MET EOYS3 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! )
which part of the stomach is the dominant pacemaker? [1]
corpus
human stomach movement:
- random depolarisation of interstitial cells of cajal is communicated to smooth muscle cells, via gap junctions
- slow waves of electrical activity propagte from dominant pacemake in corpus (see photo)
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
what normally prevents defecation? (2)
defecation prevented by:
- Tone of internal anal sphincter & puborectalis
- Mechanical effects of acute anorectal angle. The pubic symphysis and angle act as a mechanical obstruction to defecate moving to the anus.1
the hard palatine is composed of which bones (2)
where is the soft palate in relation to the hard palate?
what does soft palate do when eating?
hard palate: maxilla & palatine
soft palate: composed of muscles posterior to the hard palate - elevates during swallowing to prevent food entering nasal cavity
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)
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 hormone is released when have hypocalcemia?
what is it effects? (3)
what is 1. inhibited by?
which three strucutres do you find in the free border of the lesser omentum?
- bile duct
- hepatic artery proper
- hepatic portal vein
* what is the net gain / loss of ATP during: *
a) glycolysis?
b) TCA cycle?
c) cori cycle?
what is the net gain / loss of ATP during:
a) glycolysis: Net 2 ATP gain via susbtrate level phosphorylation
b) TCA cycle: Net 38 ATP gain via oxidative phosphorylation
c) cori cycle: Net 4 loss . Anaerobic
to make glucose, you need a source of energy and carbon units.
what are 3 sources of carbon that can be used in gluceoneogenesis?
what are 2 sources of energy that can be used in gluceoneogenesis?
- *sources of carbon:**
- lactate (from muscle - glycolysis). exported to liver can be made into pyruvate as a carbon source
- amino acids - from muscle. (from proteolysis) sent to liver & can be made into pyruvate as a carbon source
- glycerol (from lipolysis). sent to liver
- *sources of energy:**
- ATP (from glycolysis and Krebs cycle)
- fatty acids (but cannot be used as C source !!)
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)
the cori cycle spares pyruvate be ensuring that pyruvate is NOT converted to what?
where is a source of ^ instead?
the cori cycle only works if you conserve pyruvate, by removing it from muscle and recycling in the liver. cori cycle has to avoid pyruvate’s conversion to acetyl Co-A
INSTEAD
fatty acid metabolism produces acetyl co-A, creating another source of acetyl co-A & means that cori cycle can go ahead for gluconeogenesis. otherwise the pyrvate from cori cycle would be used to make actetly co-A . good thing !!
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
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
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)
the cori cycle spares pyruvate be ensuring that pyruvate is NOT converted to what?
where is a source of ^ instead?
the cori cycle only works if you conserve pyruvate, by removing it from muscle and recycling in the liver. cori cycle has to avoid pyruvate’s conversion to acetyl Co-A
INSTEAD
fatty acid metabolism produces acetyl co-A, creating another source of acetyl co-A & means that cori cycle can go ahead for gluconeogenesis. otherwise the pyrvate from cori cycle would be used to make actetly co-A . good thing !!
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)
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)
to make glucose, you need a source of energy and carbon units.
what are 3 sources of carbon that can be used in gluceoneogenesis?
what are 2 sources of energy that can be used in gluceoneogenesis?
- *sources of carbon:**
- lactate (from muscle - glycolysis). exported to liver can be made into pyruvate as a carbon source
- amino acids - from muscle. (from proteolysis) sent to liver & can be made into pyruvate as a carbon source
- glycerol (from lipolysis). sent to liver
- *sources of energy:**
- ATP (from glycolysis and Krebs cycle)
- fatty acids (but cannot be used as C source !!)
the dorsal mesogastrium forms connections between which structures? [2]
dorsal mesogastrium forms connections between:
stomach & spleen [1]
spleen and posterior ab. wall [1]
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)
which arteries do u find in the greater omentum?
= gastroepiploic arteries
what is v general overview of role of:
chylmicron
VLDL
IDL
LDL
HDL
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
which enzyme converts IDLs to LDLs? [1]
what doe LDLs only have on them? [1]
which enzyme converts IDLs to LDLs? [1]
hepatic TAG lipsase
what doe LDLs only have on them? [1]
Apo B100
what is familial hypercholeserolemia ? caused by mutation of which 3 genes?
- 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
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**
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**
explain mech. of HDLs reducing body cholesterol
- 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)
explain the two ways statins reduce blood chol levels
- statins block the activity of HMG-Co A reductase. so less cholesterol is made [1]
- more LDL receptors to be made & take in MORE LDLs -> reducing blood LDLs [1]
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
which vitamins can be stored? how? where?1
- *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)
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 are the clinical features of deficiences in
vitamin A
vitamin D
vitamin E
vitamin K
(fat soluble vitamins)
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
what is the biological activity of vitamin D? [3]
biological activity:
- *i) increases gut Ca2+ absorption
ii) increases bone calcification
iii) increases reabsorbtion of calcium**
