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IC > Tx of Diabetes > Flashcards

Tx of Diabetes Flashcards

1
Q

Type 1 DM

A

AI disease
Lack of endogenous insulin

replace insulin

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2
Q

Type 2 DM

A

Noninsulin dependent diabetes
b cells desensitized to glucose challenge
peripheral tissues resistant to insulin actions

improve insulin sensitivity at early stages and replace insulin in later stages

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3
Q

Type 3 DM

A

non pancreatic causes

Drugs impair glucose tolerance- corticosteroids, thiazides, oral contraceptives

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4
Q

Type 4 DM

A

gestational

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5
Q

Goals of treatment of DM

A

Treat hyperglycemia to avoid long term complications
-fasting glucose 90-120 mg/dl
2 hr post prandial- below 150 mg/dl
HbA1c- below 7%

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6
Q

Insulin

A

51 AA peptide
Two peptide chains linked by disulfied bond
Preproinsulin>proinsulin> insulin + free C peptide

Acts in liver, muscle, and adipose tissues to decrease blood glucose levels and shift from energy use to storage
-Acts through stimulation of tyrosine kinase receptor

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7
Q

Insulin secretion and effects

A

Stimulated by increase ATP/ADP ratio which is modulated by glucose, AA, FA, parasympathetic activity

Glucose causes Increase in ATP which closes the K+ channel in the islet cell, stopping K efflux and depolarizing the cell (glucose is low, cell is hyperpolarized). Depolarizing cell will signal Ca++ influx which causes exocytosis of insulin

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8
Q

Sulfonyl urea drugs

A

Block K+ channels and depolarize islet cells, causing Ca++ influx and insulin vesicle release

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9
Q

Exogenous insulin

A

Subq administration- allowing for slower absorption
Tailored to pts activity and diet
AE: hypoglycemia, insulin allergy, lipoatrophy, weight gain, insulin edema

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10
Q

Rapid acting insulin

A

insulin lispro, insulin aspart, insulin glulisine

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11
Q

Short acting insulin

A

novolin R, humulin R

regular length insulin
-8 hrs

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12
Q

Intmdt acting insulin

A

Humulin N

Novolin N

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13
Q

Long acting insulin

A

insulin detemir, insulin glargine (levemir and lantus)

lasts 24 hrs

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14
Q

Tx of DKA

A

IV infusion of regular insulin at low rate

-administer glucose along to prevent hypoglycemia and fluid and electrolytes

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15
Q

Sulfonylureas

A

secretagogues

  • inhibit activity of K+ channel on islet cell
  • activate residual b cells to release insulin by binding to and activating SUR1 (subunit of the K/ATP channel)
  • some pts may be allergic
  • decrease hepatic clerance of insulin and decrease serum glucagon by stimulating somatostatin release
  • can cause weight gain because using more glucose, hypoglycemia
  • orally available, metabolized by liver, metabolites excreted in urine
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16
Q

First generation sulfonylureas

A

Tolbutamide, tolazamide, chlorpropamide

for those prone to hypoglycemic episodes

17
Q

Second gen sulfonylureas

A

binds to SUR1 with higher affinity, lower dose req’d

Glyburide, glipizide, glimepiride

18
Q

Contraindications of sulfonylureas

A

type 1 DM
pregnancy
lactation
significant hepatic or renal insufficiency

19
Q

Meglitinides

A

Secretagogues

  • similar MOA to sulfonylurea
  • Repaglinide, nateglinide (more rapid)
  • cleared by liver (not for those with hepatic insufficiency)
  • hypoglycemia AE
20
Q

Biguanides

A

Metformin
Insulin sensitizers
Euglycemic effect- helps maintain normal blood glucose levels without producing hypoglycemia

21
Q

MOA of Metformin

A
  • inhibits gluconeogenesis in the liver, helpful in maintaining normal blood glucose level
  • inc peripheral insulin sensitivity
  • actings AMP-activated protein kinase
  • Inhibits mTOR-C1
22
Q

Clinical use of metformin

A

1st line for type 2 DM
Taken with food
also used for PCOS or fatty liver disease

23
Q

Metformin toxicity

A

Lactic acidosis- impair hepatic metabolism of lactic acid, but rare

Most AE are GI related- diarrhea, abd discomfort, nausea, metabollic taste, reduced B12 absorption

24
Q

Thiazolidinediones (TZDs)

A

Rosiglitazone and Pioglitazone
-PPARy agonists with PPARa agonist activity
(rosiglitazine 10x ppary affinity than pioglitazone)

25
Q

MOA of TZD

A

IN adipose tissue, PPARy activators promote transport of serum lipids to adipose tissue

  • may activate ppary in other tissues to promote insulin sensitivity- dec hepatic gluconeogenesis, enhance uptake of glucose by skeletal muscle cells
  • reduce glucose and triglycerides

metabolized by liver, so can cause hepatic toxicity
chf, weight gain

26
Q

alpha-glucosidase inhibitors

A

Inhibitor of intestinal glucose absorption

-competitive and reversible inhibitors of pancreatic alpha-amylase and intestinal alpha-glucosidase enzymes

27
Q

Acarbose and miglitol

A

a-glucosidase inhibitors
-inhibits intestinal glucose absorption

-reduces fasting glucose, a1c and post prandial glucose
no risk for hypoglycemia

can cause flatulence, bloating, diarrhea
not recommended for pts with ibd

28
Q

Incretins

A

glucagon like peptide1 (GLP1) and glucose dependent insulinotropic peptide (GIP)

Released by cells in ileum, which is stimulated by nutrients entering the gut
-increase insulin secretion, decrease glucagon secretion, delay gastric emptying, decrease appetite

29
Q

GLP1

A

Exenatide, liraglutide (victoza), albiglutide, duraglutide
(tide ending)
-increase insulin secretion, decrease glucagon secretion, delay gastric emptying, decrease appetite

  • low risk of hypoglycemia, AE- nausea, vomiting, diarrhea
  • promote weight loss
30
Q

DDP4- Inhibitors of Dipeptidyl peptidase 4

A

Inhibitor of enzyme that degrades endogenous incretins (GLP-1 and GIP)

  • increase level of endogenous incretins
  • Sitagliptin, Saxagliptin, Linagliptin, Alogliptin
  • Monotherapy or in combo with metformin (not with GLP1 analogs)
31
Q

SGLT2 inhibitors

A

-Canagliflozin, dapagliflozin, empagliflozin

  • Glucose reabsorbed in proximal tubules by sodium glucose transporter (SGLTs)
  • Inhibition causes glycosuria and lowers glucose levels
  • Efficacy reduced in chronic kidney disease

Side effects- inc incidence of genital infections and UTI

  • manageable with better hygiene
  • can also lead to intravascular volume contraction and hypotension

-SGLT2 inhibition promotes weight loss

32
Q

Pramlintide

A

Amylin analog

  • increase insulin secretion, decrease glucagon secretion, delay gastric emptying, decrease appetite, decreases appetite (hypothalamus)
  • preprandial as adjunct to insulin improves post prandial glucose control

AE: hypoglycemia and GI symptoms

33
Q

Covesevalam

A

Bile acid sequestrant, cholesterol lowering drug
-Can reduce glucose absorption via decreasing FXR nuclear receptor activation

may exacerbate hypertriglyceridemia

34
Q

Bromocriptine

A

Dopamine agonist
-lowers glucose levels
AE- nausea, fatigue, dizziness, vomiting, headache

35
Q

Combo therapy of diabetes

A

different MOA
target diff proteins

Begin with monotherapy with metformin, GLP1 mimic, SGLT2 inh, GPP-4 inh
Sulfonylureas and TZDs are second choice
Add additional agents as needed
Add insulin therapy to other agents

IC (31 decks)

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