digestion, motility and absorption Flashcards
What is the oral cavity made up of?
- lips and cheeks → skeletal muscle embedded in elastic fibro CT
- lined with stratified squamous epithelium (protection)
- tongue body + root → skeletal muscle, both intrinsic (change shape) and extrinsic (allow movement)
Where does the oesophagus pierce the diaphragm and how is it innervated?
- oesophageal hiatuse (T10)
- via vagus nerve
Describe the mucosa, submucosa and the types of muscle present in the oesophagus
- mucosa: non-keratinised stratified squamous epithelium
- submucosa: mucus secreting glands
- skeletal muscle = upper 1/3 transitional muscle = middle
- smooth muscle = lower 1/3
Describe the upper and lower oesophageal sphincter.
- upper: hypopharyngeal sphincter
- skeletal muscle fibres
- lower: gastro-oesophageal sphincter
- high pressure
In gustation, what are the 5 primary tastes and which taste buds can detect them?
- sour (acid), salt (Na+), bitter (most sensitive), sweet (organic substance), umami (meat)
- all taste buds can detect all tastes, although each most sensitive to 1 type
- tip = sweet, sides of tip = salty, back = bitter, sides = sour
What are the papillae of tastebuds and where are the different types found?
- papillae are where most taste buds are found on the epithelium of tongue
- filiform papillae not involved with taste
- fungiform papillae scattered on dorsal surface of tongue
- foliate papillae on tip and sides of tongue
- circumvallate at intersection of anterior/posterior tongue
(also receptor membranes bathed in saliva and dendrites of sensory nerves around gustatory cells)
Describe the process of taste.
- substance dissolves in saliva
- enters taste pore and attaches to chemoreceptor membrane
- induces change in membrane permeability
- depolarisation of taste cell (generator potential)
- NT released to stimulate sensory neurone → neural pathway to brain (7th, 9th, 10th cranial)
- impulses to tractus solitarius of medulla oblongata → thalamus → taste area of parietal cortex,
hypothalamus, limbic system
What is aguestia?
- loss of taste
- may result from medications or neuronal damage maybe drug-induced or metabolic or specific genetic deficiencies
Describe the secretions of saliva from the three major pairs of salivary glands.
- parotid (serous) = water and α-amylase
- submandibular (serous and mucous) = weak α-amylase and lysozyme
- sublingual (mucous) = thick, viscous secretion
(+ other glands scattered throughout mucosa)
What is the the composition of saliva?
- > 99% water, <1% solids
- ions (Na, K, Mg, HCO3-, supersaturated with Ca phosphates)
- 50+ proteins including α-amylase, mucins
- pH 6.2-8.0
What are the functions of saliva and what can lack of saliva cause?
- lubrication for movement
- taste sensation
- digestion at optimum pH
- protection
- thirst (water intake)
- speech, dentures
- absorption of dissolved drugs
- chemical balance (tooth enamel)
- can make swallowing difficult, cause halotis (bad breath) problems, dental caries, gum disease, mucousal ulceration
Name some disorders of salivary gland and their causes.
- mumps: infection of parotid gland by myxovirus - sterility in males
- xerostomia: dry mouth
- causes: autoimmune, diabetes, age-related atrophy, medication side-effect, Sjogrens syndrome (autoimmune disease)
What is mastication and how does it work?
(chewing)
• tooth shape adapted for different functions:
- incisors chisel-shaped for cutting
- canines for tearing
- molars for grinding
• movement controlled by touch, pressure and stretch receptors
- up-and-down movement of mandibles (biting by incisors)
- side-to-side movement of mandibles (crushing and breaking by molars)
- each assist mixing food with saliva, to lubricate + allow taste
How is chewing controlled?
- jaw movements voluntary, involve cerebral cortex and skeletal muscles
- strength of bite controlled by sensory receptors in teeth, send signals to brain stem area to stop/reduce
What is deglutition (swallowing) and what are its 3 phases?
- swallowing, initiated voluntarily, but becomes involuntary
- voluntary phase - tongue separates food into bolus + moves backwards/upwards
- pharyngeal phase - food into pharynx, pressure receptors in palate activated, impulses from trigem + glossophar nerves to swallowing centre in medulla → elevation of soft palate
- voluntary phase - tongue separates food into bolus + moves backwards/upwards
- impulses from swallowing centre inhibit respiration, raise larynx + close glottis
- bolus tilts epiglottis over closed glottis and upper oesophageal sphincter opens to allow bolus then closes
- glottis opens, breathing resumes
3. oesophageal phase - peristalsis of food co-ordinated by vagus nerve influenced by swallowing centre - lower oesophageal sphincter relaxes to allow food to enter stomach + closes preventing acid reflux into oesophagus
- increased gastrin increases tone of sphincter (when stomach filled)
Describe types of dysphagia (disorders of deglutination) and provide examples.
• dysphagia:
- damage to cranial nerves or to swallowing centre in medulla i.e. stroke
- degenerative diseases of skeletal muscle/transmission process
- defects in autonomic nerves/intrinsic nerves of oesophagus
• i.e.
- inactive swallowing reflex
- hiatus hernia
- diffuse oesophageal spasm → thickening of SM
- gastro-oesophageal reflux disease (GORD) → gastric contents into oesophagus (heartburn)
Describe control of salivary secretion and how it depends on the nervous system.
- tastebuds + mechanoreceptors activated by food
- sensory info sent to salivary nucleus in medulla
- unconditional reflex activated by sensory input to brain
- impulses via autonomic nerves (parasympathetic, cranial nerves 7 and 9) to salivary glands
- increased secretion of fluids/enzymes/mucins and dilated vessels
- composition depends on flow rate (low FR = low pH)
Name some gastric secretions and the cells which secrete them.
- mucus: gel formed from glycoprotein w/ water - from surface epithelial + mucous neck cells
- bicarbonate: protective against acid, trapped in mucus layer - surface epithelial cells
- hydrochloric acid - parietal cells
- intrinsic factor: protection of vit B12 - parietal cells
- pepsinogens: protein digestion - chief cells
What are pepsins? Write out its structure.
- endopeptidase enzymes which hydrolyse specific peptide bonds w/in protein chain
- NH-CH₂-C(=O)- | -NH-CH₂-⬣(H)-C(=O) -NH-CH(R)- etc…
- (| = cleavage point, exopeptidases hydrolyse terminal peptide bonds and generate free AAs)
State the five functions of gastric acid secretion.
- activates pepsinogens
- maintains pepsin activity
- bactericidal
- disrupts CT proteins
- dissolves particulate matter (from air) in food
On which on 3 factors does stimulation of gastrin secretion depend on?
- M1, acetylcholine: NT released from vagus nerve and local intrinsic nerves
- gastrin: hormone released from G-cells of antral mucousa by Ach, stretch, dietary proteins; circulates
in bloodstream to parietal and other secretory cells - H₂, Histamine: local hormone released from cells close to parietal cells by gastrin + Ach; acts alongside to give strong secretory response (= synergistic)
Describe the 3 phases of gastric secretion including their triggers and control.
- cephalic phase (“head”)
• triggered by thought, smell, sight, taste of food
• controlled by nervous mechanisms (CNS impulses via vagus nerve), causing:
- release of acid and pepsin
- small release of gastrin from antral G-cells - gastric phase (“stomach”)
• triggered by:
- distension (enlargement) of stomach by food
- action of food components i.e. peptides, caffeine, alcohol, calcium
• controlled by hormonal mechanisms:
- gastrin release from G-cells of antrum, then circulating to glands in fundus/body
- increases acid and pepsin secretion - intestinal phase (“intestine”)
• triggered by:
- emptying of stomach contents into duodenum
- low pH in gastric antrum
• controlled by nerves + hormones:
- release of hormones from duodenal mucousa which inhibit gastric secretion (secretin, CCK, gastric inhibitory peptide)
- local and long CNS nervous reflexes which inhibit gastric secretion
What is peptic ulcer disease (PUD), its causes and treatment?
- protective mechanisms in epithelium of stomach + upper small intestine fail
- epithelial/sub-epithelial cells become inflamed + damaged by acid/pepsins
- causes:
• excess acid/pepsin/histamine
• steroidal/nonsteroidal anti-inflammatory drugs
• Helicobacter pylori infection - treatment:
• antibiotics
• change medication
• block acid secretion using H⁺ pump inhibitors
What is Zollinger-Ellison syndrome and what effects does it have?
- raised gastrin levels in secretory gastrinomas
- effects: excess basal acid, stimulated acid + pepsin production, hypertrophy of gastric mucousa, ulceration, abnormal motility