Diabetes/DKA

Question 1

Most severe adverse effect is lactic acidosis

Answer 1

metformin

Question 2

MC side is hypoglycemia

Answer 2

= sulfonylureas

Question 3

Recommended first line tx in Type 2 DM

Answer 3

= metformin

Question 4

Not safe in settings of hepatic dysfunction or CHF?

Answer 4

TZDs

Question 5

Should not be used in patients with elevated serum creatinine?

Answer 5

Metformin ( due to risk of lactic acidosis)

Question 6

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

Answer 6

alpha glucosidase inhibitors

Question 7

Not associated with weight gain?

Answer 7

Metformin, DPP-4 inhibitors, GLP-1 analogs

Question 8

metabolized by liver, safe in renal disease pt?

Answer 8

TZDs (Pioglitazone, rosiglitazone)

Question 9

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

Answer 9

sulfonyureas (glimepiride, glipizide, glyburide)

Question 10

Inhibits alpha glucosidase at intestinal brush border?

Answer 10

alpha glucosidase inhibitors

Question 11

MOA: TZDs

Answer 11

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

Question 12

MOA: Metformin

Answer 12

Stimulate AMPK by decreasing glucose production and insulin resistance

Question 13

PPAR gamma is found where? Function?

Answer 13

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

Question 14

Exenatide,

liraglutide (sc injection)

Answer 14

GLP-1 analogs

Question 15

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

Answer 15

GLP-1 analogs

Question 16

GLP-1 analog MC SE?

Answer 16

pancreatitis

Question 17

saxagliptin, sitagliptin

Answer 17

DPP-4 inhibitors

Question 18

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

Answer 18

DPP-4 inhibitors

Question 19

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

Answer 19

Block reabsorption of glucose in PCT.

which increases renal glucose excretion

Question 20

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

Answer 20

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

Question 21

good for weight loss

Answer 21

GLP-1 agonists

Question 22

best for organ failure

Answer 22

insulin

Question 23

Tx for type 1 DM

Answer 23

Low-carbohydrate diet, insulin replacement

Question 24

Tx for type 2 DM

Answer 24

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

Question 25

Tx for DKA

Answer 25

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

Question 26

Insulin, rapid acting | Lispro, Aspart, Glulisin

Answer 26

Binds insulin receptor (tyrosine kinase activity) rapidly,

Question 27

Postprandial glucose control (GDM)

Answer 27

Insulin, rapid acting | Lispro, Aspart, Glulisin

Question 28

Insulin, long acting | Detemir, glargine

Answer 28

Basal glucose control (GDM)

Question 29

Hepatotoxic, risk of fractures

Answer 29

TZDs

Question 30

Require some islet cell function. So avoid in Type___DM

Answer 30

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

Question 31

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

Answer 31

Type 1 DM

Question 32

Type 2 DM | 

Answer 32

resistance to insulin, progressive pancreatic β-cell failure

Question 33

Insulin always necessary during treatment

Answer 33

Type 1 DM

Question 34

Classic symptoms of polyuria, polydipsia, poylphagia, weight loss

Answer 34

Type 1 DM

Question 35

DKA causes:

Answer 35

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

Question 36

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

Answer 36

DKA

Question 37

DKA lab findings

Answer 37

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

Question 38

Hyperosmolar hyperglycemia nonketotic syndrome

Answer 38

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

Question 39

Hyperosmolar hyperglycemia nonketotic syndrome

Answer 39

There is some insulin present so there is no lipolysis, beta oxidation or ketones made; you won’t have an acidosis or kusshmal breathing

Question 40

MC SE: fluid retention, heart failure, weight gain

Answer 40

Glitazones/ Thiazolidinediones

Question 41

MC SE: hypoglycemia, weight gain

Answer 41

Sulfonylureas & Meglitinides

Question 42

MC SE: Nasopharyngitis

Answer 42

DPP4 inhibitors

Question 43

MC SE: increase urinary tract infections and hypotension

Answer 43

SGLT2 inhibitors

Question 44

MC SE: diarrhea and flatulence

Answer 44

Alpha glucosidase inhibitors

Question 45

MC SE: pancreatitis

Answer 45

GLP-1 agonist

Question 46

Symptoms of hypoglycemic reaction

Answer 46

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

Question 47

Treatment of hypoglycemic reaction

Answer 47

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

Question 48

MOA: Stimulates insulin release from pancreatic beta cells ; *has adjunctive use in type 2 diabetes - administer just before meals due to short half life

Answer 48

repaglinide

Question 49

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

Answer 49

inhibin B

Question 50

Best for post meal hyperglycemia

Answer 50

lispro, aspart, glulisine

Question 51

Best for DKA

Answer 51

insulin

Question 52

Increases intestinal production of lactate by anaerobic glycolysis?

Answer 52

metformin

Question 53

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

Answer 53

metformin