METSS2

Question 1

which amino acids are glucogenic? [2]

which a.a are ketogenic? [2]

Answer 1

glutamine
Alanine

lysine and leucine are ketogenic

Question 2

which cells regulate water contents in the gut?

what is the mechanism of this?

Answer 2

secretory cells of the intestinal crpyts:

- CFTR channel within these cells controls this:

a) Cl- moves from ECF via Na/K/CL2 cotransporter (as does Na & K)
b) Cl- enters lumen through CFTR channel
c) Na+ is reabsorbed via Na/K ATPase
d) negative Cl- in lumen attracts Na by paracellular pathway (through cell gaps)
e) water follows the Na into the lumen

Question 4

gastric epithelial cells

• parietal cells produce HCl. But HCl is actually quite toxic. how does the body cell overcome this issue of not causing self harm via the HCl? (2)

Answer 4

1. HCl is only produced when food is in the stomach = get unstimualted and stimulated parietal cells:
a) unstimulated parietal cells have H+ ATPase Pumps in the cytosol
b) stimulated parietal cells have H+ ATPase Pumps on apical surface

• *2. surface mucus cells secrete mucus**
• without mucus = would directly interact with cells
• mucus works as:
  a) physical barrier; gel layer
  b) chemical barrier; bicarbonate

Question 5

explain how diabetes disrupts gluconeogensis pathway ox

Answer 5

insulin doesnt work:
SO
- pyruvate dehydrogenase remains phosphorylated & therefore inactive
- = less acetyl co-A to go into krebs cycle from pyruvate
- instead fats are broken down to produce fatty acids & acetyl co-A & goes into krebs cycle instead
- means that pyruvate is available for gluconeogenesis

Question 6

explain what happens to the stomach when food enters the intestines?

a) hormonal control
b) nervous control

Answer 6

Primarily inhibits gastric acid secretion when FOOD AND ACID ENTERS THE INTESTINES

NERVOUS CONTROL:

• *It signals the sympathetic system to stop gastric secretions**
• Inhibition of parietal and chief cells

HORMONAL CONTROL:

• *- Cholecystokinin, secretin and GIP (gastric inhibitory protein) produced by duodenum –> inhibit gastric secretions**
• Cholecystokinin and GIP released by presence of lipids and carbohydrates
• Secretin released when pH decreases (due to entrance of acidic chyme into the duodenum)

Question 7

Q

PDH is regulated in two ways:

1. PDH is de/-phosphorylated by which enzymes? what do they add / remove? what is their effect?

which substances control 1.?

Answer 7

:)

• PDH Kinases inhibit PDH by adding PO4
• PDH Phosphatases activate PDH by removing PO4

//

• *control of PDH kinases**
• PDH kinases are activated: by ATP, acetyl Co-A and NADH (last two are products of PDH) = switch off PDH.
• Pyruvate & insulin inhibits PDH Kinasese (as pyruvate wants PDH to be active to break pyruvate down) = switch on PDH.

control of PDH phosphatases
- Ca2+ ions activate PDH phosphatises - increases PDH. occurs in muscle -> eventually get more ATP production = switch on PDH
- insulin activates PDH phosphatases - actives PDH

Question 8

what does Akt do in muscle?

Answer 8

Akt: phosphorylates and inactivates glycogen synthase kianse = activates glyocgen synthase

Question 9

how is the TCA cycle controlled in response to exercise?

(3)

Answer 9

1.

• Ca2+ is an allosteric keeps the pyruvate deyhyrogenase complex activated.
• therefore causes **quicker conversion of pyruvate -> acetly co-A
• increases TCA to occur more**

(PDH controls the entry to the TCA, it’s activity is regulated. The enzyme is phosphorylated and dephosphorylated depending on whether it is active or inactive. The calcium is promoting essentially the active state of PDH, by influencing PDH phosphatase (this PDH phosphatase will remove phosphates from the PDC and activate it)

2:
calcium and ADP drive activity of two dehydrogenase enzymes in the TCA to maintain high ATP production

3.

Low levels of ATP/NAD pushes PDH into its active state.

Question 10

what are the step changes in metabolism that undergo during starvation? (5)

Answer 10

1. glucose starts falling; insulin goes down, glucagon up
2. glycogen can keep brain alive for 2/3 days / 30 hrs
3. swith to FA break down = energy for 2-3 days due to gluconeogenesis
4. FA then switches to ketone bodies. (ketone bodies can go into brain - important !)
5. final resource = break down proteins to release amino acids for gluconeogenesis

Question 11

to put simply - insulin has what effect on PDH?
what effect does insulin have of kinases & phosphatases?

what do adrenaline and glucagon do to PDH? - why?

Answer 11

insulin caueses the activation of PDH & eventual production of acetyl co-A

insulin = -ve effect on kinases (which inhibit PDH)
+ve effect on phosphatases (which activate PDH)

adrenaline and glucagon: want pyruvate untouched, so it can be used to make glucose via gluconeogenesis = inhibit PDH

Question 12

NADPH is a co-factor created by immune cells.

Name 2 functions of NADPH

Answer 12

• as a reducing agent (like NADH)
• to generate ROS: immune cells use NADPH oxidase to reduce O2 to free radical and the H202. H202 then used to kill engulfed pathogens = respiratory burst

Question 13

what covers the rectus abodminis?

Answer 13

rectus sheath

Question 14

what does tissue transglutaminase (tTG) do to gliadin in CD patients? [1]

Answer 14

removes amide group / deamination

Question 15

Name the cells bordering the lumen [1]

Answer 15

paneth cell

Question 16

what region of the GI tract is this? [1]
how can you tell? [1]

Answer 16

duodenum [1]
brunners glands [1]

Question 17

label A-E

Answer 17

A = **enterocyte brush border**
B = **lacteal**
C = **goblet cell**
D = **immune cells (lymphocytes)**
E = **lamina propria**

Question 18

name this region of the intestine [1]
how can you tell [1]

Answer 18

jejunum
plicae circularis

Plicae circulares are out foldings of both the mucosa and submucosa. Projecting from these folds are numerous villi that are outfoldings of the mucosa.

Question 19

label A-H of the lymph node

Answer 19

A = afferent lymphatic, B =subcapsular sinus, C = cortex, D = medullary cords, E = medulla, F = efferent lymphatic, G = hilus, H = secondary follicles

Question 20

label A-H of the lymph node

Answer 20

A = afferent lymphatic, B =subcapsular sinus, C = cortex, D = medullary cords, E = medulla, F = efferent lymphatic, G = hilus, H = secondary follicles

Question 21

name this region of the intestine [1]
how can you tell [1]

Answer 21

jejunum
plicae circularis

Plicae circulares are out foldings of both the mucosa and submucosa. Projecting from these folds are numerous villi that are outfoldings of the mucosa.

Question 22

what is the squamocolumnar junction? - chang

Answer 22

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 23

what is the squamocolumnar junction? - chang

Answer 23

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 24

label A-E

Answer 24

A = **enterocyte brush border**
B = **lacteal**
C = **goblet cell**
D = **immune cells (lymphocytes)**
E = **lamina propria**

Question 25

what region of the GI tract is this? [1]
how can you tell? [1]

Answer 25

duodenum [1]
brunners glands [1]

Question 26

Name the cells bordering the lumen [1]

Answer 26

**paneth cell**

Question 32

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

Answer 32

_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 33

what does a lack of cAMP doe regarding glucose release? [1]

Answer 33

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

Question 34

what does a lack of cAMP doe regarding glucose release? [1]

Answer 34

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

Question 35

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 35

**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 36

IgA anti-gliadin, anti-tTG and anti-endomysial\* (EMAs) are produced by which immune cell? [1]

Answer 36

B cells

Question 37

which inflammatory cytokines are associated with CD? IFN-γ TNF-a IL-1 IL-6

Answer 37

which inflammatory cytokines are associated with CD? **IFN-γ** TNF-a IL-1 IL-6

Question 38

which inflammatory cytokines are associated with CD? IFN-γ TNF-a IL-1 IL-6

Answer 38

which inflammatory cytokines are associated with CD? **IFN-γ** TNF-a IL-1 IL-6

Question 39

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

Answer 39

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

Question 40

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

Answer 40

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

Question 41

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

Answer 41

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

Question 42

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

Answer 42

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

Question 43

which inflammatory cytokines are associated with CD? IFN-γ TNF-a IL-1 IL-6

Answer 43

which inflammatory cytokines are associated with CD? **IFN-γ** TNF-a IL-1 IL-6

Question 44

which inflammatory cytokines are associated with CD? IFN-γ TNF-a IL-1 IL-6

Answer 44

which inflammatory cytokines are associated with CD? **IFN-γ** TNF-a IL-1 IL-6

Question 45

IgA anti-gliadin, anti-tTG and anti-endomysial\* (EMAs) are produced by which immune cell? [1]

Answer 45

B cells

Question 46

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 46

**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 47

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

Answer 47

_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 48

describe the structure of the rectus sheath a) above arcuate line b) below arcuate line

Answer 48

* *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 50

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

Answer 50

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 51

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

Answer 51

_glycogen synthase_ is **activated by removing P**, i**nactivated by adding P** _glycogen phosphorylase_ is **activated by adding P,** **inactivated by removing b** therefore work antagonistically !

Question 52

label 1-3

Answer 52

1: posterior belly of digastric muscle 2: mylohyoid muscle (cut) 3: geniohydoid muscle

Question 53

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

Answer 53

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 55

name the three papillae in the tongue which have taste buds (2)

Answer 55

* *- fungiform papillae**: located anteriorly * *- filiform papillae**: loacted centrally * *- circumvallate papillae:** located posteriorly fungiform and circumvallate = taste buds

Question 56

upper oesophageal sphincter is made from which muscle?

Answer 56

EOS: **cricopharnyngeus muscle**

Question 57

for **anterior 2/3 tongue:** which nerve supplies the a) special sensory (taste) b) general sensory (pressure etc) c) motor sensory?

Answer 57

**_anterior 2/3 tongue:_** nerve supplies the a) special sensory (taste): **CN VII - facial nerve** b) general sensory (pressure etc): **CN V - trigeminal nerve (V3, mandibular nerve)** c) motor sensory: **hypoglossal nerve - CN XII** _for **posterior 1/3 tongue:**_ nerve supplies the a) special sensory (taste): **glossopharnyngeal nerve (CN IX)** b) general sensory (pressure etc): **glossopharnyngeal nerve (CN IX)** c) motor sensory: **hypoglossal nerve - CN XII**