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physio > Q2: Pancreas > Flashcards

Q2: Pancreas Flashcards

1
Q

what are the storage sites, percent of total body energy content (& calories), and the reservoir capacity of carbs fats and proteins

A

Fat: free fatty acids in circulation, triglycerides in storage. stored in adipose tissue. makes up 77% (143,000 calories) of our energy. about TWO MONTHS worth of energy. primary energy RESERVOIR , energy source during fastss

protein: circulates as amino acids, stored as body proteins. storage in MUSCLE. 22% of energy, 41,000 calories. would die before capacity is used because of structural and functional impairment! but protein is a source of glucose for the brain during a fast, its a last resort to meet other energy needs..

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2
Q

what is the normal range of glucose in the blood

A

70 to 100 mg per 100 ml

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3
Q

when glucose is low what are other sources of energy

A

first, liver glycogen reserve is used (limited storage tho)

  • fatty acid used as an energy source in tissues where glucose is not essential (cant be made into glucose)
  • amino acids are converted to glucose via gluconeogenesis. (glucose supply to the brain from this)
  • lactate: made by incomplete catabolism of glucose via glycolysis and lactate dehydrogenase. converted to glucose by the liver!!
  • glycerol: from triglyceride hydrolysis
  • ketone bodies (acetone, acetoacidic acid, beta hydroxybutyric acid) - produced during glucose sparing times. liver oxidizes fatty acids only to acetyl CoA- in hepatocytes acetyl coa is unable to enter CAC. acetyl CoA is converted into ketone bodies.
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4
Q

in the absorptive/postabsorptive states; describe carbohydrate

A

Absorptive:

  • glucose acts as the major energy source
  • glycogen synthesis and storage occurs
  • excess is converted and stored as triglyceride fat

Postabsoprive state:

  • glycogen degradation and depletion
  • glucose sparing to conserve glucose for the brain
  • production of new glucose through gluconeogenesis
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5
Q

in the absorptive/postabsorptive states; describe fat

A

absorptive:
-triglyceride synthesis and storage

postabsorptive: triglyceride catabolism, fatty acids provide major energy source for non-glucose dependent tissues

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6
Q

in the absorptive/postabsorptive states describe protein

A

absorptive: protein synthesis, excess converted and stored as triglyceride fat

postabsorptive; protein catabolism, amino acids used for gluconeogenesis

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7
Q

what are the major metabolic adaptations to prolonged starvation

(protein?)

A

-decrease protein catabolism (prevention of muscle degradation)
-increase concentration of ketone in blood (inhibits protein degradation in muscle, brain uses ketone bodies instead of glucose)
-gluconeogenesis is reduced
-death from starvation is due to protein wasting (loss of proteins/protein function) not hypoglycemia/ not due to a lack of energy!
brain converts to using ketone bodies instead of glucose,
—>

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8
Q

what do duct cells/acinar cells of pancreas secrete?

A

exocrine cells
-duct; nahco3
acinar; digestive enzymes

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9
Q

what do : alpha, beta, delta, and F (PP) cells secrete

A

alpha; glucagon

beta; insulin,

delta; somatostatin

F cells (PP cells) pancreatic polypeptide

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10
Q

what does somatostatin (GHIH) do from the pancreas?

A
  • inhibitory effect on digestion (reduces rate of digestion and absorption. Its released from D cells in response to increase in blood glucose and amino acids during absorption of meal)
  • regulates pancreatic hormone secretion; decreases insulin , glucagon and somatostatin (dono why)
  • also synthesized by cells lining digestive tract and brain
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11
Q

what is somatostatin synthesized by?

A
  • pancreas (D cells)
  • cells in digestive tract
  • hypothalamus
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12
Q

WHAT ARE THE TWO TYPES of somatostatin and where they are/what they are more potent at doing

A

116 amino acid preprosomatostatin is cleaved into two options :

  • somatostatin-14 : pancreas (100%), brain (90-95%) –> this one is more potent in inhibiting glucagons release!
  • somatostatin-28: digestive tract (70-75%) , more potent in inhibiting GH and insulin release
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13
Q

what is the half life of somatostatin

A

3 minutes

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14
Q

what are the\ endocrine and paractine effects of insulin

A

endocrine: promotes storage of ingested nutrients. decrease blood glucose concentration by promoting glucose uptake from blood by cells for use and storage
paracrine: reduce secretion of glucagon from pancreatic A cells

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15
Q

what is insulin synthesized as and what are the 3 chains in it? how does it make insulin

A

preproinsulin!
-has A, B and C chains and a signal sequence. the signal sequence is removed to make PROINSULIN. proteases then remove the C chain to produce functional insulin, which has A and B chains, connected by a disulfide bride.

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16
Q

which cells require insulin for glucose uptake?

A

myocytes, adipocytes, and hepatocytes. they require insulin dependent receptors to aid function of glucose transporter to bring the glucose into the cytosol. in the pancreas insulin will reduce the secretion of glucagon from A cells.

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17
Q

whats th fasting level of glucose

A

approx 100 mg/dL

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18
Q

what influences islet beta cells

A

(insulin making cells)
-MAJORLY = glucose concentration
-gastrointestinal hormones (incretins) increase insulin
-blood amino acid concentration increases insulin release
parasympathetic stimulation (increased by food intake) increases islet beta cells to make inslun too
-sympathetic simulation and epinephrine INHIBITS insulin secretion by beta cells

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19
Q

what are all the actions of insulin secretion

A
  • decrease glucose in blood
  • decrease fatty acids in blood
  • decrease amino acids in blood
  • increase protein synthesis
  • increase feul storage
20
Q

how does excitation-secretion coupling stimulate insulin (describe how this process works)

A

glucose enters beta cell via GLUT2 (facilitated diffusion- this is an insulin independent receptor)

  • glucose gets converted to glucose6-phosphate , glycolysis and oxidative phosphorylation-> atp!
  • high concentration of ATP then binds to and inactivates ATP sensitive potassium channels. the potassium channel is different from voltage gated on neurons. It is normally open, allowing potassium to leak Out of the beta cell. the amount of flux depends on atp concenrations. so when the ATP is high bc of glucose, the channel closes and decreases flux.
  • next potassium in cytoplasm increases, which depolarizes the cell. depolarization activates the voltage gated calcium channels, and increases calcium flux. Increase in cytoplasmic calcium allows activation of a physiological process- this allows exocytosis of vesicles containing insulin. Insulin secretion from pancreatic beta cells.
21
Q

what anabolism/catabolism occurs in the liver due to insulin??

A

anabolism: increase glucose storage via synthesis of glycogen (glycogenesis)- and increase protein and triglyceride synthesis

catabolism: inhibits the following :
- glycogenolysis (breakdown of glycogen to glucose)
- ketogenesis (conversion of fatty acids and amino acids to keto acids)
- gluconeogenesis (conversion of amino acids to glucose)

22
Q

what type of receptors are on insulin dependent cells

A

tissues that require insulin for glucose uptake (muscle, liver, fat)

  • express insulin dependent GLUT4 transports and insulin receptors.
  • insulin activates the insulin receptors, which activates GLUT4. glucose then can be taken up by GLUT4..
23
Q

what does insulin stimulate in muscles vs liver??

-how do liver vs muscle release energy into the blood?

A

MUSCLE: -promotes protein synthesis and increases amino acid transpor into muscle cells.
-promotes glycogen synthesis: increasing glucose transport into the cell, activity of glycogen synthase (enzyme for glycogenesis).. inhibit activity of glycogen phosphorylase (enzyme for glycogenolysis)

-muscles lack glucose6phosphate-> cant be used to increase blood glucose!

liver cells act similar but stored glycogen in liver will be released as glucose into blood when blood glucose goes down. stored glycogen in muscle cells CANT be released back into the blood!!!! muscle cells lack glucose 6 phosphatase, which turns it back into glucose so it can leave. liver does have it so it can transport glucose out into the blood.

muscles release enegy into the blood n the form of LACTATE. the lactate is used by the liver to make glucose. lactate release from muscles only occurs it he muscle cell has insufficient levels of oxygen for oxidative phosphrylation. in this state glycolysis becomes the major means for atp in the muscle, and then lactates a byproduct!

24
Q

how does insulin impact adipose tissue

A

increase glucose transport into the fat cells.

  • promotes triglyceride storage - enhances the activity of lipoprotein lipase which hydrolyzes triglycerides from circulating lipoproteins!
  • increases alpha glycerol phosphate (which converts fatty acids to triglycerides)
  • inhibits activity of lipase (enzyme for lipolysis of stored triglycerides)
25
Q

what is glucagons major target cell?

A

the liver.. high glucose levels increase insulin, decrease glucagon

26
Q

what are the effects of glucagon

A
  • increase conc of blood glucose
  • increase hepatic glucose production and release. inhibit glycogenesis and stimulate glycogenolysis AND gluconeogenesis
  • increase in blood fatty acids and ketones (promote lipolysis and inhibit triglyceride synthesis. enhance hepatic ketone production)
  • inhibit hepatic protein synthesis (promotes protein catabolism in the liver, no significant effect on blood amino acid)
27
Q

what causes insulin secretion

A

increased blood glucose and increased amino acids in blood

28
Q

what causes glucaon release

A

decreased blood glucose, increased amino acids

29
Q

what effect does glucagon have on blood amino acids and muscle protein?

A

NONE

30
Q

what effect does epinephrine have on blood glucose

A

increase glycogenolysis, increase gluconeogenesis, decrease insulin secretion, increase glucagon secretion

31
Q

what effect does epinephrine have on fatty acids, amino acids, and muscle protein?

A

fatty acids: INCREASE lipolysis (breakdown!)

-no effect on amino acids OR muscle protein!

32
Q

what stimulates epinephrine release/ whats its funciton

A

synpathetic stimulation stress/exercise

function: provide energy for emergencies/exercise

33
Q

what effect on blood glucose, fatty acids, amino acids, and muscle protein does Cortisol have?

A

bloog glucose: increase gluconeogenesis, decrease glucose uptake by tissues other than the brain. glucose sparing!

fatty acids: increase lipolysis

amino acids: increase protein degradation

muscle protein: decrease protein degradation.

34
Q

whats a stimulus for cortisol, and its primary role in metabolism?

A

stimuli is stress

mobilization of metabolic fuels, building blocks during adapting to stress times.

35
Q

what effect on blood glucose, fatty acids, amino acids and muscle protein does growth hormone have?

A

-blood glucose: increases glucose uptake by muscles, glucose sparing action

fatty acids: increases lipolysis

amino acids: decreases uptake

protein: increase synthesis, decrease degredation of protein. and increase synthesis of DNA and RNA

36
Q

what stimulates GH secretion? whats its primary role in metabolism

A

deep sleep, stress, exercise, hypoglycemia = STIMULI for GH secretion

role: promotion of growth, normally a little role in metabolism, mobilization of fuels and glucose sparing (sometimes?)

37
Q

what occurs in type 1/2 diabetes

A

1: lack of insulin secretion at all due to death of pancreatic B cells
2: normal/increased insulin secretion but reduced sensitivity of target cell to insulin

other type is gestational: mother is diabetic but fetus is not. THIS INCREASES risk of geting type 2 diabetes for mom!

38
Q

what type of risks are posed to type 1 and type 2 diabetes (hyper/hypoglycemia)

A

type 1 is at risk for BOTH hypo and hyperglycemia

type 2 is greater risk for hyperglycemia

39
Q

are there oral medications for type 1 diabetes

A

no , they have to take insulin

40
Q

what are polyuria, polydipsia, and polyphagia (& their causes in diabetes)

A

polyuria; excessive urine (caused by osmotic diuresis)
polydipsia; excessive thirst (caused by dehydration from excessive urine/polyuria which is due to so much glucose in the urine)
polyphagia; excessive hunger (caused by glucose deficiency in cells)

41
Q

how does insulin deficiency impact amino acid /repercussions? lipids/ repercussions?

A

amino acids;
=decreases uptake by cells and increases protein degradation. these both cause an increase in amino acids in the blood. protein degradation causes muscle wasting/weight loss.
-an increase in amino acid in the blood causes gluconeogenesis to increase, and this aggravates hyperglycemia (which is already an issue in diabetes) this adds on to the issues like dehydration, hunger

42
Q

what are the repercussions of hyperglycemia with insulin deficiency (pathway to death)

A
  • it causes osmotic diuresis because of excessive glucose in the urine. this causes excessive urination and dehydration. the dehydration causes excessive thirst. but also cell shrinking which causes nervous system malfunctions and death
  • dehydration also causes a decreased blood volume, which causes circulatory failure ->renal failure and low cerebral flow -> death
43
Q

how does diabetes/insulin deficiency impact nourishment of cells

A

brain; fully nourished! doesnt require insulin/Glut4 to uptake glucose.
other cells are starved for energy , including muscles. stimulates hunger (polyphagia)

44
Q

how does glucose reabsorption change in diabetes

A

normally its reabsorbed in the kidneys but the mechanism can be overwhemlded under exterme hyperglycemia so glucose is in urine- this draws out water! osmotic diuresis (polyuria)

45
Q

how does circulatory failure occur in diabetes

A

loss of fluid from excess urine (due to osmotic diuresis) -> dehydration, decreased blood volume and then circulatory failure (nervous system malfunction, low cerebral blood flow. renal failure from inadequate filtration pressure)

46
Q

why does ketosis occur in diabetes and which type more (why)

A

increased fatty acids in the blood, due to lack of insulin .. lipolysis increases and triglyceride synthesis decreases because of insulin..

  • so we have fatty acids from triglyceride stores
  • increased fatty acids- used as alternative energy source by cells.
  • increased use of fatty acids in liver releases ketone bodies.
  • high concentrations of ketone bodies -> ketosis which causes blood pH decrease (metabolic acidosis) this depresses brain activity.. can cause a coma

-

47
Q

why might a diabetic patient have sweet/fruit smellin breath

A

ketosis can cause this

-body tries to lower acetone levels (a ketone) by breathing it out and this is a sweet/fruity smell..

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