S2L2 - Diabetes Flashcards

1
Q

What does insulin do?

A

Regulates glucose storage

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2
Q

What does glucagon do?

A

Modulates glycogen stores for release

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3
Q

What does somatostatin do?

A

Inhibits secretory cells

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4
Q

What does gastrin do?

A

Stimulates gastric acid secretion

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5
Q

What is type III and IV diabetes?

A

Type III is induced by other causes like pancreatitis or drug therapy
Type IV is gestational

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6
Q

How is insulin formed?

A

From pro-insulin within beta cell golgi

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7
Q

What is formed in equal amounts with insulin?

A

C-peptide

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8
Q

What degrades insulin?

A

60% liver and 40% kidney but reversed in insulin treated patients

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9
Q

What stimulates insulin release?

A

Vagus nerve stimulation and blood glucose levels

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10
Q

What are the target tissues of insulin?

A

Liver, fat and muscle

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11
Q

What is the insulin effect on the liver?

A

Inhibits glycogenolysis, conversion of AAs to glucose and FAs and AAs to keto acids, promotes glucose storage as glycogen and increases TG synthesis

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12
Q

What is the insulin effect on muscle?

A

Increases AA and glucose transport and glycogen and protein synthesis

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13
Q

What is the insulin effect on adipose tissue?

A

Increases TG storage and glucose transport into cells

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14
Q

What are the routes of insulin administration and the formulations

A

Inhaled not well tolerated, SQ most often, IV in emergency

Rapid, short, intermediate and long

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15
Q

How is DKA managed?

A

saline hydration, regular insulin infusion every 2 hours, potassium serum level maintenance which can translate to hyponatremia

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16
Q

What is HHS?

A

Hyperosmolar hyperglycemic syndrome - elevated blood glucose level complication in T2D with similar symptoms to DKA, but management more focused on hydration

17
Q

What are the symptoms and management of hypoglycemia? Why does it happen?

A

Tachycardia (fast HR), diaphoresis (sweating), tremor, nausea, confusion - treat with glucose or glucagon (oral or injectable) - complication of therapy

18
Q

What are sulfonylureas and how do they work?

A

Insulin secretory agents that stimulate the pancreas - they close K channels depolarizing the cell and causing calcium influx to stimulate insulin release

19
Q

Why are sulfonylureas not used anymore?

A

Can give hypoglycemia and increased drug activity because of liver and kidney dysfunction

20
Q

What are the sulfonylurea drugs?

A

Glyburide, glipizide and glimepiride

21
Q

What are the newer insulin secretory drugs?

A

Meglitinide class - repaglinide
D-Phenylalanine - nateglinide
Used in patients with sulfur allergy - similar MOA and benefits of sulfonylurea

22
Q

What is metformin?

A

A biguanide - inhibits the conversion of lactic acid to glucose via gluconeogenesis in the liver by activating AMPK - stimulates glycolysis in tissues and reduces plasma glucagon levels

23
Q

What can happen in chronic metformin use? and how is it treated?

A

lactic acidosis - MALA - drug builds up with no way to metabolize or clear - treated by sodium bicarbonate administration (to balance acid) or given dialysis (to clear drug)

24
Q

What are thiazolidinediones?

A

Pioglitazone and rosiglitazone
Regulate PPAR-gama to regulate muscle and fat expression to increase insulin sensitivity by helping glucose metabolism and adipose storage

25
What else are thiazolidinediones used for and what are the risks?
Cholesterol profile | Low hypoglycemia risk - but increase cardiac event risk
26
What are alpha-glucosidase inhibitors?
Acarbose and miglitol | Inhibit intestinal alpha-glucosidase - delays absorption of starch and disaccharides
27
What are amylin analogs?
Pramlintide Suppress glucagon release and cause delayed gastric emptying and anorectic effects Used in patients who need additional therapy
28
What is incretin therapy?
Exenatide - analog of GLP-1 to decrease glucagon release and increase insulin release Sitagliptin - inhibits DDP-4 which will increase GLP-1 and GIP levels (also increase insulin release) Given in combination to T2D patients with high blood sugar