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Pharm > Diabetes/DKA > Flashcards

Diabetes/DKA Flashcards

1
Q

Most severe adverse effect is lactic acidosis

A

metformin

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2
Q

MC side is hypoglycemia

A

= sulfonylureas

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3
Q

Recommended first line tx in Type 2 DM

A

= metformin

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4
Q

Not safe in settings of hepatic dysfunction or CHF?

A

TZDs

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5
Q

Should not be used in patients with elevated serum creatinine?

A

Metformin ( due to risk of lactic acidosis)

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6
Q

Should not be used in patients with cirrohsis or inflammatory bowel disease?

A

alpha glucosidase inhibitors

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7
Q

Not associated with weight gain?

A

Metformin, DPP-4 inhibitors, GLP-1 analogs

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8
Q

metabolized by liver, safe in renal disease pt?

A

TZDs (Pioglitazone, rosiglitazone)

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9
Q

Closes K+ channels on beta cells and ultimately increase insulin secretion

A

sulfonyureas (glimepiride, glipizide, glyburide)

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10
Q

Inhibits alpha glucosidase at intestinal brush border?

A

alpha glucosidase inhibitors

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11
Q

MOA: TZDs

A

increase insulin sensitivity in peripheral tissue. Binds to PPAR-γ nuclear transcription regulator.a

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12
Q

MOA: Metformin

A

Stimulate AMPK by decreasing glucose production and insulin resistance

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13
Q

PPAR gamma is found where? Function?

A

are found in skeletal muscle and adipose tissue ; they regulate FA storage and glucose metabolism ; they bind to the PPAr gamma transcription factor and activate it

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14
Q

Exenatide,

liraglutide (sc injection)

A

GLP-1 analogs

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15
Q

increase glucose-dependent insulin release, increase glucagon release, decrease gastric emptying,  increase satiety.

A

GLP-1 analogs

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16
Q

GLP-1 analog MC SE?

A

pancreatitis

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17
Q

saxagliptin, sitagliptin

A

DPP-4 inhibitors

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18
Q

Inhibits DPP-4 enzyme that deactivates GLP-1, thereby increase glucose-dependent insulin release, decrease glucagon release, decrease gastric emptying, increase satiety.

A

DPP-4 inhibitors

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19
Q

Sodium-glucose co-transporter 2 (SGLT-2) inhibitors ( Canagliflozin, dapagliflozin)

A

Block reabsorption of glucose in PCT.

which increases renal glucose excretion

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20
Q

Not really popular among patients; avoid in patients with bowel issues

A

Sodium-glucose co-transporter 2 (SGLT-2) inhibitors ( Canagliflozin, dapagliflozin)

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21
Q

good for weight loss

A

GLP-1 agonists

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22
Q

best for organ failure

A

insulin

23
Q

Tx for type 1 DM

A

Low-carbohydrate diet, insulin replacement

24
Q

Tx for type 2 DM

A

dietary modification and exercise for weight loss; oral agents, non-insulin injectables,
insulin replacement

25
Q

Tx for DKA

A

IV fluids, IV insulin, and K+ (to replete intracellular stores); glucose if necessary to prevent hypoglycemia.

26
Q

Insulin, rapid acting

Lispro, Aspart, Glulisin

A

Binds insulin receptor (tyrosine kinase activity) rapidly,

27
Q

Postprandial glucose control (GDM)

A

Insulin, rapid acting

Lispro, Aspart, Glulisin

28
Q

Insulin, long acting

Detemir, glargine

A

Basal glucose control (GDM)

29
Q

Hepatotoxic, risk of fractures

A

TZDs

30
Q

Require some islet cell function. So avoid in Type___DM

A

Sulfonyureas

Avoid in Type 1 because you have no islet cell function here.

31
Q

Autoimmune destruction of β cells (eg, due to glutamic acid decarboxylase antibodies)

A

Type 1 DM

32
Q

Type 2 DM



A

resistance to insulin, progressive pancreatic β-cell failure

33
Q

Insulin always necessary during treatment

A

Type 1 DM

34
Q

Classic symptoms of polyuria, polydipsia, poylphagia, weight loss

A

Type 1 DM

35
Q

DKA causes:

A

Usually due to insulin noncompliance or insulin requirements fromstress (eg, infection).

36
Q

Kussmaul respirations (rapid/deep breathing), Abdominal pain/nausea/vomiting, Dehydration. Fruity breath odor (due to exhaled acetone).

A

DKA

37
Q

DKA lab findings

A 
Hyperglycemia
increased H+
decreased HCO3– (increased anion gap metabolic acidosis)
increased blood ketone levels
leukocytosis
Hyperkalemia
38
Q

Hyperosmolar hyperglycemia nonketotic syndrome

A

State of profound hyperglycemia-induced dehydration andserum osmolarity, classically seen
in elderly type 2 diabetics

39
Q

Hyperosmolar hyperglycemia nonketotic syndrome

A

There is some insulin present so there is no lipolysis, beta oxidation or ketones made;

you won’t have an acidosis or kusshmal breathing

40
Q

MC SE: fluid retention, heart failure, weight gain

A

Glitazones/ Thiazolidinediones

41
Q

MC SE: hypoglycemia, weight gain

A

Sulfonylureas & Meglitinides

42
Q

MC SE: Nasopharyngitis

A

DPP4 inhibitors

43
Q

MC SE: increase urinary tract infections and hypotension

A

SGLT2 inhibitors

44
Q

MC SE: diarrhea and flatulence

A

Alpha glucosidase inhibitors

45
Q

MC SE: pancreatitis

A

GLP-1 agonist

46
Q

Symptoms of hypoglycemic reaction

A

lip/tongue tingling, lethargy, confusion, sweats, tremors, tachycardia, coma and seizures

47
Q

Treatment of hypoglycemic reaction

A

oral glucose, IV dextrose if unconscious or glucagon (IM or inhalation)

48
Q

MOA: Stimulates insulin release from pancreatic beta cells ;

*has adjunctive use in type 2 diabetes - administer just before meals due to short half life

A

repaglinide

49
Q

defective FSH receptors will prevent spermatogenesis and cause low ______ levels; because FSH is responsible for both spermatogenesis and _____________production.

A

inhibin B

50
Q

Best for post meal hyperglycemia

A

lispro, aspart, glulisine

51
Q

Best for DKA

A

insulin

52
Q

Increases intestinal production of lactate by anaerobic glycolysis?

A

metformin

53
Q

Normally the lactate produced in the intestine is converted to glucose via gluconeogenesis in the liver, but this drug inhibits the same process of gluconeogenesis, which results in elevated circulating lactate levels and puts them at risk of lactic acidosis

A

metformin

Pharm (9 decks)

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