METSSS

Question 2

how does peristalsis occur in oesophagius ? (primary / secondary waves?)

Answer 2

peristalsis:

• bolus enters striated muscle, initiates primary peristaltic wave. pressures changes / waves of contraction push bolus down.
• this stimulates stretch receptors = secondary peristaltic wave of smooth muscle (back up secondary wave) pushes the bolus into the stomach

Question 3

how does pit. gland control FSH & LH hormone release?

why is it more complex in women then men?

Answer 3

hypothalamic hormones: GnRH + kisspeptin

regulate release of: FSH and LH from pituitary.

FSH & LH cause sex steroid release (testosterone / oestrogen) , ovulation, spermatogenesis.

in women: estradiol +ve and -ve feedback depends on stage of menstruation

Question 4

what are two seperate roles of aldosterone? [2

Answer 4

1. restores BP, reabsorbed salt & water lvls (not excrete as much)
2. restores K loss !

(two totally differnet systems! )

Question 5

what type of hormones are thyroid hormones?

produced from what?

what is active / inactive names?

how does it circulate around body?

Answer 5

biological amines - produced from tyrosine

T4 (inactive) is produced by thyroid gland -> converted to T3 to be active (via deiodinise enzyme)

circulates as T3, but attached to thryoid binding globulin1

Question 6

main role of thryoid hormones? (1)

how controlled?

• negative feedback - how? (1)
• how else (4)

Answer 6

- increases metabolic rate

• negative feedback control: T3 inhibits pituitary release of TSH

- local control mechanism:

i) deiodinase expression
ii) thyroid hormone uptake transporter expression
iii) thyroid hormone receptor expression
iv) release from thyroid binding globulin

Question 7

how does hypothalamus communicate with the anterior pit. gland? and posterior pit gland?

Answer 7

• hypothalamic hormone binds to anterior pituitary cell target (all are stimulatory except Dopamine which is inhibitory) via portal system
• causes release of anterior pituitary hormone - releaed into blood
• hypothalamus have long axons that cause release of posterior pituitary hormones (ADH and oxytocin)

Question 9

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

Answer 9

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

Question 10

what are the 3 steps of glycolysis that are metabolically irrervisble and need to be side stepped to in order to produce glucose in gluconeogenesis?

Answer 10

3 irreversible steps are in glycolysis:

• *1. Glucose –> glucose-6-phosphate.
  2. P + fructose-6-phosphate –> fructose-1-6-bisphosphate.
  3. pyruvate -> PEP (complicated)**

enyzmes used to reverse ^^ reactions:

1. enzyme = gluocse-6-phosphatase (removes the P)
2. enzyme = fructose, 1,-6-biphosphatase
3. enzyme = (more complicated -> will come to later)

Question 11

Acetyl co-A is a product of of fatty acid break down.

how do high levels of acetyl co-a influence gluconeogenesis?

Answer 11

high levels of Acetyl Co-A:

activates pyruvate carboxylase (used in step 1 of malate cycle: drives gluconeogenesis from pyruuvate -> PEP & eventually glucose)

inhibits: pyruvate dehydrogenase complex (prevents pyruvate being turned into acteyl co A & sparing it, leaving for gluconeogenesis)

Question 12

gluconeogensis from glycerol:

what is glycerol converted to? what does this get converted to?
where? (2)

Answer 12

• glycerol is converted to dihydroxyacetone phosphate only in the liver & kidneys
• dihydroxyacetone phosphate then reacts with glyceraldehyde-3-phosphate to produce fructose-1,6, bisphosphate (and from there .. = fructose-6-phosphate -> glucose-6-phosphate -> glucose)

Question 13

Q

specifically, how is gluconeogensis controlled by:

• insulin?
• glucagon?
• adrenaline?

(.i.e. which enzymes blocked etc)

Answer 13

• *insulin:**
• inhibits gluconeogensis
• insulin dephosphorylates pyruvate dehydrogenase. this makes pyruvate dehydrogenase active & converts pyruvate -> acetyl coA, which enters krebs cycle. pyruvate is therefore not available to be made into glucose
• *glucagon & adrenaline:**
• promotes gluconeogensis
• glucagon increases cAMP levels. this causes pyruvate dehydrogenase to be phosphorlayed (by pyruvate dehydrogenase kinase) & inactive. pyruvate is then available for glucose production

Question 14

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 14

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 15

how can ur body create cholesterol? (which enzyme)

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

Answer 15

- 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 16

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

Answer 16

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

Question 17

why is commensal bacteria gut overgrowth clinically significant regarding vitamins?

Answer 17

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

overgrowth: likely to have B12 deficiency & high B9

Question 18

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

Answer 18

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

Question 19

describe pathway of common hepatic artery –> hepatic artery proper —> ?? :)

Answer 19

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 20

what are the 3 branches of the IMA?

what connects the SMA & IMA?

Answer 20

inferior mesenteric artery branches:

• left colic artery
• sigmoidal artery
• superior rectal artery
• SMA & IMA connected by marginal artery

Question 21

what are the 3 branches of the IMA?

what connects the SMA & IMA?

Answer 21

inferior mesenteric artery branches:

• left colic artery
• sigmoidal artery
• superior rectal artery
• SMA & IMA connected by marginal artery

Question 22

Answer 22

Question 23

Answer 23

Question 24

describe pathway of common hepatic artery –> hepatic artery proper —> ?? :)

Answer 24

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 25

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

Answer 25

• gonadal vein
• renal vein
• internal iliac vein
• external iliac vein

Question 26

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

Answer 26

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

Question 27

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

Answer 27

**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 28

Answer 28

get a fusion of the dorsal mesogastrium & the transverse mescolon !

Question 29

Answer 29

get a fusion of the dorsal mesogastrium & the transverse mescolon !

Question 30

what are glucogenic and ketogenic amino acids?

Answer 30

* *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 31

Answer 31

Question 32

Answer 32

Question 33

what is glutamine used for? (4)

Answer 33

 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 34

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 34

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 35

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

Answer 35

**- 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

Question 36

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

Answer 36

**- 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

Question 37

the mesentary connects which two structures? [2] the greater omentum connects which two structures? [2]

Answer 37

small intestine to the posterior abdominal wall stomach (greater curvature) to transverse colon !!

Question 38

Three main branches of the coeliac trunk?

Answer 38

Left gastric Splenic Common hepatic

Question 39

Three main branches of the coeliac trunk?

Answer 39

Left gastric Splenic Common hepatic

Question 40

the mesentary connects which two structures? [2] the greater omentum connects which two structures? [2]

Answer 40

small intestine to the posterior abdominal wall stomach (greater curvature) to transverse colon !!

Question 41

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 41

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 42

what is glutamine used for? (4)

Answer 42

 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 43

what are glucogenic and ketogenic amino acids?

Answer 43

* *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 44

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

Answer 44

**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 45

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

Answer 45

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