Where the ventrolateral nuclues (feeding) stimulated by hunger and hyperphasia and the ventromedial nuclues for satiety stimulated by fullness
Anorexia causes damage to ventrolateral nuclues while hyperphagia causes damage to ventromedial nuclues
When the stomach extends the impulse is carried by the vagus nerve to nucluestractus soliatrius (fullness) then the food is in duodenum ( CCK and peptide yy) are released sending an excitaroty signal to vagus nerve
concentration of glucose amino acids and fatty acids in the blood sends signals to VMN in hypothalamus
When fastingghrelin is secreted VLN is stimulated - hunger
If youre fat, adipose tissue produce lectin which inhibits ghrelin
Fluid intake is regulated in the the thirst centre which is located in the anterolateral region of the hypothalamus - thirst feeling when there is an increase in the plasma osmolality (hypothalamic osmoreceptor) decreased salivation (oropharyngeal osmoreceptor) and decrease in blood volume
2 muscles that open the mouth temporalis and lateral pterygoid
2 muscles that close the jaw masseter and medial pterygoid
Automatic pharyngeal muscle contraction,
soft palate up to prevent the reflux of food to nasopharynx
Palatopharyngeal folds are pulled medially to approximate each other forming a sggital slit
Vocal cords are tensed
Larynx is pulled upward and anteriorly by neck muscles
Epiglottis swings backward over the opening or larynx
The upper esophageal sphincter is made from 2 muscles
inferior pharyngeal constrctor muscle
Cricopharyngeus muscle
UES and swallowing
Resting - high vagal tone UES is closed
Swallowing - low to none vagal tone UES is open
Esophagus upper 1/3 - straited muscle
the motor supply is nuclues ambigous > vagal nerve > axon terminus > Ach > Nictonic receptors > contraction only
Esophagus lower 2/3 - smooth muscle
pathway: Dorsal motor nuclues > myenteric plexus >
Inhibitory > NO and VIP
Excitatory >Ach and Substance P
LES opens up by NO and VIP
Secondary preistalsis clears esophagus when there is residual
upper >vagovagal reflex
lower > peristaltic reflex
Achlasia is a dilated esophagus since the LES isnt relaxing for the bolus to go through giving a birds beak apperaence
No actual cause but theory is that its an autoimmune disorder of the enteric system
Factors that contirbute to LES competence / Tone
Tonic contraction (Ach and Substance P) of circular muscle fibres
Oblique gastro-esophageal angle forms mucosal flap- valve emchanism
Crura of th diaphgram forms pinch-cock mechanism
Positive intra-abdominal pressure
To increase LES tone
Increase Intraabdominal pressure
Decrease intrathoracic pressure
Cough/sneezing > chronic cases > damage
Gastrin, motilin, alpha-adrenergic stimulation
To decrease LES tone
Secretin, glucagon, VIP, GIP, progestrone
Parotid gland gives off serous fluid (protein, water and electrolytes)
Sub- lingual and mandibular gives off viscous fluid which has mucins in serous secretions
In the acini saliva is isotonic because its the site of production but when it enters the striated duct it becomes hypotonic as Na+ and Cl- are absorbed and K+ and HCO3- are secreted
Channels in straited duct:
Na+ is aborbed back into the blood via Na+/K+ pump
Cl- aborbed and HCO3- secreted via exchanged fueled by CFTR
HCO3- enters using HCO3- Na+ cotransporter
K+ is secreted where more Na+ Cl- absorbed than K+ HCO3- secreted
Stimulants to glands
Mainly parasympathetic - Ach > water and salts > where parotid is supplied by glossopharyngeal and the subs is by facial nerve
Sympathetic - norepinepherine in the superior cervical ganglion T1 to T3 through cAMP > exocytosis of music and amalyase