:) 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
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?)
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
