back 44

PS reflex response is not intact, so no slowing of HR. Massive increase in BP can lead to stroke

Front 45

agonist-induced desensitization

Back 45

due to phosphorylation, can occur w/in minutes due to continued presence of agonist. Dephosphorylation activates it once again when agonist is no longer present

Front 46

agonist downregulation

Back 46

receptor protein degradation after longer duration exposure to agonist. must synthesize new receptors in order to be activated again.

Front 47

supersensitivity

Back 47

upregulation of receptors after lack of stimulation >> suprasensitive response when activated

Front 48

E is what type of agonist

Back 48

alpha 1, beta 1, beta 2

Front 49

effects of E

Back 49

beta 1: increase CTY of heart, systolic BP; beta 2: vasodilation to skeletal muscles, lowering periph resis and diastolic pressure. Mean increase in BP and moderate increase in HR

Front 50

clonidine

Back 50

alpha 2 agonist used to treat hypertension, addiction withdrawal

Front 51

epinephrine, phenylepinephrine

Back 51

alpha 1 agonists used to treat decongestion, hemmorage, hypertension, etc.

Front 52

dobutamine

Back 52

beta 1 agonist used after heart surgery or for heart fialure, has positive ionotropic effects w/ little change in HR. Also used for shock

Front 53

albuterol

Back 53

short-term beta 2 agonist used for acute asthmatic symptoms

Front 54

salmeterol

Back 54

long-term beta 2 agonist used with ICS for maintenance therapy of asthma

Front 55

treating allergic rxn

Back 55

alpha 1 and beta 2 effects: epinephrine intramuscularly stops mast cell release (prevents edema) (beta 2) and also supports BP (alpha 1)