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Metabolism > :)) > Flashcards

:)) Flashcards

1
Q

* What is the rate controlling step of glycolysis? What factors regulate it’s function. [3] *

A

Fructose-6-phosphate to Fructose-1,6-bisphosphate via the enzyme Phosphofructokinase-1.

Is regulated by:

1.ATP:AMP ratio
2.Citrate (decreases activity)
3.Fructose-2,6-bisphosphate (increased activity)

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2
Q

where does bile enter the dudeonum? which part of the duodenum?

A

at the Ampulla of Vater: 2nd part of duodenum

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3
Q

what are th 5 pancreatic enyzmes made?

A
  • Procarboxypeptidase
  • Trypsinogen
  • Chymotripsinogen
  • Amylase
  • Lipase
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4
Q

which cells release pepisogen?
how is it activated?

A

Chief cells (1) release pepsinogen –> activated to pepsin using hydrochloric acid released from parietal cells!!

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5
Q

explain how trypsin is activated (and from what?) and what it does subsequently to activation (2)

A
  • Trypsinogen from pancreas converted to trypsin via enterokinase (a brush border enzyme)
  • Trypsin then activates chymotrypsinogen to chymotrypsin and procarboxypeptidase to carboxypeptidase
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6
Q
A

pink = parietal !!

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7
Q

Vitamin B12 - absorbed where?

which population needs supplementts/

A
  • Complexed with intrinsic factor in stomach
  • Absorbed in terminal ileum!!
  • Vegans need to be supplemented with vitamin B12
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8
Q

name two genes that cause dissacaride deficiences and what they cause a deficiency in?

what happens as a result?

A
  • Mutation in the gene encoding for lactase: known as LCT
  • Mutation in the gene encoding for SGLT1 co-transporter (known as SLC5A1)

Consequence of both is osmotic diarrhea due to the fermentation of the unprocessed sugars by gut flora

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9
Q

which cells transport gut antigens from lumen across epithelium?

A

M cells (microfold cells) transport gut antigens from the lumen across epithelium into the tissue.

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10
Q

Gut honing mechanism:

dendritic cells create WHAT in the gut? - what does this cause gut homing T cells to make? (2)

A
  • dendritic cells produce retinoic acid (vitamin A) which induce gut homing T cells to express α4β7 and CCR9.
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11
Q

gut honing mechanism:

what do epithelial cells lining the gut home T cells by expressing? (2)

A

Epithelial cells lining gut home T cells by expression of CCL25 (ligand for CCR9) while endothelial cells express MadCAM (ligand for α4β7).

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12
Q

IgA:
how much is secreted per day?

(what residue does it have?)

A
  • > 3g of secretory IgA per day
  • 18 amino acid C-region tailpiece with cysteine residue required for polymerisation
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13
Q

what can lack of B12 cause?

A

pernicious anaemia

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14
Q

what resists being broken down in CD?

what type of MHCs do CD patients have/

A

gliadin !!! pls remember

HLA-DQ2 or HLA-DQ8

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15
Q

as a result of CD, CD4 cells are activated in the gut.
what do they cause to be released? (5)

A

•macrophages present gliadin via MHC to CD4 T cells:

CD$ cause the release of inflammatory cytokines like IFN-γ which destroys epithelia of small intestine

  • CD4 T cells also activate B cells to produce IgA anti-gliadin, anti-tTG and anti-endomysial* (EMAs)
  • CD4 T cells also recruit CD8 T cells which further destroys epithelia of small intestine
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16
Q

what does deficiency in B1 cause a subsequent a deficency in? [1]

A
  • Pathology from VitB1 deficiency = B1 used as a cofactor to produce actetyl co-A from pyruvate. inability for cells to produce Acetyl CoA
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17
Q

acetyl co-A is the input for TCA. acetyl co-A can be produced by three ways. What are they?

A

1.Glycolysis of glucose to pyruvate
•Converted to acetyl-CoA using pyruvate dehydrogenase complex (PDC)
•Produces 2 reduced NAD molecules per glucose
•1 reduced NAD per pyruvate

2.Transamination of glucogenic amino acids to pyruvate
• Converted to acetyl-CoA using pyruvate dehydrogenase complex (PDC)

3.Beta-oxidation of fatty acids directly to acetyl-CoA
•Produces 1 NADH and 1 FADH2 per acetyl-CoA

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18
Q

what do chief cells secrete? [1]
what do chief cells secrete in children? [1]

A

Chief cells:

  • secrete: pepsinogen (–> pepsin by gastric acid)
  • in children: also secret chymosin (rennin) ->a protease that helps coagulate milk allowing it to be retained more longer in the stomach
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19
Q
A
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20
Q

describe the structure of the rectus sheath

a) above arcuate line
b) below arcuate line

A
  • *rectus sheath:**
  • surrounds rectus abdominis muscle
  • made from: aponeuroses of external oblique, internal oblique and transverse abdominis
  • structure:
  • *a) above arcuate line**
    i) external oblique aponeuroses runs anterior to rectus abdmonis & inserts into the midline: forms linea alba
    ii) i_nternal oblique aponeuroses splits in half_: half goes anterior of rectus abdominis, other half goes posterior. again insets onto linea alba
    iii) transversus abdominis runs posterior to rectus abdominis
    iv) transversalid fascia runs posterior to rectus abdominis
  • *b) below arcuate line:**
    i) all of aponeuroses run anterior to rectus abdominis
    ii) transveralis fascia runs posterior to rectus abdominis
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21
Q

what is the blood supply to the abdominal wall like? (3) where from?

A

internal thoracic artery –> superior epigastric artery
external iliac artery –> inferior epigastric artery
lower intercost and lumbar arteries - blood to lateral aspect of ab wall.

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22
Q

what two anatomical features are found under the inguinal ligament? [2]

A
  • under inguinal ligament:
    a) passageway for the femoral artery, vein and nerve pass & enter thigh.
    b) spermatic cord:
  • femoral artery and vein are below inguinal ligament
  • spermatic cord goes through the abdominal wall and inguinal canal (which is inside inguinal ligament) and towards scrotum
23
Q

what are anatomical differences between jejunum and ileum? (3)

A

jejunum:

  • most absorbtion
  • greater vascularity
  • lots of plicae circularis (folds of mucosa)

ileum:

  • less vasucularity
  • less plicae circularis
  • peyers patches present
24
Q
A
25
Q

colon ha longitudinal muscle separated into 3 bands known as what? [1]

A

Longitudinal muscle separated into 3 bands known as taenai coli

26
Q

where are bile acids absorbed?

A

ileum

27
Q

why is water needed in the digestive system? (4)

A

Hydrolysis reactions of digestion

Facilitation of absorption (brings products of digestion into close proximity to microvilli)

Facilitation of propulsion of gut contents

Combination with mucin granules to make mucus

28
Q

what is the enterohepatic circulation?

A
  • *Enterohepatic circulation: recycling of bile salts**
  • liver: makes bile salts
  • stored in gall bladder
  • goes into duodenum: help digest fats
  • reabsorbed in ileum
  • bulk of bile salts are absorbed in liver
29
Q

** why do vitamins need to be absorbed from the food?

what are two type of vitamins?
how are each absorbed?^
into which system are they absorbed? **

A

vitamins cant be manufactured by body

  1. fat soluble vitamins: A, D, E & K
    - absorbed with lipids: readily dissolve in lipid droplets, micelles and chylomicrons
    - absorbed into lymph fluid
  2. water soluble vitamins: B & C
    - follow flux of water (B&C)
    - absorbed into portal vein
30
Q

which 3 antibodies in the body is a sign of CD?

A

antigliadin
tissue transgluataminase
antiendomyisial

31
Q

what isoform do CD patients have?

A
  • (95% of CD) have isoform of DQ2 or DQ9 of human leukocyte antigen (HLA) HLA-DQ protein
  • due to HLA-DQ, get high levels of antibodies: antigliadin, tissue transgluataminase, antiendomyisial
32
Q

what do mutations in:

  • LCT gene
  • SLC5A1 gene

cause?

A

mutation in gene LCT - affects mucosal phase of dissachardide absorption. lactose intolerance

gene SLC5A1 - encodes for Sodium dependent GLucose tranpsorter one: SGLT1. so mutation causes glucose-galactose malabsorption. again: mucosal phase

33
Q

what is the name for primer used in glycogen synthesis?

A

glycogenin

34
Q

Q

  1. in muscle - how can glucose-6-phosphate produce ATP (aerobically and anaerobically?
  2. why does muscle not have a role in raising blood glucose levels?
A

in muscle, glucose-6-phosphate can produce ATP:
- aerobically (via Acetyl coA, krebs cycle & oxidative phosphorylation) - b (via lactate)

  • free glucose cannot be produced / released from skeletal muscle bc it doesnt have glucose-6-phosphatase (to convert G6P -> glucose)
35
Q

Q

what is glycogen breakdown aka?
explain how this occurs (4)

A

glycogenolysis:

1. debranching enzyme: breaks down the a-1,6 glycosidic bonds (the branches of glucose)
2. glycogen phosphorylase: breaks down a-1,4 glycosidic bonds: free G1Ps
3. phosphoglucomutase: converts G1P to G6P
4. in the liver: glucose-6-phosphatase removes the P group = free glucose
(but step 4 does not occur in the muscle - instead, it is immediately used in glycolysis)

36
Q

when is insulin / glucagon released?

what do insulin and glucacon to do: & how?

a) glycogen synthase
b) glycogen phosphorylase

* key - learn this *

A

insulin: released after meal. insulin works via protein phosphatase (removes Ps):
- activates glycogen synthase - by removing P
- inhibits glycogen phosphorylase - by removing P

glucagon & adrenaline: released between meals / when fasting: works via cAMP, protein kinase A and phosphorylase kinase: adds P
- inhibits glycogen synthase - adds P
_- activates glycogen phosphorylas_e - adds P

37
Q

what is the mechanism of adrenaline, glucagon and calcium activating glycogen -> glucose

A
  • *- adrenaline, glucagon and calcium activate adenylate cyclase**
  • adenylate cyclase causes: ATP –> cAMP
  • cAMP inhbits glycogen synthase by phosphorylasing it AND cAMP promotes phosphorylation of phosphorylase kinase
  • phosphorylase kinase promotes phosphorylation of glycogen phosphorylase
  • glycogen phosphorylase breaks down glycogen into glucose
38
Q

glycogen production and breakdown is carried out by which hormone signalling molecules (4) and which do they act on - liver or muscle?

A
  1. insulin: muscle and liver - builds glycogen stores
  2. glucagon: only liver - breaks down glyocgen stores to release glucose
  3. adrenaline: muscles via a & b adrergic receptors - release glucose

4 calcium: muscles via a & b adrergic receptors - release glucose

39
Q

Q

whats the MoA of insulin

  • activating phosphodiesterase?
  • activating protein phosphastase?
A

1. - insulin activates phosphodiesterase
- phosphodiesterase breaks down cAMP -> AMP
- this means protein kinase A is not activated
- this means that glycogen synthase is not phosphorylated andswitched off
- glycogen synthase: glucose -> glycogen
AND
- phosphorlase kinase is not active: glycogen phosphorylase not activated = glycogen break down inhibited

2. insuline activates protein phosphatase -> downstream consequences also: - glycogen synthase: glucose -> glycogen

40
Q

* why doesnt glucagon work on liver, not muscle ? *

A

muscle doesnt have glucagon receptors

41
Q

what is the effect of a lack of cAMP?

A

lack of cAMP causes glucagon and adrenaline effects to be stopped (and less glucose released)

42
Q

in the production / break down of glucagon, glycogen synthase and glycogen phosphorylase are made active / inactive by the addition of what?

A

glycogen synthase is activated by removing P, inactivated by adding P

glycogen phosphorylase is activated by adding P, inactivated by removing b

therefore work antagonistically !

43
Q

what is von Gierkes disease?

A

deficiency in glucose-6-phosphastase: means liver cant produce glucose via glycogen breakdown.

44
Q

Mc Ardle’s disease:

A

Mc Ardle’s disease:

autosomal recessive disease

caused by: deficiency in glycogen phosophorylase gene: PYGM. cant breakdown glycogen in the muscle = muscle weakness

when exercise: can only exercise in short bursts, otherwise muscles will cramp, lock and they will fall over in intense pain. This is due to their muscles running out of energy.

second wind: muscles use alternative fuel to glucose

45
Q

what is Her’s disease caused by? & treatment?

A

Her’s disease:

caused by: deficiency in glycogen phosphorylase in liver = severe problems maintaining their blood glucose

Treatment: regular, often feeding. This is because they cannot maintain their blood glucose like we can

46
Q

what are the two pathways that insulin causes glycogen synthase to be activated and cause glucose -> glycogen?

A

insulin:

  • *- activates phosphodiesterase
  • activates protein phosphastase**

which are two different pathways that both end up in the glucose –> glycogen

47
Q 
intrinsic innervation (communication within the gut) anatomy:
what are the 4 layers of the gut wall?
what are their functions?
A

gut wall layers & roles

  • mucosa: epithelial cells - contain and secrete hormones. highly innervated with neurons
    above the mucosa:
    - longitudinal muscle & circular muscle: both important for srretch: peristalsis & expelling of faecal matte
    - myenteric plexi: primarily focused on contraction and relaxtion of peri
    - submucosal plexi: involved in regulating absorbtion and secretion of nutrients
48
Q

extrinisc innervation of the GI tract:

  • which nerve controls communication between gut and CNS?
  • after enetering the brain stem, where does & synapse?
A

extrinsic innervation - vagus nerve mediates communication gut and CNS

  • has central terminals that enter brain stem and synapse to neurons of nucleus tractus solitarus
49
Q

where is the largest microbial colony found in GI?

A
  • largest microbial colony: colon
50
Q

Q

faecal microbiota transfer:

a) aim?
b) who are donors?
c) results in? (2)
d) approved for treatment of what infection?

A
  • *faecal microbiota transfer:**
    a) aim: increase microbial diveristy
    b) who are donors: healthy relative, super donors
    c) results in: obesity phenotype reversed - due to transfer of facees rfom fit healthy to obese
    d) approved for: treatment of C. difficile infection
51
Q

gastroparesis:

  • caused by?
  • symptoms?
  • which disease is it associated with?
  • what can it lead to?
A
  • caused by: delayed gastric emptying
  • inability to remove stomach content causes: nausea, vomiting, feeling of fullness, pain and bloating
  • associated with diabetes: diabetic gastroparesis
  • subsquently can lead to malnutrition (bc people dont eat) and changes in blood sug
52
Q

inflammatory bowel disease:
collective term that refers to chronic inflammation of the lower GIT.
which two diseases main?

A

inflammatory bowel disease:
collective term that refers to chronic inflammation of the lower GIT.
a) Crohns Disease
b) Ulcerative colitis

53
Q

Clostridium difficile:

a) associated / caused by what?
b) results in what symptoms? (2)
c) treatment? (3)

A

Clostridium difficile:

a) associated / caused by: broad spectrum antiobiotic usage - opportunistic overgrowth
b) results in: watery diarrhoea & abdominal pain
c) treatment: stop antibiotic use, vancomycin, fecal microbiota transfer

54
Q

link between gut and brain:
what two things have been shown to be altered in brain as a result of altered gut microbiota?

A
  • activity of macrophages / microglia within brain
  • development and plasticity in brain (leads to ageing)

Metabolism (35 decks)

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