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Pharm Exam IV > Diabetes > Flashcards

Flashcards in Diabetes Deck (45):
1

Whats up with K in diabetic ketoacidosis?

Pt is probably hypokalemic, even if their serum K is WNL. When pt is acidotic, K enters blood from cellular compartment (via H+-K+ antiporter) making serum K relatively high compared to status. Insulin will push K into the cellular compartment, as will treating volume status. Be sure to check serum K continuously when treating pt and supplement if low.

2

How do you correct measured Na in a hyperglycemic patient?

true Na= Na + 0.016*(Glc-100)

3

Diabetic ketoacidosis: treatment approach

1- fluids to correct acidosis- give 1L NS (0.9%) then switch to 0.45% once Na is corrected. Add D5 once glucose >200. 2- Insulin 1-2 hours after fluids (beware, this could push hypokalemia further)- 0.1 units/kg bolus then 0.1u/kg/hr infusion (make sure they arent hypokalemic first). 3- Treat for K depletion (if K

4

Anion gap calculation:

AG= Na-(Cl + HCO3)

5

Diagnostic criteria for DM:

HgA1c>=6.5% OR FPG>=126 OR Sx + rPG>=200 OR 2 hr PG>=200 after OGTT

6

Diabetic ketoacidosis: treatment approach

1- fluids to correct acidosis- give 1L NS (0.9%) then switch to 0.45% once Na is corrected. Add D5 once glucose >200. 2- Insulin 1-2 hours after fluids (beware, this could push hypokalemia further)- 0.1 units/kg bolus then 0.1u/kg/hr infusion3- Treat for K depletion (if K

7

Diagnostic criteria for DM:

HgA1c>=6.5% OR FPG>=126 OR Sx + rPG>=200 OR 2 hr PG>=200 after OGTT

8

Which physiologic states stimulate insulin release?

Glucose (or any food) PO, GI hormones: Secretin, Incretins (GLP-1, GIP); parasympathetic stimulation.

9

Which physiologic states inhibit insulin release?

Sympathetic stimulation; somatostatin (released by Delta cells in pancreas); glucocorticoids (cortisol); beta blockes. Sympathetic stimulation is biphasic, initially inhibiting, then stimulating via b2 while inhibiting via a2

10

GLUT2 and GLUT4 transporters: role

GLUT2- located in Beta cells of pancreas. High Km- respond to high plasma glucose. GLUT4- located in muscle and adipose. Glucose uptake stimulated by insulin.

11

Lispro

ultra short acting insulin formulation- useful t bring down glucose immediately (not crystaline). 10-30 mins onset, peaks in 30-60;; total duration 3-5 hrs.

12

Aspart

ultra short acting insulin formulation. 10-30 mins onset, peaks in 30-60;; total duration 3-5 hrs.

13

Glulisine

ultra short acting insulin formulation. 10-30 mins onset, peaks in 30-60;; total duration 3-5 hrs.

14

NPH

Intermediate-acting insulin- (AKA isophane). Onset: 1-2 hrs; peak 4-8hrs; duration: 10-20 hrs.

15

Detemer

Long-acting insulin (not as long as glargine)- fatty acid attached increases albumin bindingOnset: 1-2 hrs; peak: 2-4 hrs; duration 12-20 hrs

16

Glargine

Lantus- Longest acting insulin. Inject sc at bedtime. No peak. Onset: 2-6 hrs; Duration: 22-24hrs

17

Insulin: safety

Preg cat B; hypoglycemia is largest risk

18

Metformin

1st line for type 2 DM (after diet and exercise). "Sensitizer" enhancing insulin effect by activating AMP-dependent protein kinase in muscle and liver (encourages FA oxidation, less fat in liver, inc. insulin sensitivity). Largest effect is blocking GNG and increasing glucose uptake. Inhibits microvascular complicatoins.

19

Metformin: safety

Side-effects: NV transient, dose-dependent. EtOH can cause lactic acidosis. half-life is 1.5-3h; CI in renal OR liver disease. Not metabolized, but renal clearance. Preg: B

20

Metformin (biguanides)

1st line for type 2 DM (after diet and exercise). "Sensitizer" enhancing insulin effect by activating AMP-dependent protein kinase in muscle and liver (encourages FA oxidation, less fat in liver, inc. insulin sensitivity). Largest effect is blocking GNG and increasing glucose uptake. Inhibits microvascular complicatoins.

21

Sulfonylureas- Glipizide

Stimulates insulin release in pancreas by binding to ATP-sensitive K channel (SU subunit)- closing it, causing depolarization, Ca influx, and exocytosis of insulin. Inexpensive!

22

Glipizide (sulfonylurea): safety

Can cause weight gain, hypoglycemia. CI in hepatic or renal disease. Preg: CNSAIDs exacerbate hypoglycemia induced by glipizide.

23

Meglitinides: Repaglinide

Same target as glipizide (ATP-sensitive K channel, SU subunit), same effect- enhanced insulin release. Vs Glipizide: Shorter-acting, faster response. Liver metabolism (CI in liver but NOT renal disease)Preg: CSame interaction profile, weight GAIN, hypoglycemia risk.

24

Pioglitazone (Thazolidinedione)

This is the only med that increases insulin sensitivity at target cells. Target is PPAR-gamma (peroxisome proliferator-activated gamma receptor) located in nucleus in adipose and muscle. Adipose: Modifies gene expression with effect of:Decreasing lypolysis and FFAs; reducing TNF-alpha, Leptin excretion; increasing adiponectin secretion (increases insulin activity)Muscle: increases glucose utilization.

25

Pioglitazone: safety

Increased risk of heart failure, fluid retention, weight GAIN; CI in liver disease, CVD. Black box warning for CVD. NOT hypoglycemic.

26

Exenatide: GLP-1 mimetics

GLP-1 (endogenous insulin stimulator) agonist- causes glucose-dependent increase in insulin secretion, better kinetic profile than endogenous GLP. Injectable route.

27

Exantide (GLP-1 agonist): safety

Inc. risk of hypoglycemia when combined with secretagogues. GI side effects, weight LOSS/neutral. Preg: C

28

Sitagliptin (DPP-4 inhibitor)

Inhibits DPP-4, increasing the activity of endogenous GLP-1 (from GI tract) after meals. Increases glucose-mediated insulin secretion.

29

Sitagliptin (DPP-4 inhibitor): safety

Increased risk of hypoglycemia when combined with secretagogue. Long term safety unknown. No CIs, but can cause hepatic failure. Weight neutral. Preg: B

30

Acarbose (alpha-glucosidase inhibitor)

Acts in GI tract slowing digestion/absorption of carbohydrates. V. effective at reducing postprandial hypoglycemia.

31

Acarbose (alpha-glucosidase): safety

Side effects are GI. CI in chronic GI disease. Increased risk of hypoglycemia with insulin and sulfonylureas (Glipizide) (tx is oral glucose). Preg: B

32

Which agents are CI in renal disease?

Metformin, GlipizideOK: Repaglimide*, Pioglitazone*, exantide, sitagliptan, acarbose, canagliflozin*- CI in liver disease, but ok in kidney disease.

33

Canagliflozin (SGLT-2 inhibitor)

Inhibits SGLT-2 in prox renal tubule, inhibiting glucose reabsorption in kidney.

34

Which agents are CI in hepatic impairment? Which are ok?

Metformin, Glipizide, Repaglinide, PioglitazoneOK: Exantide (GLP-1 mimetic), sitagliptin, acarbose, canagliflozin, insulin

35

Which agents are safest in pregnancy?

Insulin, metformin, acarbose, sitagliptin are all BRest are cat C.

36

Best way to initiate therapy in type II DM (how do you assess)?

Start with lifestyle change, then add metformin. F/U in 3 months- if A1c is not at target (7 for most people), then add a second oral agent.

37

You have a pt. on two oral drugs for DM, how do you assess?

F/u in 3 months. If A1c target not met, add a 3rd agent that isn't CI

38

You have a pt on 3 oral drugs for DM, how do you assess?

F/u in 3 months. If A1c target not met, consider injectible agents (GLP-1 agonist- exantide, insulin). Ideally, give Metformin+ basal insulin + exantide OR mealtime insulin.

39

Pt is on basal insulin plus exantide for DM, but its still refractory. What now?

Add pioglitizone OR canagliflozin to existing regimen.

40

What are the target lipid and BP levels for patients with DM:

BP 130/85 = HTN threshold. LDL>100 is hyperlipidemia. If microalbuminurea (30-300 mg/24 hours) is present, treat with ACEi or ARB starting now.

41

What labs do you get for your DM patients?

FBG, HgA1c; Urine Albumin! Urine albumin is the most important for identifying early signs of diabetic nephropathy when it's still reversible.

42

WTF is HHNS?

Hyperosmolar hyperglyucemic nonketotic syndrome. Pt will have seizures, focal neuro defects, lethargy, confusion, polyuria/dipsiaProfound hyperglycemia (>900), hyperosmolarity, pH>7.3 NO ACIDOSIS!!! HCO3>15

43

How do you treat HHNS?

FLUIDS 1L in fisrt hour, then another in nest 2 hours. Switch to 0.45% saline once pt is stabilized. Switch to D51/2NS once glucose reaches 250. 2. Insulin- 5-10 units bolus, followed by low-dose infusion.

44

What is the danger of reducing blood glucose too fast?

Cerebral edema, in both HHNS and DKA.

45

Canagliflozin: safety

Long term safety unknown. Increased risk of UTI, mycotic infections. Weight LOSS. Preg: C