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Physiology I F2015 > 18. ANS Pt 1 > Flashcards

18. ANS Pt 1 Flashcards

1
Q

What is role of ANS?

A
  • To help the body respond to internal environmental stresses and bring today back down to homeostasis.
    • Resting state allows for growth + metabolism
    • Reactive state is ineffective + inefficient, damaging to organs
    • ANS can respond to real or perceived stresses (emotional stresses (esp. non-physical) that aren’t normally stressful become stressful)
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2
Q

(T/F) Unregulated + prolonged sympathetic state can cause end organ dysfunction.

A

True.

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3
Q

What molecules regulate PNS + SNS?

A
  • SNS: epinephrine + related molecules (dopamine, norepi)
  • PNS: ACh
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4
Q

Which responds faster? PNS or SNS?

A

SNS. Sympathetic burst followed by slow return to homeostatic state.

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5
Q

(T/F) An increase in epi is equivalent to a decrease in PNS?

A

True

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6
Q

Describe adaptive + maladaptive ANS.

A
  • Adaptive: typically short lived response of SNS followed by return to homeostasis via PNS.
  • Maladaptive: long-lasting, uncontrolled sympathetic state causing chronic stress leading to organ damage + dysfxn
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7
Q

What cardiac problems appear in maladapted, unregulated, hypersympathetic state?

A
  1. Diastolic dysfunction (heart doesn’t relax + fill well)
  2. Tachycardia
  3. Tachyarrhymthias
  4. Ischemia (leading to necrosis)
  5. Cardiac stunning (heart doesn’t pump well)
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8
Q

What pulmonary problems appear in maladapted, unregulated, hypersympathetic state?

A
  1. Pulmonary edema (increased outflow cardiac failure w leaky pulm capillaries)
    • Maladaptive effects of heart causes decreased CO –> increased P in LV –> increased P in pulmonary veins + capillaries –> fluid into alveoli
  2. Pulmonary HTN (causes increased RV strain –> fluid back up in periphery –> swelling in extremeties + liver + other tissues)
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9
Q

What hematologic problems appear in maladapted, unregulated, hypersympathetic state?

A
  1. Hypercoagulation
  2. Anemia
  3. Bone marrow suppression (leading to decreased production of WBC + RBC –> anemia)
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10
Q

What endocrinological problems appear in maladapted, unregulated, hypersympathetic state?

A
  1. Decreased thyroid fxn (thyroid releases hormones that regulate growth and rate of fxn for many organ systems –> impt for cellular growth + metabolism)
  2. Decreased growth hormone (GH impt for long-term cellular growth + short-term tissue repair)
  3. Glucose intolerance (hyperglycemia)
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11
Q

What gastroinestinal problems appear in maladapted, unregulated, hypersympathetic state?

A
  1. Hypoperfusion (leads to ulcers + break down of intestinal walls –> gut bacteria leak through –> sepsis)
  2. Decreased peristalsis (lim digestion + uptake of nutrients –> malnourished despite eating)
  3. Ulcerations
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12
Q

What immunological problems appear in maladapted, unregulated, hypersympathetic state?

A
  1. Immune suppresion
  2. Stim. of bacterial growth (due to increased cathecholamine + decreased immune syst)
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13
Q

What metabolic problems appear in maladapted, unregulated, hypersympathetic state?

A
  1. Increased cellular metabolism (requires increased O2, nutrients, E, + CO2 removal; if body can’t provide –> cellular death)
  2. Hyperglycemia (for heart + brain, which primary uses glu for E)
  3. Catabolism
  4. Lipolysis
  5. Electrolyte fluxes
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14
Q

What muscular problems appear in maladapted, unregulated, hypersympathetic state?

A
  1. Cellular death (use aa to prod more glu)
  2. Apoptosis (can lead to muscle wasting + weakness if cells don’t regen.)
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15
Q

How is ANS organized?

A
  • Two nerve system: pre-glanglionic nerve –> ganglion (where nerve synapses) –> post-ganglionic nerve
    • SNS: pre-ganglionic comes from spinal cord, ganglion at symathetic chain (b/w T1-L2) close to cords
    • PNS = cranial-sacral system: pre-ganglionic from cranial pt near brainstem + sacral region of cords, ganglion close to innervated​ organ
  • Connects CNS to end organs
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16
Q

What is a second way of generating sympathetic response outside of ANS?

A

Through medulla of adrenal glands, which secrete catecholamines (epi/norepi) during stress –> global response

17
Q

Where does SNS preganglionic nerves originate?

A

Spinal cord between T1-L2, from intermediolateral nuclei (intermediate, lateral part of vertebra where pre-ganglionic nerve originates)

18
Q

What is the NT used for both SNS + PNS at the ganglion?

A

ACh

19
Q

What happens when you give an injection of ACh?

A

Both SNS + PNS will be upregualted becuase ACh = NT used at ganglion for both systems. However, much harder to get ACh into ganglion than end organ receptors –> greater increase in PNS than SNS –> overall down regulation of SNS (increase in PNS = decrease in SNS)

20
Q

(T/F) Somatic motor nerves are 2 nerve systems.

A

False. Somatic is 1 nerve system

21
Q

What is the difference in speed between SNS + PNS?

A
  • SNS: input tends to be more fast on b/c each nerve innervates one organ
  • PNS: ganglions located more in periphery from where nerves branch off before innervating multiple organs –> slower onset
  • e.g. During stressful situation, tachycardia appears almost immediately (SNS) but bringing HR back down takes a while (PNS)
22
Q

What is the pathway to make epinephrine?

A
  • Tyrosine –> –> Dopamine –> Norepiephrine –> Epinephrine
  • Not many changes b/w the molecules –> similar responses but different potencies based on what receptors the molecules bind to
23
Q

What are the four types of adrenergic receptors and where is each generally found?

A
  • α1 receptors = post-synaptic, located on end organs
    • Commonly on smooth muscle, esp of blood vessels
  • α2 receptors = primarily pre-synaptic membrane w some post-synaptic
    • Mostly smooth muscle + CNS
  • β1 receptors are post-synaptic
    • Primarily on heart
  • β2 receptors are post-synaptic
    • Primarily on smooth muscle, esp bronchiole smooth muscle, skeletal muscle, arterioles, + glands
24
Q

What happens when ɑ1 receptors are stimulated?

A
  • G protein activation of phospholipase C
  • Phosphatidylinositol –> inositol 1,4,5-trisphosphate (IP3) + diacylglycerol (DAG)
  • IP3 initiates Ca++ release from ER into cytosol
25
Q

What are the smooth muscle effects of α1 receptor activation?

A
  1. Eyes: dilate (constrict muscle) –> get as much light into eyes as possible to see as much as possible during stressful situation
  2. Lungs: constrict –> pulm HTN + bronchoconstriction
    • Effects can be overcome by β2 bronchodilation
  3. Blood vessels: vasoconstriction –> increased BP
  4. Uterus: contraction
  5. Genitourinary: constrict sphinctors
  6. Gut: constrict sphinctors –> “stomach in knots” feeling
  7. Endocrine: inhibits insuline release –> increased glu in system to be used
    • Insuline drives glucose into cells to be stored
26
Q

Neosynephrine + norepinephrine are ______ agonists.

A

α1

27
Q

What happens when presynaptic ɑ2 receptors in the periphery are stimulated?

A
  • Feedback control: release of epi/norepi from presynaptic neuron circles back + binds to ɑ2 receptors
  • G-protein mediated inhibition of adenylyl cylase –> fall in second messenger cAMP –> decreases Ca++ in post ganglionic nerve terminals –> inhibits exocytosis of NT
  • Decreases amount of epi/norepi that reaches postsynaptic ɑ1 receptors –> decreased symathetic tone –> indirect vasodilation
  • Epi/norepi are both agonists of ɑ2 receptors leading to their own down regualtion
28
Q

What happens when postsynaptic ɑ2 receptors are stimulated?

A
  • Smooth muscle: contristrion, similar to ɑ1 effects
  • CNS: sedation, reduced CNS output via inhibitory effect (decreased release of NT in CNS)
29
Q

What is clonidine?

A
  • Selective for ɑ2 receptors in CNS (brain) –> decreases ANS output –> decreased sympathetic tone –> decreased smooth muscle contraction + decreased BP
  • Antihypertensive
  • Negative chronotrope (brady due to increased vagal stim to SA node due to sympathetic withdrawl)
  • Sedative –> decreases anesthetic + analgesic requirements
30
Q

What is dexmedetomidine/precedex?

A
  • Lipophylic derivative, highly selective ɑ2 receptor agonist –> decreased CNS NT release
  • Sedation
  • Analgesic
  • Sympatholytic –> brady, negative chronotrope
  • No respiratory depression + hypotension
31
Q

What happens when β1 receptors are stimulated?

A
  • Increased adenylyl cylase activity –> increased second messenger cAMP –> increased intracellular Ca++
  • Chronotropic: increased rate
  • Dromotropic: increased conduction
  • Inotropic: increased F of contraction
32
Q

What happens when β2 receptors are stimulated?

A
  • G-protein increases adenylyl cylase activity –> increased cAMP –> activates various proteins
    • Has more of an inhibitory effect on smooth muscle contraction
  • Relaxes smooth muscle
  • Gluconeogensis (making glu from non-carbohydrate C sources)
  • Insulin release (stores glu as glycogen or fat)
  • Stim. Na-K pump to drive K intracellular
    • Think pumpkin –> Pump-K-in
    • Can give to pt w hyperK
33
Q

What is the diff in affinity to epi/norepi b/w ɑ1 + ɑ2 receptors?

A
  • ɑ1 respond better to norepi than epi
  • Smooth muscle cells in vascular system in resp to ɑ1 receptors = excitatory –> vascular smooth muscle contraction –> increase BP
  • ɑ2 are inhibitory when stimulated –> decreased release of NT or glandular product (e.g. insulin from pancreas)
  • HOWEVER, postsynaptic ɑ2 receptors on vascular smooth muscle behave in similar way at ɑ1 receptors –> vasoconstriction
34
Q

What receptors do these adrenergic agonists bind to?

  • Phenylephrine
  • Epinephrine
  • Ephedrine
  • Dopamine
  • Dobutamine
  • Albuterol
  • Methyldopa
  • Clonidine
  • Terbutaline
  • Fenoldopam
A
  • Phenylephrine - ɑ1
  • Methyldopa - ɑ2
  • Clonidine - ɑ2
  • Dobutamine - β1
  • Albuterol - β2
  • Terbutaline - β2
  • Epinephrine - ɑ + β
  • Ephedrine - ɑ + β
  • Dopamine - dopaminergic receptors
  • Fenoldopam –> vasoconstriction
35
Q

What is the diff b/w direct + indirect adrenergic agonists?

A
  • Direct: looks like catecholamines, stim. receptor directly
  • Indirect: depends on body’s stores of NT in nerve cell, increase endogenous NT
    • Increased release
    • Decreased uptake
    • Inhibit metabolism
    • E.g. ephedrine –> norepi release
    • E.g. when someone uses cocaine, depletes body of catecholamines (epi + norepi) such that indirect agonsts have no effect
36
Q

How are NT broken down?

A
  1. Reuptake: put NT back into storage
  2. Degradation: degrade in synapse (catechol-O-methyl transferase, monoamine oxidase, which oxidizes w removal of amine group)
37
Q

What are MAO inhibitors?

A
  • Blocks metabolism of catecholamines –> prolonged + pronounced response from SNS, esp w indirect agonists
  • Pt taking MAO inhibitors can have huge swings in SNS response
38
Q

Summary of receptor, receptor location, agonist/antagonist effects

A

Physiology I F2015 (13 decks)

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