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Pharm > Pancreatic Hormones & antidiabtic drugs > Flashcards

Pancreatic Hormones & antidiabtic drugs Flashcards

Test 4

1
Q

What are the 2 major types of tissues in the pancreas? What are their functions?

A

Exocrine gland: Releases secretions on body surface
-Releases digestive enzymes into the duodenum to help with protein, lipid, & carbohydrate digestion

Endocrine gland: Release hormones into the bloodstream to regulate physiological processes

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2
Q

What is an example of exocrine gland secretions?

A

sweat

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3
Q

What is the smallest portion of the pancreas?

A

endocrine gland

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4
Q

Where is the endocrine gland?

A

Scattered amongst pancreatic cells called pancreatic islet

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5
Q

What are the cells associated with the endocrine gland? What are the main subtypes & their functions?

A

pancreatic islets of Langerhans

  1. Alpha (20% of islet): Secretes Glucagon
  2. Beta (75%): Secretes Insulin, C-peptide, proinsulin, amylin
  3. Delta (3-5%): Secretes somatostatin
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6
Q

What cell releases insulin when BGS is high?

A

Beta islet cell

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7
Q

What cell releases glucagon when BGS is low?

A

Alpha islet cell

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8
Q

Which cell is associated with pancreatic function?

A

Beta islet cell

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9
Q

Which 2 cells counter each other? How?

A

Alpha & Beta islet cells
Alpha secretes glucagon
Beta secretes insulin

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10
Q

Describe amylin

A

Supress production of glucagon

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11
Q

Why is Somatostatin so important?

A

It is released immediately after eating

Suppresses both glucagon and insulin
-allows for spikes & allows sugars to be distributed through bloodstream before insulin released

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12
Q

Which cells are associated with gastric emptying?

A

G and F islet cells

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13
Q

What type of receptors are insulin-R?

A

Tyrosine Kinase

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14
Q

Describe the insulin pathway

A
  1. Insulin from pancreatic beta islet cells bind the insulin-R
  2. They phosphorylate, which requires an ATP molecules, dimerize and elicit a response throughout the cell.
  3. This translocates glucose transporters to the cell membrane
  4. Glucose is now able to enter the cell from the bloodstream which lowers the BGS
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15
Q

What is the normal range for BGS?

A

70-110 mg/dL

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16
Q

What is a Insulin Secretagogue?

A

Stimulant for insulin release

Ex) Elevated glucose levels

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17
Q

What type of receptor is a Glucagon-R?

A

GCPR

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18
Q

What is the stimulant for glucagon?

A

Blood sugar dropping

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19
Q

What is glyconolysis?

A

Breaking down glycogen

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20
Q

What is the liver’s role in the endocrine system?

A

-takes up some extra glucose when BGS high and stores as glycogen

  • breaks down stored glycogen and releases as glucose when BGS low
  • inhibits glucogenolysis
  • inhibits conversion of fatty acids & amino acids to keto acids
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21
Q

What is fasting sugar?

A

When you start the day and havent eaten

Your BSG should be around 70mg/dL

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22
Q

What is a renal threshold?

A

> 160 mg/dL

threshold where you will start to see glucose in the urine

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23
Q

F/T: glucose in the urine is OK

A

F

Should be filtered in reabsorbed in PCT

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24
Q

What are the glucose transporters in the PCT?

A

SGLT –> GLUT

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25
Q

T/F: There is always insulin being released in the body

A

T

Called “constitutive insulin”

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26
Q

What is “constitutive insulin”

A

Small amount of insulin that’s always being released

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27
Q

What are the four types of Diabetes Mellitus? Briefly compare them

A
  1. Type 1: insulin-dependent
  2. Type 2: non-insulin-dependent
  3. Type 3: temporary increase in BGS
  4. Type 4: Gestational, associate it with pregnancy
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28
Q

What does Mellitus mean?

A

Sugar

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29
Q

What are symptoms in ALL DM?

A

Polyuria: increase urine
polydipsia: increased thirst
polyphagia: increase hunger

HYPERGLYCEMIA

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30
Q

What are the two most common types of DM?

A

Type 1 and 2

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31
Q

Describe Type 1 DM

A

Insulin-dependent -> “IDDM”

-Idiopathic/autoimmune (seen as a child)
-Caused by destruction of beta islet cells
-Insulin is the only way to treat this

SE: Increased BGS; PPP; Wt loss, fatigue

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32
Q

What can type 1 DM lead to?

A

DKA
Diabetic ketoacidosis

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33
Q

Describe Type 2 DM

A

Non-insulin-dependent -> “NIDDM”

Causes: genetics & metabolic syndrome (obesity, HTN, CVD)

Caused by: Chronic increase in BGS, body stops responding

AE: recurrent infections, vision problems, neuropathy, dehydration

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34
Q

What is pre DM? How can you treat this?

A

Fasting BSG 100-110 mg/dL

Lifestyle changes and lastly medcation (metformin)

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35
Q

What can type 2 DM lead to?

A

HHS
Nonketotic hyperosmolar coma

36
Q

What is A1C in a regular person vs what we want it to be in a person with DM?

A

normal 4%
With DM < 7%

37
Q

Describe the sorbitol pathway, and why it leads to peripheral neuropathy and blindness

A
  1. When glucose is too high, it converts to fructose
  2. Fructose then converts to sorbitol (sugar alcohol)
  3. sorbitol goes into cells but cannot leave & draws in water.
  4. The excess water causes the cell to burst

This happens in RBC in the eye lense and peripheral nerves leading to retinopathy and diabetic neuropathy caused by lysis of RBC in that area.

38
Q

Why is it important to have food foot care with DM?

A

Diabetic neuropathy

Lysis of RBC in the feet will cause nerve damage which will make it difficult for you to feel if your foot is hurt/injurded

This increases your risk for prolonged infection & amputation

39
Q

What protein is activated by hyperglycemia?

A

Protein kinase C

40
Q

Why do we measure hemoglobin A1C in DM?

A

In prolonged increase BGS, glucose molecules attach to hemoglobin

Looks at glucose levels for 90-120 days

41
Q

Describe Type 4 DM

A

Gestation - pregancy related

Caused by: Hormones block insulin release

AE: higher birth wt; increased risk for DM2 & with subsequent pregencies; infant risk for DM

42
Q

What are the different tests associated with DM?

A

Dx
1. Fasting blood glucose
2. Glucose tolerance test

Monitoring
3. Self Glucose POC
4. Hemoglobin A1C
5. Insulin

43
Q

Which DM test do you take during pregnancy?

A

Glucose tolerance test

44
Q

Describe the structure of insulin

A

Peptide hormone made of long string of amino acids

Not a protein

-Consist of an Alpha & Beta chain + C-Peptide
-Alpha & Beta chain held together by disulfide linkages (S-S)

-Alpha & Beta chains are activated in the granules before released in the bloodstream
-C-peptide, which has no function, is cleaved before release but is also released into blood stream as well

45
Q

What is a good way to measure the functioning of your beta islet cells?

A

Measurement of C-peptide at the beginning of regiment and at that moment to see if there is a decrease in the functioning of your beta islet cells

46
Q

What are insulin secretagogues?

A

Glucose primary
Amino acids
hormones
fatty acids
incretins (from intestines)
drugs: sulfonylureas (block K+ channels); isoproterenol (beta agonist/increases insulin release)

47
Q

Describe the Glucose/Insulin pathway

A
  1. BGS levels are increased
  2. Sugar goes into the beta islet cell via GLUT 2 transporter
  3. That sugar is used through metabolism and Glycolysis to create ATP
  4. ATP causes an efflux K+ channel to close; this depolarizes the cell membrane
  5. This opens the VG Ca++ channel, which allows Ca++ to come into the cell
  6. Ca++ helps move the insulin vessicle to the cell membrane for exocytosis
  7. Insuline is released into the blood stream
48
Q

How long do endogenous insulin last in the bloodstream?

A

6 minutes

49
Q

What part of the insulin TK-R is activated? and what happens when this is activated

A

Beta unit

“insulin repsonse substrates” are activated and causes a downstream response

50
Q

Where are your GLUT transporters?

A

GLUT 1: All tissues, esp, RBC; brain
GLUT 2: Beta cells of pancreas
GLUT 3: Brain
GLUT 4: Muscle; adipose
GLUT 5: Gut, Kidney

51
Q

Which glucose transporter is on the beta islets? What is its function? What is its K(m)? What does that mean?

A

GLUT 2

Regulation of insulin release

K(m) is high: 15-20
-This means that affinity is low
-if glucose levels are low, the transporter doesnt work well; if glucose levels are high, transporter works very well

52
Q

Which glucose transporter is the most common throughout the body? What is its function?

A

GLUT 4

Muscle & adipose tissue insulin mediated uptake of glucose

53
Q

Which transporters have low K(m)? What does this mean?

A

All except GLUT 2

affinity is high and that regardless of the amount of glucose, the glucose will be transported into the cell via the transporter.

54
Q

What things endogenous inhibit insulin secretion?

A

exogenous insulin
leptin
SNS (alpha adrenergic)
Chronically high BGS
Drugs: diazoxide, phenytoin, vinblastine, colchicine

55
Q

How does Leptin inhibit endogenous insulin secretion?

A

Leptin is produced by adipose & causes feelings of fullness -> decrease in insulin secretion

56
Q

Drugs: Rapid acting Insulin

A

Lispro, Aspart, Glulisine

Take w/ meals

57
Q

Drugs: Short acting insulin & Intermediate acting Insulin

A

Short: Novolin, Humulin
Intermediate: Neutral protamine Hagedor

These can be taken in conjunction 2x/day

58
Q

Drugs: Long acting Insulin

A

Glargine, detemir

Take 1x/day to mimic constituative levels

59
Q

Which combination of insulin is not tightly controlled? Which is?

A

Not: NPH w/ regular or short

Is tightly controlled: long acting with short

60
Q

What is the best way to deliver insulin for the tight control?

A

Continuous subcutaneous insulin in fusion device (CSID) “Insulin Pump”

61
Q

What are the ways Insulin can be delivered?

A

-SQ with injection or pen
-insulin pump best practice for tight control
-Inhaled
-IV

62
Q

How often should you change the needle in an insulin pump?

A

Sterile needle changes should occur every 2-3 days

63
Q

How do you Calculate your insulin dose?

A
  1. Start your day with giving yourself 1 injection of long acting insulin
  2. Calculcate your carb coverage:
    - 1 unit of Rapid acting insulin covers 12-15 grams of carbs.
    - Ex) if you plan to eat 60 carbs for lunch –> take 4 units of RA insulin
    - Do this for all your meals
  3. Correction dose calculation:
    - 1 unit of RA unit needed to drop BGS by 50 mg/dL.
    - Ex) sugar is 200 –> take 2 units to drop BGS to 100 mg/dL
64
Q

For carb coverage, what do we take?

A

Rapid acting insulin

1 unit per 12-15 grams of carbs

65
Q

For correction coverage, what do we take?

A

Rapid acting insulin

1 unit will drop BGS by 50 mg/dL

66
Q

What type of control do we need for IDDM?

A

This is type 1 DM

This is insulin dependent.

Tight control

Rapid & Long acting

67
Q

Insulin needs _______ when patients are ill.
Explain why.

A

Increase

Metabolic rate increases, especially when on parenteral nutrition

68
Q

Describe S/S and Tx for Hypoglycemia

A

S/S: anxiety, blurred vision, palpitations, shakiness, slurred, speech, sweating

Tx: Alert pt: 3/4 glucose tabs; 1/2 can of soda
- NPO: 1mg glucagon; may repeat in 20 mins

69
Q

T/F: You can take PO antidiabetic for type 1 DM

A

F

70
Q

Drugs: Metformin

A

Class: Biguanides
(Bi - 2; Guanine molecules joined together by a NH)

MOA: decrease glucose production in the liver

1st line therapy in type 2 DM

Take with meals

71
Q

What is Gluconeogenesis?

A

Production of glucose in the liver

72
Q

Drugs: Sulfonylurea

A

Class: Insulin Secretagogues
MOA: Bind to K+ receptor to depolarize beta islet cells –> Ca++ channel opens –> promotes insulin vessel exocytosis

** SULFA DRUG ALLERGY!!**

1st generation: need a higher dose
2nd gen: more effective at a lower dose

BLACK BOX WARNING
-Increase in Cardiovascular events
-Do not take at all if you have heart problems
-Not even a 1st line drug because of this…

73
Q

Drugs: Thiazolidinediones

A

Class: Thiazolidinediones
MOA: Decrease insulin resistance by acting on the Peroxisome proliferator-Activated Receptor (PPAR) –> increasing insulin signaling & GLUT 4 transporters to the surface

Increase risk of MI if using insulin or nitrates!!!!
-Monitor patients very closely on this!!!! tf

74
Q

Drugs: Acarbose

A

Class: Alpha-Glucosidase Inhibitor
MOA: Block digestion of complex carbohydrates –> sucrose goes straight to large intestines

Beneficial in people with high carb diets

SE: Prominent GI disturbances

75
Q

Drugs: Bile acid binding resins

A

Class: Bile acid binding resins
MOA: Large catioon exchange resins bind with bile acids and are not absorbed

SE: Prominent GI disturbances

76
Q

Drugs: Amylin

A

Class: Amylin analog
MOA: Suppresses glucagon release –> increases insulin efficiency

Taken in conjunction with insulin

77
Q

What cell secretes endogenous amylin?

A

Beta islet cells

78
Q

Drugs: Semaglutide (Ozempic)

A

Class: Incretin-Based Therapies
Glucagon-Like Polypeptide-1 agonist (GLP-1)

MOA: Mimics Incretins (GI hormone) –> Stimulates insulin release & inhibits glucagon release

Increases pancreatic cancer risk

79
Q

______ inhibits GLP-1 agonists/incretin & _______ glucose levels.

A

DPP-4 enzyme

increase

80
Q

Drugs: Sitagliptin

A

Class: DDP-4 inhibitor

Decrease glucose levels

Act as incretin/GLP-1

81
Q

Drugs: Gliflozins

A

-flozin

Class: SGLT2 inhibitor
MOA: Prevents glucose reabsorption in the PCT –> Glucose excreted in urine

SE: Wt loss, decrease in BP, dehydration (acts as an osmotic diuretic)
AE: Necrosis/infection in genital area d/t high glucose

82
Q

What does glycosuria mean?

A

positive glucose in urine

83
Q

If taking Gliflozins, where is sugar reabsorbed at?

A

SGLT-1 in the descending loop of Henle

84
Q

What type of transporter is the SGLT transporter?

A

Glucose & Na+ cotransporter

SGLT2: 1 glucose & 1 Na+

SGLT1: 2 Na+ & 1 glucose

85
Q

What is the best way to combat type 2 diabetes?

A

Combination therapy that targets different areas/pathways

86
Q

What are Adjunctive therapies for type 2 DM?

A
  1. Diet (low carb/fat/calories)
  2. Exercise
  3. Correction of metabolic syndrome
    -CVS/HTN (<130): ACE inhibitors (-prils); ARBs (-sartans); daily low dose aspirin (81 mg)
  4. LDL <100 mg/dL
  5. Stop smoking
  6. Screen for mental conditions
  7. Assess/screen for diabetic neuropathy & foot care
  8. Eye exams
  9. Monitor kindey functions

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