Buzzwords 3 Flashcards

1
Q

What are three indications of IV regular insulin?

A
  1. DKA
  2. Hyperkalemia (with glucose)
  3. Stress hyperglycemia
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2
Q

List the 4 categories of insulin, tie to peak, and their names.

A
  1. Rapid (1 hour) - Lispro, Aspart, Glulisine (LAG)
  2. Short (2-3 hours) - regular insulin
  3. Intermediate (4-10 hours) - NPH
  4. Long (no peak) - detemir, glargine
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3
Q

Name the 2 categories of non-insulin injectables and the drugs in each category.

A
  1. Amylin analogs (Pramlintide)

2. GLP-1 analogs (Exenatide, Liraglutide)

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4
Q

MOA of Pramlintide?

A

Decrease glucagon release, decrease gastric emptying, increase satiety

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5
Q

MOA of Exenatide and Liraglutide?

A

Decrease glucagon release, decrease gastric emptying, increase satiety, increase glucose-dependent insulin release

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6
Q

Drugs used to treat diabetes that may lead to weight LOSS

A
  1. GLP-1 analogs
  2. Metformin
  3. SGLT-2 inhibitors
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7
Q

Diabetes drug - AE - lactic acidosis

A

Metformin

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8
Q

Diabetes drug - AE - B12 deficiency

A

Metformin

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9
Q

MOA - metformin

A

Inhibit hepatic gluconeogenesis and the action of glucagon via inhibition of mGPD

Increase glycolysis, peripheral glucose uptake

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10
Q

Diabetes drugs that increase insulin sensitivity

A
  1. Metformin

2. Glitazones

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11
Q

Compare the MOA of sulfonylureas and meglitinides.

A

Both close the K+ channel in the beta cell membrane -> cell depolarization -> increased calcium influx -> insulin release

Binding sites differ

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12
Q

Drugs used to treat diabetes that may lead to weight GAIN.

A
  1. Sulfonylureas
  2. Meglitinides
  3. Glitazones
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13
Q

Name the first generation sulfonylureas.

A

Chlorpropamide

Tolbutamide

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14
Q

Name the second generation sulfonylureas.

A

Glimepiride, Glipizide, Glyburide

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15
Q

Diabetes drug - AE - disulfiram-like effects

A

1st generation sulfonylureas (Chlorpropamide, tolbutamide)

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16
Q

List the 2 meglitinides.

A

Nateglinide

Repaglinide

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17
Q

MOA - DDP-4 inhibitors?

A

Inhibit DDP-4 enzyme, which deactivates GLP-1

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18
Q

List the common suffix of DDP-4 inhibitors.

A

–agliptin

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19
Q

MOA - glitazones

A

Bind to PPAR-gamma nuclear transcription regulator -> increase insulin sensitivity and levels of adiponectin

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20
Q

Diabetes drug - AE - edema and Heart Failure

A

Glitazones (also increased risk of fractures)

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21
Q

Which diabetes drug has a delayed onset of action (several weeks)?

A

Glitazones

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22
Q

Common suffix for SGLT2 inhibitors

A

–Agliflozin

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23
Q

Diabetes drug - AE - vaginal yeast infections and UTIs

A

SGLT2 inhibitors

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24
Q

List the 2 alpha-glucosidase inhibitors.

A

Acarbose, miglitol

inhibit intestinal brush border enzyme, delay glucose absorption

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25
Q

List the 2 thioamides.

A

Propylthiouracil and methimazole

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26
Q

MOA - block TPO, which inhibits oxidation of iodide and organification of iodine -> inhibition of TH synthesis

A

Thioamides (propylthiouracil and methimazole); PTU also inhibits 5’deiodinase -> decreased peripheral conversion of T4 to T3

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27
Q

Discuss how to safely treat hyperthyroidism in pregnancy.

A

1st trimester - PTU (methimazole is teratogenic)

2nd and 3rd trimesters - Methimazole (risk of PTU-induced hepatoxicity)

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28
Q

Rx - hypothyroidism and myxedema

A

Levothyroxine (T4) and liothyronine (T3)

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29
Q

Rx - SIADH

A
  1. ADH antagonists at the V2 receptor -> conivaptan and tolvaptan
  2. Demeclocyline (ADH antagonist in the tetracycline family)
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30
Q

Desmopressin indications

A

Central DI (not nephrogenic)
VW disease
Sleep eneuresis
Hemophilia A

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31
Q

MOA - cinacalcet

A

Sensitizes the calcium sensing receptor (CaSR) in the parathyroid gland to circulating calcium -> decreased PTH

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32
Q

MOA - sevelamer

A

Prevents phosphate absorption in the GI tract by binding phosphate (non-absorbable)

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33
Q

MOA - activates antithrombin -> decreases action of 2a (thrombin) and 10a

A

Heparin

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34
Q

List the LMW heparins.

A

Enoxaparin

Dalteparin

35
Q

How do LMW heparins and fondaparinux differ from heparin?

A

These act predominantly on or only on (fondaparinux) factor 10a.

Pro - better bioavailability, longer half-life, no lab monitoring

Con - NOT EASILY REVERSIBLE

36
Q

In HIT, IgG antibodies develop against what?

A

Heparin-bound platelet factor 4 (PF4)

37
Q

List the 3 direct thrombin inhibitors.

A

Bivalirudin, Argatroban, Dabigatran (D - oral)

“BAD”

38
Q

MOA - interferes with gamma-carboxylation of vitamin K dependent clotting factors 2, 7, 9, 10 and proteins C and S

A

Warfarin

39
Q

AE - heparin vs. warfarin - skin and tissue necrosis

A

Warfarin

40
Q

Heparin vs. warfarin - route of administration

A

H - parenteral (IV, SC)

W - oral

41
Q

Heparin vs. warfarin - site of action

A

H - blood

W - liver

42
Q

Heparin vs. warfarin - onset and duration of action

A

H - rapid onset (seconds), hours (duration)

W - Slow onset (limited by the half-lives of normal clotting factors), days (duration)

43
Q

Heparin vs. warfarin - reversal?

A

H - protamine sulfate

W - vitamin K, FFP, PCC

44
Q

Heparin vs. warfarin – monitoring?

A

H - PTT (intrinsic)

W - PT/INR (extrinsic)

45
Q

Heparin vs. warfarin - crosses placenta?

A

H - no

W - yes (teratogenic)

46
Q

Heparin vs. warfarin - indications?

A

H - immediate anticoagulation for PE, ACS, MI, DVT + in pregnancy

W - chronic anticoagulation for prophylaxis of venous thromboembolism and a stroke due A-Fib

47
Q

List the two 10a inhibitor.

A

Apixaban, rivaroxaban

48
Q

Indications for thrombolytic therapy.

A

Early MI
Early ischemic stroke
Severe PE

49
Q

List the 4 ADP receptor inhibitors. Which one is reversible?

A

Clopidogrel
Prasugrel
Ticagrelor (reversible)
Ticlodipine

50
Q

MOA - inhibit platelet aggregation by irreversibly blocking ___ receptor. This prevents expression of GP 2b3a.

A

ADP receptor inhibitor

51
Q

Cilostazol and dipyridamole are phosphodiesterase inhibitors. How do they function in platelets?

A

Increase cAMP -> inhibition of platelet aggregation (in addition to vasodilation)

52
Q

List the GP2b3a inhibitors.

A

Abciximab, eptifibatide, tirofiban

53
Q

Rx - hairy cell leukemia

A

Cladribine

54
Q

Enhances effects of 5-FU?

A

Leucovorin

55
Q

Cancer drug - AE - hand-foot syndrome

A

5-FU

56
Q

Leucovorin rescue

A

Used in MTX treatment to reverse myelosuppression

57
Q

Cardiotoxic cancer drug + prevention?

A

Doxorubicin; prevent with dexrazoxane (iron chelating agent)

58
Q

Prevent hemorrhagic cystitis caused by cyclophosphamide

A

Mesna

59
Q

Prevent cisplatin/carboplatin nephrotoxicity?

A

Amifostine (free radical scavenger) and chloride (saline) diuresis

60
Q

MOA - TK inhibitor of BCR-ABL (CML) and c-Kit (GI stromal tumors)

A

Imatinib

61
Q

MOA - proteasome inhibitors that induce arrest at G2-M phase -> apoptosis

A

Bortezomib, carfilzomib

62
Q

MOA - SERMs

A

Estrogen receptor antagonists in the breast and agonists in bone

63
Q

Indications for SERMS?

A

Both - breast cancer prevention
Tamoxifen - breast cancer treatment
Raloxifene - osteoporosis

64
Q

Compare AE of tamoxifen and ralofixfene

A

Tamoxifen - partial agonist in endometrium -> increases risk of cancer

Raloxifene - antagonist in endometrial tissue, no increase

Both increase risk fo thromboembolism

65
Q

AE - trastuzumab?

A

Cardiotoxicity

66
Q

MOA - small molecule inhibitor of BRAF oncogene + melanom

A

VemuRAFenib for V600E-mutated BRAF inhibition

67
Q

Prevention and treatment of tumor lysis syndrome - use ___

A

Rasburicase

68
Q

Chemotoxicity - ototoxicity

A

Cisplatin/Carboplatin

69
Q

Chemotoxicity - peripheral neuropathy

A

Vincristine

70
Q

Chemotoxicity - pulmonary fibrosis

A

Bleomysin, Busulfan

71
Q

Redirection of emotions or impulses to a neutral person or object vs. Attributing an unacceptable internal impulse to an external source

A

Displacement vs. Projection

72
Q

Partially remaining at a more childish level of development vs. Involuntarily turning back the maturational clock and going back to earlier modes of dealing with the world

A

Fixation vs. Regression

73
Q

Replacing a warded-off idea or feeling with an unconsciously derived emphasis on its opposite vs. Replacing an unacceptable wish with a course of action that is similar to the wish but socially acceptable

A

Reaction formation vs. sublimation

74
Q
  1. Neuromuscular hyperactivity (clonus, hyperreflexia, hypertonia, tremor, seizure
  2. Increased autonomic stimulation (hyeprthermia, diaphoresis, diarrhea)
  3. Agitation
A

Serotonin syndrome

75
Q

Treat serotonin syndrome

A

Cyproheptadine (5-HT2 receptor antagonist)

76
Q

Rx - carcinoid syndrome

A

Octreotide

77
Q

Rx - hypertensive crisis

A

Phentolamine

78
Q

Cause of neuroleptic malignant syndrome?

A

Antipsychotics + genetic predisposition

79
Q

Symptoms of neuroleptic malignant syndrome?

A
Mygolobinuria
Fever
Encephalopathy
Vitals unstable
Increased enzymes (CK, etc.)
Rigidity of muscles (lead pipe)
80
Q

Rx - neuroleptic malignant syndrome

A

Dontrolene, dopamine agonist (eg. bromocriptine)

81
Q

Rx - acute dystonia

A

Benztropine or diphenhydramine

82
Q

Serum Gamma-glutamyltransferase?

A

Sensitive indicator of alcohol use

83
Q

List the low-potency typical antipsychotics.

A

Chlorpromazine, Thioridazine

Cheating Thieves are LOW

84
Q

List the high-potency typical antipsychotics.

A

Trifluoperazine, Fluphenazine, Haloperidol

Try to Fly High