Smooth Muscle, Mastication, Salivation Flashcards
(98 cards)
1
Q
What are the main structural and functional characteristics of smooth muscle?
A
- No sarcomeres
- uses dense bodies containing alpha-actinin for actin attachment
- Intermediate filaments also bind to dense bodies
- During contraction, cells twist into a corkscrew shape
- Gap junctions allow synchronized contractions
2
Q
Where is smooth muscle manly found?
A
- GI tract (peristalsis)
- uterine smooth muscle
- blood vessels
- urinary bladder
3
Q
How does smooth muscle differ from skeletal and cardiac muscle?
A
- smooth muscle lacks T-tubules and has a rudimentary sarcoplasmic reticulum
- Contains tropomyosin but lacks troponin
- Anchored by dense bodies instead of Z-discs
- Contracts about 20 times slower than skeletal and 15 times slower than cardiac muscle
- Achieves 100% maximal tension with only 40% ATP phosphorylation
4
Q
How does smooth muscle produce movement in the GI tract?
A
Through peristalsis, which is a wave-like contraction that propels content along the tract
5
Q
How does smooth muscle’s tension development compare to skeletal and cardiac muscle?
A
When normalized for cross-sectional area, smooth, skeletal, and cardiac muscle have nearly equal tension development
6
Q
How many nuclei are typically found in smooth muscle cells compared to striated muscle?
A
- smooth muscle has one nucleus per cell
- striated muscle can have one or more nuclei per cell
7
Q
What are the two types of smooth muscle and their main characteristics?
A
- Multi-Unit: Few gap junctions, most cells are individually innervated for fine control (ciliary muscles of the eye, erector pili of the skin)
- Single Unit: Many gap junctions; cells behave as a syncytium allowing synchronized contraction (GI tract, uterine smooth muscle, blood vessels, and urinary bladder)
8
Q
What is the role of varicosities in smooth muscle?
A
so smooth muscle can behave as a syncytium
9
Q
How is excitation-contraction coupling achieved in smooth muscle?
A
Calcium Entry: Through three main pathways:
- Voltage-Gated Ca²⁺ Channels (VGCC): Opens with changes in membrane potential.
- Receptor-Activated Channels (ROC): Activated by neurotransmitters or hormones
- IP₃ Pathway: Stimulates calcium release from the sarcoplasmic reticulum
10
Q
What mechanisms are involved in smooth muscle relaxation?
A
Voltage-Gated Calcium Channels close.
- SERCA Pumps move calcium back into the sarcoplasmic reticulum
- Na⁺/Ca²⁺ or H⁺/Ca²⁺ Exchangers expel calcium from the cell
- Ca²⁺-ATPase Pumps are always active, continuously pumping calcium out of the cytosol
11
Q
What triggers contraction in smooth muscle and what occurs after the trigger?
A
- increase in intracellular calcium (Ca²⁺) through voltage-gated channels or release from the SR
- Ca²⁺ binds to calmodulin (CaM), activating myosin light chain kinase (MLCK)
- MLCK, phosphorylates myosin light chains, increasing myosin ATPase activity, allowing for cross-bridge formation with actin
- filament sliding occurs
12
Q
How does smooth muscle relaxation occur?
A
- relaxation occurs when calcium is pumped back out of the cytosol, reducing Ca²⁺ levels, and myosin light chain phosphatase (MLCP) dephosphorylates the myosin light chains
- Nitric oxide (NO) increases cGMP production, activating protein kinase G (PKG), which enhances MLCP activity
- Rho kinase inhibits MLCP, maintaining phosphorylation of myosin light chains
13
Q
What are the main functions of the GI system?
A
- Breakdown of food (physical and chemical)
- Absorption of nutrients
- Waste elimination
- Immune system contribution
- Symbiotic relationship with microbiota
**pH is important
14
Q
what are the components of the GI tract and the major accessory glands?
A
- mouth, esophagus, stomach, small intestines, and large intestines
- Salivary glands, liver (bile), gallbladder, and the pancreas
15
Q
What are the key components of GI anatomy?
A
- Circular and longitudinal muscle layers (“tube within a tube”)
- Enteric nervous system (submucosal and myenteric plexuses)
- Parasympathetic (vagus, pelvic nerves) and sympathetic innervation
- Glandular tissue responsive to hormones
16
Q
What is the function of the Myenteric Plexus (Auerbach plexus) and Submucosal Plexus (Meissner plexus)?
A
- MP: Modifies motility of the GI tract
- SP: Modifies secretion and blood flow in the GI tract
17
Q
What is the role of Circular and Longitudinal Muscles in the GI tract?
A
- Circular muscle: thick and densely innervated, controls constriction
- Longitudinal muscle: thin and less innervated, controls shortening
18
Q
What are the four control systems involved in GI regulation?
A
- Enteric nervous system (ENS) - local neural control
- Endocrine - hormone secretion into the bloodstream
- Paracrine - local signaling by diffusion
- Unitary smooth muscle - gap junction communication
19
Q
How do GI peptides act as hormones, paracrines, or neurocrines?
A
- Hormones: Enter the bloodstream, act on distant targets
- Paracrines: Diffuse locally, act on nearby cells
- Neurocrines: Released from neurons after an action potential
20
Q
What are varicosities and how do they influence smooth muscle cells?
A
- swellings along postganglionic autonomic neurons that run along smooth muscle membranes, enabling neurotransmitter release over large areas
- allow one neuron to influence many effector cells without specialized synaptic clefts, called synapse en passant.
21
Q
What is Single Unitary Visceral Smooth Muscle (SUVSM)?
A
type of smooth muscle found in the GI tract, uterus, bladder, arteries, and veins that contracts as a single unit due to gap junctions
22
Q
What role do Interstitial Cells of Cajal (ICC) play in smooth muscle?
A
act as pacemaker cells, generating slow waves that initiate and regulate contractions in the GI tract
23
Q
What are slow waves in smooth muscle and do they require neural or hormonal input?
A
- baseline electrical rhythms that set the pace for GI motility, varying in rate across different segments
- no, slow waves are independent of neural or hormonal influences
24
Q
What triggers spike potentials in smooth muscle and how do they relate to muscle contractions?
A
- occur when threshold potential is reached, triggering calcium-sodium channels to open
- frequency and strength of spike potentials correlate directly with the force of muscle contraction
25
How do inhibitory signals affect smooth muscle contraction?
open potassium channels, causing hyperpolarization and reducing contraction strength
26
What are the main characteristics of phasic and tonic smooth muscle contractions?
- Phasic Contractions: rhythmic contraction and relaxation, found in esophagus, distal stomach, and intestines, requires pacemaker and Ca²⁺ influx.
- Tonic Contractions: constant contraction without relaxation, found in upper stomach, esophagus, ileocecal region, and sphincters, does not require action potentials or pacemakers
27
How do phasic and tonic contractions contribute to GI motility?
- Phasic: Involved in mixing and propulsion of contents through the GI tract
- Tonic: Maintains sustained tone to prevent backflow and regulate sphincter control
28
What are Excitatory and Inhibitory Junctional Potentials (EJPs and IJPs)?
- EJPs: Summated to induce action potentials and trigger smooth muscle contraction
- IJPs: Cause hyperpolarization, making it harder to reach action potential and relaxes the muscle
29
What is the role of the sympathetic and parasympathetic systems in smooth muscle?
- Parasympathetic: Stimulates motility via acetylcholine and stretch
- Sympathetic: Can contract sphincters (stimulatory) or lengthen smooth muscle (inhibitory)
30
What is the role of the Enteric Nervous System (ENS) in GI function?
- functions independently of the CNS but communicates with the ANS
- regulates smooth muscle contraction, gut motility, and fluid secretion through the submucosal and myenteric plexuses
31
How does the ENS receive sensory input and manage gut motility?
- receives input from mechanoreceptors and chemoreceptors in the mucosa
- responsible for moment-to-moment control of peristalsis and secretion adjustments
32
What does the parasympathetic nervous system stimulate and what is it supplied by?
- stimulating digestion, promoting peristalsis (movement of food), and increasing secretions
- supplied by the vagus nerve which innervates the upper GI tract including the stomach and small intestine and pelvic nerve, which innervates the lower GI tract like the colon and rectum
33
what are the fibers of the parasympathetic nervous system and what are the neurotransmitters released?
long preganglionic fibers (extend from the spinal cord to the organ) and short postganglionic fibers (located near or within the target organ)
- Acetylcholine (ACh): Activates smooth muscle contractions and increases secretions
- Vasoactive Intestinal Peptide (VIP): Promotes smooth muscle relaxation and increases intestinal secretions
34
What does the sympathetic nervous system stimulate, what are the fibers and what neurotransmitters are released?
decrease in digestive activities by reducing motility, and constricting blood vessels to the GI tract during "fight or flight" responses
- contains short preganglionic fibers (travel short distances to the ganglia) and long postganglionic fibers (extend from ganglia to the target organ)
- Norepinephrine (NE) is released to induces smooth muscle relaxation in the wall of the GI tract, cause contraction of sphincters to control movement through the GI sections and reduce salivary secretion (results in a dry mouth during stress)
35
what is co-release and co-transmission of the Enteric Nervous System (ENS)?
- Co-Release: multiple neurotransmitters are packaged in the same vesicle and released together (ATP and Norepinephrine (NE) are released simultaneously to cause contraction in smooth muscle)
- Co-Transmission: different neurotransmitters are packaged in separate vesicles and released at different times or locations which allows for precise control over various aspects of GI function (Acetylcholine (ACh) is released to stimulate smooth muscle contraction, while VIP is released later to relax the muscle)
36
What are the three types of gastrointestinal reflexes and what do they control?
1. Local Reflexes: controls GI secretion, peristalsis, mixing contractions, and local inhibition
2. Regional Reflexes: gastrocolic reflex, enterogastric reflex, and colonoileal reflex
3. Systemic Reflexes: defecation and pain reflexes that travel to the colon, rectum, and abdominal wall
37
How do local, regional, and systemic reflexes differ in their pathways?
- Local: confined to the ENS without CNS involvement
- Regional: go through sympathetic ganglia and return to the GI
- Systemic: processed in the spinal cord or brainstem to control overall GI activity via the vagus nerve
38
What are the four main GI hormones, their sites of secretion and actions?
1. Gastrin: G cells of the stomach →↑ H⁺ secretion, stimulates gastric mucosa growth
2. Cholecystokinin (CCK): I cells of the duodenum and jejunum → pancreatic enzyme secretion, gallbladder contraction, and relaxation of the sphincter of Oddi
3. Secretin: S cells of the duodenum → HCO₃⁻ secretion from the pancreas and liver; inhibits gastric H⁺ secretion
4. Glucose-dependent Insulinotropic Peptide (GIP): K cells of the duodenum and jejunum → insulin release, inhibits H⁺ secretion, and delays gastric emptying
39
What are the triggers for the release of each GI hormone?
- Gastrin: Small peptides, amino acids, stomach distention, vagal stimulation (GRP)
- CCK: Fatty acids, amino acids, small peptides
- Secretin: Acidic pH (H⁺) and fatty acids in the duodenum
- GIP: Fatty acids, amino acids, oral glucose load
40
what are the two mechanisms of gastrin that stimulate H⁺ secretion from parietal cells?
1. Direct Mechanism: gastrin binds directly to receptors on parietal cells, leading to the activation of the H⁺/K⁺ ATPase pump which results in the secretion of hydrochloric acid (HCl) into the stomach lumen, which is necessary for food digestion and activating pepsinogen to pepsin
2. Indirect Mechanism: gastrin stimulates Enterochromaffin-like (ECL) cells to release histamine which binds to H₂ receptors on parietal cells, further amplifying acid secretion through cAMP-dependent pathways
41
what are the types of Gastrin and when are they released?
1. G₃₄ "Big Gastrin": Secreted between meals to maintain basal acid levels
2. G₁₇ "Little Gastrin": Secreted during meals to boost acid secretion
*Both require a C-terminal tetrapeptide for biological activity
42
what are the stimulators and inhibitors of Gastrin?
- Stimulated by: Phenylalanine, tryptophan, stomach distension, and gastrin-releasing peptide (GRP) also known as bombesin
- Inhibited by: Low gastric pH (high acidity) and somatostatin
43
what is Zollinger-Ellison Syndrome?
where tumors cause excessive gastrin production, leading to hypersecretion of acid and inactivation of pancreatic enzymes in the duodenum
44
what are the key functions of Cholecystokinin (CCK)?
1. Gallbladder Contraction: Stimulates the release of bile acids into the duodenum, which emulsify fats to enhance digestion.
2. Pancreatic Secretion: Triggers the exocrine pancreas to release digestive enzymes (lipase, amylase, trypsinogen) essential for fat, carbohydrate, and protein breakdown.
3. Sphincter of Oddi Relaxation: Allows bile and pancreatic secretions to flow into the duodenum.
4. Stomach Emptying Inhibition: Slows gastric emptying to optimize nutrient absorption
5. Induce Growth: induces pancreatic and gallbladder growth
45
what are the receptors for CCK and what can they bind?
- CCKₐ Receptors: Selective for CCK
- CCKᵦ Receptors: Can bind both CCK and Gastrin
46
How is CCK secretion inhibited?
when high levels of triglycerides (TAGs) are present, slowing its release to prevent excessive bile secretion.
47
what are the main roles of Secretin?
1. Stimulates Bicarbonate (HCO₃⁻) Secretion: promotes the release of HCO₃⁻ from the pancreas and bile ducts and neutralizes the acidic chyme entering from the stomach
2. Inhibits Gastric Acid Secretion: reduces H⁺ secretion from parietal cells to prevent excess acidity.
3. Prevents Metabolic Alkalosis: secretion is given if vomiting or severe loss of H⁺ occurs which causes HCO₃⁻ buildup in the blood, leading to metabolic alkalosis (secretin is not released due to low H+)
48
what are the main functions of GIP (Glucose-dependent Insulinotropic Peptide)?
1. Stimulates Insulin Secretion: response to an oral glucose load, GIP enhances insulin release from pancreatic beta-cells which is part of the incretin effect, where oral glucose stimulates more insulin than intravenous glucose
2. Inhibits Gastric Activity: slows gastric emptying and H⁺ secretion, allowing more time for nutrient absorption in the intestine
49
How is GIP (Glucose-dependent Insulinotropic Peptide) regulated?
- Degradation: GIP is rapidly broken down by Dipeptidyl Peptidase-4 (DPP4), resulting in a short half-life
- Pharmacological Target: DPP4 inhibitors are used clinically to prolong the action of GIP and GLP-1, enhancing insulin release in diabetic patients
50
What is the role of Histamine in the GI tract and what drugs are used for treatment?
- secreted by enterochromaffin-like (ECL) cells in the stomach and mast cells
- stimulates H⁺ secretion by activating H₂ receptors on parietal cells
- H₂ receptor antagonists (e.g., ranitidine, famotidine) are used to treat peptic ulcers
51
What is the role of Somatostatin in the GI tract and what drugs are used for treatment?
- secreted by D cells in the GI tract, hypothalamus, and delta cells of the pancreas
- Inhibits the secretion of gastrin, H⁺, and pancreatic enzymes
- Octreotide (Analog); used for reducing hormone-related GI tumors and variceal bleeding
52
What is the role of Serotonin in the GI tract and what drugs are used for treatment?
- secreted by enterochromaffin (EC) cells in response to gastric distension
- Increases GI motility and secretion through the ENS
- 5-HT3 receptor antagonists are used to treat nausea and vomiting, especially in chemotherapy-induced nausea (CINV)
53
What is the function of Ghrelin?
Hypoglycemia causes the secretion from X cells and the stomach to promote food intake and growth hormone secretion from the hypothalamus
54
What is the role of Motilin?
the fasting state causes the release from intestinal cells of the duodenum which increases GI motility by initiating interdigestive myoelectric complexes
** Erythromycin can bind to motilin receptors, enhancing gastric emptying
55
What is the role of Pancreatic Polypeptide (PP)?
ingestion of a meal causes the release from the pancreas to inhibit pancreatic secretion of HCO₃⁻ and enzymes
56
What is the role of Enteroglucagon?
hypoglycemia causes the secretion from intestinal cells to stimulate liver glycogenolysis and gluconeogenesis to increase blood glucose levels
57
What is the role of Glucagon-like Peptide-1 (GLP-1)?
ingestion of glucose causes secretion from L cells of the small intestines to
- Enhances insulin secretion from pancreatic beta-cells
- Inhibit glucagon release and gastric emptying
- Reduce appetite through central mechanisms
58
What are the three main functions of chewing (mastication)?
- Mixes food with saliva to lubricate and facilitate swallowing
- Reduces the size of food particles for easier digestion
- Begins carbohydrate digestion with salivary amylase and fat digestion with lingual lipase
59
Is chewing (mastication) voluntary or involuntary?
Both:
- Involuntary: Triggered by reflexes when food is present in the mouth; mechanoreceptors signal the brainstem.
- Voluntary: Can override involuntary control at any time.
60
What are the primary, secondary, and tertiary functions of the oral cavity?
- Primary: trituration of food (breaking down into smaller particles) by interaction of the mandible and maxilla.
- Secondary: protection of teeth, starts starch and fat digestion (amylase and lipase), lubricates the food bolus for smooth swallowing and provides an airway and is involved in speech.
- Tertiary: Maintains oral health, which is linked to cardiovascular health and poor oral health (periodontal disease) is associated with a higher risk of cardiovascular issues
61
How do teeth and bite force impact mastication?
- Food fragmentation depends on the number of teeth.
- Bite force is influenced by: muscle volume, jaw muscle activity, and muscle coordination.
62
What type of lever system is mastication and what is its advantage?
Class III Lever System:
- Fulcrum: Located at the jaw joint.
- Effort: Applied by the jaw muscles.
- Load: The food being chewed.
Advantage: Allows more control over the bite force, making it effective for grinding and tearing food
63
How much bite force can humans generate?
- Maximum: 975 lbs./in²
- Average: 162 lbs./in²
- Varies based on tooth position (e.g., molars have greater force than incisors)
64
What are the four basic reflexes involved in mastication?
1. Myotatic Reflex (Stretch Reflex):
- Keeps the jaw closed with a resting tone of jaw muscles
2. Inverse Myotatic Reflex (Golgi Tendon Reflex):
- Activated by pressure on TMJ or periodontal ligament
- Inhibits jaw closing and stimulates jaw opening
3. Low Threshold Mechanoreceptor Reflex:
- Activated by pressure or touch on the tongue dorsum
- Stimulates jaw closing during swallowing
4. High Threshold Mechanoreceptor Reflex:
- Triggered by nociceptive (pain) stimuli
- Causes rapid jaw opening to protect from harmful substances
65
What is the main jaw-opening force?
Gravity: The jaw naturally opens due to gravity, and jaw muscles work to close it
66
What is the Myotatic Reflex and where is it found?
- Also called the jaw jerk reflex
- Found only in jaw-closing muscles (resting state)
- Gravity stretches the jaw, activating muscle spindles (gravity --> stretch spindles --> stimulates closing)
67
How does the Myotatic Reflex work?
- Muscle spindles detect stretching and send signals to jaw-closing muscles to contract
- Ensures the mouth remains shut and maintains the tone of the masseter muscle
- Jaw opening muscles do not have spindles, preventing confusion in CNS signaling
68
What triggers the Inverse Myotatic Reflex?
Triggered by stimulation of Golgi tendon organs in the periodontal ligament or TMJ (Temporomandibular Joint)
69
What are the three main actions of the Inverse Myotatic Reflex?
1. Stimulates jaw-opening muscles.
2. Inhibits jaw-closing muscles.
3. Modulates pressure applied to the teeth (dentition protection)
70
What activates Low Threshold Mechanoreceptors and what does it cause?
Pressure on the dorsum of the tongue
- Stimulates jaw-closing muscles
- Prepares the oral cavity for swallowing by sealing it.
- There is no reciprocal innervation to jaw-opening muscles in this reflex
71
what are the High Threshold Receptors and what does stimulation cause?
Golgi tendon like organs in gingiva and periodontal
ligament and pain receptors (nociceptors) in gingiva, periodontal ligament and in peri-oral mucosa
* Stimulation of motor nerves to jaw opening
muscles
* Reciprocal inhibition of jaw muscle closing motor
nerves
* Rapid opening of oral cavity
* Expulsion of offending stimulus
72
What is occurring during the At Rest (Pre-Chewing State)?
The entire system is in a low-activity state with minimal neural signaling
- Gamma efferents are quiet: Minimal activity to keep the jaw slightly closed
- TMJ (Temporomandibular Joint) afferents: Pressure and rotation receptors are at a low level; nothing is actively pressing or rotating the jaw
- 1A afferents from muscle spindles: Low activity, indicating muscles are relaxed
- Periodontal ligament receptors: Low activity as there is no pressure or significant movement
73
what is occurring during the start of the chewing cycle?
CNS sends a command to motor nerves to initiate chewing and as the jaw begins to close and compress the object (e.g., a peanut):
- Gamma efferents are stimulated → Feedback from muscle spindles adjusts tension
- Muscle spindles stretch → This feedback helps maintain optimal force
- TMJ and periodontal ligament receptors sense increasing pressure and send signals to the CNS
- TMJ rotation receptors fire as the jaw rotates during the chewing motion
!!!The force applied is strong enough to crack the food but not the teeth!!!
!!!CNS adjusts gamma motor activity to optimize force without damaging the dentition!!!
74
what is occurring during the splitting the peanut phase (crisis point)?
When the peanut splits, several things happen simultaneously:
- Jaw closure accelerates
- Alpha and gamma neurons continue firing based on previous activation
- TMJ pressure sensors detect a drop in pressure and go silent
- Periodontal ligament receptors also decrease activity since the food is no longer providing resistance
- TMJ rotational receptors increase their firing rate to detect rapid movement
- 1A spindle activity decreases sharply as muscles shorten
!!! jaw is now in a ballistic arc and moves rapidly, risking impact with opposing teeth !!!
75
How does out body protect against cracked dentition (protection mechanism)?
1. **Warning Signal to the CNS: If the spindle output goes silent and TMJ + periodontal ligament pressure drops suddenly, it triggers the CNS to rapidly adjust
2. **Rapid Inhibition of Jaw Closing Muscles: CNS inhibits motor nerves to jaw-closing muscles, stopping forceful closure and motor nerve activity falls to zero, then resumes at a much lower level to ensure light contact.
3. **Gamma efferent activity is rapidly reset: TMJ and periodontal ligament receptors slightly increase input to stabilize the jaw and jaw-opening muscles are stimulated reciprocally to prevent hard collision.
!!! rapid adjustments prevent cracking or damaging teeth by softening the final closure force !!!
76
what happens when the system resets to the initial resting state before the next chewing cycle begins?
1. **Information from low-threshold pressure receptors helps determine if food is ready for swallowing and if not, the cycle repeats until proper consistency is achieved
2. **CNS Circuitry: Chewing is managed by central pattern generators (CPGs) in the brainstem and is modulated by basal ganglia
3. **Chewing Reflexes: Occur within tenths to hundredths of a millisecond and maximal chewing rate: 4 Hz (4 cycles per second)
77
What are the main functions of saliva?
1. Lubricates the food bolus for easy swallowing
2. Initiates digestion of carbohydrates (salivary amylase) and fats (salivary lipase)
3. Protects teeth and esophagus: neutralize acid, provides immunoglobulins for antibacterial action and adheres proteins to enamel
4. Hormone Secretion: Cortisol, DHEA, and others can be detected in saliva, useful for non-invasive testing
78
What are the three major salivary glands and their characteristics?
1. Parotid Gland: composed mostly of serous cells, produces a watery fluid rich in enzymes and ions.
2. Submandibular (Submaxillary) Gland: mixed serous and mucous cells, secretes mucins for lubrication and enzymes
3. Sublingual Gland: primarily mucous cells with some serous and produces thicker saliva for lubrication
79
What is the major cause of dry mouth (xerostomia)?
Anticholinergic drugs reduce salivary secretion
80
What types of cells are found in salivary glands?
1. Acinar cells: Produce the initial saliva, which is isotonic to plasma
2. Ductal cells: Modify saliva by reabsorbing Na⁺, Cl⁻ and secreting K⁺ and HCO₃⁻
3. Myoepithelial cells: Contract to eject saliva into ducts
81
How do sympathetic and parasympathetic systems affect saliva?
- Parasympathetic: Increases volume and flow rate of watery saliva
- Sympathetic: Produces thicker, protein-rich saliva
82
How does salivary flow rate affect its composition?
- High Flow Rate: Saliva is more like plasma but remains hypotonic
- Low Flow Rate: More time for ductal modification → more Na⁺ and Cl⁻ reabsorption (less in saliva)
- HCO₃⁻ secretion increases with high flow rates to buffer acids
83
Which glands contribute most to saliva volume?
- Basal (Resting): Mostly from submandibular gland (71%)
- Stimulation (e.g., eating): Parotid gland increases output significantly and becomes a major producer
- Sublingual gland contributes the least overall
84
What controls salivary secretion?
- Parasympathetic (CN VII and CN IX): Stimulates IP₃ and Ca²⁺ → watery secretion
- Sympathetic (T1–T3): beta-adrenergics activate cAMP → thick, protein-rich saliva
- Alpha-adrenergic agonists: Vasoconstriction → reduces volume and enzyme content
85
What are the three classical phases of salivation?
1. Cephalic Phase: Triggered by sight, aroma, or thought of food (Pavlov's experiment)
2. Oral Phase: Largest volume, initiated by mechanical stimulation (eating, chewing gum)
3. Esophageal (Gastric) Phase: Triggered by distension of the esophagus and stomach
86
What important components are found in saliva?
- Mucus and Water: Lubricates and protects the oral cavity
- Amylase: Begins starch digestion
- Lingual Lipase: Starts lipid digestion
- Kallikrein: Converts to bradykinin, increasing blood flow to salivary glands
- R-protein (Haptocorrin): Binds Vitamin B12 for transport
- Immunoglobulins (IgA): Provides antibacterial protection for teeth
87
What are the three phases of swallowing?
Oral Phase (Voluntary)
Pharyngeal Phase (Involuntary)
Esophageal Phase (Involuntary)
88
what happens during the Oral Phase (Voluntary) of swallowing?
- Chewed food (bolus) is pushed to the back of the mouth by the tongue
- Reflexive closure of the lips and activation of somatosensory receptors initiate the next phase
89
what happens during the Pharyngeal Phase (Involuntary) of swallowing?
- mediated by CN IX (Glossopharyngeal) and X (Vagus) the soft palate elevates to close off the nasopharynx.
- Epiglottis covers the larynx to prevent food from entering the airway
- Upper Esophageal Sphincter (UES) relaxes to allow food to enter the esophagus
- Peristaltic wave is initiated to move the bolus down
- Breathing is temporarily inhibited during this phase
90
what happens during the Esophageal Phase (Involuntary) of swallowing?
- Controlled by the swallowing reflex and ENS (Enteric Nervous System).
- Primary Peristaltic Wave: Moves food towards the stomach
- If food remains, a Secondary Wave (ENS mediated) clears it
- Transit time: 5–6 seconds
91
How does serotonin (5-HT) regulate peristalsis?
- Stretch receptors activate serotonin release in the ENS.
- In front of the bolus (anad side): stimulates longitudinal muscle contraction → widens lumen and inhibits circular muscle contraction → allows movement forward.
- Behind the bolus (orad side): inhibits longitudinal muscle contraction → narrows lumen and stimulates circular muscle contraction → pushes bolus forward.
!!!This coordination ensures smooth and directed movement of food!!!
92
What are the characteristics of the LES?
- Not a true anatomical sphincter, but a high-pressure zone created by thickened muscularis
- At rest, the LES is contracted to prevent reflux
93
what other structures also contribute to LES control?
Diaphragm and oblique stomach fibers
94
What is receptive relaxation, what mediates it and what does it require?
- LES and stomach relax when swallowing begins after ENS and vagal reflexes initiate the process.
- Mediated by NO and VIP, allowing food to enter the stomach smoothly
- Requires a functional myenteric plexus; any damage affects this relaxation
95
Why does negative pressure in the thoracic cavity cause issues?
negative pressure, increasing the risk of:
- Air entering the esophagus (belching)
- Acid reflux from the stomach if the LES is not properly sealed
96
what is GERD (Gastroesophageal Reflux Disease) and what are common causes?
Occurs when the LES fails to prevent backflow of acid
- Hiatal Hernia: LES moves above the diaphragm, disrupting pressure.
- Obesity: Increased abdominal pressure.
- Pregnancy: Elevated progesterone relaxes the LES.
- Calcium channel blockers: Reduce muscle tone of LES.
- Overfilling the stomach: Increases pressure on the LES.
- Exercise after a large meal: Aggravates reflux.
97
what is Achalasia?
disorder of swallowing (dysphagia) in which the LES fails to relax (likely due to lack of nitric oxide) and there is impaired peristalsis in the lower 2/3rds of the esophagus which will cause for a dilation to occur above the LES
98
What is the difference between a wet and dry swallow?
Wet Swallow:
- Contains solid food or liquid
- Generates strong peristaltic contractions and LES inhibition.
Dry Swallow:
- Only air is swallowed
- Produces weaker peristaltic contractions
