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Pharmacology > Diabetes Mellitus Type I/II: Final Exam > Flashcards

Diabetes Mellitus Type I/II: Final Exam Flashcards

1
Q

Define Alpha Cells.

A

Found within the Islets of Langerhans of the pancreas, these cells synthesize and secrete glucagon, which increases the blood sugar levels

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2
Q

Define Beta Cells.

A

Found within the Islets of Langerhans of the pancreas, these cells synthesize and secrete insulin

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3
Q

How is Insulin released?

A
  1. Glucose enters the beta cell through GLUT-2 transporters
  2. Once inside the cell, glucose is metabolized by Glucokinase to make ATP
  3. The ATP will bind to ATP sensitive potassium channels in the cell membrane
    - This causes the channels to close and depolarizes the cell (Action potential, Na+ ions enter and K+ ion exit the cell)
  4. The depolarization of the cell triggers the Ca++ voltage-gated channel
  5. The calcium (Ca+) enters the beta cell and stimulates the vesicles within (these vesicles contain insulin and amylin)
  6. These vesicles are propelled to the cell membrane and through exocytosis release insulin and amylin into the blood
  7. The insulin will bind to insulin receptors (tyrosine kinase) on muscles/fat cells
  8. The binding of insulin to its receptor leads to the activation of a second messenger system which causes translocation of the glucose transporter GLUT-4 into the cell membrane
  9. GLUT-4 uptakes glucose from the bloodstream and enters the muscle and fat cells so the glucose can be converted to fat stored, as glycogen or can be utilized to make ATP
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4
Q

Define Glucagon.

A

Glucagon produces an increase in blood glucose
Therefore it is triggered when the blood glucose levels are LOW
- Triggered by low plasma glucose levels (between meals; hypoglycemia) => mobilize stores and replenish blood glucose for cellular use

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5
Q

Glucose Regulation.

A
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6
Q

Define Diabetes Mellitus Type I.

A

Diabetes Mellitus type one occurs when the pancreatic cells are damaged (mainly caused by an auto-immune disorder) causing the inability to regulate blood glucose levels with endocrine hormones; leaving the cells in need of energy and decreasing their function)

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7
Q

How Does the body react to Decreased Insulin Production?

A

Hyperglycemia (cells not able to uptake glucose therefore, issues are not able to produce ATP)

Protein and Fat are metabolized instead and used as a constant supply of energy

  • The metabolism of fatty acids causes the production of ketone bodies (such as acetone)
  • Acetone is excreted through the lungs (which gives the characteristic of fruity breath)

Ketonuria: Ketones found within the urine

Polyuria: Frequent urination

  • The glucose within the blood is excreted through urine, due to osmotic pressure the water leaves the cells and exits the body through urine output
  • This osmotic shift of fluid concentration causes cellular dehydration and increases urine production
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8
Q

Hyperglycemia: The Three P’s Acronym.

A

Polyuria: Frequrent urintaion

Polydipsia: Increased thirst (the blood is trying to prevent the body from becoming dehydrated from excessive urination so it signals to the body to drink more water)

Polyphagia: Very hungry! (the body will start to burn fatty acids for energy since glucose is unable to uptake glucose into the cells)

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9
Q

Hyperglycemia: SUGAR Acronym.

A

S: Slow wound healing

BluUrred: Blurry vision

G: Glycosuria (presence of glucose in the urine)

A: Acetone smell of breath (when ketones are burned acetone is a byproduct and is excreted through the lungs, causing fruity-smelling breath)

R: Rashes on the skin

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10
Q

Hyperglycemia VS Hypoglycemia.

A

Hypoglycemia:

  • Shakiness
  • Dizziness
  • Sweating
  • Increased hunger
  • Headache
  • Pallor
  • Confusion
  • Fainting

Hyperglycemia:

  • Polyuria
  • Polydipsia
  • Lethargy
  • Weakness
  • Blurred Vision
  • Increase Hunger
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11
Q

Define Ketoacidosis.

A

When the cells enter starvation due to the lack of glucose; they switch to metabolizing the fatty acids (fats). This type so metabolism results in ketones as a byproduct, causing a decrease in cellular pH. The decrease in Ph will lead to cellular dysfunction.

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12
Q

What are Ketones?

A

Present when the body metabolizes fatty acids for ATP (when glucose is not being metabolized by the cells). This causes the production of ketone bodies which after time will put the body into acidosis.

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13
Q

Pathophysiology of Diabetic Ketoacidosis

A
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14
Q

How to Manage DKA?

A
  1. Promote Circulation
  2. Ensure airways are open and monitor RR
  3. Administer IV fluids
  4. Admisnter insulin as needed
  5. Measure pH in the blood
  6. Monitor ketones In urine
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15
Q

Types of Insulin.

A
  1. Rapid Acting
  2. Short-Acting
  3. Long-acting
  4. Intermediate
  5. Insulin Infusion Pump
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16
Q

Characteristics of Rapid Acting Insulin.

A
  • Onset: 10-15 minutes
  • Peak: 1-2 hour
  • Duration: 3-5 hours
  • Ensure patient eats right away (HAS TO HAVE A MEAL)
  • No IV
  • Rapid-acting Insulin: Do not LAG

LAG= Lispro, Aspart, Glulisine

17
Q

Characteristics of Short-Acting Insulin.

A
  • Onset: 30 minutes
  • Peak: 2-3 hours
  • Duration: dose dependant, 6.5 hours
  • Must eat 30-45 minutes BEFORE
  • ONLY ONE WITH IV
18
Q

Characteristics of Long-Acting Insulin.

A
  • NO peak (no dependency on a meal)
  • NO mix (do not mix with other insulins in the same syringe-CONTAMINATION Decreases efficiency)
  • Onset: 90 minutes
  • Never IV
  • 1-2 times daily
19
Q

Characteristics of Intermediate Insulin.

A
  • Onset: 1-3 hours
  • Peak: 5-8 hours (long peak so ensure to monitor glucose levels and have a snack ready!!)
  • Duration: 18 hours (dose dependant)
  • 1-2 times a day
  • NEVER IV
20
Q

Types of Insulin Therapy.

A
  1. Basal Bolus Insulin Therpsay (BBIT)
  2. Sliding Scale Insulin Therapy
21
Q

Define Basal Bolus Insulin Therapy (BBIT).

A

Mimics of how the body naturally makes insulin: It is a set of orders indicating how and which insulin medications are required, this kind of therapy is mainly for hospital patients and better replicates the body’s natural insulin production.

B = basal (long-acting Insulin)

B = bolus (short/rapid-acting Insulin)-3x per day

I = Insulin correction if necessary (short/rapid-acting)

T = titrate doses to achieve glucose levels 5-8 (monitor glucose 4x/day)

22
Q

Define Sliding Scale Insulin Therapy.

A

The sliding scale allows for the nurse to measure how much insulin is required based on the glucose levels

  • Always check blood sugar levels before meals!
  • Give insulin, based on their blood sugar levels
  • The insulin dose required is based on the sugar levels BEFORE the meal.
23
Q

Define Diabetes Mellitus.

A

Type 2 diabetes is an adult-onset disease. It is caused by insulin resistance due to a high intake of sugar. It is a chronic disease characterized by insufficient insulin production in the pancreas or when the body cannot efficiently use the insulin it produces. This leads to an increased concentration of glucose in the bloodstream (hyperglycemia).

24
Q

Treatments for DM Type II (Medications).

A
  1. Oral antidiabetic Agents (oral hypoglycemic agents)
  2. Managing blood glucose levels
  3. Biguanides
  4. SGLT2 inhibitors
  5. Insulin therapy
25
Q

Define Biguanides.

A

Reduces GI glucose absorption while also increasing cell glucose uptake and insulin release

  • By reducing GI glucose absorption we decrease the amount of energy in the intestines, stomach etc. This will ultimately slow down digestion and GI function overall. This increases metabolism but slows down digestion at the cellular level.
  • By increasing cell glucose uptake and insulin release, the blood glucose levels will decrease and the cells with be able to function (create ATP and carry out cellular functions)
26
Q

Biguanides Medications

A

Metformin (Glucophage)

27
Q

Define SGLT2 Inhibitors.

A

Increase glucose diuresis (gets rid of glucose through the urine in order to decrease serum glucose levels)

  • SGLT2 = transporter of glucose in proximal nephron tubule, increasing glucose reabsorption by the kidney
  • Inhibition = decreases glucose uptake and increases glucose excretion through the urine
28
Q

SGLT2 Inhibitor Medications.

A

Canagliflozine (Invokana)

29
Q

Define Sulfonylureas.

A

Increases insulin release and receptor sensitivity!

This allows for more insulin secretion to assist in glucose uptake by the cells as well as increases the sensitivity of the insulin receptor sites.

30
Q

Sulfonylureas Medications.

A

Glyburide (DiaBeta)

31
Q

Incretin Enhancers function and Medications

A

Stimulates Insulin release

Meds: Dulaglutide (Trulicity)

32
Q
A

Pharmacology (27 decks)

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