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AG1 > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

Drugs for T1 DM

A
  1. Bolus insulins
    -rapid acting: Lispro
    -short acting: Humulin R
  2. Basal insulins
    -intermediate: Isophan (NPH)
    -long-acting: Glargine
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2
Q

What is a rapid-acting drug for T1 DM?

A

Lispro

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3
Q

What is a short-acting drug for T1 DM?

A

Humulin R

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4
Q

What is an intermediate-acting drug for T1 DM?

A

isophane (NPH)

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4
Q

What is the long-acting drug for T1 DM?

A

Glargine

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5
Q

Drugs for T2 DM

A
  1. sulphonylurea: glyburide
  2. biguanides: metformin
  3. meglitinides: repaglinide
  4. glucosidase inhibitors: acarbose
  5. thiazolidinediones: rosiglitazone
  6. SGLT inhibitors: dapagliflozins
  7. DPP-4 inhibitors: sitagliptin
  8. Incretin mimetics/GLP-1 agonist: exenatide
  9. amylin analog: pramlintide

7 and 8 are drugs that improve incretin action and act via GLP-1.

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6
Q

Pathogenesis of the long-term complication of diabetes

A
  1. formation of advanced glycation end products (AGE): natural rate of AGE formation is accelerated in the presence of hyperglycemia. AGE binds to RAGE which is expressed on inflammatory cells like macrophage and T cell, and in endothelium and vascular smooth muscle. It then release pro-inflammatory cytokines and growth factors from macrophages. Generate ROS in endothelial cells. increase procoagulant activity on endothelial cells and macrophages. enhance proliferation of vascular smooth muscle cells and synthesis of ECM. AGE can enhance protein deposition like LDL, accelerating atherosclerosis. while albumin gets trapped within capillaries aka hyaline arteriosclerosis (diabetic microangiopathy)
  2. activation of PKC: pro-angiogenic molecules like VEGF causes neovascularization (diabetic retinopathy), increase deposition of ECM & basement membrane material.
  3. disturbances of polyol pathways: in tissues that dont require insulin for glucose transport like nerves, lens, kidneys, hyperglycemia increases intracellular glucose which is then metabolised > sorbitol aka polyol> fructose. The reaction sorbitol converting into fructose requires NADPH. NADPH is also needed in a reaction that reproduces GSH. GSH is an antioxidant, hence any reduction in GSH causes high risk of oxidative stress to cells. Thus, diabetic neuropathy (glucose neurotoxicity) in neurons with persistant hyperglycemia.
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7
Q

Late complications of diabetes

A

Pancreas: reduced number & size of islets (mostly T1), leukocytic infiltration of islet (lymphocytes and macrophages), amyloid replacement of islets in T2, fetal islet hyperplasia in response to maternal hyperglycemia
1. macrovascular disease (arteries)
* atherosclerosis
* hyaline arteriolosclerosis
2. microangiopathy (basement membranes of small vessels)
* diabetic capillaries are more leaky to plasma protein
3. diabetic nephropathy (kidneys)
* glomerular lesions
* renal vascular lesions
* pyelonephritis
4. retinopathy (retina)
* divided into nonproliferative retinopathy and proliferative retinopathy
* nonproliferative retinopathy: retinal exudates
* proliferative retinopathy is a process of neovascularization and fibrosis: leads to blindness
5. neuropathy (nerves)
* motor and sensory function

list not exhaustive, please refer robbins 9 ed pg762

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8
Q

What are the insulin secretagogues?

A

Glyburide (sulfonylurea)
Repaglinide (meglitinide)

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9
Q

What are the insulin sensitisers?

A

Metformin ( biguanide)
Rosiglitazone (thiazolidinedione)

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10
Q

What is an alpha-glucosidase inhibitor?

A

Acarbose

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11
Q

What is a SGLT inhibitor?

A

Dapagliflozin

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12
Q

What is a DPP-4 inhibitor?

A

Sitagliptin

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13
Q

What is an incretin mimetic/GLP-1 agonist?

A

Exenatide

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14
Q

What is an amylin analog?

A

Pramlintide

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15
Q

Which of the following statements is correct regarding insulin glargine?
A. It is primarily used to control postprandial hyperglycemia.
B. It is a ‘peakless’ insulin.
C. The prolonged duration of activity is due to slow dissociation from albumin.
D. It should not be used in a regimen with insulin lispro or glulisine.
E. It may be adminsitered intravenously in emergencies.

A

B.
It is used for basal glucose control, not postprandial. The prolonged duration is due to its low pH, which leads to precipitation at injection site and resultant extended action.

*glargine should not be combined with other insulins in SAME syringe

16
Q

A pt with T2 DM has a blood glucose of 400mg/dL today at his office visit. The physician would like to give some insulin to bring glucose down before he leaves the office. Which would lower the glucose in the quickest manner?

A

insulin aspart
as it is a rapid-acting insulin with an onset of action within 15 to 20 mins.

17
Q

Which pairing is correct?
A. DPP-4 inhibitor: inhibits breakdown of complex carb
B. glinide: increases insulin sensitivity
C. sulfonylurea: increase insulin secretion
D. thiazolidinedione: decrease hepatic gluconeogenesis

A

C.
DPP-4 inhibitors work by inhibiting breakdown of incretins, thereby increasing postprandial insulin secretion, decreasing postprandial glucagon.
Glinides increase insulin secretion. TZD work primarily by increasing insulin sensitivity.

18
Q

What is the characteristic of metformin?

A

Metformin decreases hepatic glucose production.
It inhibits hepatic gluconeogenesis. It is the preferred initial agent for management of T2 DM.

19
Q

Which is the most appropriate initial oral agent for managements of T2 DM in pt with no other comorbid conditions?
A. glipizide
B. insulin
C. metformin
D. pioglitazone

A

C

20
Q

A woman with T2 DM is diagnosed with heart failure. Which med is CI?

A

pioglitazone/rosiglitazone
TZDs can cause fluid retention and lead to worsening of heart failure.

21
Q

A 69yo man with T2 DM and advanced chronic kidney disease, which med is CI?

A

metformin.
Possibility of lactic acidosis

22
Q

Which drug for diabetes would be least likely to cause weight gain?
A. glimepiride
B. liraglutide
C. pioglitazone
D. repaglinide
E. insulin glulisin

A

B. incretin mimetics/GLP-1 agonist are associated with weight loss due to their ability to enhance satiety. The rest causes weight gain

23
Q

Pt with T2 DM taking metformin, fasting glucose level are in range but postprandial glucose is uncontrolled. All the following drugs would be appropriate to add to metformin to target postprandial glucose except:
A. acarbose
B. exenatide
C. insulin aspart
D. pramlintide

A

D. Pramlintide should be used only in conjunction with mealtime insulin. All drugs target postprandial gllucose.

24
Q

Which pairing is correct?
A. canagliflozin: lactic acidosis
B. metformin: UTI
C. nateglinide: heart failure
D. liraglutide: pancreatitis

A

D. incretin mimetics>pancreatitis. Lactic acidosis is rare but a serious side effect of metformin. AE of canagliflozin are genital mycotic infxn, UTI and urinary freq. Nateglinide causes hypoglycemia. TZD> heart failure.

AG1 (2 decks)

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