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Semester 4 > case 6 - extra > Flashcards

case 6 - extra Flashcards

1
Q

where does the Kreb’s/citric cylce occur

A

occurs in the matrix of the mitochondrion

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2
Q

what happens in this step and what does this release

A

in this step, the acetyl CoA is degraded into carbon dioxide and hydrogen atoms

the release of hydrogen atoms will be used later

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3
Q

describe the steps 1-6 of what happens next

A

Acetate is offloaded from CoA and joins with Oxaloacetate to form citrate.

Citrate is decarboxlyated and dehydrogenated to form a 5C compound.
The hydrogen atoms are accepted by NAD, which take them to the Electron Transport Chain
The Carboxyl group becomes CO2.

The 5C compound is decarboxylated and dehydrogenated to form a 4C compound.

The 4C compound is changed into another 4C compound, and a molecule of ATP is phosphorylated.

The second 4C compound is changed into a third 4C compound and a pair of hydrogen atoms are removed, reducing FAD.

The third 4C compound is further dehydrogenated to regenerate oxaloacetate.

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4
Q

what is entered into the cycle for the net reaction per molecule of glucose

A

2 acetyl-CoA molecules
6 molecules of water

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5
Q

what is released from the cycle

A

4 carbon dioxide molecules
16 hydrogen atoms
2 molecules of coenzyme
2 molecules of ATP are formed (one acetyl CoA molecule = one ATP molecule)
6 NADH

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6
Q

for every molecule of glucose, the first three stages of carbohydrate metabolisms makes:

A

4 molecules of ATP
24 molecules of hydrogen atoms

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7
Q

what enters oxidative phosphorylation

A

20/24 hydrogen atoms that were formed before combine with nicotinamide adenine dinucleotide (NAD+) under the influence of a dehydrogenase enzyme.

This forms NADH and H+, which enter oxidative phosphorylation.

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8
Q

what is the final stage of respiration

A

oxidative phosphorylation

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9
Q

what does oxidative phosphorylation involve

A

electron carriers embedded in the mitochondrial membrane

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10
Q

describe oxidative phosphorylation

A

These membranes are folded into cristae, which increases the surface area for electron carriers and ATP synthase enzymes.

Oxidative phosphorylation is the formation of ATP by the addition of an inorganic phosphate to ADP in the presence of oxygen.

As protons flow through ATPsynthase, they drive the rotation part of the enzyme and join ADP to Pi to make ATP.

The electrons are passed from the final electron carrier to molecular oxygen, which is the final electron acceptor.

Hydrogen ions also join, so oxygen is reduced to water

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11
Q

does anaerobic or aerobic respiration produce a higher yeild

A

anaerobic respiration produces a much lower yield of ATP than aerobic respiration because only glycolysis takes place in anaerobic respiration

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12
Q

what are the 5 steps in carbohydrate metabolism overall

A
  1. glycolysis
  2. link reaction
  3. citric acid cycle
  4. oxidative phosphorylation
  5. The remaining four hydrogen atoms are released by their dehydrogenase. Two ATP molecules are usually released for every two hydrogen atoms oxidized, thus giving a total of 4 more ATP molecules.
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13
Q

what are ketone bodies

A

are an emergency fuel that the liver can produce to preserve glucose.

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14
Q

can the liver use these ketone bodies itself

A

no

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15
Q

what happens during starvation

A

the ability of the liver to oxidise fatty acids released from adipocytes may be limited

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16
Q

features of ketone bodies

A

are highly soluble and unlike lipids can be transported without carriers

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17
Q

what is observed in uncontrolled type I diabetes

A

increased levels of ketone bodies in blood and urine - ketonemia and ketonuria

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18
Q

what does the acidity of ketone bodies do

A

lowers blood pH - ketoacidosis

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19
Q

what do delta cells in the pancreas secrete

A

somatostatin

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20
Q

what do the PP cells of the pancreas do

A

secrete pancreatic polypeptide

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21
Q

what inhibits glucagon secretion

A

insulin

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22
Q

what inhibits insulin secretion

A

amylin

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23
Q

what inhibits the secretion of both insulin and glucagon

A

somatostatin

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24
Q

what are the two things the insulin does in the blood

A

Binds to insulin receptors in target cells.

The remainder is degraded by the enzyme insulinase mainly in the liver, to a lesser extent in the kidneys and muscles, and slightly in most other tissues.

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25
Q

how does insulin initiate its effects on target cells

A

it first binds with and activates a membrane receptor protein

it is the activated receptor, not the insulin that causes the subsequent effects

26
Q

what does the insulin bind to

A

the alpha subunits on the outside of the cell, but because of the linkages with the beta subunits, the portions of the beta subunits protruding into the cell become autophosphorylated

27
Q

what is the insulin receptor an example of

A

an enzyme linked receptor

28
Q

what is required for insulin’s effects to manifest

A

one insulin molecule can only bind to one alpha subunit, therefore two insulin molecules are required for its effects to manifest

29
Q

what does autophosphorylation of the beta subunits of the receptor activate

A

a local tyrosine kinase, which in turn causes phosphorylation of multiple other intracellular enzymes, including a group called insulin-receptor substrates (IRS)

30
Q

what is the net effect of activating IRS

A

is to activate some of these enzymes while inactivating others

31
Q

what does this produce

A

in this way, insulin directs the intracellular metabolic machinery to produce the desired effects on carbohydrate, fat and protein metabolism

32
Q

when do muscles use large amounts of glucose

A

moderate to heavy exercise

during the few hours adter a meal

33
Q

what is the mechanism via which insulin causes glucose uptake into hepatocytes

A

Insulin binds to its receptor on the hepatocytes.

Autophosphorylation of the B subunit occurs.

Tyrosine kinase is activated and intracellular changes happen.

Insulin inactivates ‘glycogen phosphorylase’, the principal enzyme that causes liver glycogen to split into glucose.
This prevents breakdown of the glycogen that has been stored in the liver cells.

Insulin causes enhanced uptake of glucose from the blood by the liver cells.
It does this by increasing the activity of the enzyme ‘glucokinase’, which is one of the enzymes that causes the initial phosphorylation of glucose after it diffuses into the liver cells.
Once phosphorylated, the glucose is temporarily trapped inside the liver cells because phosphorylated glucose cannot diffuse back through the cell membrane.

Insulin also increases the activities of the enzymes that promote glycogen synthesis, including especially ‘glycogen synthase’, which is responsible for polymerization of the monosaccharide units to form the glycogen molecules.

34
Q

what is the net effect of this mechanism

A

is to increase the amount of glycogen in the liver, without it being broke down

35
Q

what does insulin promote the conversion of

A

Insulin promotes the conversion of all this excess glucose into fatty acids.
These fatty acids are subsequently packaged as triglycerides in very-low-density lipoproteins (VLDLs) and transported in this form by way of the blood to the adipose tissue and deposited as fat.

36
Q

what does insulin inhibit gluconeogenesis by

A

Decreasing the quantities and activities of the liver enzymes required for gluconeogenesis.

Decreasing the release of amino acids from muscle and other extrahepatic tissues and in turn the availability of these necessary precursors required for gluconeogenesis.

37
Q

how does insulin promote fat storage in adipose cells

A
  1. insulin inhibits the action of hormone-sensitive lipase
  2. insulin promotes glucose transport through the cell membrane into the fatty cells
38
Q

describe how insulin is required for the storage of protein

A

insulin stimulates transport of many of the amino acids into the cells

insulin increases the translation of messenger RNA, thus forming new proteins

insulin also increases the rate of transcription of selected DNA genetic sequences in the cell nuclei

insulin inhibits the catabolism of proteins

in the liver, insulin depresses the rate of gluconeogenesis

39
Q

in summary what does insulin do for protein metabolism

A

promotes protein formation and prevents the degradation of proteins

40
Q

what does insulin promote glucose as

A

promotes glucose storage as glycogen

insulin lack promotes glycogenolysis

41
Q

what is the rate limiting step in glucose metabolism

A

the glucose is phosphorylated to glucose-6-phosphate by glucokinase

42
Q

what inhibits the exocytosis of insulin

A

somatostatin and norepinephrine (by activating a-adrenergic receptors)

43
Q

what drugs stimulate insulin secretion and how

A

sulfonylurea drugs stimulate insulin secretion by binding to the ATP sensitive potassium channels and blocking their activity

44
Q

what does this result in

A

results in a depolarising effect that triggers insulin secretion, making these drugs very useful in stimulating insulin secretion in patients with type II diabetes

45
Q

what is insulin secretion primarily controlled by

A

controlled by blood glucose concentration

46
Q

what factors stimulate insulin secretion

A

amino acids
incretin hormoones

47
Q

what are the incretin hormones

A

GLP-1 and GIP

48
Q

what is the mechanism of action of GLP-1 and GIP

A

GIP and GLP-1 are secreted by enterocytes into the blood.

The enzyme dipeptydylpeptidase-4 (DDP4) degrades these hormones and makes them inactive.

§But, the degradation isn’t sufficient enough and so majority of these hormones remain active and can therefore pass to the pancreas and exhibit their effects of stimulating insulin secretion and decreasing glucagon secretion.

49
Q

what are the different somatostatin inhibitory effects

A

acts locally within the iselts themselves to supress the secretion of both insulin and glucagon

somatostatin decreases the motility of the stomach and gallbladder

decreases both secretion and absorption in the gastrointestinal tract

50
Q

what is the role of somatostatin

A

is to extend the period of time over which the food nutrients are assimilated into the blood

51
Q

what can viral infections do

A

destroy the beta cells

52
Q

how many of the islet of Langerhans need to be destroyed to develop type I diabetes

A

90%

53
Q

describe insulin resistance

A

This occurs as a compensatory response by the pancreatic beta cells for diminished sensitivity of target tissues to the metabolic effects of insulin (intracellularly) - insulin resistance.
The decrease in insulin sensitivity impairs carbohydrate utilization and storage, raising blood glucose and stimulating a compensatory increase in insulin secretion.

Excess weight gain and obesity lead to development of insulin resistance and impaired glucose metabolism. This is usually a gradual process.

54
Q

what are the main reasons for insulin resistance

A

there are fewer insulin receptors, especially in the skeletal muscle, liver and adipose tossie

Most of the insulin resistance appears to be caused by abnormalities of the intracellular signaling pathways that link receptor activation with multiple cellular effects.
Impaired insulin signaling appears to be closely related to toxic effects of lipid accumulation in tissues (obesity) – TNF-α.
This can also occur as a result of gene mutations then encode dysfunctional intracellular proteins involved in this signaling.

55
Q

what is HbA1c

A

glycated haemoglobin - when Hb in the blood joins with glucose

56
Q

what does HbA1c indicate

A

your glucose levels for the past three months

target is <48mmol/L

57
Q

what are the blood arterial gases in diabetes

A

pO2 - in the state of acidosis, this will deplete
pCO2 - in the state of metabolic acidosis, this will increase greatly to provide respiratory compensation

58
Q

what controls the thirst mechanism

A

the osmoreceptor-ADH feedback system

59
Q

how does this feedback system operate

A

An increase in extracellular fluid osmolarity (increase in plasma sodium concentration) causes osmoreceptor cells, located in the anterior hypothalamus near the supraoptic nuclei, to shrink.

Shrinkage of the osmoreceptor cells causes them to send nerve signals to additional nerve cells in the supraoptic nuclei, which then relay these signals down the stalk of the pituitary gland to the posterior pituitary.

these action potentials conducted to the posterior pituitary stimulate the release of ADH, which is stored in secretory granules (or vesicles) in the nerve endings.

ADH enters the blood stream and is transported to the kidneys, where it increases the water permeability of the late distal tubules, cortical collecting tubules, and medullary collecting ducts.

The increased water permeability in the distal nephron segments causes increased water reabsorption and excretion of a small volume of concentrated urine.

60
Q

what is the result

A

water is conserved in the body while sodium and other solute continue to be excreted in the urine

this causes dilution of the solutes in the extracellular fluid, thereby correcting the initial excessively concentrated extracellular fluid

Semester 4 (80 decks)

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