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Physiology 2 Exam 2 > Exam 2 Review > Flashcards

Exam 2 Review Flashcards

1
Q

Describe the upper motor neuron

A
  • descends the spinal cord to level of the appropriate spinal nerve root
  • synapses with lower motor neuron or interneuron
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2
Q

Neurotransmitter of UMN and LMN is ____, which binds to _____ receptors

A

glutamate, glutamatergic

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3
Q

Describe the lower motor neuron

A

typically found in anterior gray portion of SC or cranial nerve nuclei of brainstem

  • terminate at effector with acetylcholine as neurotransmitter
  • cranial nerves are unique LMN
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4
Q

Describe renshaw cells

A

inhibitory cells in anterior horns of spinal cord that receive collateral branches from alpha moron neurons

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5
Q

Renshaw cells transmit inhibitory signals to surrounding motor neurons which results in what?

A

lateral inhibition and enhanced fluidity of limb movement

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6
Q

When renshaw cells transmit inhibitory signals to the same motor neuron, it results in what?

A

in recurrent inhibition

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7
Q

Sensory fiber types are either:

A

A-alpha or A-beta fibers
A-delta fibers
C fibers

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8
Q

What is the conduction rate of A-alpha or A-beta fibers

A

30-120 m/sec

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9
Q

What is the conduction rate of A-delta fibers

A

4-30 m/sec

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10
Q

What is the conduction rate of C fibers

A

less than 2.5 m/sec

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11
Q

What fibers are nociceptors and thermoreceptors related to?

A

C fibers or A-delta fibers

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12
Q

Describe the muscle spindle

A

3-10 mm long

consists of 3012 intramural fibers innervated by small gamma motor neuron

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13
Q

With finer moments, the number of muscle spindles required ____

A

increases

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14
Q

Central region of spindle has no _____; function as ____ receptor

A

contractile fibers; sensory

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15
Q

What fibers make up the ‘muscle fibers’ which are innervated by alpha motor neurons?

A

extrafusal fibers

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16
Q

What are the types of intrafusal fibers?

A

nuclear bag fibers

nuclear chain fibers

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17
Q

Describe the nuclear bag fibers

A
  • detect create of change in muscle length
  • innervated by group Ia afferent and dynamic gamma efferents
  • multiple nuclei located in a central bag- like configuration
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18
Q

Describe nuclear chain fibers

A
  • detect static change in muscle length
  • innervated by group II afferents and static gamma efferents
  • more numerous than bag fibers
  • multiple nuclei arranged in a single row
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19
Q

stimulation of sensory fibers from central region of intramural fiber results from

A

lengthening of entire muscle

contraction of ends of intramural fibers

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20
Q

What are the types of sensory fibers?

A

Ia (primary fibers)

II (secondary fibers)

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21
Q

when muscle is stretched, spindle is _____

A

stretched

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22
Q

muscle spindle gamma motor neurons innervate _____

A

intrafusal fibers

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23
Q

what does a Golgi tendon organ do?

A

detect muscle tension

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24
Q

What is the golgi tendon organ?

A

encapsulated sensory receptor through which muscle tendon fibers pass

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25
Q

Golgi organ is stimulated by _____ or _____ of muscle

A

contracting or stretching

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26
Q

premotor and supplementary motor cortices generate a plan for _____

A

movement

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27
Q

anterior part of the premotor cortex develops a _____ of the total muscle movement that is to be preformed

A

motor image

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28
Q

Supplementary motor cortex programs complex _____ and is responsible for mental rehearsal for a movement

A

motor sequences

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29
Q

What does the medial activation system innervate?

A

postural and girdle muscles

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30
Q

What is the lateral activation system associated with?

A

distally located muscles used for fine movements

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31
Q

What does the nonspecific activating system facilitate?

A

local reflex arc

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32
Q

What is the origin of the corticospinal tract?

A
  • Primary motor cortex
  • Premotor cortex
  • Somatosensory area
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33
Q

What is the pathway of the corticospinal tract?

A

Site of origin → internal capsule → medullary pyramids → X in lower medulla (most
fibers) → lateral columns of spinal cord (lateral corNcospinal tract)

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34
Q

Describe the lateral corticospinal tract

A
  • Made up of corticospinal fibers that have crossed in medulla.
  • Supply all levels of spinal cord.
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35
Q

Describe the anterior corticospinal tract

A
  • Made up of uncrossed corticospinal fibers that cross near level of synapse with LMNs.
  • Supply neck and upper limbs
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36
Q

What are the functions of the corticospinal tract?

A
  • Adds speed and agility to conscious movements: Especially movements of hand.
  • Provides a high degree of motor control: (i.e., movement of individual fingers)
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37
Q

Where are giant pyramidal (Betz) cells located?

A

motor cortex

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38
Q

What happens if the corticospinal tract has lesions?

A 
- Reduced muscle tone
• Clumsiness
• Weakness
• Not complete paralysis
• Note: complete paralysis results if both pyramidal and extrapyramidal systems are involved (as is often the case).
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39
Q

describe the corticobulbar tract

A

Upper motor neurons of the cranial nerves – innervating the face, head and neck
• Innervates the head
• Most fibers terminate in reticular
formation near cranial nerve nuclei.

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40
Q

What happens with the associated neurons of the corticobulbar tract?

A
  • Leave reticular formation and synapse in cranial nerve nuclei.
  • Synapse with lower motor neurons.
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41
Q

what is the red nucleus?

A

evolutionarily primitive portion of the brain

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42
Q

Fibers from the primary motor cortex and branches from corticospinal tract synapse in ______ portion of red nucleus

A

magnocellular

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43
Q

large neurons from the magnocellular region of the red nucleus give rise to what?

A

rubrospinal tract which decussates in lower brain stem

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44
Q

stimulation of red nucleus results in :

A
  • Stimulation of flexors

* Inhibition of extensors (antigravity muscles)

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45
Q

describe the vestibulospinal tract and apparatus

A
  • originates in vestibular nuclei
  • descends in anterior funicular column
  • synapses with LMNs to extensor muscles
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46
Q

components of the vestibulospinal tract and apparatus

A

utricle
saccule
semicircular canals

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47
Q

the utricle and saccule each contain a _____

A

macula

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48
Q

Each macula is covered by a ______ layer

A

gelatinous

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49
Q

What are the functions of the cerebellum?

A

Not essential for locomotion
• Helps sequence motor activities
Cerebellum: Functions
• Monitors and makes corrective adjustments to motor activities while they are being executed
• Removal of the cerebellum causes body movements to become highly abnormal.
• The cerebellum plays major roles in the timing of motor activities and in rapid, smooth
progression from one muscle movement to the next.
• Compares actual movements with intended movements
• Aids cortex in planning next sequential movement
• Learns by its mistakes
• Functions with spinal cord to enhance the stretch reflex
• Functions with brain stem to make postural movements
• Functions with cerebral cortex to provide accessory motor functions.
• Turns on antagonist at appropriate time
• Helps program muscle contraction in advance
• Functions mainly when muscle movements have to be rapid

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50
Q

What is the vermis?

A

Location for control functions for muscle movements of the axial body, neck, shoulders, and hips

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51
Q

What is the intermediate zone?

A

Concerned with controlling muscle contractions in the distal portions of the upper and lower limbs, esp. hands, feet, fingers, and toes

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52
Q

What is the lateral zone?

A

Associated with cerebral cortex with planning of sequential motor movements

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53
Q

If there are lesions in the dentate, emboliform and globose nuclei what can occur?

A

extremity ataxia

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54
Q

dentate, emboliform and globose nuclei project where?

A

red nucleus

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55
Q

dentate, emboliform and globose nuclei are related to what?

A

limb musculature and fine manipulative movement

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56
Q

lesion in the fastigial nuclei cause what?

A

trunk ataxia

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57
Q

fibers of fastigial nuclei project where?

A

to reticular formation and vestibular nuclei

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58
Q

What is fastigial nuclei related to?

A

postural activity and limb movements via reticulospinal and vestibulospinal tracts

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59
Q

describe the granular layer of the cerebellar cortex

A

• Innermost layer
• Made up of granule cells, Golgi type II cells, and glomeruli
cortex (+)
• Axons of mossy fibers synapse with granular cells and Golgi type II cells in the glomeruli

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60
Q

describe the purkinje cell layer of the cerebellar cortex

A
  • Middle layer

* Contains Purkinje cells

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61
Q

describe the molecular layer of the cerebellar cortex

A 
• Outermost layer
Purkinje dendrites (-)
• Contains stellate cells, basket cells, Purkinje dendrites, Golgi type II cells, and axons of granule cells (parallel fibers)
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62
Q

_____ cells axons form parallel fibers in cortex (+)

A

granular

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63
Q

____ cells project from parallel fibers to granular cell bodies (-)

A

golgi

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64
Q

_____ cells project from parallel fibers to purkinje axon hillock (-)

A

basket

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65
Q

_____ cells parallel fibers to purkinje dendrites (-)

A

stellate

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66
Q

Purkinje cells only output from _____

A

cortex

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67
Q

Purkinje cell output is always _____

A

inhibitory

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68
Q

describe climbing fibers

A
  • Originate from medullary olives
  • Make multiple synapses with Purkinje cells
  • Provide high frequency bursts (complex spikes)
  • “Condition” the Purkinje cells
  • Play a role in motor learning
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69
Q

describe fossy fibers

A
  • Originate from multiple centers in brainstem and spinal cord, including vestibulocerebellar, spinocerebellar, and pontocerebellar tracts
  • Make multiple synapses on Purkinje cells and result in simple spikes
  • Synapse on granule cells in glomeruli
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70
Q

Vestibulocerebellum consist of what?

A

flocculonodular lobes and vermis

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71
Q

Vestibulocerebellum receives fibers from where?

A

vestibular system

oculomotor system

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72
Q

what changes occur when cerebellum is removed

A
  • Movements are slow to develop.
  • Force developed is weak.
  • Movements are slow to turn off.
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73
Q

what is vestibulocerebellular syndrome?

A
  • Starts with abnormal eye movement including nystagmus (eyes make repetitive, uncontrolled movements)
  • Progressive genetic disease of the flocculonodular lobe
  • Vertigo, tinnitus
  • Ataxia
  • Eventually fine motor skills are lost
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74
Q

What does the spinocerebellum consist of?

A

vermis and intermediate zone

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75
Q

What is the function of the spinocerebellum?

A

functions in synergy: control of rate, force, range, and direction of movement

76
Q

What does the spinocerebellum receive?

A

-Information from motor cortex and red nucleus telling cerebellum intended sequential plan of movement for the next few fractions of a second.
• Feedback information from periphery telling cerebellum what actual movements result

77
Q

The spinocerebellum compares two sources of information and sends corrections to

A
  • Motor cortex via thalamus

* Magnocellular portion of red nucleus

78
Q

the cerebrocerebellum consist of what?

A

lateral parts of hemispheres

79
Q

the cerebrocerebellum is mostly associated with what?

A

the premotor and primary and association somatosensory areas of the cerebral cortex

80
Q

what does the cerebrocerebellum receive?

A

corticopontocerebellar projections

81
Q

What is the cerebrocerebellum involved in?

A

coordination of skilled movement and speech

82
Q

Describe the corticopontocerebellar

A
  • Motor and premotor corNces/Somatosensory cortex → PonNne nuclei → Lateral divisions of cerebellum
  • Main link between cortex and cerebellum
  • Lesions result in muscle weakness
83
Q

Describe the vestibulocerebellar

A

• Terminates in flocculonodular lobes

84
Q

Describe the termination of the reticulocerebellar

A

terminates primarily in vermis

85
Q

describe the spinocerebellar

A
  • Dorsal and ventral
  • Transmit signals at 120 m/sec.
  • Sends proprioceptive information to cerebellum
86
Q

olivocerebellar axons form _____

A

climbing fibers

87
Q

What is the efferent tract of the cerebelloreticular?

A

Fastigial nuclei → reNcular nuclei in pons and medulla

88
Q

What is the efferent tract of the cerebellothalmocortical?

A

Dentate, emboliform, globose nuclei → thalamus → motor cortex

89
Q

What is the efferent tract of the cerebellorubral?

A

Dentate, emboliform, globose nuclei → red nucleus

90
Q

What is the efferent tract of the cerebellovestibular?

A

Cerebellum → vestibular nuclei

91
Q

What can damage to the cerebellum lead to?

A
  • The inability to judge distance and when to stop (dysmetria)
  • Uncoordinated movement (ataxia)
  • The inability to perform rapid alternating movements (adiadochokinesia)
  • Past pointing
  • Movement tremors (intention tremor) are common in cerebellar lesions
  • Staggering, wide based walking (cerebellar lesion gait)
  • Tendency toward falling
  • Weak muscles (cerebellar hypoplasia)
  • Slurred speech (ataxic dysarthria)
  • Abnormal eye movements (nystagmus)
  • Dystonia (ballistic movements)
92
Q

What are the functions of the basal nuclei?

A
  • Plan and execute motor commands in concert with cerebral cortex; help cortex execute subconscious but learned pattern
  • Help plan multiple parallel sequential patterns
  • Control complex patterns of motor activity
93
Q

Where does the basal nuclei receive most of their input? output?

A

Basal nuclei receive most of their input from the cerebral cortex and return most of their output to the cerebral cortex.

94
Q

What is the principal role of the basal nuclei?

A

Principal role is to work with corticospinal system to modulate thalamic output to the motor cortex to plan and execute smooth movements.

95
Q

Dopamine is _____ on the indirect pathway and uses ____ receptors

A

inhibitory; D2

96
Q

Dopamine is ____ on the direct pathway and uses ____ receptors

A

excitatory; D1

97
Q

What is the direct pathway an example of?

A

disinhibition via GABA signaling at the thalamus

98
Q

Lesions in the globus pallidus results in what?

A

Result in inability to maintain postural support.

• Result in continuous spontaneous writhing movements of a hand, arm, neck or face = athetosis

99
Q

Lesions in the sub thalamic nuclei result in what?

A
  • Result in the release of inhibition on the contralateral side.
  • Result in sudden, flailing movements of an entire limb = hemiballismus
100
Q

Lesions in the striatum result in what?

A
  • Results in the release of inhibition
  • Results in flicking movements in hands, face, or elsewhere = chorea.
  • Occur in patients with Huntington disease.
101
Q

Lesions in substantia nigra result in what?

A

Caused by destruction of dopaminergic neurons.
• Occur in patients with Parkinson’s disease.
• Results in rigidity, akinesia, and tremors.
• Since dopamine inhibits the indirect (inhibitory) pathway and excites the direct (excitatory) pathway, destruction of the dopaminergic neurons results in an overall inhibitory effect.

102
Q

Describe the putamen circuit (direct pathway)

A
  • For subconscious execution of learned patterns of movement

* Overall excitatory – tends to increase motor activity

103
Q

describe the caudate circuit (indirect pathway)

A

For cognitive planning of sequential and parallel motor patterns.
Plays major role in cognitive control of motor activity.
Overall inhibitory – tends to decrease motor activity.

104
Q

Substantia nigra → caudate nucleus and putamen neurotransmitter

A

dopamine (inhibitory)

105
Q

Caudate nucleus and putamen → globus pallidus and substantia nigra neurotransmitter

A

GABA (inhibitory)

106
Q

Cortex → caudate nucleus and putamen neurotransmitter

A

acetylcholine (excitatory)

107
Q

Multiple pathways from brain stem neurotransmitters

A

Norepinephrine, serotonin (inhibitory), enkephalin

108
Q

What are the principal areas of the brain that affect body temperature?

A

anterior hypothalamic nuclei
medial pre optic area
(called the anterior Oreo-tic hypothalamus)

109
Q

describe the anterior preoptic area

A

Contains warm-sensitive, cold- sensitive, and temperature insensitive neurons

110
Q

heating the pre optic anterior hypothalamus causes what

A
  • Dilation of skin blood vessels over the entire body
  • Profuse sweating over the entire body
  • Inhibition of excess heat production
111
Q

What causes the vasodilation of skin blood vessels

A

Caused by inhibition of sympathetic centers in posterior hypothalamus that
cause vasoconstriction.

112
Q

What are the mechanisms to reduce body heat?

A
  • preoptic anterior hypothalamus
  • vasodilation of skin blood vessels
  • sweating
  • decrease in heat production
113
Q

What mechanisms to increase body heat?

A
  • skin vasoconstriction
  • piloerection
  • increase in thermogenesis
114
Q

What happens in increase in thermogenesis?

A

shivering
basal metabolic rate
thyroxin secretion
norepinephrine

115
Q

Define fever

A

Body temperature above the usual range of normal

116
Q

Causative factors of fever

A

Brain abnormalities
Surgery in the region of the hypothalamus Prostaglandins
Lipopolysaccharide toxins

117
Q

How does IL-1 and prostaglandins effect fever?

A

increase set point temperature

118
Q

How does aspirin effect fever?

A

decrease set point temperature by inhibiting cyclooxyrgenase which results in decrease in production of prostaglandins

119
Q

_____ becomes the final common pathway for the transport of almost all the carbohydrates to the tissue cells

A

glucose

120
Q

Where does transport of glucose via active sodium glucose co transport occur?

A

GI tract and renal tubules

121
Q

Where does transport of glucose via facilitated transport occur?

A

in most tissues

122
Q

What does phosphorylase do?

A

promotes conversion of glycogen to glucose, so glucose can be released from blood

123
Q

What factors can activate phosphorylase?

A

epinephrine

glucagon

124
Q

What are the end products of glycolysis?

A

pyruvic acid
hydrogens
ATP

125
Q

what are the end products of the citric acid cycle?

A

hydrogens
ATP
carbon dioxide

126
Q

Increased blood glucose levels lead to:

A
  • Increased osmotic pressure
  • Osmotic diuresis (increased urine output)
  • Damage to tissues and blood vessels
127
Q

Where does oxidative phosphorylation occur?

A

mitochondrial cristae

128
Q

what is the efficiency of oxidative phosphorylation?

A

66%

129
Q

Describe the pentose phosphate pathway

A

-The pentose phosphate pathway is a cyclical pathway in which one molecule of glucose is metabolized for each revolution of the cycle.
• For every six molecules of glucose that enter the pathway, five molecules of glucose are resynthesized.
• This pathway is mostly used for the synthesis of fats and other substances.
• Hydrogens generated from this pathway are bound to NADP+ instead of NAD+

130
Q

Chylomicrons are removed from blood by various tissues, especially:

A

adipose tissue
skeletal muscle
heart

131
Q

conditions that increase utilization of fat for energy

A
  • Starvation

* Diabetes mellitus

132
Q

lipoproteins synthesized by intestinal cells

A

Chylomicrons

133
Q

lipoproteins synthesized by liver

A
  • Very low density lipoproteins (VLDLs)
  • Intermediate density lipoproteins (IDLs)
  • Low density lipoproteins (LDLs)
  • High density lipoproteins (HDLs)
134
Q

describe VLDLs

A

• High concentrations of triglycerides and moderate amounts of cholesterol
and phospholipids.
• Transport lipids mainly from liver to adipose tissue.

135
Q

describe LDLs

A

high concentration of cholesterol and moderate concentration of phospholipids

136
Q

describe HDLs

A

high concentration of proteins and low concentration of cholesterol and fatty acid

137
Q

Acetoacetic acid, β-hydroxybutyric acid, and acetone are ketone bodies that diffuse back into cells and converted into ____

A

acetyl-CoA

138
Q

If concentration of ketone bodies increase above normal in blood what occurs?

A

ketosis

139
Q

conditions favoring ketosis

A

starvation
diabetes
diet composed almost entirely of fat

140
Q

Rate of overall chemical reaction is determined by what?

A
  • Concentration of the enzyme

* Concentration of the substrate

141
Q

when substrate concentration is high what is reaction rate determined almost entirely by?

A

concentration of enzyme

142
Q

When enzyme concentration is high what does reaction rate become?

A

directly proportional to concentration of substrate and enzyme

143
Q

____ is the major rate limiting factor for almost all energy metabolism in the body

A

ADP

144
Q

factors that influence metabolic rate

A

arousal vs sleeping Skeletal muscle Age
Thyroid activity Testosterone Growth hormone Fever
Note that cold is one of the best known stimuli for increasing the rate of thyroid stimulating hormone.
Sleep Malnutrition

145
Q

_____ is one of the best known stimuli for increasing the rate of thyroid stimulating hormone

A

cold

146
Q

how does thyroxine affect the basal metabolic rate?

A

Thyroxine increases rate of chemical reactions in cells and increases metabolic rate.
• Maximal secretion may increase metabolic rate 50 to 100 percent above normal.
• Loss of thyroid secretion decreases metabolic rate to 40 to 60 percent of normal.

147
Q

How does testosterone affect basal metabolic rate?

A

Testosterone can increase metabolic rate 10 to 15 percent.

• Mainly related to anabolic effect of increase in skeletal muscle mass.

148
Q

How can malnutrition affect basal metabolic rate?

A

Malnutrition results in reduced food substances in the cells.
• Maximal secretion may increase metabolic rate 50 to 100 percent above normal.
• This results in a marked reduction in metabolic rate.
• Loss of thyroid secretion decreases metabolic rate to 40 to 60 percent of normal.
• This process may accompany final stages of many disease conditions

149
Q

describe mixing movements

A
  • May be caused by peristaltic contractions themselves.
  • Contractile ring moves forward after it appears.
  • At other times local intermittent constrictive contractions occur every few centimeters in the gut wall.
150
Q

what are slow waves?

A

Slow waves are slow, oscillating potentials inherent to the smooth muscle itself in some parts of the digestive tract and spread through gap junctions

151
Q

What are spike potentials?

A

• Spike potentials excite muscle contraction.
• Action potentials.
• Occur automatically when resting membrane potential of GI smooth muscle
becomes more positive than -40 mv.
• The higher the slow wave potential, the greater the frequency of the spike potentials.
• Last 10-40 times as long as a typical action potential in a large nerve fiber (10-20 ms).
• Spike potentials are responsible for opening calcium-sodium channels in GI smooth muscle cells.
• Channels open and close slowly.

152
Q

types of gastrointestinal reflexes

A
  • Reflexes that are integrated entirely within the gut wall enteric nervous system
  • Reflexes from the gut to the prevertebral sympathetic ganglia and then back to the GI tract
  • Transmit signals long distance to other areas of the gut tract
  • Reflexes from the gut to the spinal cord or brain stem and then back to the GI tract
153
Q

Reflexes that are integrated entirely within the gut wall enteric nervous system control

A
  • Much of the GI secretion
  • Peristalsis
  • Mixing contractions
  • Local inhibitory effects
154
Q

Reflexes from the gut to the prevertebral sympathetic ganglia and then back to the GI tract:

A

• Transmit signals long distance to other areas of the gut tract

  • Cause evacuation of the colon (gastrocolic reflex)
  • inhibit stomach motility and secretion (enterogastric reflex)
  • empty ileal contents into the colon (colonoileal reflex)
155
Q

Gastrin stimulus for secretion

A

• Small peptides and amino acids in stomach lumen, especially phenylalanine and tryptophan
• Stimulates gastric acid secretion by parietal cells
• Distension of stomach
• Vagal stimulation mediated by GRP
• Stimulates mucosal growth by stimulating synthesis of RNA and new protein.
(gastrin-releasing peptide)

156
Q

Inhibition of secretion of gastrin

A
  • Acid from stomach

* Somatostatin

157
Q

site of secretion for gastrin

A

Secreted from G cells of small intestines in response to stimuli associated with ingestion of a meal

158
Q

Actions of gastrin

A
  • Stimulates gastric acid secretion by parietal cells

- Stimulates mucosal growth by stimulating synthesis of RNA and new protein.

159
Q

Pathology behind gastrin

A

-Patients with gastrin-secreting tumors have hypertrophy and hyperplasia of gastric mucosa.
• Zollinger-Ellison syndrome occurs from gastrin-secreting non-β cell tumors of pancreas.

160
Q

Cholecystokinin (CCK) stimulus for secretion

A
  • Small peptides and amino acids

* Fatty acids and monoglycerides

161
Q

CCK site of secretion

A

• I cells of the small intestines

162
Q

CCK actions

A
  • control feedback of duodenum
  • stimulates pancreatic enzyme secretion
  • stimulates pancreatic bicarbonate secretion
  • stimulates growth of exocrine pancreas
  • inhibits gastric emptying
  • inhibits appetite
  • stimulates contraction of gallbladder and relaxation of sphincter of Oddi for secretion of bile
163
Q

Secretin stimulus for secretion

A

acid and fat in lumen of duodenum

164
Q

Secretin site of secretion

A

S cells of the small intestines

165
Q

secretin actions

A
  • stimulates pepsin secretion
  • stimulates pancreatic bicarbonate secretion
  • stimulates biliary bicarbonate
  • stimulates growth of exocrine pancreas
  • inhibits gastric acid secretion by parietal cells
166
Q

GIP stimulus for secretion

A
  • only GI hombre released in response to protein, fat, and carbohydrate
  • released in response to orally administer glucose
167
Q

GIP site of secretion

A

K cells of duodenum and jejunum

168
Q

GIP actions

A

stimulates insulin release to bring blood glucose down

inhibits gastric acid secretion by parietal cells

169
Q

motilin stimulus for secretion

A

fat, acid, nerve action

170
Q

motilin site of secretion

A

M cells of duodenum and jejunum

171
Q

motilin actions

A
  • stimulate gastric and intestinal motility

- secreted during fasting

172
Q

composition of saliva

A
  • High potassium ion and bicarbonate concentrations
  • Low sodium and chloride ion concentrations
  • Hypotonicity
  • Contains α-amylase, lingual lipase, and kallikrein
173
Q

what is saliva production controlled by?

A

parasympathetic system, but also sympathetic system-both results in increase in saliva production

174
Q

The _____ nerve and the ____ are involved in regulating the secretion of saliva

A

facial and glossopharyngeal

175
Q

secretory cell types of in gastric glands

A

mucous neck cells
chief peptic cells
parietal oxyntic cells

176
Q

what do chief cells do

A

secrete pepsinogen

177
Q

release of pepsinogen by chief cells is stimulated by

A
  • Ach from vagus nerves or gastric enteric nervous plexus

* Response to acid in stomach

178
Q

describe the Direct parasympathetic vagal stimulation pathway to increase H+ secretion

A
  • CN X innervates parietal cells
  • Stimulates H+ secretion directly
  • Utilizes Ach and muscarinic (M3) receptor
179
Q

describe the indirect parasympathetic vagal pathway to increase H+ secretion

A
  • CN X innervates G cells
  • Stimulates gastrin secretion
  • Gastrin stimulates secretion of H+
  • Neurotransmitter is GRP (gastrin-releasing peptide)
180
Q

describe gastrin stimulation

A
  • Secreted by gastrin (G) cells in pyloric glands
  • Released in response to presence of protein in pylorus
  • Causes enterochromaffin-like cells to release histamine
  • Stimulates H+ secretion
  • Second messenger on parietal cell is IP3/Ca2+
181
Q

describe histamine stimulation

A
  • Stimulates secretion of H+ by activating H2 receptors on parietal cell membrane.
  • H2 receptor is coupled to adenyl cyclase via Gs protein.
  • Second messenger is cAMP.
182
Q

what secretes somatostatin

A

delta cells of pancreas

183
Q

describe what somatostatin does

A

-Inhibits secretion of insulin, glucagon, and gastrin
-Decreases motility of stomach, duodenum, and gallbladder.
-Decreases secretion and absorption of GI tract
Inhibits gastric H2 secretions by direct and indirect pathway:
• Direct:
• Somatostatin binds to receptors on parietal cell that are coupled to
adenyl cyclase via a Gi protein.
• Antagonistic to stimulatory action of histamine
• Indirect:
• Inhibits the release of histamine and gastrin

184
Q

What do prostaglandins do?

A

Inhibit gastric H2 secretions by activating Gi protein, inhibiting adenyl cyclase

185
Q

What are the cell types in the crypts of lieberkuhn

A

goblet cells
enterocytes
paneth cells
enteroendocrine cells

186
Q

What do paneth cells do

A

Secrete antimicrobial proteins to limit bacteria- enterocyte contact

187
Q

What do enter endocrine cells do

A

Secrete peptide hormones controlling several GI system functions

Physiology 2 Exam 2 (1 decks)

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