Endo Pharm mechanisms/toxicity Flashcards

1
Q

Lispro

A

rapid acting insulin

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2
Q

Insulin mechanism

A

M:Bind insulin receptor (tyrosine kinase act)
Liver - increase glucose stored as glycogen
mm - inc glycogen & protein synth; K+ uptake
Fat - aids TG storage

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3
Q

Insulin Toxicity

A

Hypoglycemia; hypersensitivity (rare)

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4
Q

Insulin Clinical use

A

DM I, DM II, gestational diabetes, life-threatening hyperkalemia, stress-induced hyperglycemia
Always injected

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5
Q

Aspart

A

Rapid acting insulin

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6
Q

Glulisine

A

rapid acting insuling

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7
Q

Regular Insulin

A

short acting; only one used IV

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8
Q

NPH

A

intermediate insulin

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9
Q

Glargine

A

long acting insulin

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10
Q

Detemir

A

long-acting insulin

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11
Q

Biguanide mechanism

A

(Metformin)

decrease GNG, increase Glycolysis, increase peripheral glucose uptake (insulin sensitivity)

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12
Q

Biguanide clinical use

A

(Metformin)

oral 1st line for type 2. Can be used if no islet fx

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13
Q

Biguanide tox

A

(Metformin)

GI upset, lactic acidosis (serious), Contraindicated in renal failure so CHECK creatinine!

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14
Q

Sulfonylurea mechanism

A

closes K+ channel in beta cell membrane –> depolarization –> insulin release via Ca2+ influx. Also increases protein C

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15
Q

Sulfonylurea Use

A

stimulate endogenous insulin in type 2 diabetes. Requires some islet fx

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16
Q

Sulfonylurea tox

A

1st gen: disulfiram-like

2nd gen: hypoglycemia

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17
Q

Tolbutamide, Chlorpropramide

A

1st gen sulfonylurea

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18
Q

Glyburide, Glimepiride, Glipizide

A

2nd Gen sulfonylurea

19
Q

Glitazones/thiazolidinediones mech

A

increase insulin sensitivity in peripheral tissue by binding PPAR gamma nuclear transcription regulator

20
Q

Glitazones/thiazolidinediones use

A

monotherapy in DM 2 or in combo

21
Q

Glitazones/thiazolidinediones tox

A

weight gain, edema, hepatotox, Heart failure (makes this last choice)

22
Q

Pioglitazone, rosiglitazone

A

Glitazones/thiazolidinediones

23
Q

alpha glucosidase inhibitors mechanism

A

inhibit intestinal brush border on surface membrane. delayed sugar hydrolysis & glucose absorption –> decreases postprandial hyperglycemia

24
Q

alpha glucosidase inhibitors use

A

monotherapy DM 2 or in combo

25
Q

alpha glucosidase inhibitors tox

A

GI disturbances

26
Q

Acarbose, miglitol

A

alpha glucosidase inhibitors

27
Q

Amylin analogs (Pramlintide)

A

decrease glucagon in DM 1&2; hypoglycemia, nausea, diarrhea

28
Q

GLP-1 analogs

A

increase insulin, decrease glucagon; DM2; tox = nausea, vomit, pancreatitis

29
Q

Exenatide, Liraglutide

A

glucose-like peptide 1 analogs

30
Q

DPP-4 inhibitors

A

increase insulin, decrease glucagon; DM2; tox mild urinary/respiratory infection

31
Q

Linagliptin, saxagliptin, sitagliptin

A

DPP-4 inhibitors

32
Q

TNF-alpha

A

decreases glucose uptake by increasing sering p’lation

33
Q

Propylthiouracil, methimazole mech

A

block peroxidase, inhibits organification of iodide & TH synth. (Prop. also blocks 5’-deiodinase, decreasing peripheral T4->T3)

34
Q

Propylthiouracil, methimazole Tox

A

Skin rash, agranulocytosis, aplastic anemia, hepatotox, teratogen

35
Q

Levothyroxine, triiodothyronine

A

Thyroxine replacement
hypothyroid, myxedema
Tox: tachy, heat intolerance, tremor, arrythm

36
Q

Growth hormone

A

Gh deficiency, Turner’s

37
Q

Octreotide

A

Somatostatin analog;

Tx- Acromegaly, carcinoid, gastrinoma, glucagonoma, esophageal varices

38
Q

oxytocin

A

stimulates labor & contractions, milk letdown, controls uterine hemorrhage

39
Q

Desmopressin

A

ADH

Tx-central DI (not nephrogenic)

40
Q

Demeclocycline

A

M: ADH antag (tetracycline)
TX: SIADH
TOX: Nephrogenic DI, photsens, bone/teeth abnorm

41
Q

Glucocorticoids mechanism

A

decreases LTs & PGs by inhibiting phospholipase A2, and expression of COX-2

42
Q

Glucocorticoid use

A

Addison’s. inflammation, immune suppression, asthma, adrenal crisis

43
Q

Glucocorticoid Tox

A

Iatrogenic Cuching’s syndrome

Adrenal insufficiency if stopped abruptly after chronic use