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Endocrine > Pancreas > Flashcards

Pancreas Flashcards

1
Q

Match each pancreatic hormone with the cell type that produces it:

1.) Pancreatic polypeptide
2.) Glucagon
3.) Somatostatin
4.) Insulin

A.) Beta cells
B.) Alpha cells
C.) Delta cells
D.) PP cells

A

Pancreatic peptide: PP cells
Glucagon: Alpha cells
Somatostatin: Delta cells
Insulin: Beta cells

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2
Q

What are Acini glands, and what are they responsible for?

A

-secrete digestive juices into the duodenum

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3
Q

What are Acinar cells?

A

Make up the exocrine portion of the pancreas and accounts for 98% of the gland’s weight.

Gastrointestinal enzymes and bicarb are synthesized in the acinar cells and secreted into the pancreatic ducts to aid in digestion

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4
Q

What do the Islets of Langerhans do?

A

Make up the endocrine portion of the pancreas
-produce hormones that do not enter ducts but secrete directly into capillary blood vessels.

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5
Q

What cell type makes up the largest portion of the islet?

A

Beta cells (60%)

Beta cells also secrete amylin

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6
Q

What is somatostatin?

A

type of inhibitory hormone produced from the hypothalamus that may restrict the rate at which nutrients are absorbed after a meal

Inhibits insulin and glucagon. It also inhibits the splanchnic blood flow, gastric motility and gallbladder contraction.

AKA growth hormone-inhibiting hormone., regulates hormone output from the islet cells.

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7
Q

What does pancreatic polypeptide do?

A

Inhibits pancreas’ exocrine function

inhibits pancreatic exocrine secretion, gallbladder contraction, gastric acid secretion and gastric motility

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8
Q

Define glycogenesis

A

storage of glucose as glycogen in liver and muscle

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9
Q

Define lipogenesis

A

Formation and storage of fat as triglycerides, occurs in adipose tissue

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10
Q

Define gluconeogenesis

A

Formation of glucose from lactate, pyruvate, amino acids, and glycerol.
-important hepatic glucose production mechanism during fasting and starvation

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11
Q

Define Glycogenolysis

A

the breakdown of glycogen into glucose- occurs primarily in the liver

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12
Q

Define Lipolysis

A

the breakdown of stored triglycerides to free fatty acids and glycerol- stimulated by the enzyme hormone-sensitive lipase

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13
Q

Glucagon in high concentrations also causes what?

A

1.) relaxation of bile ducts and promotes bile flow
2.) enhances cardiac contraction

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14
Q

Exocrine hormones are secreted into the ________ for digestion

A

Duodenum

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15
Q

Endocrine hormones are secreted into the ______ _______ for metabolism

A

systemic circulation

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16
Q

What stimulates insulin release from pancreatic beta cells?

A

-High blood glucose (plasma glucose is by far the most important regulator of insulin release from the beta cells)

-amino acids
-beta-keto acids
-acetylcholine (parasympathetic stimulation)
-gastrointestinal hormones
-beta agonists

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17
Q

What inhibits insulin secretion?

A

-Low blood glucose
-fasting (80 mg/dL)
-glucagon
-cortisol
-catecholamines (alpha-agonists)
-growth hormone
-somatostatin

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18
Q

What cells/organs do not need insulin to utilize glucose?

A

BRAIN
-erythrocytes
-retina
-epithelium
-gonads
-liver

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19
Q

Cerebral function generally declines when serum glucose falls below what level?

A

50 mg/dL

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20
Q

What effects on the heart does glucagon produce?

A

-increased myocardial contractility
-increased heart rate
-increased AV conduction

by increasing the intracellular concentration of cAMP. This occurs independently of ANS function

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21
Q

What is the main function of insulin?

A

Insulin is an anabolic hormone that promotes energy storage.

It works in all cells, but especially in the liver, adipose, and muscle beds.

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22
Q

How is insulin eliminated?

A

-Insulinase degrades unused insulin in the liver, with some degraded by the kidneys and muscles

-circulates almost entirely unbound w plasma half-life of 5-7 mins

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23
Q

After a meal, insulin secretion increases and plays a significant role in capturing and storing energy. How is this accomplished?

A

-Increasing glucose permeability in skeletal muscle, live, and fat

-converts carbs to glycogen in the liver and skeletal muscle

-converts excess carbs to fats. These fats can be oxidized if blood sugar becomes low

-Promoting cellular uptake of amino acids, potassium, magnesium and phosphate.

-Encouraging protein synthesis and discouraging protein breakdown

-Stimulating the Na/K-ATPase. (This decreases serum potassium and is why we give insulin and D50 for hyperkalemia)

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24
Q

Describe the insulin receptor:

A

Consists of 2 alpha and 2 beta subunits that are joined together by disulfide bonds.

When insulin binds to the receptor, the beta subunits activate tyrosine kinase, which then activates insulin receptor substrates (IRS). The insulin cascade turns on the GLUT4 transporter, which increases glucose uptake by skeletal muscle and fat.

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25
Q

What does glucagon do?

A

-Hormone of energy release

-glucagon is a catabolic hormone that promotes energy release from adipose tissue and the liver.

-Enhance hepatic glucose output (glycogenolysis and gluconeogenesis)

-it a physiologic antagonist to insulin

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26
Q

How is glucagon eliminated?

A

eliminated by the kidneys and liver and has a half-life of 3-6 minutes

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27
Q

What does glucagon in high concentrations cause?

A

1.) relaxation of bile ducts and promotes bile flow
2.) enhances cardiac contraction

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28
Q

What stimulates glucagon release?

A

-Hypoglycemia
-amino acids
-beta-adrenergic stimulation
-exercise
-cholecystokinin
-gastrin
-cortisol
-surgery/stress/trauma/sepsis

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29
Q

What inhibits glucagon release?

A

-High glucose levels
-somatostatin
-free fatty acids
-ketones
-insulin

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30
Q

What are other uses for glucagon? (IV 1-5mg)

A

-beta-blocker overdose
-CHF
-Low cardiac output after MI or CPB
-improving MAP during anaphylaxis

-also administered during ERCP to relax the biliary sphincter

(N/V are key side effects of glucagon)

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31
Q

Compared to type 1 diabetes mellitus, choose the statements that MOST accurately describe type 2 diabetes mellitus (select 2)

a.) peripheral sensitivity to insulin is reduced
b.) it is more likely to cause hyperglycemic hyperosmolar syndrome
c.) it is usually associated w a thin body habitus
d.) it is usually caused by an autoimmune response

A

a.) peripheral sensitivity to insulin is reduced
b.) it is more likely to cause hyperglycemic hyperosmolar syndrome

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32
Q

Diabetes shifts metabolism towards:

A

protein catabolism and lipid oxidation

-insulin deficiency produces a shift from carbohydrate to fat metabolism
-free fatty acids become main energy substrate for essentially all tissues

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33
Q

What is the diagnostic criteria for diabetes?

A

-Fasting plasma glucose >126 mg/dL
-random glucose level > 200 mg/dL + classic symptoms
-Two hour plasma glucose > 200mg/dL during an oral glucose tolerance test
-Hemoglobin A1C >6.5%

pre-diabetes: FPG 100-125
fasting defines as no caloric intake for at least 8 hrs.

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34
Q

At what blood glucose levels will you see glucosuria?

A

When blood glucose concentration increases to approx 180mg/dL, the amount of glucose filtered at the kidney glomerulus cannot be totally reabsorbed.

-Excess glucose spills into urine (glucosuria) and acts as osmotic diuretic

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35
Q

Causes of DM type 1

A

causes:
-autoimmune
-genetic
-virus

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36
Q

Causes of DM type 2

A

Obesity

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37
Q

What is the typical BG in diabetic ketoacidosis?

A

> 250 mg/dL
-Usually occurs in type 1

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38
Q

At what blood glucose level does insulin begin to be released?

A

100 mg/dL

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39
Q

At what blood glucose level is insulin’s max response?

A

400-600 mg/dL

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40
Q

At what blood glucose level is insulin’s max response?

A

400-600 mg/dL

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41
Q

What do the anabolic effects of insulin increase/inhibit?

A

-increase glycogenesis (glycogen is storage form to glucose)

-inhibition of glycogenolysis
-inhibits gluconeogenesis
-phosphorylates glucose (traps) for use in glycolysis, glycogenesis
-increases lipogenesis

42
Q

What is hypoglycemia defined as?

A

Less than 70 mg/dL

43
Q

What is the treatment for hypoglycemia?

A

10-25 gIV of 50% dextrose (20-50mL)
glucose infusion: 5% dextrose

44
Q

What are the manifestations of DKA?

A

-dehydration (5-10L)
-ketoacidosis (ketone bodies = beta-hydroxybutyrate, acetoacetate, acetone)
-metabolic decompensation
-tachycardia
-metabolic acidosis (pH <7.3)
-anion gap greater than 10-20 mEq/L
-electrolyte depletion
-hyperosmolarity (>300 mOsm/L)
-nausea
-abdominal pain
-lethargy
-lactic acidosis
-kussmaul respiration

45
Q

How high is blood sugar in Hyperglycemic Hyperosmolar State (HHS)

A

> 600mg/dL
-common in elderly pts w Type 2

46
Q

Causes of HHS

A

infection
sepsis
pneumonia
stroke
MI
inuslin resistance or inadequate production
Enough insulin is produced to prevent ketosis but not hyperglycemia

47
Q

Manifestations of HHS

A

-pH >7.3
-mentally obtunded
-hypovolemia/dehydration (9L)
-mental confusion
-lethargy
-coma
-increased serum osmolarity (>330 mOsm/L)
-HoTN
-Tachycardia
-increased plasma viscosity
-arterial and venous thromoembolic events are common
-NO anion gap

48
Q

Besides the presence of hyperglycemia, what is the classic triad of symptoms associated w diabetes mellitus?

A

1.) polyuria
2.) dehydration
3.) polydipsia

48
Q

Besides the presence of hyperglycemia, what is the classic triad of symptoms associated w diabetes mellitus?

A

1.) polyuria
2.) dehydration
3.) polydipsia

49
Q

What is DKA usually caused by?

A

infection

50
Q

Acute symptoms of diabetes:

A

polyuria (osmotic diuresis)
polydipsia (intravascular volume depletion)
polyphagia and wt loss (protein catabolism

CNS irritability/confusion (hypertonic ECF leads to cell shrinkage)

Visual disturbances- sorbitol formation in lens cuases osmotic swelling, cylcation leads to opacification
-microvascular disease affects perfusion of retina

51
Q

What are normal A1C levels?

A

4-5.6%

the higher the hgbA1C, the higher the risks of developing complications related to diabetes

51
Q

What are normal A1C levels?

A

4-5.6%

the higher the hgbA1C, the higher the risks of developing complications related to diabetes

52
Q

The following factors can mask the signs of intraoperative hypoglycemia EXCEPT:

a.) general anesthesia
b.) propranolol
c.) diabetic autonomic neuropathy
d.) hydrochlorothiazide

A

d.) hydrochlorothiazide

thiazide diuretics have a unique side effect in that they increase serum glucose (hydrochlorothiazide, metolazone, and indapamide)

53
Q

Key anesthetic considerations of Diabetes Mellitus

A

-Diabetic autonomic neuropathy (inability to mount a sympathetic response to hypovolemia and the cardio-depressant effects of anesthetic drugs)

-orthostatic hypotension
-increased risk of aspiration
-increased risk of hypothermia
-reduced ROM of AO joint
-the prayer sign suggests and increased risk of diffucult intubation
-peripheral neuropathy
-hypoglycemia can be masked by general anesthesia, or BB
-schedule surgery early in the day

54
Q

Hyperglycemic hyperosmolar syndrome rarely produces significant

A. hyperglycemia
B. dehydration
C. hyperosmolarity
D. ketoacidosis
A

D. ketoacidosis

Hyperglycemic hyperosmolar state, or HHS, is a condition that occurs most commonly in acutely ill patients older than 60 years of age who have type II diabetes. It is characterized by severe hyperosmolarity, hyperglycemia, and dehydration. In HHS, the patient is able to secrete enough insulin to prevent lipolysis, so ketoacidosis, if present, is rarely severe. Signs and symptoms include confusion, lethargy, coma, hypokalemia, a high incidence of thromboembolism, and a life-threatening dehydration. On average, patients with HHS have a water deficit of 9 liters.

55
Q

What is the leading cause of death in patients with diabetes mellitus?

A. Cardiovascular disease

B. Diabetic ketoacidosis

C. Hyperosmolar hyperglycemic nonketotic coma

D. Emphysema

A

A. Cardiovascular disease

56
Q

All of the following are symptoms of hypoglycemia except

A. Hypotension
B. Tachycardia
C. Diaphoresis
D. Lacrimation

A

A. Hypotension

Hypoglycemia is associated with a sympathetic response and symptoms such as hypertension, tachycardia, diaphoresis, and lacrimation.

57
Q

Which of the following classes of oral hypoglycemic agents increase insulin secretion?

A. Alpha-glucosidase inhibitors

B. Thiazolinediones

C. Sulfonylureas

D. Biguanides

A

C. Sulfonylureas

Sulfonylureas increase insulin secretion by beta cells, thiazolinediones and metformin (a biguanide) enhance tissue sensitivity to insulin, and alpha-glucosidase inhibitors decrease postprandial glucose absorption.

58
Q

What is the best predictor of silent coronary artery disease in diabetic patients?

A. U waves on the electrocardiogram

B. Autonomic neuropathy

C. First degree heart block

D. Obesity

A

B. Autonomic neuropathy

59
Q

Which of the following is most consistent with Hyperglycemic Hyperosmolar State (HHS)?

A. dehydration
B. ketoacidosis
C. hyperkalemia
D. hypomagnesemia

A

A. dehydration

Hyperglycemic hyperosmolar state, or HHS, is a condition that occurs most commonly in acutely ill patients older than 60 years of age who have type II diabetes. It is characterized by severe hyperosmolarity, hyperglycemia, and dehydration. Signs and symptoms include confusion, lethargy, coma, hypokalemia, a high incidence of thromboembolism, and a life-threatening dehydration. On average, patients with HHS have a water deficit of 9 liters. Ketoacidosis is rare in HHS.

60
Q

What is the best assessment for long-term glucose control in a diabetic?

A. Hemoglobin A1C
B. Fasting glucose
C. Sodium to glucose ratio
D. 24-hour urine glucose

A

A. Hemoglobin A1C

A fasting plasma glucose greater than 100 mg/dL is considered a positive screen for impaired glucose tolerance indicative of diabetes. The hemoglobin A1C test is considered a more informative measurement of glucose tolerance because it is a measurement of long-term glucose control. The normal hemoglobin A1C level is between 4 and 6 percent.

61
Q

What conditions comprise the biochemical triad of diabetic ketoacidosis?

A. Proteinuria, hyperglycemia, acidemia

B. Ketonemia, hyperglycemia, alkalemia

C. Acidemia, ketonemia, hyperglycemia

D. Proteinuria, ketonemia, acidemia

A

C. Acidemia, ketonemia, hyperglycemia

Diabetic ketoacidosis is described as the biochemical triad of hyperglycemia, acidemia, and ketonemia.

62
Q

What does insulin increase?

A

Glycogenesis (glycogen is the storage form of glucose)
Lipogenesis (formation of fat)
Protein synthesis
Glucose transport
Stimulates intracellular amino acid transport
Increases translation of mRNA into proteins
increased formation of glycerol and fatty acids = triglycerides

63
Q

What does insulin inhibit?

A

gluconeogenesis (formation of new glucose)
glycogenolysis (break down of glycogen)
protein catabolism

64
Q

What does glucagon increase?

A

Gluconeogenesis (formation of glucose)
Glycogenolysis (breakdown of glycogen)

65
Q

What doesn’t insulin facilitate glucose entry into?

A

Brain
Kidney tubules
RBC

66
Q

What increases the uptake of insulin?

A

Exercise and insulin

67
Q

What is used for energy while exercising?

A

increased glycogenesis and protein synthesis

68
Q

When are ketone bodies produced?

A

When insulin levels are low

69
Q

What do epinephrine and glucagon work on in the liver?

A

Catabolism effect: breaks down amino acids, glycerol, and glycogen into glucose to be released into vascular system

70
Q

What cardiovascular effects does glucagon have?

A

enhances heart strength- can be used for beta-blocker overdose

enhances bile secretion
increased blood flow to some tissues
inhibits gastric acid secretion

71
Q

What does glucagon help with during ECPR and colonoscopy?

A

ECPR: dilate bile ducts

Colonoscopy: help with spasms of the colon

72
Q

type 2:

A

Decreased sensitivity to receptors on the cell.

73
Q

Insulin insufficiency leads to:

A

hyperglycemia from decreased cell entry, increased gluconeogenesis and glucose released from liver

74
Q

Glucose is reabsorbed by the kidney until

A

180mg/dL = osmotic diuresis, loss of Na+ , K+ and glucosuria

Hypovolemic HoTN, dehydration, polyuria, polydipsia, polyphagia (increased appetite from hypothalamus ventromedial nucleus)

75
Q

Low insulin leads to:

A

muscle catabolism increased fat catabolism

increases the release of keto acids (acetoacetic acid, beta-hydroxybutyric acid) and causes anion gap metabolic acidosis

76
Q

Polyuria:

A

osmotic diruesis

77
Q

Polydipsia:

A

intravascular volume depletion

78
Q

Polyphagia and weight loss:

A

protein catabolism

78
Q

Polyphagia and weight loss:

A

protein catabolism

79
Q

Why do you see CNS irritability and confusion with diabetes?

A

Hypertonic extracellular fluid leads to cell shrinkage

80
Q

Why would someone have visual disturbances with diabetes?

A

Sorbitol formation in the lens= osmotic swelling, glycation leads to opacification

microvascular disease affects perfusion of retina

81
Q

Why would someone have visual disturbances with diabetes?

A

Sorbitol formation in the lens= osmotic swelling, glycation leads to opacification

microvascular disease affects perfusion of retina

82
Q

Chronic symptoms of diabetes:

A

Infection
Non-alcoholic fatty liver
Macrovascular disease (CAD, PAD, AMI, CHF, CVA)
Microvascular: nephropathy, retinopathy, neuropathy (stocking-glove, orthostatic HoTN, delayed GI emptying )

83
Q

What can the autoimmune disorder causing type 1 be caused by?

A

environmental factors, viral infections, exposure to antigenic proteins

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

RECEPTOR AND CELLULAR MECHANISMS PRESERVED (coming from beta cells in pancreas)

84
Q

is joint stiffness more common in type 1 or type 2?

A

TYPE 1

85
Q

How long should you hold metformin before surgery?

A

24-48hrs

86
Q

What is the risk of Biguanides (METFORMIN)?

A

First line
LACTIC ACIDOSIS in surgical pts especially in liver/kidney/CHF

-PCOD

decreases hepatic glucose production, increase peripheral insulin uptake

87
Q

Risk of Sulfonylureas:

A

HYPOGLYCEMIA RISK d/t increase INSULIN SECRETION

88
Q

Meglitidies risk:

A

Hypoglycemia= INCREASE INSULIN SECRETION

89
Q

Thiazolidindiones:

A

decrease glucose production in liver
Decrease insulin resistance

90
Q

Alpha-glucosidase inhibitors:

A

Slows digestion and absorption of carbs in the GI tract

don’t give to anyone with an intestine disorder

91
Q

Glucagon-like peptide 1 (GLP-1):

A

Delays gastric emptying= aspiration risk

blackbox: pancreatitis, tumor

92
Q

SGLT2 inhibitors

A

decreases renal glucose reabsorption

osmotic diresis= hypovolemia

93
Q

Dipeptidyl-peptidase 4- inhibitors

A

Potentiates insulin release

94
Q

What counter regulatory hormones are elevated in DKA?

A

glucagon
cortisol
GH
catechols

95
Q

anion gap

A

Anion gap = Sodium – (Chloride and Bicarb) which is equivalent to (most prevalent cation) minus (the sum of the most prevalent anions)

DKA = anion gap >10

96
Q

how dehydrated is a DKA pt?

A

4-6 L

97
Q

what electrolytes are low in DKA?

A

potassium (severe hyperkalemia in the face of total body K depletion)
Na+
Mag+
cl-
phos

Endocrine (7 decks)

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