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Pharmacology fall 2024 > 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
Q

What are the results of gestational diabetes mellitus?

A
  • ↑ child birth weight
  • ↑ risk for 2nd pregnancy
  • ↑ risk for development of Type 2 DM.
26
Q

What should a fasting blood glucose be in a healthy individual?
Describe the glucose tolerance test.

A
  • < 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
Q

Porcine insulin administration can cause local ______ at the injection site.

A

atrophy

28
Q

What are insulin secretagogues?
What non-drug insulin secretagogues should be known?

A
  • Anything that causes insulin release
    1. Glucose
    2. Amino acids
    3. Hormones
    4. Fatty acids
    5. Incretins
29
Q

What drugs were noted in lecture to be insulin secretagogues?

A
  • Sulfonylureas
  • Isoproterenol
30
Q

GLUT-4 has an _______ affinity for glucose.
GLUT-2 has a _______ affinity for glucose. What does this mean?

A
  • Intermediate
  • Low; this means that high levels of blood glucose are required to stimulate this transporter.
31
Q

What is the complete process for how insulin is stimulated & released from a cell via extracellular glucose?

A
  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
Q

What effects are elicited by insulin reacting with the insulin tyrosin kinase receptor?

A
  • ↑ uptake of glucose via more GLUT proteins
  • ↑ glycogen formation
  • Activation of more transcription factors.
33
Q

What GLUT transporters have a very high affinity?

A
  • GLUT-3; Brain
34
Q

What GLUT transporters have a very low affinity?

A
  • GLUT-2; β cells of pancrease, liver, & kidney
35
Q

What GLUT transporters have an intermediate affinity?

A
  • GLUT-4; Muscles & adipose tissue.
36
Q

What are the 3 endocrine effects of insulin?

A
  1. ↓ glycogenolysis = ↓ release of liver glucose.
  2. ↓ conversion of fatty acids & amino acids to keto acids.
  3. ↑ glycogen formation/storage.
37
Q

What non-drug factors inhibit insulin secretion?

A
  • Insulin itself, Leptin, SNS activity, chronically high glucose, & amylin
38
Q

What drugs inhibit insulin secretion?
What type of DM do these then cause?

A
  • Diazoxide, phenytoin, vinblastine, colchicine
  • Type III DM
39
Q

70/30 insulin is a combination of what?
How effective is the combination?

A

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
Q

Why is nasal insulin not in more frequent use?

A

Nasally administered insulin causes bronchoconstriction.

41
Q

What method is preferable for tight blood glucose level control?

A
  • Continous subcutaneous insulin infusion devices (CSIID)
  • Basal Bolus method with long acting (next best)
42
Q

1 unit of rapid-acting insulin “covers” how many carbs that are eaten?

A
  • 1 unit RA insulin = 12-15g carbs (ex. 75g carb meal requires 5 units RA insulin)
43
Q

1 unit of rapid-acting insulin drops blood glucose by _____ mg/dL.

A
  • 50mg/dL
44
Q

When metabolic rate increases, what occurs with insulin requirements?

A
  • Insulin requirement increases as well
45
Q

At what blood glucose level is one considered hypoglycemic?

A
  • < 60mg/dL
46
Q

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?

A
  • Biguanides =Metformin
  • Reduces hepatic glucose production
  • Dosing starts at 500mg & maxes out at 2500mg/day
47
Q

What drug classes are insulin secretagogues? Which of these can have trigger sulfa- allergies?
What is this drug classes MOA?

A
  • 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
Q

1st generation sulfonylureas have a ______ dose than 2nd generation sulfonylureas. What does this mean for safety?

A
  • higher
  • 1st generation have a higher doses = more side effects. 2nd generation is safer with its lower doses.
49
Q

Which sulfonylurea is associated with bad outcomes and increased instances of MI?

A
  • Tolbutamide.
50
Q

Which class of insulin secretagogues has much less efficacy due their very short T½ & duration of action?

A
  • Meglitinides
51
Q

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?

A
  • ↓ insulin resistance by ↑ GLUT-4 prevalence.
  • Rosiglitazone = risk of MI, especially with nitrate & insulin use.
52
Q

What is the mechanism of action of α-glucosidase inhibitors?
When is this drug beneficial?
What side effects are typical?

A
  • 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
Q

What is the mechanism of action of bile-acid binding resins?
What side effects are typical?

A
  • BABR’s bind to food & prevent absorption of glucose.
  • GI upset.
54
Q

How do Amylin Analogs treat DM?
What is this drug’s route of administration?
Where is Amylin naturally produced in the body?

A
  • ↓ glucose release.
  • IV/IM (not oral)
  • Amylin is produced in the βcells of the pancreas.
55
Q

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?

A
  • 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
Q

Gliflozins are also known as ______ ________.
What suffix is denoted by this drug class?

A
  • SLGT2 Inhibitors
  • -flozin
57
Q

How do Gliflozin’s work?
What is the result of this & what side effects can occur?

A
  • Prevention of glucose reabsorption in the PCT
  • Glycosuria (perineal necrosis, ↓BP, weight loss, & dehydration).
58
Q

Where do SLGT-2 inhibitors work in the kidneys?
How much glucose is reabsorbed despite administration of these drugs?

A
  • S1 segment of the PCT.
  • 20-30% glucose reabsorption in S2 (increased by SLGT-2 inhibition, normally 10% in S2 segment)

Pharmacology fall 2024 (23 decks)

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