GIT tract 3 Flashcards
net absorption
Take in a certain amount, excrete a certain volume alongside secretion and absorption
aborption and secretion noral
volume moving from blood to gut lumen is less than lumen to blood
malabsroption
absent or defective digestive enzymes - defects in transported protein - diseases/infections of the small intestine examples of malabsroption 1) lactase deficiency - lactose intolerance 2) coeliac disease - abnormal immune response to gluten - loss of mucosal epithelium
diarrhoea
Increase stool volume or increased frequency of defecation
osmotic involvemtn in diarrhoea
increased solutes in lumen causes less water reasoprtion
- poorly absorbed substrate, high conc of substrate that cannot cross lumen so water moves into the lumen rather than increasing water levesl in gut
secretory involvemetn in diarrohea
Increases secretion of water into the lumen (secretion exceeds absorption)
not due to osmotic effect
- cholera toxin (defect function of chloride channel opening up Cl- channel, too much chloride into gut, water follows increased secretion of water)
- laxatives, hormones, drugs (antidepressants), caffeine
- bile acid malabsorption
cholera caused by
bacterial toxins from cholerae
how does cholera work
toxin enters cells and is activated in the ER
binds a G protien
activates adenylate cyclase
production cyclic AMP
activates chloride channel
chrlodie moves out of channel into lumen of gut, followe by soidum and water
inflammaiton involvemtn in diarrhoea
pathogens breach and damage the absorptive epithelium
- clostridium difficile
- invasive parasites
degranged motility in diarrhoea
Altered transit time hence less time for water reabsorption
- irritable bowel syndrome
colon motility and what it allows
segmented contractions in segmented region
allows
- mixing contents
- retain material in the proximal colon (fermentaion, water absroption)
gasto colic repsonce
mass movement of material into aboral end of colon - ready for defection
what allows defecation
regualting movemnt of material and opening of sphincters
defecation
Faeces moved into rectum (via gasto colic response) – leads to dissension
- activates stretch receptors
- afferent signals to the spinal cord
when convinemtn to defecate and what is involved
- voluntary motor nerves are inhibited allowing the external anal sphincter to relax
Automimic informs need, voluntary decides whether it is convent
Symp and parasymp
- stimulate contraction of the rectum and relaxation of the internal anal sphincter
voluntary and involuntary defacation
External is voluntary , internal is autonomic controlled
incontinence and what it leads to
pelvic floor damage
pudendal nerev damaged
Alters ability to control and regulate
- can cause loss of control of emptying, defecation could occur involuntarily or problems being unable to defecate
defecation failure causes
spinal injuries
outlet blockages
storage vs empyting defacation muscles
storage
- contracted spincters and relazaiton of colon/rectum
emptying
- relaxation of spincters and contraction of colon/rectum
emesis
protective mechanisms to prevent damafe to GI tract and ingestion of contaminated/toxic substances
detectors of toxins
pre ingestion
pre absoption
post absroption
pre ingestion - sight, smell ,tastes pre absoption - toxin dectection in lumen - mechano/chemo receptors - explusion post absroption - chemoreceptive trigger zone induced nausea to prevent further ingestion activates voimiting centters
thngs that make us sick
1) food poisoning
2) bowel disease
3) motion/vestibular disease
4) pregnancy
5) head injury
6) radiation/chemotherapy
7) surgery/ anaesthesia
8) drugs
9) pain
nausea symptoms
- pallor
- sweating
- salivation
- irregular breathing
- increased HR
- retching (several, increased force)
GI motor control of nausea steps
1) contraction of small intestine
- retrograde giant
- contracts return intestinal contents to the stomach
2) stomach relaxes
- proximal stomach relates to accommodate returning intestinal contents
- antral motility inhibited to prevent gastric emptying
3) contraction of diapgragm and abdominal wall
- expulsion
steps for vomiting
Deep inspiration allows closure of glottis, protects respiratory tract
- air and saliva drawn into oesophagus
- protection and decrease in oesophageal pressure
- soft pallet elevated to prevent entry into the nasopharynx and nose
- expiration against closed glottis and abdominal contraction
- increase intra abdominal pressure
- relaxation of lower oesophageal sphincter
- passage of contents into oesophagus
- relaxation of the UOS
- violent expulsion force stomach and abdominal contraction
during retching
upper oesophageal spincter remains closed (open for vomiting)
where is the vomiting centre
4th ventricel in medulla oblongata
vomiting centre
contains cheoreceptors sampling blood
sigals from higher centres
what detects motion sickness
vestibular system
emetic repsonce to anticancer therapry
acute recognise toxins
delayed responce due to damae to epithelium as the entero chromaffin cells damaged
- anticipatory senssros to
anti emetics work by
blocking activation of vomiting centre
Chemoreceptor trigger zone – Ondanstron (5-HT antagonist)
Block receptors for the histamines
