:) Flashcards
what is the name for what dietary lipid is transported in?
which system are dietary lipids transported in/
Nearly all dietary lipid is transported in chylomicrons from the gut to the blood through the lymphatic system (too big for blood) by entering specialized lymphatic vessels, referred to as lacteals
B12 can be only observed where? & what must it first be complexed with?
what is B12 aka?
describe the absorptive pathway of B12 :)
- B12: absorbed only in terminal ileum, after being complexed with stomach-derived intrinsic factor
- B12: aka cobalamin
absorptive pathway:
- bound to dietary protein
- first dissociated by HCl and pepsin, in stomach
- reattaches itself via haptocorrin (from saliva thats now in stomach)
- dissociated from haptocorrin and binds with stomach-derived intrinsic factor
- absorbed only in terminal ileum in enterocytes (although 60-80% still goes into faeces)
- reassociates with transcobalamin and then goes to portal circulation
what causes coeliac disease? - what isoform do they have? which 3 antibodies this this create?
what does it cause in the cells ? (3)
coeliac disease:
- autoimmune disease
- (95% of CD) have isoform of DQ2 (more common) or DQ9 of human leukocyte antigen (HLA) HLA-DQ protein
- due to HLA-DQ, get high levels of antibodies: antigliadin, tissue transgluataminase, anti endomysial
causes
- complete villi atrophy
- marked crypt hyperplasia (bc trying to replace the villi, which are being replaced)
- major inflammation
give two examples of things that are a specific malabsorbed lol
- e.g B12 or dissacharide sugars
how do commensal bacteria regulate digestion?
what happens if we have bacterial overgrowth?
dynamic equilibrium between diet-gut microbiome-bile acid pool size:
normally - we have conjugated bile acids, created by liver. Conjugated bile acids (primary bile acids): more efficient in emulsifying fats because at intestinal pH they become more ionized than the unconjugated bile acids.
Commensal bacteria: participate in the synthesis of bile acids. Microbial enzymes de-conjugate bile acids & make them less effecient: (secondary bile acids).
so we have a pool of primary and secondary bile acids: if have bacterial overgrowth in gut: form too much secondary bile acids = struggle to digest fats
what do mutations in:
- LCT gene
- SLC5A1 gene
cause?
which phase of digestion they effect?
mutation in gene LCT - affects mucosal phase of dissachardide absorption. lactose intolerance
gene SLC5A1 - encodes for Sodium dependent GLucose tranpsorter one: SGLT1. so mutation causes glucose-galactose malabsorption. again: mucosal phase
** why do vitamins need to be absorbed from the food?
what are two type of vitamins?
how are each absorbed?^
into which system are they absorbed? **
vitamins cant be manufactured by body
- *1. fat soluble vitamins: A, D, E & K**
- absorbed with lipids: readily dissolve in lipid droplets, micelles and chylomicrons
- absorbed into lymph fluid
- *2. water soluble vitamins: B & C**
- follow flux of water (B&C)
- absorbed into portal vein
- what type of bonds connect the monomer in glycogen?
- attached by alpha 1-4 glycosidic bonds (but forms branches by using 1-6 links)
- why does muscle not have a role in raising blood glucose levels? [2]
- why does muscle not have a role in raising blood glucose levels?
- free glucose cannot be produced / released from skeletal muscle bc it doesnt have glucose-6-phosphatase (to convert G6P -> glucose) [1]
- muscle doesnt have glucagon receptors [1]
where is glucagon made?
it is produced by the alpha cells, found in the islets of Langerhans, in the pancreas
what is glycogen breakdown aka?
explain how this occurs (4)
glycogenolysis:
- debranching enzyme: breaks down the a-1,6 glycosidic bonds (the branches of glucose)
- glycogen phosphorylase: breaks down a-1,4 glycosidic bonds: free G1Ps
- phosphoglucomutase: converts G1P to G6P
- in the liver: glucose-6-phosphatase removes the P group = free glucose
(but step 4 does not occur in the muscle - instead, it is immediately used in glycolysis)
what do two starting materials do you need before glycogen synthesis?
- *glycogen synthesis needs:**
- a primer (protein that glucose will attach to): glycogenin.
- *- glucose-6-phosphate (G6P)**
BUT: NEED TO CONVERT G6P -> UDP-glucose before can be added to glycogen:
- *a) G6P –> G1P
b) G1P –> UDP-glucose**
glycogen production and breakdown is carried out by which hormone signalling molecules (4) and which do they act on - liver or muscle?
- insulin: muscle and liver - builds glycogen stores
- glucagon: only liver - breaks down glyocgen stores to release glucose
- adrenaline: muscles via a & b adrergic receptors - release glucose
4 calcium: muscles via a & b adrergic receptors - release glucose
when is insulin / glucagon released?
what do insulin and glucacon to do: & how?
a) glycogen synthase
b) glycogen phosphorylase
* key - learn this *
insulin: released after meal. insulin works via protein phosphatase (removes Ps):
- *- activates glycogen synthase - by removing P
- inhibits glycogen phosphorylase - by removing P**
glucagon & adrenaline: released between meals / when fasting: works via cAMP, protein kinase A and phosphorylase kinase: adds P
- *- inhibits glycogen synthase - adds P
- activates glycogen phosphorylase - adds P**
what is the effect of a lack of cAMP?
lack of cAMP causes glucagon and adrenaline effects to be stopped (and less glucose released)
what are the two pathways that insulin causes glycogen synthase to be activated and cause glucose -> glycogen?
insulin:
- activates phosphodiesterase
- activates protein phosphastase
which are two different pathways that both end up in the glucose –> glycogen
Mc Ardle’s disease:
- what type of disease (autosomal dom etc?)
- caused by?
what does this mean with regards to exercise ? second wind can occur from?
Herrs Disease
same>?
Mc Ardle’s disease:
autosomal recessive disease
caused by: deficiency in glycogen phosophorylase gene: PYGM. cant breakdown glycogen in the muscle = muscle weakness
when exercise: can only exercise in short bursts, otherwise muscles will cramp, lock and they will fall over in intense pain. This is due to their muscles running out of energy.
second wind: muscles use alternative fuel to glucose
//
Her’s disease:
caused by: deficiency in glycogen phosphorylase in liver = severe problems maintaining their blood glucose
Treatment: regular, often feeding. This is because they cannot maintain their blood glucose like we can
what is von Gierkes disease?
deficiency in glucose-6-phosphastase: means liver cant produce glucose via glycogen breakdown.
feed patients with carbs day and night
which type of cells are bile salts secreted from?
bile salts - produced by hepatocytes
intrinsic innervation (communication within the gut) anatomy: what are the 4 layers of the gut wall? what are their functions?
gut wall layers & roles
-
mucosa: epithelial cells - contain and secrete hormones. highly innervated with neurons
above the mucosa: - longitudinal muscle & circular muscle: both important for srretch: peristalsis & expelling of faecal matte
- myenteric plexi: primarily focused on contraction and relaxtion of peri
- submucosal plexi: involved in regulating absorbtion and secretion of nutrients
which plexi in gut is focused on peristalsis?
which plexi in gut is focused on absorbtion of nutrients?
- myenteric plexi: primarily focused on contraction and relaxtion of peri
- submucosal plexi: involved in regulating absorbtion and secretion of nutrients
faecal microbiota transfer:
a) aim?
b) who are donors?
c) results in? (2)
d) approved for treatment of what infection?
faecal microbiota transfer:
a) aim: increase microbial diveristy
b) who are donors: healthy relative, super donors
c) results in: obesity phenotype reversed - due to transfer of facees rfom fit healthy to obese
d) approved for: treatment of C. difficile infection
inflammatory bowel disease:
collective term that refers to chronic inflammation of the lower GIT. which two disease is it split into?
A
inflammatory bowel disease:
collective term that refers to chronic inflammation of the lower GIT.
a) Crohns Disease
b) Ulcerative colitis
* both go through periods of active disease and non-active disease *
- *gastrooesphageal reflux disease (GERD):**
- caused by?
- associated with? (3)
- what can chronic condition lead to? (3)
- treatments?
gastrooesphageal reflux disease (GERD):
- caused by:
a) movement of stomach contents from fundus -> distal oesophagus after lower oesophagus sphincter is relaxed
b) then get increased frequency of transient relaxations of lower oesph. sphincter
- associated with:
- **weight gain
- gastroparesis
- stress**
- chronic condtion leads to:
- *a) ulcer formation
b) inflammation** - treatment: antacids and alginates - like gaviscon
Q
gastroparesis:
- caused by?
- symptoms?
- which disease is it associated with?
- what can it lead to?
- caused by: delayed gastric emptying
- inability to remove stomach content causes: nausea, vomiting, feeling of fullness, pain and bloating
- associated with diabetes: diabetic gastroparesis
- subsquently can lead to malnutrition (bc people dont eat) and changes in blood sugar
how do u diagnose gastroparesis?
how u treat?
diagnosis:
- gastric emptying study: C13 meal ingested. time-course compared to normal values
treatment:
- domperidone or erythomycin - stimulate stomach muscle contraction
- anti-emetics for nausea
- dietary changse
what is the squamocolumnar junction? - chang
squamocolumnar junction
- abrupt change in the mucosa from stratified squamous to columnar cells (and glands)
- Oesophagus joins at an acute angle
- only the mucosa changes, the underlying layers stay the same !!
(oespahus -> stomach?)
in the stomach: what is this describing
a series of ridges produced by folding of the wall of an organ.
rugae
which cells in stomach secrete:
- pepsinogen?
- HCl?
where in the stomach do u find them?
how do u differientate? (2)
- pepsinogen: chief cells
- HCl: parietal cells
- *- chief cells:** deep in fundic glands
- *- parietal cells:** neck of fundic segment
- chief cells: smaller, paler
- *- parietal cells**: bigger, darker
- what are the folds called in the small intestine?
- what are the main histological feature of small intestine? (2)
- what are the lieberkuhns crpyts?
- what are the folds called in the small intestine: plicae circularis
- what are the main histological feature of small intestine: villi (projections of the mucosa) & microvilli
- lieberkuhns crpyts: gland found in between villi
what are the main histological differences between the duodenum, jejunum and ileum?
duodenum:
- have brunner’s glands in submucosa: produce secretion that neutralises acidic chyme from stomach
- villi are shorter
jejunum:
- no brunners glands
- long, finger like villi with well developed lacteal (lympathic vessel) in the core
ileum:
- peyers patches (lymphoid aggregations / nodules in the mucosa. form part of GALT
- shorter villi
- most goblet cells
- prominant fat in submucosa
how do u tell the difference between paneth cells and endocrine?
Paneth granules are above nucleus (supranuclear) & appear pink
endocrine granules are beneath the nucleus (subnuclear)
name the 5 different types of celsl find in the body / fundic mucosa?
body / fundic mucosa:
mucous neck cells: secrete mucous
- chief cells: deep at bottom of fundic glands. secrete pesinogen !
- parietal cells: neck of fundic segment: secrete HCl and intrinsic factor !
- stem cells
- endocrine cells
what are the small intestine cells? (5)? roles
- enterocytes: secretory and absorb functions
- goblet cells: secrete mucous
- paneth cells: secrete antimicrobe substances; H&E= pink
- enteroendocrine cells: release horomones
- m cells: modified enterocytes that cover lymphoid nodules
in the colon, where are paneth sides found?
only on the right side!
the external anal sphincter is formed by X muscle?
the external anal sphincter is formed by skeletal muscle
- describe difference in structure between large and small intestine (2)
- difference: circular folds and villi = ABSENT
- similarities: same mucosal cells:
a) paneth cells are found in right side of colon only
how do u tell histoligcally if you have significant oesophagitis? (2)
how do u tell histoligcally if you have barret oesph? (1)
how do u tell histoligcally if you have CD? (3)
significant oesophagitis: eosinophils in squamous mucosa & neutrophils
barret oesophagus: complication of chronic gastro reflux disease (GERD). characterised by change of squamous mucosa in oesph to simple columnar epithelim
CD: atrophy of villi (1), hyperplasia of intestinal crypts, more lymphocytes
what happens to C&L muscle in anal sphincter?
circ muscle: becomes internal anal sphincter
long muscle: extends over sphincter & attaches to CT
what are the three zones of the anal canal? what are the cells like there?
colorectal zone: simple columnar epi
anal transitional zone: transition betwen simple columnar and and stratified squamous epi
squamous zone: stratified squamous
what two things specifically make u hungry?
- release of hormone ghrelin
- *- phase three** of migrating motor complex
which cells cause depolarisation to initiate stomach muscle contraction?
interstitial cells of cajal
functions of the proximal stomach:
- what happens when bolus enters stomach? (2 steps)
- what is each step innervated by?
- what method can u do to relieve pressure of stomach? - how does this occur?
functions of the distal stomach? (3)
functions of the proximal stomach:
- receptive relaxation: makes proximal stomach stretch so not immediatly full (vagal-vagal relflex, causes release of CCK)
- adaptive relaxation: ENS releases NO to allow relaxation
- can relieve pressure by burping (lets gas out of stomach) via relaxation of LOS
- *functions of the distal stomach:**
- propulsion, retropulsion and further grinding and mixing (propels food agaisnt closed pylorus)
- gastric acid digestion
- only particles of 1-2 mm empty into duodenum
what anatomical features of the colon ensure that peristalsis is modified? (2)
- get bulges of outer circular muscle (haustra), which are held together by three bands of circular muscle: taenia
- taenia can contract in either direction
explain what the duodenal and jejunal breaks are
dudenal and jejunal brakes:
- food goes into the duodenum, might be too big - like long chain fatty acids / amino acids. causes the release of CCK
2. release of CCK activates vagal efferents
- *3. as a result of vagal efferents:**
- reduces opening of pyloric sphincte
- reductions contractions in corpus
- enhances relaxation of fundus
whats the ileal brake?
- fats reach the ileum (even tho theyre meant to have been absorbed in duodenum)
- causes release of peptide YY & glucagon-like peptide-1 (GLP-1) by enteroendocrine cells
= slows gastric emptying
out of the stomach and small intestine is vagus dependent and independent migrating motor complex?
what is function of MMC in stomach? and small intestine?
originates:
a) stomach - vagus dependent
b) small intestine - vagus independent
functions:
a) clear undigested material
b) prevents bacteria overgrowth
describe how the ENS and peristaltic reflex works:
- how this reflex activated? (2)
- describe the difference between the different motor neurons causing ascending and descending wave of peristalsis:
- what type of NT released?
- what does that cause?
- *1. Activation of enteric reflexes: can be chemical or mechanical.**
- Chemical activation can be through substances from endocrine cells (e.g. 5-HT), nutrients or low Ph
- mechanical via muscle deformation or stretch
motor neurons:
Ascending wave of peristalsis: excitatory neuro-transmission to muscle, mostly by the release of acetylcholine. This causes the contraction and initiate the push.
Descending wave of peristalsis: Inhibitory neurotransmission to muscle, mostly by release of the gas nitric oxide
which are the main antibodies that protects you in the gut? which one is more?
- *IgA** - 80% of the antibodies in the gut are IgA
- *IgM** - 13%
(in lymphoid organs, like lymph nodes / bone marrow - IgG is the majority)
describe the structure of IgA and IgM - how many binding sites do they have?
what do they both contain?
IgA: dimer !! (know this) - can form 4 binding sites
IgM: pentamer - can form 10 bindings sites
= form multimers
- both have J chain: (The joining (J) chain is a small polypeptide, expressed by mucosal and glandular plasma cells)
why is breast feeding important immunologically?
- Newborn babies have no IgA, which is why it’s a really good idea to be breast-feed as you are getting passive immunity
how does IgA get into where its needed?
- polymeric Ig receptor is made by the epithelial cells of the gut
- IgA & IgM J chains bind to polymeric Ig receptor, and IgA & IgM is actively transported across epithelium.
- IgA & IgM transcyosied (moved by cytosis) in to gut lumen
what is function of IgA and IgM?
- good at: agglunation: the IgA in the mucus and agglutinates pathogens to keep them away from the epithelial, and therefore it keeps them in a hostile environment and they will be washed away, prevented from binding and entering gut cells. They are usually swept away by peristalsis
what is
passive transfer of gastrointestinal pathogen immunisation to the baby from the mother
passive transfer of gastrointestinal pathogen immunisation to the baby from the mother
- During lactation, B cells leave the peyer’s patch and move to the breast via the thoracic duct
- breast blood vessels cells express MADCAN
- epithelial cells express secretory component
- peyers patches immune activation depends on the what?
gut flora !
without gut flora = no immune activation
