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Endocrine - Troutmanm > Pancreas > Flashcards

Pancreas Flashcards

1
Q

The pancreas is a glandular organ with both digestive ______ &______ functions

A

(exocrine) and endocrine

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2
Q

The pancreas is about ___ inches long and rests in the back of the abdomen behind the stomach

A

6

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3
Q

The pancreas secretes insulin and glucagon which are vital in the regulation of ____, _____, and _______ metabolism

A

glucose, lipid, and protein

The pancreas secretes other hormones with lesser and uncertain importance (e.g. amylin, somatostatin, pancreatic polypeptide)

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4
Q

What is the Acini?

A

glands secreting digestive juices into the duodenum

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5
Q

What are the 3 islets of Langerhans?

A

Alpha cells
Beta cells
Delta cells

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6
Q

What do alpha cells secrete?

A

secrete glucagon

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7
Q

What do beta cells secrete

A

secrete insulin

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8
Q

What do delta cells secrete

A

secrete somatostatin and pancreatic polypeptide

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9
Q

Insulin is a hormone associated with energy abundance and

A

storage of this excess energy

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10
Q

Insulin causes carbohydrates to be stored as

A

glycogen in muscle and liver

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11
Q

Insulin causes fat storage in

A

adipose tissue

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12
Q

Insulin causes excess carbohydrates that cannot be converted to glycogen to be

A

converted to fats and are stored in adipose tissue

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13
Q

Insulin promotes uptake of amino acids and

A

conversion to protein

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14
Q

What is insulin stimulated by? (7)

A 
High blood glucose
Amino acids
Beta-keto acids
Glucagon
Acetylcholine, intestinal hormones
Insulin resistance: obesity
Sulfonylurea drugs (glyburide)
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15
Q

What is insulin inhibited by? (4)

A

Low blood glucose
Fasting
Catecholamines (alpha-agonists)
Somatostatin

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16
Q

How is insulin circulating?

A

Circulates almost entirely unbound with plasma half-life of 6 minutes

(Circulates almost entirely unbound with plasma half-life of 6 minutes)

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17
Q

Insulin: highly specific receptor leads to _______. Within seconds, adipose and muscle cells markedly

A

endocytosis

increase their uptake of glucose

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18
Q

T/F: neurons in the brain respond differently to insulin as the rest of the body

A

true

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19
Q

how do neurons in the brain respond to insulin

A

Neurons permeable to glucose

Normal blood glucose required to prevent hypoglycemic shock

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20
Q

With insulin, the cell membrane increases intake of

A

amino acids, potassium and phosphate

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21
Q

Storing glucose for later use is what type of effect?

A

anabolic effect

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22
Q

Anabolic effects increases muscle storage of glucose, fatty acids and amino acids. What 4 things do these do?

A

Increases glycogenesis
Inhibits glycogenolysis
Inhibits gluconeogenesis
Phosphorylates glucose (traps) for use in glycolysis, glycogenesis

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23
Q

anabolic effects of insulin facilitates entry of glucose into cells of all tissues except

A

brain, kidney tubules, intestinal mucosa and RBCs

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24
Q

T/F: an anabolic effects of glucose is that it increases hepatic uptake, storage, and use of glucose

A

true

Liver releases glucose between meals

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25
Q

anabolic metabolism increases ________ and protein synthesis in the liver

A

lipogenesis

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26
Q

Does anabolic metabolism increase or decrease protein synthesis?

A

Increases protein synthesis

Stimulates intracellular amino acid transport, increases translation of mRNA into proteins

Inhibits protein catabolism and depresses gluconeogenesis

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27
Q

Does insulin increases fat synthesis and storage

A

YES

Increases formation of glycerol and fatty acids and the resulting triglycerides

Insulin promotes transport of glucose as well as
Conversion of excess glucose into fatty acids

Inhibits lipolysis enzymes

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28
Q

Des insulin increase protein synthesis and storage

A

YES

Increases amino acid uptake as well as glucose entry

Normally only slightly permeable to glucose, exercise and insulin increase permeability and uptake

Increases glycogenesis and protein synthesis

Used for energy if exercising

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29
Q

*** What is glycogen secreted by? and when does it happen?

A

alpha cells of the islets of Langerhans when the blood glucose falls

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30
Q

Glucagon has effects that ______ the effects of insulin

A

oppose

It increases blood glucose concentration and can cause hyperglycermia

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31
Q

What type of reaction os glucagon?

A

catabolic - generally opposes insulin but stimulates insulin release

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32
Q

info about glucagon

A

Activates enzymes for glycogenolysis

Increases gluconeogenesis

Increases lipolysis and ketogenesis

Inhibits triglyceride storage in liver

Increases proteolysis and flow of amino acids from muscle to liver for gluconeogenesis

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33
Q

What does glucagon enhance?

A

enhances heart strength, increases blood flow in some tissues, enhances bile secretion, and inhibits gastric acid secretion

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34
Q

What is glucagon stimulated by? (5)

A

Fasting hypoglycemia

Amino acids (protein meal)

Beta-adrenergic stimulation

Exercise
Not associated with hypoglycemia, but may be a response to increased circulating amino acids

Cholecystokinin, gastrin and cortisol

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35
Q

What is glucagon inhibited by? (5)

A 
High glucose levels
Somatostatin
Free fatty acids
Ketones
Insulin
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36
Q

For carbohydrate metabolism, what is the anabolic (synthesis) phase?

A

postprandial (after a meal)

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37
Q

During the anabolic phase, when energy intake exceeds sugar requirements, what is energy stored as?

A

glycogen, structural proteins and fat

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38
Q

What is anabolic phase mediated by?

A

insulin

Release begins at 100mg/dl glucose, peaks at 4-600mg/dl

After eating, plasma insulin concentration increases almost 10-fold in 3-5 minutes due to dumping of preformed, stored insulin

Level decreases in 5-10 minutes

At 15 minutes, new insulin
plateau is reached due to more release and synthesis

Shut off is in 3-5 min after level under 80 mg/dl

39
Q

For carbohydrate metabolism, what is the catabolic phase?

A

Fasting

40
Q

During the catabolic phase, how are body needs met?

What is this mediated by?

A

endogenous (internal) sources

glucagon

41
Q

T/F: During the catabolic phase of carbohydrate metabolism, there is a breakdown of glycogen, protein, triglyceride stores for energy supply: glucose, ketones.

A

TRUE

42
Q

Can the brain function on glucose and ketones?

A

YES

43
Q

How long is liver glycogen sufficient for the brain?

At what time does gluconeogenesis uses AAs, glycerol and lactate to make glucose?

A

12-24 hours

24 hrs

44
Q

Amino acids from breakdown of muscle protein are a good source of _____ formation

A

glucose

Muscle wasting significant in first few days of fasting

Gluconeogenesis primarily in liver, some kidney

45
Q

when fasting, days 2-4 Fat stores broken down to free fatty acids for tissues, some glucose, but primarily ____ for brain.

A

ketones

Ketones formed in liver

At this point, most glucose used by CNS, protein loss minimized by fat loss

After weeks, brain uses primarily ketones

Measurable in urine

46
Q

What is the greek word diabetes mean

What mellitus latin for?

A

to pass through, a siphon

honey sweet (Thomas Willis)

47
Q

What is the definition of DM

A

A syndrome of impaired carbohydrate, fat, and protein metabolism caused by either a lack of insulin or a decreased sensitivity of the tissues to insulin

48
Q

T/F: DM is the most common endocrinopathy

A

TRUE

49
Q

What is type 1 DM caused by?

A

caused by lack of insulin secretion

50
Q

What is type 2 DM caused by?

A

caused by decreased sensitivity of target tissues to the metabolic effects of insulin (insulin resistance)

51
Q

how does insulin insufficiency lead to hyperglycemia?

A

decreased cell entry, increased gluconeogenesis, and glucose release from the liver

52
Q

Glucose is reabsorbed by the kidney until about

A

180gm/dl

53
Q

*** What does hyperglycemia lead to?

A

Leads to osmotic diuresis, loss of Na, K, glucosuria

Hypovolemic hypotension, dehydration, POLYURIA, POLYDIPSIA, POLYPHAGIA (increased appetite from hypothalamus ventromedial nucleus)

54
Q

Low insulin leads to _____ catabolism, increased ___ catabolism

A

muscle, fat

Increases the release of keto acids
causes an anion gap metabolic acidosis

55
Q

CNS acute symptoms

A

Polyuria – osmotic diuresis
Polydipsia – intravascular volume depletion
Polyphagia and weight loss – protein catabolism

CNS irritability/confusion – hypertonic ECF leads to cell shrinkage

Visual disturbances

56
Q

how do visual changes happen with diabetes

A

sorbitol formation in lens causes osmotic swelling, glycation leads to opacification

Microvascular disease affects perfusion of retina

Often present in 10-15 years

57
Q

Chronic symptoms of diabetes

A 
Infection
Macrovascular disease (CAD, PAD, AMI, CHF, CVA)
Microvascular disease (nephropathy, retinopathy, neuropathy)
58
Q

How does type 1 DM happen?

A

Destruction of Beta islet cells results in loss of insulin release

(responds well to insulin, just doesn’t have enough)

59
Q

What is DM1 caused by?

A

Caused by viral infections or autoimmune disorders

Heredity plays a role in determining susceptibility of beta cells to insults

60
Q

What is DM 2 caused by?

A

Caused by greatly diminished sensitivity of target tissues to metabolic effects of insulin

61
Q

are high levels of Keto Acids present in type 2

A

not usually

62
Q

which type of DM is more common

A

2

63
Q

How are plasma insulin levels in DM2?

A

Plasma insulin is elevated in type II DM

Levels still insufficient for regulation, beta-cells become exhausted in some patients

64
Q

T/F: most patients with DM are obese

A

true

65
Q

Was was DM historically diagnosed?

A

glucose tolerance test

look at side 24 is you want to read more about this

66
Q

Hgb A1C reflects average glucose over

A

3 months (RBC life span)

67
Q

What is a normal Hbg A1C

A

4-5.6%
(the chart shows less than 6.5% still in the okay range)

The higher the HgbA1C, the higher the risks of developing complications related to diabetes

68
Q

Majority of diabetics develop secondary disease in one of more organ systems. what are they are increased risk of>

A

Increased risk of CAD, HTN, CHF, perioperative MI (often silent), CVA

69
Q

Increased risk of cerebral vascular, peripheral vascular, renal vascular, and microvascular disease with DM patients, what do you need to consider Intraoperative?

A

increased risk of positioning injuries, autonomic neuropathy and hemodynamic instability, gastroparesis and pulmonary aspiration

joints will become stiff resulting in difficult intubation

70
Q

hyperglycemia causes increased

A 
CHF
18x mortality
2x length of stay
greatly increased risk of infection
sepsis
ARF
illness related neuropathy
Increased susceptibility to positioning injuries
CVA
poor fetal outcomes

(look at slide 28 for stats)

71
Q

Perioperative stress may increase serum glucose concentrations (cortisol and catecholamine release). When should glucose be treated?

A

> 200

72
Q

When should diabetes be scheduled for surgery?

A

1st case in the day

73
Q

should oral hypoglycemics be given?

A

No, Oral hypoglycemics are held day of surgery to prevent hypoglycemia until oral intake is restarted

74
Q

T/F:Type I diabetics should continue basal insulin administration to avoid ketoacidosis

A

true

75
Q

In ketoacidosis, DM1, there is profoundly low insulin levels and elevated regulatory hormones (glucagon, cortisol, GH, catechols) that do what?

A

that render insulin ineffective

76
Q

Primary features of DKA

A

Dehydration, acidosis, electrolyte depletion

77
Q

In DKA, Blood glucose rises without effective insulin leading to

A

osmotic diuresis and lyte losses

Dehydration up to 4-6L
Loss of up to 10% body K+
Lesser degrees of Na, Mag, cl, phos losses

78
Q

DKA leads to accelerated protein breakdown that leads to

A

increased liver gluconeogenesis, worsening hyperglycemia

79
Q

DKA leads to Activation of _______ of fatty acids

A

B-oxidation

80
Q

Symptoms of pts in DKA

A

Nausea/Vomiting, polyuria, polydipsia, polyphagia, anorexia, orthostatic changes, Kussmaul breathing, acetone halitosis

(Level of consciousness related to pts osmolality, not acidosis)

81
Q

What are precipitating factors in DKA?

A

MI, trauma, etoh, infection, non-compliance

82
Q

treatment for DKA

A

Massive fluid resuscitation, electrolyte replacement, insulin therapy

Will present with often severe hyperkalemia in face of total body K depletion

83
Q

Nonketotic hypersomolar state

A

in type 2 diabetics

84
Q

primary features of HHNK

A

Severe hyperglycemia, dehydration, severe hyperosmolar state (Na down 1.6/100 glucose) and lack of ketoacidosis

85
Q

symptoms of HHNK

A

Thrombosis from hyperviscosity, focal neuro/reflex signs, global neuro signs, confusion, seizures, coma

86
Q

treatment for HHNK

A

Fluid resuscitation

Add sugar to IVF when BG ~250 to avoid precipitous drop and cerebral edema

K+, phosphate, insulin if needed

87
Q

equation for osmolarity

A

2[Na+] + [Glucose]/18 + [ BUN ]/2.8

88
Q

Hypoglycemia symptoms

A

Profound effects on CNS (confusion, convulsions, coma)

89
Q

hypoglycemia
Early
Late
Very late

A

Early - liver glycogen breakdown
Glucagon response less important early, becomes increasingly important progressively

Late - Sympathetic stimulation, epi release

Very late - GH and cortisol secreted

90
Q

What is insulinoma and how do you treat it?

A

beta cell adenoma

Insulin shock: coma under 20mg/dl

Treat: glucose, (glucagon, epinephrine)

91
Q

hypoglycemic shock happens in what range

A

20-50

92
Q

in hypoglycemic shock, the brain uses glucose if available, what else can it use

A

can use fats/ketones with difficulty in times of stress

93
Q

how to treat hypoglycemia

A

Treat with D50 + infusion of D5

94
Q

Prolonged hypoglycemia leads to

A

brain cell death and apoptosis

Endocrine - Troutmanm (7 decks)

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