Autonomic Nervous System Flashcards
The ANS is a component of what system?
PNS
It involves what types of actions and controls what functions?
acts as a control system for involuntary actions and visceral functions
What types of actions does if affect?
HR, digestion, RR, salivation, perspiration, diameter of pupils, micturition and sexual arousal
It consists of what two components?
sympathetic and parasympathetic NS
What involves a 3rd component? Name?
GI tract has a third component - enteric NS
What do the terms sympathetic and parasympathetic refer to?
anatomic origin of preganglionic neurons in CNS
Where do the preganglionic neurons in SNS originate?
thoracolumbar spinal cord (T1-L3)
Where do the preganglionic neurons in PNS originate?
in brainstem (CN 3,7,9,10) and sacral spinal cord (S2-S4)
Describe the anatomic pathways for PNS and SNS
PNS: 1) preganglionic cholinergic neuron –> ACh –> N(ganglia); post-ganglionic cholinergic neuron–> ACh –> M
SNS: 1) preganglionic cholinergic neuron –> ACh –> N(ganglia); postgang adrenergic neuron –> NE –> alpha, beta receptors
2) pregang cholinergic neuron –> ACh –> N(ganglia); postgang dopaminergic neuron –> D –> D1
3) pregang cholinergic neuron –> ACh –> N(adrenal glands); systemic circulation –> NE or Epi –> alpha, beta
Describe differences btw symp and parasymp:
origin of pregang:
location of autonomic ganglia:
length of preg:
length of post:
effector organs:
neurotransmitter and receptor type in gang:
neurotransmitter in effector organs
receptor types in effector organs
Sympathetic Parasympathetic
1) T1-L3 CN 3,7,9,10 and S2-S4
2) para and pre-vert in or near effector organs
3) short long
4) long short
5) smooth and cardiac muscle, glands
6) ACh; N ACh; N
7) NE ACh
8) a1 a2, b1 b2 M
Describe the effects of the Parasympathetic and Sympathetic
Parasympathetic Sympathetic
eyes
salivary glands
heart
lungs
stomach
liver
kidneys
intestines
bladder
RR
Operation
Metabolism
Circulation
1) constrict pupil dilate pupil
2) stimulate inhibition
3) slow HR accelerate HR
4) constrict bronchi dilate bronchi
5) stimulate dig inhibit dig
6) stim bile release stim glu release
7) stim Epi and NE release
8) stim peristalsis and secretion; inhibit
9) contract relaxes
10) decreased increased
11) all the time all the time, plus stress
12) normoglycemia hyperglycemia
13) smooth muscle skeletal muscle
1) What is the adrenal medulla?
2) Where are the cell bodies of its preganglion neurons located?
3) Where do those axons travel?
4) Where do they synapse?
5) What do they release and what does it activate?
6) What do the chromaffin cells secrete?
7) What is the difference btw sympathetic postganglion neurons and adrenal medulla?
1) a specialized ganglion in the sympathetic division of ANS
2) thoracic spinal cord
3) in the greater splanchnic nerve to the adrenal medulla
4) on the chromaffin cells
5) releases ACh which activates nicotinic receptors
6) catecholamines (epi and NE) into general circulation
7) sympathetic release only NE; whereas adrenal medulla secretes 80% epi and 20% NE
1) Describe mechanism of action of A and B receptors
`
NE and Epi –>
a1 –> phospholipase C –> PIP3, DAG, IP3 –> Ca+2 –> smooth muscle contraction
a2 –> adenylylcyclase –> ATP –> cAMP –> smooth muscle contraction; a2 –> Ca+2 –> inhibition of transmitter release
B –> adenylylcyclase –> ATP –> cAMP –> heart muscle contraction, smooth m relaxation, glycogenolysis
1) Where are adrenoreceptors found?
2) How are they activated?
3) Where is NE released from?
4) What secretes Epi? and what does it reach?
5) What are the two types of adrenoreceptors?
6) Each of the receptor types has a different mechanism of action resulting in what?
1) in target tissue of the sympathetic NS
2) by the catecholamines NE and Epi
3) postganglion neurons of SNS
4) adrenal medulla and reaches the target tissue via circulation
5) alpha and beta –> a1, a2, b1, b2
6) different physiological effects
1) What are the two types of cholinoreceptors?
2) Where are nicotinic receptors found?
3) Where are muscarinic receptors found?
1) nicotinic and muscarinic receptors
2) on teh motor end plate in all autonomic ganglia and on chromaffin cells of adrenal medulla
3) in all effector organs of the PNS and in a few effector organs of SNS
1) The ANS innervates the GI tract with what two components?
2) What does the extrinsic involve?
3) What does the intrinsic involve?
4) Where is the intrinsic contained?
5) Who does the enteric NS communicate with?
1) intrinsic and extrinsic components
2) parasympathetic and sympathetic NS
3) enteric NS
4) wholly within the submucosal and myenteric plexuses
5) witht he sympathetic and parasympathetic NS
1) What supplies parasympathetic innervation of GI?
2) What does the vagus nerve innervate?
3) What does the pelvic nerve innervate?
4) Describe the parasympathetic neurons
5) How are the postganglionic neurons classified?
1) vagus nerve and pelvic nerve
2) upper GI
3) lower GI
4) it has long preganglionic fibers that synapse in ganglia in or near target organs
5) as either cholinergic or peptidergic
1) What do cholinergic neurons release?
2) What do peptidergic neurons release?
3) What is the vagus nerve composed of?
4) What do afferent fibers do?
5) What do efferent fibers do?
6) What do mechanoreceptors and chemoreceptors do?
1) ACh as the neurotransmitter
2) one or more enteric neuropeptides (Substance P - SP, vasoactive intestinal peptide VIP, neuropeptide Y - NPY and gastrin-releasing peptide - GRP
3) a mixed nerve –> 75% afferent fibers and 25% efferent fibers
4) transmit sensory information from mechano and chemorecdeptors in the wall of GI tract to CNS
5) deliver motor information from CNS back to target cells in periphery (sm m, secretory and endocrine cells)
6) in the GI mucosa, they relay afferent info to CNS via vagus nerve –> triggers relexes whose efferent pathway transmits back via vagus nerve as well
1) What supplies sympathetic innervation?
2) What do the sympathetic nerves innervate?
3) Describe preganglion sympathetic neurons
4) Why type is the postganglionic neuron? What do they release?
5) What comprises sympathetic nerve fibers?
6) How is info relayed?
1) spinal segments T1-L3 of thoracolumbar spinal cord
2) heart, blood vessels, bronchi and GI
3) short and synapse at ganglia outside GI tract
4) adrenergic and release NE as neurotransmitter
5) 50% afferent and 50% efferent
6) sensory and motor info relayed btw GI tract and CNS, coordinated by submucosal and myenteric plexuses
1) Where are the ganglia of ENS located?
2) What do they control?
3) Where do they receive inputs from?
4) What types are enteric neurons?
1) in submucosal and myenteric plexuses
2) control contractile, secretory and endocrine fns of gut
3) from parasympathetic and sympathetic NS which serve to modulate their activity
4) cholinergic, adrenergic and peptidergic –> may secrete one or more neurotransmitters
1) What nerves comprise the peripheral nervous system?
2) What is it divided into?
3) Describe general characteristics of SNS
4) Describe general characteristics of ANS
5) When is ANS activated?
1) all cranial and spinal nerves?
2) somatic and autonomic NS
3) innervates skeletal muscle, General Somatic Sensory, voluntary control
4) innervates visceral organs, muscle/glands/adipose, involuntary control
5) during digestion
1) What type of motor system is SNS?
2) What type of control is it under?
3) What comprises the unit?
4) Where are the cells bodies?
5) Where do axons synapse?
6) What does the pre-synaptic terminal release?
7) Where is nicotinic cholinergic receptor located?
8) What does the motor neuron AP result in?
1) voluntary
2) conscious
3) single motor neuron and skeletal muscle fiber
4) in the CNS - brainstem ro spinal cord
5) directly on skeletal muscle
6) ACh
7) motor end plate
8) muscle AP
1) What is the unit of the ANS?
2) Where are the cell bodies of preganglion?
3) Where do axons synapse?
4) Where do axons of postganglion synapse?
5) What do preganglion neurons release?
6) What do postganglion neurons release?
1) two neurons, pre and post ganglion –> ANS arborizes, branches
2) cell bodies of preganglion neurons –> in CNS
3) on cell bodies of postganglionic neurons in autonomic ganglia outside CNS
4) on visceral effector organs
5) ACh
6) ACh, NE, neuropeptides
1) Name the enteric neuropeptide families
2) What fns are they involved in?
1) Tachykinins, VIP/PIH - secretin, Opioids, Bombesins, Gastrin-CCk, Pancreatic polypeptides
2) substance P (SP) - tachykinin
propagagtion of peristalsis of gut
visceral sensitivity
vomiting response
1) Describe mechanism of neuropeptides
2) What are opioids involved in with GI?
3) Consequences of regulation?
4) What’s involved in peristalsis?
5) What is Loperamide?
1) bind to own receptors –> stimulates Ca+2 release/influx and K+ efflux –> Ca-CaM –> MLCK (myosin light chain kinase) –> myosin phosphorylation
2) increases segmentation –> circular smooth muscle
3) if no regulation –> loss of nutrition (seg causes ingesta to slow down - nutrient loading in proximal GI)
4) longitudinal smooth muscle contraction –> movement of ingesta uninhibited (distal GI)
5) anti-diuretic; inhibits fluid secretion, promotes absorption, stimulates segmentation
1) What are the phases of Gastric secretion?
2) What is the basal phase?
3) What is the cephalic phase?
4) what is the gastric phase?
5) What is the intestinal phase?
6) Which species has an increased risk of gastric ulcers and why?
1) gasal, cephalic, gastric and intestinal
2) that which occurs in the absence of a cephalic, gastric and intestinal stimulation (hasn’t tasted/eaten)
3) that mediated by sight, smell, taste and swallowing (chewed and swallowed)
4) that mediated by gastric distention and protein
5) that mediated by duodenal secretions (stomach –> intestine)
6) humans –> higher % in intestinal phase than other species
What distinct physical feature does the stomach contain?
What produces the gastric acid response
What are there receptors for on the gastric parietal cell?
1) rugae folds
2) parietal cells
3) histamine, ACh and gastrin
1) when contronted with a stressful situation, animals behave how?
2) Neurohormonal regulation of this behavior has been linked to what?
3) what does this lead to?
4) What does stress provoke?
5) What is the outcome of this?
6) How do the neural (SNS) and hormonal components operate?
1) in a predictable way –> default set or rxns directed toward flight or fight endpt
2) activation of neurons in hypothalamus and brain stem
3) increased input to sympathetic preganglionic neurons –> regulating cardiac and adrenal medullary fns
4) release of corticotropin-releasing factor CRF –> incnrease release of adrenocorticotropic hormone ACTH –> production orf corticosteroids and ANS-induced release of catecholamines
hypothalamus(-) –> CRF –> ant pit(-) –> ACTH –> adrenal cortex –> cortisol
5) beneficial (modulation of E, met, hemodynamics, immune and inflammatory response) and deleterious (stress ulcer and systemic hypertension)
6) neural components operate in short term (sec to min) ; hormonal components operate long term ( hrs to days)
1) What is autonomic regulation crucial for?
2) what two activities change in opposite phases during sympathetic stimulation?
3) What stage is where the 1st is high and 2nd is low?
4) What stage is where thw 1st is low and 2nd is high?
5) Where did ANS originate?
1) homeostasis in animals
2) circulatory and digestive activity
3) fight or flight
4) rest and digest
5) in early vertebrate phyla and developed to its greatest extent in mammals
1) what actions is associated with SNS acitvation of these organs?
GI sphincter tone
GI tract
metabolism
circulation
auditory
Repro
Neural
increased
inhibition of peristalsis, secretion, digestion and absorption
increased blood glucose and lipolysis
dilation of blood vessels to skeletal and cardiac muscle; constriction of blood vessels to smooth m(GI)
increased auditory acuity
inhibition of erection
disinhibition of spinal reflexes
Describe molecular mechanism
the regulation of L-type Ca currents occurs through what?
release of epi from adrenal medulla and norepi from sympathetic nerve endings –> B-adrenergic receptors –> increases in L-type Ca+2 currents in cardiac and skeletal muscle –> increases force of contraction of skeletal muscle and the beating rate and contractilityy of heart
activation of PKA-mediated phosphorylation of multiple targets in cardiac muscle including cardiac ryanodine receptor/ca release channel required for muscle contraction
1) define hibernation
2) define torpor
3) Why is torpor used rather than hibernation?
4) what are daily heterotherms?
5) How do they contrast with hibernators?`
6) define poikilothermy
1) a behavioral, physiological and molecular adaptation exhibited by diverse mammalian species to withstand protracted periods or seasons of insufficient or unpredictable food availability
2) the period in hibernation that is characterized by suppressed minimal body temp and MR
3) b/c hibernation refers to a process that encompasses several months of prolonged torpor, interrupted by and including arousal episodes
4) species that enter daily torpor exclusively, appear to rely mostly on fall of body temp for MR reduction
5) hibernators (species capable of prolonged torpor bouts) rely extenesively on metabolic inhibition, in addition to body temp effects, to reduce MR to a fraction of that observed in daily heterotherms
6) process by which an animals body temp with ambient temp
1) The ability to hibernate involves what?
2) What is the hibernation season characterized by?
3) What do many global biochemical and physiological processes do?
4) What must other critical fns do?
1) differential expression of genes common to all mammals, rather than induction of novel gene products unique to hibernating state
2) extended bouts of torpor during which minimal body temp can fall as low as -2.9C and metabolism can be reduced to 1% of euthermic rates
3) exploit low temp to lower rxn rates but retaint he ability to resume full activity upon re-warming
4) continue at physiologically relevant levels during torpor and be precisely regulated even at body temp values near 0C
1) What are cell processes suppressed at low temp?
2) What cell prcesses continue at low temp?
3) What do diving mammals and birds face in deep-diving?
4) How are they solved?
1) DNA txn, RNA tln, mitosis and cell proliferation, membrane comp and fn, mito resp, dig fn, renal fn and immune fn
2) CNS fn, CV fn, ventilation and met (adipose tissue)
3) limited oxygen stores and large hydrostatic pressures
4) increased muscle myoglobin, greater tissue O2 stores, ability to rely on anaerobic met, lung collapse at shallow depths, regional hypothermia, animal buoyancy
1) What is dysautonomia?
2) What are the clinical signs?
3) What signs are seen less frequently?
4) What is the pathophysiology?
1) generalized autonomic neuropathy originally reported in cats in UK, now in dogs and cats throughout Western Europe and US
2) reflect a generalized autonomic dysfn –> megaesophagus, esophageal hypomotility, gastric and small bowel distension and hypomotility (delayed gastric emptying), and urinary bladder distension
***acid erosion of esophagus –> dec appetite –> anorexia –> dec bcs
3) aspiration pneumonia and megacolon
4) degenerative lesions are found in autonomic ganglia, intermediate gray columns of spinal cord and some sympathetic axons
***no definitive etiology established
1) What are the most frequent clinical signs reported in dogs?
2) What are the most frequent in cats?
3) How is a diagnosis made?
4) What are additional findings consistent with diagnosis?
5) What are some differential diagnoses early in the course of illness?
6) What is tx protocol?
7) Prognosis?
1) vomiting, diarrhea, anorexia, lethargy, wt loss, dysuria and inspiratory dyspnea
2) dilated pupils, esophageal dysfn, dry nose, reduced lacrimal secretions, prolapse of 3rd eyelid, regurgitation and constipation
3) based on hisorical and PE findings
4) esophageal dilation and hypomotility on survey ro barium contrast xrays; delayed gastric emptying on barium contrast xrays; reduced tear production (schirmer tear tests); atropine-insensitive bradycardia; bladder and colonic distension on survey xrays
5) colonic or intestinal obstruction, other causes of megaesophagus and lower UT disease
6) supportive care (artificial tears, elevated feedings, expressing urinary bladder, antibiotics) is still basis of therapy; some dogs and cats show mild improvement with parasympathetic drugs; gastrostomy tube feedings or total parenteral nutrition may sustain some animals until they regain neuro fn
7) guarded to poor for long-term survival; 20-40% in affected cats likely to recover (2-12 mths); lower in dogs; complete recovery is ucommon - many left with residual impairment
1) What are pheochromocytoma?
2) What are they classified as?
3) Where do they most often arise?
4) Characteristics
5) When active, what do they cause?
6) symptoms?
1) catecholamine-secreting tumors of neuroectoderm-derived chromaffin cells
2) amine precursor uptake and decarboxylation cell tumors or APUDomas –> potential to secrete a variety of polypeptide hormones
3) from adrenal medulla but can occur at extra-adrnal sites
4) can be benign or malignant and may be functionally active or inactive
5) paraneoplastic syndrome associated with excess epi and norepi secretion
6) episodic weakness, resltessness, tachycardia, hypertension and collapse
1) What is significant about pheochromocytomas in dogs?
2) What are the clinical signs?
3) What are effective diagnostic tests?
4) Why is thorough staging of this disease important?
5) Approx 50% of these disease are what?
6) Cause of death?
1) unusual tumor type in dogs requiring a high degree of clinical suspicion to obtain a diagnosis
2) most are nonspecific
3) abdominal imaging techniques and perhaps special biochemical or provocative tests
4) to determien tumor behavior, appropriate therapy and prognosis
5) inactive adn remain clinically undiagnosed
6) tumor-related in 50% of dogs –> this disease is a clinical problem that will often require therapy
1) What are clinical signs of horner’s syndrom?
2) WHat is the pathogenesis?
3) What ist he etiology?
4) What is the therapy?
1) ptosis (drooping of eyelid), miosis (narrowing of pupil), enophthalmos, prolapsed nictitans (nictitating membrane)
2) disruption of sympathetic innervation to eye and peri-ocular facial muscles
3) idiopathic, trauma, tumor, inflammation, immune-mediated
4) supportive care, spontaneous recovery (those that don’t recover –> other underlying condition)
systemic hypertension
1) humans
2) dogs/cats
3) causes?
4) pathology?
5) signs?
1) primary hypertension is most common form
2) secondary causes most common form
3) renal and endocrine disorders (diabetes mellitus, hypothyroidism)
4) heart, kidney, eyes, CNS
5) episodic weakness, acute blindness (detached retina), arrhythmias
