:)

Question 1

what is the name for what dietary lipid is transported in?
which system are dietary lipids transported in/

Answer 1

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

Question 2

B12 can be only observed where? & what must it first be complexed with?

what is B12 aka?

describe the absorptive pathway of B12 :)

Answer 2

• 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

Question 3

what causes coeliac disease? - what isoform do they have? which 3 antibodies this this create?

what does it cause in the cells ? (3)

Answer 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

Question 4

give two examples of things that are a specific malabsorbed lol

Answer 4

• e.g B12 or dissacharide sugars

Question 5

how do commensal bacteria regulate digestion?

what happens if we have bacterial overgrowth?

Answer 5

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

Question 6

what do mutations in:

• LCT gene
• SLC5A1 gene

cause?

which phase of digestion they effect?

Answer 6

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

Question 7

** 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? **

Answer 7

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

Question 8

• what type of bonds connect the monomer in glycogen?

Answer 8

• attached by alpha 1-4 glycosidic bonds (but forms branches by using 1-6 links)

Question 9

2. why does muscle not have a role in raising blood glucose levels? [2]
3. why does muscle not have a role in raising blood glucose levels?

Answer 9

• 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]

Question 10

where is glucagon made?

Answer 10

it is produced by the alpha cells, found in the islets of Langerhans, in the pancreas

Question 11

what is glycogen breakdown aka?
explain how this occurs (4)

Answer 11

glycogenolysis:

1. debranching enzyme: breaks down the a-1,6 glycosidic bonds (the branches of glucose)
2. glycogen phosphorylase: breaks down a-1,4 glycosidic bonds: free G1Ps
3. phosphoglucomutase: converts G1P to G6P
4. 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)

Question 12

what do two starting materials do you need before glycogen synthesis?

Answer 12

• *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**

Question 13

glycogen production and breakdown is carried out by which hormone signalling molecules (4) and which do they act on - liver or muscle?

Answer 13

1. insulin: muscle and liver - builds glycogen stores
2. glucagon: only liver - breaks down glyocgen stores to release glucose
3. adrenaline: muscles via a & b adrergic receptors - release glucose

4 calcium: muscles via a & b adrergic receptors - release glucose

Question 14

when is insulin / glucagon released?

what do insulin and glucacon to do: & how?

a) glycogen synthase
b) glycogen phosphorylase

* key - learn this *

Answer 14

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**

Question 15

what is the effect of a lack of cAMP?

Answer 15

lack of cAMP causes glucagon and adrenaline effects to be stopped (and less glucose released)

Question 16

what are the two pathways that insulin causes glycogen synthase to be activated and cause glucose -> glycogen?

Answer 16

insulin:

• activates phosphodiesterase
• activates protein phosphastase

which are two different pathways that both end up in the glucose –> glycogen

Question 17

Mc Ardle’s disease:

1. what type of disease (autosomal dom etc?)
2. caused by?

what does this mean with regards to exercise ? second wind can occur from?

Herrs Disease

same>?

Answer 17

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

Question 18

what is von Gierkes disease?

Answer 18

deficiency in glucose-6-phosphastase: means liver cant produce glucose via glycogen breakdown.

feed patients with carbs day and night

Question 20

which type of cells are bile salts secreted from?

Answer 20

bile salts - produced by hepatocytes

Question 21

intrinsic innervation (communication within the gut) anatomy:
what are the 4 layers of the gut wall?
what are their functions?

Answer 21

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

Question 22

which plexi in gut is focused on peristalsis?
which plexi in gut is focused on absorbtion of nutrients?

Answer 22

• myenteric plexi: primarily focused on contraction and relaxtion of peri
• submucosal plexi: involved in regulating absorbtion and secretion of nutrients

Question 23

faecal microbiota transfer:

a) aim?
b) who are donors?
c) results in? (2)
d) approved for treatment of what infection?

Answer 23

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

Question 24

inflammatory bowel disease:
collective term that refers to chronic inflammation of the lower GIT. which two disease is it split into?

Answer 24

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 *

Question 25

* *gastrooesphageal reflux disease (GERD):** - caused by? - associated with? (3) - what can chronic condition lead to? (3) - treatments?

Answer 25

**_gastrooesphageal reflux disease (GERD):_** _- caused by:_ a) movement of stomach contents from **fundus -\> distal oesophagu**s 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

Question 26

Q **gastroparesi**s: - caused by? - symptoms? - which disease is it associated with? - what can it lead to?

Answer 26

_- 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

Question 27

how do u diagnose gastroparesis? how u treat?

Answer 27

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

Question 28

what is the squamocolumnar junction? - chang

Answer 28

**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?)

Question 29

in the stomach: what is this describing a series of ridges produced by folding of the wall of an organ.

Answer 29

**rugae**

Question 30

which cells in stomach secrete: - pepsinogen? - HCl? where in the stomach do u find them? how do u differientate? (2)

Answer 30

- **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

Question 31

2. what are the folds called in the small intestine? ## Footnote 3. what are the main histological feature of small intestine? (2) 4. what are the lieberkuhns crpyts?

Answer 31

2. what are the folds called in the small intestine: **plicae circularis** 3. what are the main histological feature of small intestine: **villi** (projections of the mucosa) & **microvilli** 4. **lieberkuhns crpyts:** gland found in between villi

Question 32

what are the main histological differences between the duodenum, jejunum and ileum?

Answer 32

_duodenum_: - **have brunner's gland**s 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

Question 33

how do u tell the difference between paneth cells and endocrine?

Answer 33

**Paneth granules** are **above nucleus** (supranuclear) & **appear pink** **endocrine granules** are **beneath** the **nucleus** (subnuclear)

Question 34

name the 5 different types of celsl find in the body / fundic mucosa?

Answer 34

**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

Question 35

what are the small intestine cells? (5)? roles

Answer 35

- **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

Question 36

in the colon, where are paneth sides found?

Answer 36

**only on the right side!**

Question 37

the external anal sphincter is formed by X muscle?

Answer 37

the external anal sphincter is formed by **skeletal** muscle

Question 38

1. describe difference in structure between large and small intestine (2)

Answer 38

- difference: circular folds and villi = ABSENT - similarities: same mucosal cells: a) paneth cells are found in right side of colon only

Question 39

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)

Answer 39

**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: a**trophy of villi (1), hyperplasia of intestinal crypts, more lymphocytes

Question 40

what happens to C&L muscle in anal sphincter?

Answer 40

_circ muscle:_ becomes **internal anal sphincter** _long muscle_: **extends over sphincter & attaches to CT**

Question 41

what are the three zones of the anal canal? what are the cells like there?

Answer 41

colorectal zone: simple columnar epi anal transitional zone: transition betwen simple columnar and and stratified squamous epi squamous zone: stratified squamous

Question 42

what two things specifically make u hungry?

Answer 42

- release of hormone **ghrelin** * *- phase three** of migrating motor complex

Question 43

which cells cause depolarisation to initiate stomach muscle contraction?

Answer 43

**interstitial cells of cajal**

Question 44

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)

Answer 44

**functions of the proximal stomach:** - **receptive relaxation**: makes proximal stomach **stretch** so not immediatly full _(vagal-vagal relflex, causes release of CCK)_ - a**daptive 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

Question 45

## Footnote what anatomical features of the colon ensure that peristalsis is modified? (2)

Answer 45

- get bulges of outer circular muscle (**haustra**), which are held together by three bands of circular muscle: **taenia** ## Footnote **- taenia can contract in either direction**

Question 46

explain what the duodenal and jejunal breaks are

Answer 46

**dudenal and jejunal brakes:** 1. 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

Question 47

whats the ileal brake?

Answer 47

- **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) b**y enteroendocrine cells **= slows gastric emptying**

Question 48

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?

Answer 48

originates: a) stomach - vagus **dependent** b) small intestine - vagus **independent** functions: a) clear undigested material b) prevents bacteria overgrowth

Question 49

describe how the ENS and peristaltic reflex works: 1. how this reflex activated? (2) 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?

Answer 49

* *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**

Question 50

which are the main antibodies that protects you in the gut? which one is more?

Answer 50

* *IgA** - 80% of the antibodies in the gut are IgA * *IgM** - 13% (in lymphoid organs, like lymph nodes / bone marrow - IgG is the majority)

Question 51

describe the structure of IgA and IgM - how many binding sites do they have? what do they both contain?

Answer 51

**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)

Question 52

why is breast feeding important immunologically?

Answer 52

- Newborn babies have no IgA, which is why it’s a really good idea to be breast-feed as you are getting passive immunity

Question 53

how does IgA get into where its needed?

Answer 53

- **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 t**o gut lumen**

Question 54

what is function of IgA and IgM?

Answer 54

**- 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**

Question 55

what is ## Footnote **passive transfer of gastrointestinal pathogen immunisation to the baby from the mother**

Answer 55

**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**

Question 56

- peyers patches immune activation depends on the what?

Answer 56

**gut flora !** **without gut flora = no immune activation**