METSSS Flashcards
how does peristalsis occur in oesophagius ? (primary / secondary waves?)
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
how does pit. gland control FSH & LH hormone release?
why is it more complex in women then men?
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
what are two seperate roles of aldosterone? [2
- restores BP, reabsorbed salt & water lvls (not excrete as much)
- restores K loss !
(two totally differnet systems! )
what type of hormones are thyroid hormones?
produced from what?
what is active / inactive names?
how does it circulate around body?
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
main role of thryoid hormones? (1)
how controlled?
- negative feedback - how? (1)
- how else (4)
- 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
how does hypothalamus communicate with the anterior pit. gland? and posterior pit gland?
- 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)
which three strucutres do you find in the free border of the lesser omentum?
- bile duct
- hepatic artery proper
- hepatic portal vein
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?
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:
- enzyme = gluocse-6-phosphatase (removes the P)
- enzyme = fructose, 1,-6-biphosphatase
- enzyme = (more complicated -> will come to later)
Acetyl co-A is a product of of fatty acid break down.
how do high levels of acetyl co-a influence gluconeogenesis?
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)
gluconeogensis from glycerol:
what is glycerol converted to? what does this get converted to?
where? (2)
- 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)
Q
specifically, how is gluconeogensis controlled by:
- insulin?
- glucagon?
- adrenaline?
(.i.e. which enzymes blocked etc)
- *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
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
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)
how can ur body create cholesterol? (which enzyme)
how does high cholesterol induce negative feedback of cholesetol production? (3)
- 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**
name two differences in the structure of HDLs & LDLs [2]
- Low-density lipoproteins contain B-100 proteins
- HDL particles contain mostly A-I and A-II proteins. high protein content, low fat cotent
why is commensal bacteria gut overgrowth clinically significant regarding vitamins?
commensal bacteria: providers AND consumers of B vitamins & vitamin K.
overgrowth: likely to have B12 deficiency & high B9
what two important things does niacin (B3) create? [2] roles?
- forms: NAD & NADP -> imporant hydrogen acceptors. when reduced forms: hydrogen donors
what are the 3 branches of the IMA?
what connects the SMA & IMA?
inferior mesenteric artery branches:
- left colic artery
- sigmoidal artery
- superior rectal artery
- SMA & IMA connected by marginal artery
what are the 3 branches of the IMA?
what connects the SMA & IMA?
inferior mesenteric artery branches:
- left colic artery
- sigmoidal artery
- superior rectal artery
- SMA & IMA connected by marginal artery
get a fusion of the dorsal mesogastrium & the transverse mescolon !
get a fusion of the dorsal mesogastrium & the transverse mescolon !
