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Pharm (Fall 2022) > Diabetes (Exam IV) > Flashcards

Diabetes (Exam IV) Flashcards

1
Q

What are the two types of secretory tissue found in the pancreas?
What are the functions of these two tissues?

A
  • Exocrine Glands - Digestive enzymes
  • Endocrine Glands - Hormones
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2
Q

What tissue type is located in the endocrine portions of the pancreas that produces secretory hormones? What cells make up this tissue.

A

Islet of Langerhans
- Alpha cells
- Beta cells
- Delta cells
- G cells
- F cells

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3
Q

What is produced in the Αlpha cells of the Islet of Langherhans?
What about the Βeta cells?
What about the Delta cells?

A
  • α → Glucagon
  • β → Insulin & Amylin
  • δ → Somatostatin
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4
Q

How does proinsulin become insulin?

A
  • Proinsulin is cleaved into Insulin and C-peptide.
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5
Q

What does Amylin do?

A
  • Amylin is inhibitory to Glucagon (and a little to insulin as well)
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6
Q

What does Somatostatin do?

A
  • Short acting (5min) inhibitory effect on both insulin & glucagon right after eating.
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7
Q

What receptor type are insulin receptors? What do they do when bound with insulin?

A
  • Tyrosine Kinase Receptors
  • Phophorylate effector proteins to promote GLUT transporters to bind to the cell surface.
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8
Q

What is the homeostatic level of blood glucose?

A

90mg/100mL

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9
Q

How quickly is glycogen used up?

A

Completely used up in 24 hours.

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10
Q

Why type of receptor is a glycogen receptor?
What organ takes in glycogen for energy storage & also breaks it down for use?

A
  • GPCR.
  • Liver.
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11
Q

What signs/symptoms are characteristic of diabetes mellitus? (particularly type I)

A
  • Polyuria, Polydipsia, & Polyphagia
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12
Q

What characterizes Type 1 DM?

A
  • Autoimmune destruction of βcells in the pancrease. Insulin dependent.
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13
Q

What characterizes Type 2 DM?

A
  • Usual metabolic syndrome, non-insulin dependent but will convert to Type I if untreated.
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14
Q

What characterizes Type 3 DM?

A
  • Temporary ↑ BG (pancreatitis, drug therapy, etc.)
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15
Q

What characterizes Type 4 DM?

A
  • Gestational
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16
Q

At what level of βcell destruction is a diagnosis of Type I DM official?
What two types of Type 1 DM exist & which is more common?

A
  • 80% of βcells destroyed.
    1. Immune (more common)
    2. Idiopathic (genetic)
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17
Q

Why do Type 1 diabetics often have weight loss?
What might occur if a Type 1 diabetic is not given insulin replacement.

A
  • Due to the inability to process carbohydrates.
  • Fatty acid oxidation → ↑ketones → ↓pH
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18
Q

Which Diabetes Mellitus sub-type is characterized by relative deficiency of insulin secretion & tissue insulin resistance?
What occurs at the cellular level with insulin resistance?
What would blood levels of insulin be in a type 2 DM patient?

A
  • Type II DM (the artist formerly known as “adult onset DM”)
  • Downregulation of GLUT transporters.
  • Initial ↑ insulin level; ↓ insulin level developed over time.
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19
Q

What blood glucose levels would you expect to see with non-ketotic hyperosmolar syndrome?
What symptoms would be associated with this condition?

A

> 600mg/dL
- Dehydration & eventual coma/death.

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20
Q

What are three clinical manifestations of chronic type 2 DM?

A
  1. Recurrent infections
  2. Vision problems
  3. Neuropathy
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21
Q

What is nonenzymatic glycosylation?

A
  • The process by which chronically high blood sugars attach to your hemoglobinA1C.
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22
Q

What is a normal Hemoglobin A1C?
What is a very abnormal one?

A

4-5%
> 7%

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23
Q

Describe the hyperglycemic effect on the polyol pathway.
Where is this effect most prominent?

A
  • Sorbitol & Fructose increase intracellularly = ↑ osmotic pressure = Hypotonicity of the cell & cell rupture.
  • Eye lens, nerves (neuropathy), & RBCs (anemia)
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24
Q

What microvascular areas of damage are associated with Type 2 DM?

A
  • Diabetic Retinopathy
  • Diabetic Nephropathy
25
What are the results of gestational diabetes mellitus?
- ↑ child birth weight - ↑ risk for 2nd pregnancy - ↑ risk for development of Type 2 DM.
26
What should a fasting blood glucose be in a healthy individual? Describe the glucose tolerance test.
- < 100 mg/dL - A sugary drink is imbibed and blood glucose levels are drawn 1-2 hours post ingestion. More definitive than a fasting level.
27
Porcine insulin administration can cause local ______ at the injection site.
atrophy
28
What are insulin secretagogues? What non-drug insulin secretagogues should be known?
- Anything that causes insulin release 1. Glucose 2. Amino acids 3. Hormones 4. Fatty acids 5. Incretins
29
What drugs were noted in lecture to be insulin secretagogues?
- **Sulfonylureas** - Isoproterenol
30
GLUT-4 has an _______ affinity for glucose. GLUT-2 has a _______ affinity for glucose. What does this mean?
- Intermediate - Low; this means that high levels of blood glucose are required to stimulate this transporter.
31
What is the complete process for how insulin is stimulated & released from a cell via extracellular glucose?
1. ↑ ECF glucose 2. Glucose brought to ICF via GLUT 3. Glucose metabolized & ATP created 4. ↑ ATP closes K⁺ rectifying channels 5. Closed K⁺ channels = depolarization 6. Depolarization = ↑ pCa⁺⁺ 7. ↑ pCa⁺⁺ = VP1 → VP2 & vesicular release of insulin via exocytosis.
32
What effects are elicited by insulin reacting with the insulin tyrosin kinase receptor?
- ↑ uptake of glucose via more GLUT proteins - ↑ glycogen formation - Activation of more transcription factors.
33
What GLUT transporters have a very high affinity?
- GLUT-3; Brain
34
What GLUT transporters have a very low affinity?
- GLUT-2; β cells of pancrease, liver, & kidney
35
What GLUT transporters have an intermediate affinity?
- GLUT-4; Muscles & adipose tissue.
36
What are the 3 endocrine effects of insulin?
1. ↓ glycogenolysis = ↓ release of liver glucose. 2. ↓ conversion of fatty acids & amino acids to keto acids. 3. ↑ glycogen formation/storage.
37
What non-drug factors inhibit insulin secretion?
- Insulin itself, Leptin, SNS activity, chronically high glucose, & amylin
38
What drugs inhibit insulin secretion? What type of DM do these then cause?
- Diazoxide, phenytoin, vinblastine, colchicine - Type III DM
39
70/30 insulin is a combination of what? How effective is the combination?
Combo: - Short acting (regular) - Intermediate acting (Neutral protamine hagedorn NPH). The 70/30 combo is decent but not as good as a basal/bolus method with rapid-acting & long-acting.
40
Why is nasal insulin not in more frequent use?
Nasally administered insulin causes bronchoconstriction.
41
What method is preferable for tight blood glucose level control?
- Continous subcutaneous insulin infusion devices (CSIID) - Basal Bolus method with long acting (next best)
42
1 unit of rapid-acting insulin "covers" how many carbs that are eaten?
- 1 unit RA insulin = 12-15g carbs (ex. 75g carb meal requires 5 units RA insulin)
43
1 unit of rapid-acting insulin drops blood glucose by _____ mg/dL.
- 50mg/dL
44
When metabolic rate increases, what occurs with insulin requirements?
- Insulin requirement increases as well
45
At what blood glucose level is one considered hypoglycemic?
- < 60mg/dL
46
What drug class is first-line therapy for DM? What drug is prototypical of this class and what is its mechanism of action? What is a normal dose & what is the max dose where one would want adjunct therapy?
- Biguanides =**Metformin** - Reduces hepatic glucose production - Dosing starts at 500mg & maxes out at 2500mg/day
47
What drug classes are insulin secretagogues? Which of these can have trigger sulfa- allergies? What is this drug classes MOA?
- Sulfonylureas (**sulfa**) - Meglitinide - Phenylalanine derivatives - MOA: Binds to rectifying K⁺ channel in pancreatic β cell decreasing threshold & causing depolarization. Depolarization causes Ca⁺⁺ influx & vesicular release of insulin.
48
1st generation sulfonylureas have a ______ dose than 2nd generation sulfonylureas. What does this mean for safety?
- **higher** - 1st generation have a higher doses = more side effects. 2nd generation is safer with its lower doses.
49
Which sulfonylurea is associated with bad outcomes and increased instances of MI?
- Tolbutamide.
50
Which class of insulin secretagogues has much less efficacy due their very short T½ & duration of action?
- Meglitinides
51
What is the mechanism of action for Thiazolidinediones (Tzd's)? What is the prototypical drug of this class & what is the main risk associated with it?
- ↓ insulin resistance by ↑ GLUT-4 prevalence. - Rosiglitazone = risk of MI, especially with nitrate & insulin use.
52
What is the mechanism of action of α-glucosidase inhibitors? When is this drug beneficial? What side effects are typical?
- Blockade of digestion of complex carbs & thus **blocking uptake of glucose**. - Drug is beneficial in pre-diabetics & high starch diets. (think Japan) - GI problems (flatulence, diarrhea, etc.)
53
What is the mechanism of action of bile-acid binding resins? What side effects are typical?
- BABR's bind to food & prevent absorption of glucose. - GI upset.
54
How do Amylin Analogs treat DM? What is this drug's route of administration? Where is Amylin naturally produced in the body?
- ↓ glucose release. - IV/IM (not oral) - Amylin is produced in the βcells of the pancreas.
55
What drug class treats DM through the usage of GI hormones? What are these specifically & their MOA's? What risk (though small) is conferred by these drugs?
- Incretin-based therapies. - GLP-1 (Glucagon-like polypeptide-1) = stimulates insulin release & inhibits glucagon release. - DPP-4 (Dipeptidyl Peptidase-4 Antagonist) = blocks breakdown of GLP-1 - Pancreatic cancer.
56
Gliflozins are also known as ______ ________. What suffix is denoted by this drug class?
- SLGT2 Inhibitors - -flozin
57
How do Gliflozin's work? What is the result of this & what side effects can occur?
- Prevention of glucose reabsorption in the PCT - Glycosuria (**perineal necrosis**, ↓BP, weight loss, & dehydration).
58
Where do SLGT-2 inhibitors work in the kidneys? How much glucose is reabsorbed despite administration of these drugs?
- S1 segment of the PCT. - 20-30% glucose reabsorption in S2 (increased by SLGT-2 inhibition, normally 10% in S2 segment)

Pharm (Fall 2022) (23 decks)

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