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Question 1

during fetal develop, the foregut, midgut and hindgut develop from what?

Answer 1

foregut: perotineum develops from ventral mesogastrium & dorsal mesogastrium:
i) the liver develops within the ventral mesogastrium. it exapnds
ii) dorsal mesogastrium: spleen develops in it,

get shift from

midgut & hindgut develop from dorsal mesogastrium

Question 2

Answer 2

Question 3

the dorsal mesogastrium forms connections between which structures? [2]

Answer 3

dorsal mesogastrium forms connections between:

stomach & spleen [1]
spleen and posterior ab. wall [1]

Question 4

which three strucutres do you find in the free border of the lesser omentum?

Answer 4

1. bile duct
2. hepatic artery proper
3. hepatic portal vein

Question 5

which arteries do u find in the greater omentum?

Answer 5

= gastroepiploic arteries

Question 6

where do u find the potential spaces in body? [2]

Answer 6

• *subphrenic recesses:**
• divided into L&R by falciform ligament
• *subhepatic recesses:**
• lesser sac on L
• hepatorenal recesss / pouch of morrison on the R

Question 7

Answer 7

Question 8

Q

whats the difference between primary or secondary strucutres?
give e.g.s

Answer 8

primary retroperitoneal srtuctures:
develop along posterior peritoneal wall & stay !
-great vessesl
- kidneys
- ureter
- lower rectum / anal canal

secondary retriperitoneal structures:
develop intrapetrioneally but move retro
- pancreas
- distal parts of duo
- upper rectum

Question 9

what is v general overview of role of:

chylmicron
VLDL
IDL
LDL
HDL

Answer 9

• *chylomicron**: fat transport from GI tract –> rest of body
• *very low density lipo:** (similar to chylomicrons) fat transport -> rest of body. VLDL produced in the liver
• *intermediate DL**: left over chylomicrons –> become either LDL or VLDL

LDL: deliver cholesterol to cells

HDL; pick up excess cholesterol and send back to liver

Question 10

what is the function of lipoprotein lipase?
what activates lipoprotein lipase?

where is lipoprotein lipase most active:

a) during periods of starvation?
b) after a meal

Answer 10

lipoprotein lipase: breaks down fats from inside lipoproteins and carries them into the cells

activated by: Apo C2

where is lipoprotein lipase most active:

a) during periods of starvation: muscle (where FA being used for energy in TCA)
b) after a meal: adipose cells (to form fat)

Question 11

what is the function of low density liporpotein?
where AND how made? (which enzyme)

Answer 11

low density lipoprotein:

• function: deliver cholesterol to peripheral cells of the body
• produced @: liver
• formed by: remains of VLDLS after distribiting most of triglycerides. causes them to be more dense = IDLS. hepatic TAG ligase converts IDL to cholesterol rich LDL, having only Apo B100

Question 12

what is familial hypercholeserolemia ? caused by mutation of which 3 genes?

Answer 12

• autosomal dom disease. mutation of one of three genes:

i) LDLR - receptor for receptor mediated endocytosis
ii) PCSK9: kinase that controls recyclingof LDLRs
iii) APOB: gene for ApoB which binds to LDL

= causes increased levels of cicrulating blood LDL bc not taken up into cells. increases chance of CHD.
causes heart attacks even in children

Question 13

how can ur body create cholesterol? (which enzyme)

how does high cholesterol induce negative feedback of cholesetol production? (3)

Answer 13

- acetyl co-A –> cholesterol (via enzyme HMG-coA reductase)

high cholesterol induces negative feedback of cholesetol production

• *- reduces expression of HMG co-A reductase
• reduced gene expression of LDL (which brings the cholesterol)
• XS stored as cholesterol esters**

Question 14

explain how having high LDLs leads to the formation of plaque formation & atherosclerosis

Answer 14

• high LDLs stay in blood system become damaged due to ROSs
• damaged LDLs get taken up by macrophages
• but bc there isnt anything really to kill - theyre just cholesterol: macrophages become foam cells (filled with chol)
• foam cells stick to walls of capillaries - fatty streaks -> fatty plaques -> atherosclerosis

Question 15

explain mech. of HDLs reducing body cholesterol

Answer 15

2. reverse transport pathway:
   i) ApoA1 released by liver -> goes around body and picks up cholesterols from other cells through ABCA1 / G1 receptors
   ii) changes the cholesterol -> cholesterol esters
   iii) goes back to liver
   iv) HDL transfers XS cholesterol ester to liver by binding to scavenger receptors (SR-B1)

Question 16

explain the two ways statins reduce blood chol levels

Answer 16

• statins block the activity of HMG-Co A reductase. so less cholesterol is made [1]
  causes more LDL receptors to be made & take in MORE LDLs -> reducing blood LDLs [1]

Question 17

which lipoprotein carries fats from the liver to peripheral cells?

chylomicron
very low density lipo
intermediate DL
LDL
HDL

Answer 17

which lipoprotein carries fats from the liver to peripheral cells?

chylomicron
very low density lipo
intermediate DL
LDL
HDL

Question 18

name two differences in the structure of HDLs & LDLs [2]

Answer 18

name two differences in the structure of HDLs & LDLs [2]

• Low-density lipoproteins contain **B-100 proteins
• HDL particles contain mostlyA-I and A-II proteins. high protein content, low fat cotent**

Question 19

sources of endogenous reactive species? [3]

Answer 19

endogenous sources: mito, peroxisomes, ER

Question 20

which micronutrient is important in imprinting home to the gut mucosa from peyers patches?

how does it occur (2)

Answer 20

vitmain A: precursor for retinoic acid !

• gut dendritic cells use retinoic acid to inform the niave T cells
• causes niave T cells to change transcription to express CCR9 & a4B& to do gut honing

Question 21

which population are micronutrients most important in?
WHY? (3)

Answer 21

most important in paediatric population: (body growth & development; energy supply; healthy infants have 3x energy per kg body weights than adults)

Question 22

which vitamins can be stored? how? where?

Answer 22

• *fat soluble: A D E K -**> can be stored in liver (but can be toxic in XS)
• absorbed with fats (readily absorb in micelles & chylomicrons)

Question 23

why is commensal bacteria gut overgrowth clinically significant regarding vitamins?

Answer 23

commensal bacteria: providers AND consumers of B vitamins & vitamin K.

overgrowth: likely to have B12 deficiency & high B9

Question 24

what are the clinical features of deficiences in

vitamin A

vitamin D

vitamin E

vitamin K

(fat soluble vitamins)

Answer 24

vitamin A: eyes -> xeropthalmia (Xerophthalmia refers to the spectrum of ocular disease caused by severe Vitamin A deficiency (VAD))

vitamin D: rickets (in adults = osteomalacia)

vitamin E: peripheral neuropathy

vitamin K: coagulopathy

Question 25

what are the clinical features of deficiences in - vit c - B1 - B2 - B3 - B4 - B6 - B12 - folate?

Answer 25

- vit c: scurvy - B1: beri beri - B2: angular stomatitis - B3: pellagra - B4: anemia - B6: anemia - B12: anemia (but also lots of neurological disorders) - folate: anemia

Question 26

what is the biological activity of vitamin D? [3]

Answer 26

biological activity: * *i) increases gut Ca2+ absorption ii) increases bone calcification iii) increases reabsorbtion of calcium**

Question 27

iron metabolism: - absorbed where in GI? - function in the body? (2) - stored where (2) and as what (1)?

Answer 27

iron metabolism: - absorbed where in GI: **duodenum (and proximal jejunum)** - function in the body: **oxygen transport with Hb (1) myoglobin function in skeletal muscle** - stored: **liver (1) & macrophages (1) as ferratin (1)**

Question 28

what two important things does niacin (B3) create? [2] roles?

Answer 28

**- forms: NAD & NADP** -\> imporant hydrogen acceptors. when reduced forms: hydrogen donors

Question 29

\* if the diet is deficinet in niacin (B3), cells can manufacture it from WHAT? \*

Answer 29

**trpytophan**

Question 30

what are vegans likely to be deficient in? (2)

Answer 30

``` vitamin D: (oily fish, dairy products) vitamin B12 (meat and dairy food) ```

Question 31

the spleen is the site of ? (2) is it intraperitoneal / retroperiotneal? why is the answer clincally significant?

Answer 31

``` lymphocyte proliferation (1) rbc filtration, destruction and storage (1) ``` spleen is intraperitoneal. able to move around. means that during blunt trauma to peritoneum, can be torn away from the splenic artery and cause internal bleeding

Question 32

Answer 32

A: coeliac trunk B: splenic artery C: hepatic artery proper D: gastroduodenal

Question 33

describe the branches of the SMA (6)

Answer 33

1. inferior pancreaticoduedenal artery 2. jejnunal and ileal branches 3 middle colic artery 4. right colic artery 5. ileocolic artery -\> appendicular artery

Question 34

describe pathway of common hepatic artery --\> hepatic artery proper ---\> ?? :)

Answer 34

common hepatic artery: branches into - gastroduodenal artery, which branches to give right gastroepiploic artery - which anastamoses with left gastroepiploic artery. - right gastric artery (goes to less curvature of stomach). anastamoes with left gastric artery after these two: becomes the hepatic artery proper; branches into: - right hepatic artery --\> cystic artery (gall bladder) - left hepatic artery

Question 35

Answer 35

A: jenunal B: superior mesentric C ileocolic

Question 36

what are the 3 branches of the IMA? what connects the SMA & IMA?

Answer 36

inferior mesenteric artery branches: - left colic artery - sigmoidal artery - superior rectal artery - SMA & IMA connected by marginal artery

Question 37

Answer 37

Question 38

Answer 38

Question 39

Answer 39

Question 40

Answer 40

Question 41

rectal blood supply: rectum gets supply from which 3 main arteries? where do each of these come from?

Answer 41

- superior rectal artery: from SMA - middle rectal artery: internal iliac artery - inferior rectal artery: from pudendal artery

Question 42

which veins dont go to liver & directly drain into IVC? (4)

Answer 42

- gonadal vein - renal vein - internal iliac vein - external iliac vein

Question 43

what are the 3 locations of the ganglia where splachnic nerves (sympathetic NS) synapse? (ie for foregut ? midgut? hindhut?)

Answer 43

if innervating the: foregut -\> **coelaic ganglia** midgut -\> **superior mesenteric ganglia** hindut -\> **inferior mesenteric ganglia**

Question 44

Answer 44

Question 45

explain the Para and sympathetic nerve supply to the gut. what do they normally do

Answer 45

(motor component (Parasymp and Sym) of autonomic:) sympathetic nerves effect (T1-L2) - pass through sympathetic trunk & synapse in the abdomen = splachnic nerves - inhibits digestion parasym nerves (CN III, VII, IX, X & s2-s4) - vagus nerve runs up to 2/3 transvers colon. after which sacral nerves take over and supply the hindgut: pelvic splachnic nerves - salivation - stimulates digestion - colon motility - urinatin / defecation

Question 46

Answer 46

A: left colic B: sigmoidal C: superior rectal

Question 47

what is transamination? how does it occur? where does it occur mostly? what is the enyzme used for it

Answer 47

**transamination**: transfer of an amino group. new amino acids can be made by using the carbon skeleton of other amino acids and transferreing a new side chain on it _mechanism:_ - **keto acid** / group (a.a but instead of the NH2, is replaced by C double bonded O) swaps with the amine of another amino acid - requires an intermediary**: pyridoxal phosphate (from vitamin B6)** location: liver Enzyme: tranaminase

Question 48

what are glucogenic and ketogenic amino acids?

Answer 48

* *glutogenic**: can be converted to _glucose by gluconeogenesis or enter the TCA_ - can either be transaminated to oxaloacetate or pyruvate (or other intermediates that will form oxaloacetate): - e.g. alanine or glutamate **ketogenic**: can be converted to _ketone bodies, these can feed into the TCA cycle, mostly_ via A-CoA or acetoacetyl-CoA.

Question 49

1how is ammonia produced? how is ammonia excreted from body ? why is it excreted?

Answer 49

- occurs as a reult of **amino acids** underoing **deamination** **reactions** (reactions where you lose amine groups): when amino acids are converted to other molecules, but there arent other molecules to pick up with NH4+ (which is toxic). - r**emove the NH4+ via the urea cycle:**

Question 50

the conversion of the glutamine (a.a) to glutmate and then a-ketoglutarate generates WHAT? why might this conversion occur? why is lots of NH4+ produced?

Answer 50

**_generates free ammonia (as NH4+)_** - **a-ketoglutarate i**s needed for **TCA cycle for energy**. - Glutamine has 2 amino groups, glutmate has 1, a-keto glutarate has 0 - so each step removes/adds an amino group so the **metabolism of glutamine releases a lot of ammonium**.

Question 51

what is glutamine used for? (4)

Answer 51

 Source of **fuel** during **fasting** - especially in muscles and immune cells.  Used for **gluconeogenesis**, esp. in kidney.  Produces **ammonia**, which can act as **buffer for unwanted protons.**  Glutamine has **anti-inflammatory** properties in the **gut**. **Overall: fuel, building block, needed for metabolites: a-ketoglutarate and glutamate.**

Question 52

MoA of urea cycle: a) what is the rate determining step? b) what are the two amino groups required? for it c) what is the key regulating enzyme?

Answer 52

Rate controlling step: **o HCO3- + NH4+ --\> carbamoyl phosphate (via enzyme carbamoyl phosphate synthase 1)** o Requires 2 ATP. o Controlled allosterically by glutamate metabolite: N-acetyl glutamate - this is formed in an excess of glutamate, so drives urea cycle. b) the two amino groups required from: aspartate (1) & ammonia (1) essentially is a shuttle reaction of NH4 into from aspartate and ammonia into urea

Question 53

what does the addition of ApoC2 and ApoE by HDLs do to chylomicrons? [2]

Answer 53

**- ApoC2 added:** allows chylomicrons to give its triglycerides to peripheral cells **- ApoE added: a**llows chylomicron remenant to be taken up by the liver to deliver FA & cholesterol