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Endocrine - Dr Troutman > Pancreas 1 > Flashcards

Pancreas 1 Flashcards

1
Q

A syndrome of impaired __________, fat, and Protein metabolism caused by either a lack of _________ or a decreased sensitivity of the tissues to _____________. This describes Diabetes

A

Carbohydrate
Insulin
Insulin

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2
Q

What is Type I diabetes?

A

lack of insulin secretion

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3
Q

What is Type II diabetes?

A

decreased sensitivity of the tissues to insulin (insulin resistance)

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4
Q

What does insulin insufficiency lead to?

A

hyperglycemia, increased gluconeogenesis and glucose release from the liver

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5
Q

What are some classic signs of DM (3)?

A

Polyuria - osmotic diuresis
Polydipsia - from volume depletion
Polyphagia w/ weight loss - protein catabolism

**Can also have CNS irratibility/confusion from hypertonic ECF leads to cell shrinkage

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6
Q

Diabetics can have visual disturbances. What is the cause of this?

A

Sorbitol formation in the lens causes osmotic swelling. Glycation leads to opacification.
Often present in 10-15 yrs

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7
Q

Why are diabetics more prone to infections?

A

have decreased PMN phagocytosis

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8
Q

Diabetics are prone to microvascular disease. What can this cause?

A

CAD, PAD, AMI, CHF, CVA

Nephropathy, retinopathy, neuropathy

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9
Q

What is a side effect of the neuropathy caused by DM on the GI system?

A

Delayed gastric emptying

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10
Q

T/F Retinopathy caused by DM is the leading cause of blindness in the US for ages 20-65.

A

True

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11
Q

What are the cells in the liver that create insulin?

A

Beta cells

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12
Q

What is Type II DM highly associated with?

A

Obesity - even obese children can develop this

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13
Q

What test is used to diagnosed DM?

A

Hgb A1C

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14
Q

Do people with DM II have elevated or decreased levels of insulin?

A

Elevated - tissues just don’t respond - insulin resistance

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15
Q

What is a normal Hgb A1C level?

A

4 - 5.6

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16
Q

What are DM pt’s at higher risk of happening during surgery?

A
  • *inability to compensate for changes in volume and vascular tone
  • *post induction hypotension and sudden death
  • *gastroparesis
  • *aspiration
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17
Q

Can diabetics be difficulty to intubate? Why?

A

Yes, joints can become stiff like TMJ, AA, C-spine

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18
Q

What are 3 effects of perioperative glucose control?

A
  1. inhibits lipolysis, elevated FFAs which are associated with cardiac arrythmias
  2. inhibits inflammatory growth factors important in AMI, and general inflammatory responses
  3. leads to favorable alterations in myocardial and skeletal muscle metabolism - leads to improved cardiac contractility and wean from bypass
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19
Q

What does better glycemic control do for Hospital/ICU length of stay?

A

Decreases

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20
Q

What does better glycemic control do for infection rates and wound healing?

A

decreased

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21
Q

What does better glycemic control do for a pt recuperating from MI or Stroke?

A

Improved outcomes

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22
Q

What does better glycemic control do for mortality post cardiac or carotid surgery?

A

decreased

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23
Q

What is the problem with very tight glucose control? At what level should you for sure treat a blood sugar?

A

Hypoglycemia

> 200

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24
Q

When should you plan a diabetic pt’s surgery?

A

first thing in the morning to avoid lengthy fasting times

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25
Q

How long should you hold oral hypoglycemics?

A

At least the day of surgery to prevent hypoglycemia interoperatively.

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26
Q

Should DM pt’s continue taking insulin on day of surgery?

A

yes - at a BASAL level (which may be half or less of their daily requirement). helps avoid ketoacidosis

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27
Q

What pts are susceptible to DKA, type I or II diabetics?

A

Type I, due to profoundly low insulin levels

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28
Q

What are some primary features of DKA?

A

dehydration, acidosis, electrolyte depletion

\

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29
Q

How much fluid volume can a pt with DKA be depleted?

A

4-6 liters

30
Q

Do pts with DKA typically have elevated or decreased potassium?

A

decreased - can lose up to 10% body potassium

31
Q

Symptoms of DKA?

A

N/V, poly (uria, dipsia, phagia), anorexia, orthostatic changes, Kusmaul breathing, acetone halitosis

32
Q

Treatment of DKA?

A
  • Massive fluid resuscitation
  • electrolyte replacement
  • insulin therapy
  • *Will present with severe hyperkalemia even though they’ve lost 10% of total body K+
33
Q

Which pt’s are susceptible to Nonketotic Hyperosmolar state, DM I or DM II? Why?

A

DM II - have enough insulin to prevent ketoacidosis but insulin resistance causes ultra high blood glucose levels

34
Q

What are some primary features of Nonketotic Hyperosmolar state?

A

Severe hyperglycemia
dehydration
severe hyperosmolar state (Na down 1.6/100glucose)
Lack ketoacidosis

35
Q

What is the treatment for Hyperosmolar nonketotic state?

A
  • fluid resuscitation - add sugar to iVF when BG ~ 250 to avoid precipitous drop and cerebral edema.
  • K+, phosphate, insulin (if needed)
36
Q

what is the formula for osmolarity?

A

2(Na) + (Glucose/18 + BUN)/2.8

37
Q

At what glucose levels does one experience hypoglycemic shock?

A

20-50 mg/dl

Treat with D50 and infusion of D5

38
Q

Hypoglycemia can cause CNS effects like confusion, convulsions and coma.

A

True

39
Q

An early response to hypoglycemia is the liver using glucogon to breakdown glycogen stores

A

true

40
Q

A late sign of hypoglycemia is __________stimulation and ________ release.

A

Sympathetic, Epi

41
Q

A VERY late sign of hypoglycemia is the release of growth hormone and ___________.

A

Cortisol

42
Q

The pancreas is a _________ organ with both digestive (exocrine) and endocrine functions.

A

glandular

43
Q

What two hormones does the pancreas secrete that are most vital in the regulation of glucose, lipid, and protein metabolism.

A
  • insulin

- glucagon

44
Q

Other hormones the pancreas secretes other than insulin and glucagon?

A
  • Somatostatin
  • amylin
  • pancreatic polypeptied
45
Q

T/F: Acini are glands that secrete digestive juices into the stomach.

A

FALSE (…..digestive juices into the duodenum)

46
Q

The islet of langerhans has three cells; what are they?

A
  • Alpha cells
  • Beta cells
  • Delta cells
47
Q

What does Alpha cells of the the islet of langerhans secrete?

A

-Secrete glucagon

48
Q

What does Beta cells of the the islet of langerhans secrete?

A

-Secrete insulin

49
Q

What does Delta cells of the the islet of langerhans secrete?

A

-Secrete somatostatin and pancreatic polypeptide

50
Q

T/F: Insulin is a hormone associated with energy abundance and storage of this excess energy.

A

TRUE

51
Q

List the different function insulin has?

A
  • Cause carbohydrates to be stored as glycogen in muscle and liver
  • Causes fat storage in adipose tissue
  • Excess carbohydrates that cannot be converted to glycogen are converted to fats and are stored in adipose tissue
  • Promotes uptake of amino acids and conversion to protein.
52
Q

What stimulates insulin?

A
  • high blood glucose
  • amino acids
  • beta-keto acids
  • glucagon
  • Acetylcholine, intestinal hormones
  • Insulin resistance: obesity
  • Sulfonylurea drugs (Glyburide)
53
Q

What inhibits insulin?

A
  • Low blood glucose
  • Fasting
  • Catecholamines (Alpha antagonist)
  • Somotostatin
54
Q

What is the half life of insulin?

A

6 minutes

55
Q

What does highly specific receptor lead to?

A

endocytosis

56
Q

How do neurons in the brain respond to insulin?

A
  • Permeable to glucose

- Normal blood glucose required to prevent hypoglycemia shock

57
Q

What is the anabolic effect for insulin?

A

Storing glucose for later use

58
Q

What organs does insulin not facilitate entry of glucose into the cell?

A
  • Brain
  • kidney tubules
  • intestinal mucosa and RBC
59
Q

What does insulin do?

A

-Increases glycogenesis

  • inhibits glycogenolysis
  • inhibits gluconeogenesis
60
Q

What does insulin do to the for fat synthesis and storage?

A

Increases formation of glycerol and fatty acids and the resulting

61
Q

What opposes the effects of insulin?

A

Glucagon

62
Q

What does catabolic mean for glucagon?

A

generally opposes insulin but stimulates insulin release

63
Q

What are some points that glucagon does?

A
  • Activates enzymes for glycogenolysis
  • Increases gluconeogenesis
  • Increases lipolysis and ketogenesis
  • Increases proteolysis and flow of amino acids from muscle to liver for gluconeogenesis
  • Enhances heart strength, increase in blood flow, bile secretion, an inhibits gastric
64
Q

What stimulates glucagon?

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

65
Q

What inhibits glucagon?

A
  • High glucose levels
  • Somatostatin
  • Free fatty acids
  • KetonesInsulin
66
Q

Carbohydrates are mediated by insulin at what level does release begin and when does it peaks.

A

:100 mg/dl (begin)

: 400- 600 (when it peaks)

67
Q

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

A

TRue

68
Q

How long until plasma levels decrease after eating and the initial increase in insulin levels?

A

5-10 minutes

69
Q

How long until insulin will be stopped once glucose level reach <80 mg/dL

A

3-5 minutes

70
Q

How long can liver glycogen sustain the brain for?

A

12-24 hours

71
Q

Where does gluconeogenesis happen?

A
  • Liver (primarily)

- Kidney (Some)

Endocrine - Dr Troutman (7 decks)

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