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Pharm Exam IV > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Whats up with K in diabetic ketoacidosis?

A

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.

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2
Q

How do you correct measured Na in a hyperglycemic patient?

A

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

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3
Q

Diabetic ketoacidosis: treatment approach

A

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

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4
Q

Anion gap calculation:

A

AG= Na-(Cl + HCO3)

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5
Q

Diagnostic criteria for DM:

A

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

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6
Q

Diabetic ketoacidosis: treatment approach

A

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

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7
Q

Diagnostic criteria for DM:

A

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

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8
Q

Which physiologic states stimulate insulin release?

A

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

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9
Q

Which physiologic states inhibit insulin release?

A

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

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10
Q

GLUT2 and GLUT4 transporters: role

A

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.

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11
Q

Lispro

A

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.

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12
Q

Aspart

A

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

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13
Q

Glulisine

A

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

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14
Q

NPH

A

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

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15
Q

Detemer

A

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

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16
Q

Glargine

A

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

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17
Q

Insulin: safety

A

Preg cat B; hypoglycemia is largest risk

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18
Q

Metformin

A

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.

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19
Q

Metformin: safety

A

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
Q

Metformin (biguanides)

A

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
Q

Sulfonylureas- Glipizide

A

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
Q

Glipizide (sulfonylurea): safety

A

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

23
Q

Meglitinides: Repaglinide

A

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
Q

Pioglitazone (Thazolidinedione)

A

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
Q

Pioglitazone: safety

A

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

26
Q

Exenatide: GLP-1 mimetics

A

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

27
Q

Exantide (GLP-1 agonist): safety

A

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

28
Q

Sitagliptin (DPP-4 inhibitor)

A

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

29
Q

Sitagliptin (DPP-4 inhibitor): safety

A

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

30
Q

Acarbose (alpha-glucosidase inhibitor)

A

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

31
Q

Acarbose (alpha-glucosidase): safety

A

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
Q

Which agents are CI in renal disease?

A

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

33
Q

Canagliflozin (SGLT-2 inhibitor)

A

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

34
Q

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

A

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

35
Q

Which agents are safest in pregnancy?

A

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

36
Q

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

A

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
Q

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

A

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

38
Q

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

A

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
Q

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

A

Add pioglitizone OR canagliflozin to existing regimen.

40
Q

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

A

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
Q

What labs do you get for your DM patients?

A

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

42
Q

WTF is HHNS?

A

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
Q

How do you treat HHNS?

A

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
Q

What is the danger of reducing blood glucose too fast?

A

Cerebral edema, in both HHNS and DKA.

45
Q

Canagliflozin: safety

A

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

Pharm Exam IV (7 decks)

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