MET EOYS3 Flashcards

1
Q

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

A

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
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2
Q

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

why is it more complex in women then men?

A

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

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3
Q

what are two seperate roles of aldosterone? [2

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

(two totally differnet systems! )

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4
Q

which part of the stomach is the dominant pacemaker? [1]

A

corpus

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5
Q
A

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)
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6
Q

what type of hormones are thyroid hormones?

produced from what?

what is active / inactive names?

how does it circulate around body?

A

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

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7
Q

what normally prevents defecation? (2)

A

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
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8
Q

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?

A

hard palate: maxilla & palatine

soft palate: composed of muscles posterior to the hard palate - elevates during swallowing to prevent food entering nasal cavity

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9
Q

main role of thryoid hormones? (1)

how controlled?

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

- 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

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10
Q

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

A
  • 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)
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11
Q

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

A
  • 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)
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12
Q

which hormone is released when have hypocalcemia?

what is it effects? (3)

what is 1. inhibited by?

A
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13
Q

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

A
  1. bile duct
  2. hepatic artery proper
  3. hepatic portal vein
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14
Q

* what is the net gain / loss of ATP during: *

a) glycolysis?
b) TCA cycle?
c) cori cycle?

A

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

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15
Q

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?

A
  • *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 !!)
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16
Q

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?

A

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)
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17
Q

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

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

A

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)

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18
Q

the cori cycle spares pyruvate be ensuring that pyruvate is NOT converted to what?

where is a source of ^ instead?

A

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 !!

19
Q

gluconeogensis from glycerol:

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

A
  • 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)
20
Q

Q

specifically, how is gluconeogensis controlled by:

  • insulin?
  • glucagon?
  • adrenaline?

(.i.e. which enzymes blocked etc)

A
  • *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
21
Q

Q

specifically, how is gluconeogensis controlled by:

  • insulin?
  • glucagon?
  • adrenaline?

(.i.e. which enzymes blocked etc)

A
  • *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
22
Q

gluconeogensis from glycerol:

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

A
  • 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)
23
Q

the cori cycle spares pyruvate be ensuring that pyruvate is NOT converted to what?

where is a source of ^ instead?

A

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 !!

24
Q

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

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

A

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)

25
Q

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?

A

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)
26
Q

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?

A
  • *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 !!)
27
Q
A
28
Q

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

A

dorsal mesogastrium forms connections between:

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

29
Q
A
30
Q

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

A

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)

31
Q

which arteries do u find in the greater omentum?

A

= gastroepiploic arteries

32
Q

what is v general overview of role of:

chylmicron
VLDL
IDL
LDL
HDL

A

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

33
Q

which enzyme converts IDLs to LDLs? [1]

what doe LDLs only have on them? [1]

A

which enzyme converts IDLs to LDLs? [1]
hepatic TAG lipsase

what doe LDLs only have on them? [1]
Apo B100

34
Q

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

A
  • 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

35
Q

how can ur body create cholesterol? (which enzyme)

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

A

- 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**
36
Q

how can ur body create cholesterol? (which enzyme)

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

A

- 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**
37
Q

explain mech. of HDLs reducing body cholesterol

A
  1. 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)
38
Q

explain the two ways statins reduce blood chol levels

A
  • 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]
39
Q

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

A
  • Low-density lipoproteins contain B-100 proteins
  • HDL particles contain mostly A-I and A-II proteins. high protein content, low fat cotent
40
Q

which vitamins can be stored? how? where?1

A
  • *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)
41
Q

why is commensal bacteria gut overgrowth clinically significant regarding vitamins?

A

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

overgrowth: likely to have B12 deficiency & high B9

42
Q

what are the clinical features of deficiences in

vitamin A

vitamin D

vitamin E

vitamin K

(fat soluble vitamins)

A

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

43
Q

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

A

biological activity:

  • *i) increases gut Ca2+ absorption
    ii) increases bone calcification
    iii) increases reabsorbtion of calcium**