Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology - Fall 2024 > Diabetes > Flashcards

Diabetes 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How does proinsulin become insulin?

A
  • Proinsulin is cleaved into Insulin and C-peptide.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does Amylin do?

A

*Amylin is inhibitory to Glucagon (and a little to insulin as well)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does Somatostatin do?

A

*Short acting (5min) inhibitory effect on both insulin & glucagon right after eating.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the homeostatic level of blood glucose?

A

90mg/100mL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How quickly is glycogen used up?

A

Completely used up in 24 hours.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

*Polyuria, Polydipsia, & Polyphagia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What characterizes Type 1 DM?

A

*Autoimmune destruction of βcells in the pancrease. Insulin dependent.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What characterizes Type 2 DM?

A

*Usual metabolic syndrome, non-insulin dependent but will convert to Type I if untreated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What characterizes Type 3 DM?

A

*Temporary ↑ BG (pancreatitis, drug therapy, etc.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What characterizes Type 4 DM?

A

*Gestational

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are three clinical manifestations of chronic type 2 DM?

A
  1. Recurrent infections
  2. Vision problems
  3. Neuropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is nonenzymatic glycosylation?

A

*The process by which chronically high blood sugars attach to your hemoglobinA1C.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

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

A

4-5%

> 7%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

A

*Diabetic Retinopathy
*Diabetic Nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

Continuous 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)

59
Q

Sitagliptin

A

DDP-4 antagonist (dipeptidyl peptidase-4) which enhances the effects of incretin.

pancreatic cancer risk

60
Q

semaglutide

A

Incretin (GI hormones)

  • GLP 1 agonist (glucagon-like polypeptide-1)

pancreatic cancer risk

61
Q

acarbose

A

oral antidiabetic agents

alpha-glucosidase inhibitor

62
Q

Insulin - Rapid acting (3)

A
  • Lispro, aspart, glulisine
63
Q

Insulin - Short acting (Regular) (2)

A
  • Novolin, humulin
64
Q

Insulin - Intermediate acting (1)

A
  • Neutral protamine Hagedorn
65
Q

Insulin - Long acting (2)

A
  • Glargine, detemir
66
Q

The pathway for insulin release from pancreatic beta cells involves a series of tightly regulated steps:

A
  1. Glucose Uptake
    When blood glucose levels rise glucose enters beta cells via GLUT2 transporters
  2. Increase in ATP/ADP Ratio
    Elevated ATP levels lead to the closure of ATP-sensitive potassium (K+ATP) channels on the beta cell membrane.
  3. Membrane Depolarization
    The closure of K+ ATP channels causes the beta cell membrane to depolarize (since potassium efflux is reduced).

Membrane depolarization opens voltage-gated calcium channels (VGCCs).

  1. Calcium Influx
    The opening of VGCCs allows an influx of calcium ions (Ca2+) into the cell.

The rise in intracellular calcium concentration is a crucial trigger for insulin release.

  1. Exocytosis of Insulin
    The increased intracellular Ca2+
    concentration stimulates the exocytosis of insulin-containing vesicles.

Insulin is released from these vesicles into the bloodstream to exert its effects on target tissues, such as muscle, liver, and adipose tissue.

Additional Modulatory Inputs
Incretins: Hormones like GLP-1 (glucagon-like peptide-1) enhance insulin secretion by increasing cAMP and amplifying the effect of calcium on insulin granule exocytosis.

Autonomic Nervous System: Both the sympathetic and parasympathetic nervous systems can modulate insulin release.

Pharmacology - Fall 2024 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions