Pancreas - Quiz 4 Flashcards

1
Q

Where is the Pancreas located?

A

Back of Abdomen behind the Stomach

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2
Q

What are the two main hormones that the Pancreas secrete?

A

Insulin & Glucagon - opposite functions

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3
Q

How does the body raise its blood sugar?

A

Low blood sugar –> Pancreas secretes Glucagon –> Converts Glycogen to Glucose in the Liver –> Releases Glucose into Blood

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4
Q

How does the body lower its blood sugar?

A

High blood sugar –> Pancreas secretes Insulin –> Converts Glucose to Glycogen in Liver & Stimulates Glucose uptake

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5
Q

What cell type makes of the majority of the Pancreas

A

Acini - exocrine function - secretes digestive juices into duodenum

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6
Q

Which cells make up the Islet of Langerhans of the Pancreas?

A
  • Alpha Cells - Glucagon
  • Beta Cells - Insulin
  • Delta Cells - Somatostatin
  • Pancreatic Polypeptide Cells
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7
Q

What does Insulin do to Carbs & Amino Acids?

A

Store Carbs as Glycogen in Muscle & Liver

Excess Carbs converted to Fats & stored in Adipose

Promotes uptake of Amino Acids & converts to Protein

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8
Q

What stimulates Insulin secretion?

A

High Blood Glucose

Amino Acids

Beta-Keto Acids

Glucagon

Acetylcholine

Intestinal Hormones

Beta Agonists

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9
Q

What inhibits Insulin Secretion?

A

Low Blood Glucose

Fasting

Glucagon

Cortisol

Catecholamines

Growth Hormone

Somatostatin

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10
Q

What is the Half Life of Insulin

A

Unbound - 6 to 7 minutes

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11
Q

Which enzyme degrades unused Insulin?

A

Insulinase

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12
Q

How do Neurons, Muscle, and Adipose cells react to Insulin?

A

Muscle & Adipose - Glucose uptake via Endocytosis

Neurons - Permeable to glucose

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13
Q

At what blood sugar does Insulin start to release?

A

100 mg/dL w/ max response at 400-600 mg/dL

Plasma insulin levels can increase by 10x after a meal

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14
Q

What are the Anabolic effects of Insulin?

A

↑Glycogenesis

Inhibits Glycogenolysis

Inhibits Gluconeogenesis

Traps Glucose for Later Use

↑Protein Synthesis

↑Liver Uptake, Storage, and Use of Glucose

↑Lipogenesis

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15
Q

Insulin facilitates entry of glucose into cells of all tissue EXCEPT which?

A

Brain

Kidney Tubules

RBCs

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16
Q

How does Insulin effect fatty acid when fed vs fasting?

A

Fed: Insulin suppresses fatty acid mobilization (glucose already available)

Fasting: Insulin releases free fatty acid into circulation for fuel

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17
Q

What are produced when Insulin Levels are Low during Fasting?

A

Ketone Bodies

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18
Q

What are Glucagon’s Catabolic Effects?

A

Activates enzymes for Glycogenolysis

↑Gluconeogenesis

↑Lipolysis & Ketogenesis

↑Proteolysis & Flow of Amino acids from Muscle to Liver for Gluconeogenesis

↑Heart Strength & Blood Flow

↑Bile Secretion

Inhibits Gastric Acid Secretion

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19
Q

What stimulates the release of Glucagon?

A

Fasting Hypoglycemia

Amino Acids

Beta-Adrenergic Stimulation

Exercise

Cholecystokinin

Gastrin

Cortisol

Surgery

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20
Q

What Inhibits Glucagon release?

A

High Glucose

Somatostatin

Free Fatty Acids

Ketones

Insulin

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21
Q

What is Diabetes Mellitus?

A

Syndrome of impaired Carb, Fat, and Protein metabolism

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22
Q

What is the difference between Type I & Type II Diabetes?

A

Type I
Lack of Insulin Secretion
Effects Any Age, Thin bodied, and DKA is often

Type II
Decreased Insulin Sensitivity or Insulin Resistance
Effects Obese Adults, More Prevalent, and DKA is rare

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23
Q

What would you expect when over 180mg/dL of Glucose is reabsorbed by the Kidney?

A

Osmotic Diuresis

Loss of Na, K, & Glucose in Urine

Hypovolemia, Hypotension & Dehydration

Polyuria

Polydipsia & Polyphagia

24
Q

What are the Acute Symptoms of Diabetes?

A

Polyuria

Polydipsia

Polyphagia

Irritability

Confusion

Impaired Vision

25
Q

What are Chronic symptoms of Diabetes?

A

Infection

Non-Alcoholic Fatty Liver Disease

Macrovascular Disease
(CAD, PAD, AMI, CHF, CVA)

Microvascular Disease
(Nephropathy, Retinopathy, Neuropathy)

26
Q

What is the cause of Type I Diabetes?

A

Destruction of Beta Islet Cells d/t Viral Infections or Autoimmune Disorders

27
Q

Plasma Insulin Levels are normally ______ in Type II Diabetes

A

Plasma Insulin Levels are normally elevated in Type II Diabetes, but still not enough for glucose regulation

28
Q

What are the 4 ways to Diagnose Diabetes?

A
  • A1c > 6.5%
  • Fasting Glucose > 126 mg/dL
  • Oral Glucose Tolerance after 2 hrs > 200 mg/dL
  • Random Glucose > 200 mg/dL w/ hyperglycemia symptoms
29
Q

What does a Hgb A1c reflect?

A

Average Blood Sugar over 3 Months

Normal: 4 - 5.6%

30
Q

How does Glucose Control help during the Perioperative Period?

A

Insulin inhibits inflammatory growth factors relating to MI

Insulin Improves Cardiac Contractility

Better Patient Outcomes

31
Q

How should Diabetic Meds be managed PeriOperatively?

A

Hold oral meds day of surgery

Continue Basal Insulin for Type I Diabetics

Continue Insulin Pump or Change to IV Insulin

32
Q

What is the Target A1c in regards to taking Oral Hypoglycemics?

A

A1c < 8%

33
Q

What is the First Line Oral Medication for Diabetes?

A

Biguanides - Metformin

↓Liver Glucose Production

↑Insulin Uptake

34
Q

What are the side effects of Metformin (Glucophage)?

A

Lacic Acidosis, especially for Liver/Kidney/CHF patients

35
Q

What Diabetic medication Increases Insulin Secretion?

A

Sulfonylureas -
Glimepiride (Amaryl)
Glipizide (Glucotrol)
Glyburide (Diabeta)

Meglitinides
Repaglinide (Prandin)

Both classes carry Hypoglycemia risks

36
Q

What do Thiazolidinediones do?

A

Decrease Liver Glucose Production & Insulin Resistance

Drugs ending in “-tazone”

Pioglitazone (Actos)

37
Q

How is a patient’s Insulin Regimen managed PeriOperatively?

A

Give 1/2 dose of Long Acting

&

Hold Short Acting on day of surgery

38
Q

What can be added to Insulin to prolong their effects?

A

Protamine

Careful when giving it to reverse Heparin

39
Q

What are the Rapid Acting Insulins?

A

Aspart (Novolog)

Lispro (Humalog)

Glulisine (Apidra)

Regular (Humulin/Novalin R)

40
Q

What is the Onset, Peak, and Duration of Regular Insulin?

A

Onset: 30-60 min

Peak: 2-4 hrs

Duration: 6-8 hrs

All other Rapids are 15 min, 1 hr, and 3-4 hrs respectively

41
Q

Which Insulin type is Intermediate-Acting?

A

NPH

Onset: 1-3 hrs

Peak: 6-8 hrs

Duration: 12-16 hrs

42
Q

What are the Long Acting Insulins?

A

Detemir (Levemir)

Glargine (Lantus)

Onset: 1 hr and lasts from 6 - 34 hrs

43
Q

What is the pathophysiology of DKA?

A

Dehydration

Acidosis

Electrolyte Depletion, especially Potassium

Accelerated Protein Breakdown

↑Fatty Acids

44
Q

What are symptoms of DKA?

A

N/V

Polyuria

Polyphagia

Anorexia

Kussmaul Breathing

Acetone Halitosis

45
Q

What is a patient DKA’s level of consciousness related to?

A

Osmolality, NOT Acidosis

46
Q

How is DKA treated?

A

Lots of Fluids

Replace Lytes

Insulin

47
Q

What is Nonketotic Hyperosmolar State?

A

Same as DKA, but with really high blood sugar, no ketoacidosis, and higher motality

48
Q

What are the symptoms of Nonketotic Hyperosmolar State?

A

Clots d/t Thick Blood

Neuro Signs

Confusion

Seizure

Coma

49
Q

How is Nonketotic Hyperosmolar State treated?

A

Aggressive Fluids, then add sugar at BG of 250

Replace Kphos & Insulin if needed

50
Q

What is the body’s early response to Hypoglycemia?

A

Liver Glycogen Breakdown

51
Q

What is the body’s Late response to Hypoglycemia?

A

Sympathetic Stimulation & Epi Release

52
Q

What is the body’s Very Late response to Hypoglycemia?

A

Growth Hormone & Cortisol Secretion

53
Q

What is Insulinoma?

A

Beta Cell Adenoma

Causes Insulin Shock = coma w/ BG < 20 mg/dL

Treat w/ Glucagon & Epinephrine

54
Q

At what Blood Glucose level will Hypoglycemic Shock happen?

A

20 - 50 mg/dL

Fainting, Seizure, Coma

55
Q

How is Hypoglycemic Shock treated?

A

D50 + D5 Infusion

56
Q

What happens to the brain if the sugar is low?

A

Brain will use up all the sugar, then fats/ketones, eventually leading to brain death and apoptosis