:))

Question 1

* What is the rate controlling step of glycolysis? What factors regulate it’s function. [3] *

Answer 1

Fructose-6-phosphate to Fructose-1,6-bisphosphate via the enzyme Phosphofructokinase-1.

Is regulated by:

1.ATP:AMP ratio
2.Citrate (decreases activity)
3.Fructose-2,6-bisphosphate (increased activity)

Question 2

where does bile enter the dudeonum? which part of the duodenum?

Answer 2

at the Ampulla of Vater: 2nd part of duodenum

Question 3

what are th 5 pancreatic enyzmes made?

Answer 3

• Procarboxypeptidase
• Trypsinogen
• Chymotripsinogen
• Amylase
• Lipase

Question 4

which cells release pepisogen?
how is it activated?

Answer 4

Chief cells (1) release pepsinogen –> activated to pepsin using hydrochloric acid released from parietal cells!!

Question 5

explain how trypsin is activated (and from what?) and what it does subsequently to activation (2)

Answer 5

• Trypsinogen from pancreas converted to trypsin via enterokinase (a brush border enzyme)
• Trypsin then activates chymotrypsinogen to chymotrypsin and procarboxypeptidase to carboxypeptidase

Question 6

Answer 6

pink = parietal !!

Question 7

Vitamin B12 - absorbed where?

which population needs supplementts/

Answer 7

• Complexed with intrinsic factor in stomach
• Absorbed in terminal ileum!!
• Vegans need to be supplemented with vitamin B12

Question 8

name two genes that cause dissacaride deficiences and what they cause a deficiency in?

what happens as a result?

Answer 8

• Mutation in the gene encoding for lactase: known as LCT
• Mutation in the gene encoding for SGLT1 co-transporter (known as SLC5A1)

Consequence of both is osmotic diarrhea due to the fermentation of the unprocessed sugars by gut flora

Question 9

which cells transport gut antigens from lumen across epithelium?

Answer 9

M cells (microfold cells) transport gut antigens from the lumen across epithelium into the tissue.

Question 10

Gut honing mechanism:

dendritic cells create WHAT in the gut? - what does this cause gut homing T cells to make? (2)

Answer 10

• dendritic cells produce retinoic acid (vitamin A) which induce gut homing T cells to express α4β7 and CCR9.

Question 11

gut honing mechanism:

what do epithelial cells lining the gut home T cells by expressing? (2)

Answer 11

Epithelial cells lining gut home T cells by expression of CCL25 (ligand for CCR9) while endothelial cells express MadCAM (ligand for α4β7).

Question 12

IgA:
how much is secreted per day?

(what residue does it have?)

Answer 12

• > 3g of secretory IgA per day
• 18 amino acid C-region tailpiece with cysteine residue required for polymerisation

Question 13

what can lack of B12 cause?

Answer 13

pernicious anaemia

Question 14

what resists being broken down in CD?

what type of MHCs do CD patients have/

Answer 14

gliadin !!! pls remember

HLA-DQ2 or HLA-DQ8

Question 15

as a result of CD, CD4 cells are activated in the gut.
what do they cause to be released? (5)

Answer 15

•macrophages present gliadin via MHC to CD4 T cells:

CD$ cause the release of inflammatory cytokines like IFN-γ which destroys epithelia of small intestine

• CD4 T cells also activate B cells to produce IgA anti-gliadin, anti-tTG and anti-endomysial* (EMAs)
• CD4 T cells also recruit CD8 T cells which further destroys epithelia of small intestine

Question 16

what does deficiency in B1 cause a subsequent a deficency in? [1]

Answer 16

• Pathology from VitB1 deficiency = B1 used as a cofactor to produce actetyl co-A from pyruvate. inability for cells to produce Acetyl CoA

Question 17

acetyl co-A is the input for TCA. acetyl co-A can be produced by three ways. What are they?

Answer 17

1.Glycolysis of glucose to pyruvate
•Converted to acetyl-CoA using pyruvate dehydrogenase complex (PDC)
•Produces 2 reduced NAD molecules per glucose
•1 reduced NAD per pyruvate

2.Transamination of glucogenic amino acids to pyruvate
• Converted to acetyl-CoA using pyruvate dehydrogenase complex (PDC)

3.Beta-oxidation of fatty acids directly to acetyl-CoA
•Produces 1 NADH and 1 FADH2 per acetyl-CoA

Question 18

what do chief cells secrete? [1]
what do chief cells secrete in children? [1]

Answer 18

Chief cells:

• secrete: pepsinogen (–> pepsin by gastric acid)
• in children: also secret chymosin (rennin) ->a protease that helps coagulate milk allowing it to be retained more longer in the stomach

Question 19

Answer 19

Question 20

describe the structure of the rectus sheath

a) above arcuate line
b) below arcuate line

Answer 20

• *rectus sheath:**
• surrounds rectus abdominis muscle
• made from: aponeuroses of external oblique, internal oblique and transverse abdominis
• structure:
• *a) above arcuate line**
  i) external oblique aponeuroses runs anterior to rectus abdmonis & inserts into the midline: forms linea alba
  ii) i_nternal oblique aponeuroses splits in half_: half goes anterior of rectus abdominis, other half goes posterior. again insets onto linea alba
  iii) transversus abdominis runs posterior to rectus abdominis
  iv) transversalid fascia runs posterior to rectus abdominis
• *b) below arcuate line:**
  i) all of aponeuroses run anterior to rectus abdominis
  ii) transveralis fascia runs posterior to rectus abdominis

Question 21

what is the blood supply to the abdominal wall like? (3) where from?

Answer 21

internal thoracic artery –> superior epigastric artery
external iliac artery –> inferior epigastric artery
lower intercost and lumbar arteries - blood to lateral aspect of ab wall.

Question 22

what two anatomical features are found under the inguinal ligament? [2]

Answer 22

• under inguinal ligament:
  a) passageway for the femoral artery, vein and nerve pass & enter thigh.
  b) spermatic cord:
• femoral artery and vein are below inguinal ligament
• spermatic cord goes through the abdominal wall and inguinal canal (which is inside inguinal ligament) and towards scrotum

Question 23

what are anatomical differences between jejunum and ileum? (3)

Answer 23

jejunum:

• most absorbtion
• greater vascularity
• lots of plicae circularis (folds of mucosa)

ileum:

• less vasucularity
• less plicae circularis
• peyers patches present

Question 24

Answer 24

Question 25

colon ha longitudinal muscle separated into 3 bands known as what? [1]

Answer 25

Longitudinal muscle separated into 3 bands known as **taenai coli**

Question 26

where are bile acids absorbed?

Answer 26

ileum

Question 27

why is water needed in the digestive system? (4)

Answer 27

Hydrolysis reactions of digestion Facilitation of absorption (brings products of digestion into close proximity to microvilli) Facilitation of propulsion of gut contents Combination with mucin granules to make mucus

Question 28

what is the enterohepatic circulation?

Answer 28

* *Enterohepatic circulation: recycling of bile salts** - liver: makes bile salts - stored in gall bladder - goes into duodenum: help digest fats - reabsorbed in ileum - bulk of bile salts are absorbed in liver

Question 29

\*\* 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 29

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 30

which 3 antibodies in the body is a sign of CD?

Answer 30

**antigliadin tissue transgluataminase antiendomyisial**

Question 31

what isoform do CD patients have?

Answer 31

- (95% of CD) have isoform of **DQ2 or DQ9** of human leukocyte antigen (HLA) **HLA-DQ** protein - due to HLA-DQ, get high levels of antibodies: antigliadin, tissue transgluataminase, antiendomyisial

Question 32

what do mutations in: - LCT gene - SLC5A1 gene cause?

Answer 32

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 33

what is the name for primer used in glycogen synthesis?

Answer 33

**glycogenin**

Question 34

## Footnote Q 1. in muscle - how can glucose-6-phosphate produce ATP (aerobically and anaerobically? 2. why does muscle not have a role in raising blood glucose levels?

Answer 34

## Footnote in muscle, glucose-6-phosphate can produce ATP: - **aerobically** (via Acetyl coA, krebs cycle & oxidative phosphorylation) - b (via lactate) - **_free glucose cannot be produced / released from skeletal muscle bc it doesnt have glucose-6-phosphatase (to convert G6P -\> glucose)_**

Question 35

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

Answer 35

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 36

when is insulin / glucagon released? what do insulin and glucacon to do: & how? a) glycogen synthase b) glycogen phosphorylase \* key - learn this \*

Answer 36

**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 phosphorylas_e - adds P

Question 37

what is the mechanism of adrenaline, glucagon and calcium activating glycogen -\> glucose

Answer 37

* *_- adrenaline, glucagon and calcium activate adenylate cyclase_** - adenylate cyclase causes: **ATP --\> cAMP** - cAMP **inhbits glycogen synthase** by phosphorylasing it AND cAMP promotes **phosphorylation of phosphorylase kinase** - phosphorylase kinase promotes **phosphorylation of glycogen phosphorylase** - glycogen phosphorylase breaks **down glycogen into glucose**

Question 38

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

Answer 38

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 39

Q whats the MoA of insulin - activating phosphodiesterase? - activating protein phosphastase?

Answer 39

**1. - insulin activates phosphodiesterase** - phosphodiesterase breaks down **cAMP -\> AMP** - this means protein kinase A is not activated - this means that glycogen synthase is not phosphorylated andswitched off - glycogen synthase: glucose -\> glycogen AND - phosphorlase kinase is not active: glycogen phosphorylase not activated = glycogen break down inhibited **2. insuline activates protein phosphatase -\>** downstream consequences also: - glycogen synthase: glucose -\> glycogen

Question 40

\* why doesnt glucagon work on liver, not muscle ? \*

Answer 40

muscle doesnt have glucagon receptors

Question 41

what is the effect of a lack of cAMP?

Answer 41

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

Question 42

in the production / break down of glucagon, glycogen synthase and glycogen phosphorylase are made active / inactive by the addition of what?

Answer 42

**glycogen synthase** is **activated** by **removing** **P**, **inactivated** by **adding** P **glycogen phosphorylase is** activated by **adding P**, **inactivated** by **removing** b therefore work antagonistically !

Question 43

what is von Gierkes disease?

Answer 43

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

Question 44

Mc Ardle's disease:

Answer 44

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

Question 45

what is Her's disease caused by? & treatment?

Answer 45

Her's disease: caused by: deficiency in **glycogen phosphorylase in live**r = severe problems maintaining their blood glucose Treatment: regular, often feeding. This is because they cannot maintain their blood glucose like we can

Question 46

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

Answer 46

insulin: * *- activates phosphodiesterase - activates protein phosphastase** which are two different pathways that both end up in the glucose --\> glycogen

Question 47

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

Answer 47

**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 48

extrinisc innervation of the GI tract: - which nerve controls communication between gut and CNS? - after enetering the brain stem, where does & synapse?

Answer 48

extrinsic innervation - vagus nerve mediates communication gut and CNS - has central terminals that enter **_brain stem and synapse to neurons of nucleus tractus solitarus_**

Question 49

where is the largest microbial colony found in GI?

Answer 49

- largest microbial colony: colon

Question 50

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

Answer 50

* *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 51

gastroparesis: - caused by? - symptoms? - which disease is it associated with? - what can it lead to?

Answer 51

- 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 sug

Question 52

inflammatory bowel disease: collective term that refers to chronic inflammation of the lower GIT. **which two diseases main?**

Answer 52

inflammatory bowel disease: collective term that refers to chronic inflammation of the lower GIT. **a) Crohns Disease b) Ulcerative colitis**

Question 53

Clostridium difficile: a) associated / caused by what? b) results in what symptoms? (2) c) treatment? (3)

Answer 53

Clostridium difficile: a) associated / caused by: **broad spectrum antiobiotic usage - opportunistic overgrowth** b) results in: **watery diarrhoea & abdominal pain** c) treatment: **stop antibiotic use, vancomycin, fecal microbiota transfer**

Question 54

link between gut and brain: what two things have been shown to be altered in brain as a result of altered gut microbiota?

Answer 54

- activity of macrophages / microglia within brain - development and plasticity in brain (leads to ageing)