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STEP1 > PHARM > Flashcards

PHARM Flashcards

1
Q

Cyclosporine-Tacroglimus -> Clinical Use

3

A
  • Reduce acute transplant rejection
  • Psoriasis
  • Rheumatoid Arthritis
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2
Q

Calcineurin Inhibitors

2

A
  • -Cyclosporine

- Tacrolimus

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3
Q

Cyclosporine-Mechanism

A
  • Binds cyclophilin
  • Blocks T cell activation
  • Prevents IL-2 transcription
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4
Q

Tacrolimus-Mechanism

A
  • Binds FK506 binding protein

- inhibition of IL-2 transcription

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5
Q

Binds FK506 binding protein

A

Tacrolimus-Mechanism

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6
Q

Side effects-Cyclosporine

A
  • Nephrotoxicity
  • Neurotoxicity
  • Gingival hyperplasia
  • Hirsutism
  • Hypertension
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7
Q

Side effects-Tacrolimus

A
  • ↑ risk of neurotoxicity compared to cyclosporine
  • ↑ risk of diabetes
  • -Nephrotoxicity
  • -Hypertension
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8
Q

mycophenolate mofetil-MOA

A

inosine monophosphate dehydrogenase inhibitor->By inhibiting de novo guanosine nucleotide synthesis, T and B lymphocyte proliferation is disrupted.

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9
Q

mycophenolate mofetil-Side effect

A

Bone marrow suppression

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10
Q

used in patients who cannot tolerate calcineurin inhibitors due to the frequency of neurotoxicity and nephrotoxicity.

A

mycophenolate mofetil

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11
Q

sirolimus-side effect

A

Delayed wound healing

hepatic artery thrombosis, hyperlipidemia, and dermatologic complications.

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12
Q

sirolimus-MOA

A

blocks signal transduction at the IL-2 receptor

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13
Q

anti-CD3 antigen complex monoclonal antibody-Side effect

A

associated with viral or other infectious reactivation, such as reactivation of tuberculosis or viral hepatitis

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14
Q

Skin thinning is a very common side effect associated with

A

steroids

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15
Q

Amides -> Anesthetics

A

lidocaine, mepivacaine, prilocaine, bupivacaine, etidocaine, and ropivacaine and levobupivacaine
_tienen una i antes del -caine

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16
Q

Esters -> Anesthetics

A

chloroprocaine, procaine, and tetracaine

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17
Q

serotonin syndrome->

A

SSRIs, SNRIs, TCAs,tramadol, ondansetron, triptans, MDMA, and dextromethorphan

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18
Q

Aminoglycosides

A 
Amikacin
Gentamicin
Neomycin
Tobramycin
Streptomycin
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19
Q

Binds to aminoacyl site of 16S rRNA (part of 30S subunit) → misreading of genetic code and inhibition of translocation

A

Aminoglycosides

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20
Q

Mechanism of Bacterial Resistance-> Inactivation of drug via acetylation, adenylation, or phosphorylation by bacterial transferase enzymes

A

Aminoglycosides

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21
Q

Adverse Effects->Aminoglycosides

A

Nephrotoxicity (acute tubular necrosis)
Ototoxicity (vestibular and/or cochlear damage, potentiated by loop diuretics)
Neuromuscular blockade (contraindicated in myasthenia gravis)
Teratogenic

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22
Q

PX with an acute cerebrovascular accident (CVA)

Tx

A

-Alteplase (also called tissue plasminogen activator or tPA)->increasing fibrin’s affinity for endogenous plasminogen-> increased activation of plasmin

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23
Q

inhibits vitamin K-dependent carboxylation of factors II, VII, IX, and X.

A

Warfarin

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24
Q

inhibit cyclooxygenase

A

Aspirin, ibuprofen, and naproxen

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25
Q

direct inhibitor of thrombin

A

Argatroban

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26
Q

propagates a patient’s endogenous antithrombin, which inhibits thrombin and activated factor X

A

Heparin

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27
Q

Medication for type II diabetes that should be avoided in patients with heart failure, due to the risk of fluid retention.

A

Thiazolidinediones (TZDs) -> (pioglitazone, rosiglitazone)->

Activation of peroxisome proliferator-activated receptor gamma in adipocytes

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28
Q

Activation of peroxisome proliferator-activated receptor gamma in adipocytes to promote adipogenesis and fatty acid uptake and increase insulin-dependent glucose uptake.

A

Thiazolidinediones (TZDs) -> (pioglitazone, rosiglitazone)

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29
Q

Contraindications->Thiazolidinediones

A 
Heart failure
Fluid overload
Active liver disease
Bladder cancer
Type 1 diabetes
Pregnancy
Macular edema
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30
Q

Inhibition of α-glucosidases

A

acarbose

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31
Q

oral antidiabetic agent that can cause diarrhea and gastrointestinal upset.

A

acarbose

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32
Q

work via inhibition of dipeptidyl peptidase IV, which normally functions to break down incretins (such as GIP and GLP-1) responsible for increased insulin synthesis/release and decreased glucagon release

A

Gliptins such as sitagliptin

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33
Q

works primarily via inhibition of hepatic gluconeogenesis->Increase insulin sensitivity

A

Metformin

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34
Q

also contraindicated in decompensated CHF and Renal failure, this is due to an increased risk of lactic acidosis

A

Metformin

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35
Q

work via stimulation of insulin release from the pancreas

A

Sulfonylureas

36
Q

Side effects include hypoglycemia and weight gain (DM tx)

A

Sulfonylureas

37
Q

Stimulation of glucose-dependent insulin release

A

GLP-1 agonists

38
Q

Liraglutide
Semaglutide
Dulaglutide

A

GLP-1 agonists

39
Q

DPP-4 normally degrades glucagon-like peptide-1 (GLP-1)

DPP-4 inhibitors therefore prevent degradation of GLP-1

A

DPP-4 inhibitors

40
Q

DPP-4 inhibitors

A

Sitagliptin
Saxagliptin
Linagliptin

41
Q

SGLT-2 inhibitors

A

Canagliflozin

Empagliflozin

42
Q

expressed in the proximal tubule and mediates reabsorption of approximately 90 percent of the filtered glucose load

A

SGLT-2

43
Q

Sulfonylureas

A

Glyburide
Glipizide
Tolbutamide
Chlorpropamide

44
Q

hookworm infection -> first-line therapy

A

inhibition of microtubule synthesis

**albendazole or mebendazole

45
Q

treatment of pinworm, roundworm, and hookworm.

A

Depolarizing neuromuscular blockade

  • modulates the GABAergic system to induce a neuromuscular blockade in the helminth
  • *Pyrantel pamoate
46
Q

treatment of strongyloidiasis

A

influx of Cl- ions leading to hyperpolarization of the helminth cell membranes.
(Ivermectin)

47
Q

modulates the nitric oxide and cyclooxygenase inflammatory pathways to increase the helminth’s susceptibility to phagocytosis

A

Diethylcarbamazine

-> treatment of filariasis

48
Q

treatment of schistosomiasis

A

an influx of Ca++ ions, leading to muscle spasm and paralysis of the helminth
->Praziquantel

49
Q

Cardiac Glycoside

1

A

(Digoxin)

50
Q

Adverse Effects-> Digoxin

A 
AV block
Arrhythmias
Blurry yellow vision
Cholinergic: Diarrhea,Nausea,Vomiting
Hyperkalemia
51
Q

Atrial fibrillation->Decreases conduction at AV node

Heart failure-> Increases contractility

A

> Digoxin

52
Q 
Direct inhibition of Na+/K+ ATPase
Indirect inhibition of Na+/Ca2+ exchanger
↑ Ca2+ concentration
Increases Inotropy
Stimulates Vagus nerve
↓ Heart rate
A

Digoxin

53
Q

Risk Factors for toxicity
-> Drugs that displace Digoxin from tissue-binding sites
(3)

A
  • > Amiodarone
  • > Quinidine
  • > Verapamil
54
Q

Risk Factors for toxicity->digoxin

A

Hypokalemia
Renal failure (digoxina se extreta por el rinon)
↓ Excretion

55
Q

Digoxin toxicity is characterized by electrocardiogram changes including

A

increased PR interval
decreased QT interval
scooping of the ST segment
T-wave inversion

56
Q

selectively blocking the binding of angiotensin II to AT1 receptors

A

Losartan

57
Q

alpha-1 receptor blocker and works by selectively blocking the alpha-1 receptors

A

Prazosin

58
Q

Prazosin ->Uses

A

benign prostate hyperplasia, PTSD, and hypertension treatment

59
Q

Prazosin-> secondary effects

A

Side effects include 1st dose orthostatic hypotension, dizziness, and headaches.

60
Q

β-blocker that decreases SA and AV nodal activity by decreasing cAMP and Ca2+ currents

A

Metoprolol

61
Q

Metoprolol-> side effects

A

impotence, exacerbation of COPD and asthma, bradycardia, and masking of hypoglycemia.

62
Q

vasodilation of vascular smooth muscles with increased cGMP

A

Nitroglycerin

63
Q

Nitroglycerin-> Side effects

A

reflex tachycardia, hypotension, flushing, and headaches

64
Q

angiotensin-converting enzyme inhibitor and works by inhibiting ACE and decreasing ATII

A

Lisinopril

65
Q

Side effects ->Lisinopril

A

angioedema, cough, hyperkalemia, and hypotension

66
Q

Inhibit calcium ion channel

A

Calcium channel blockers

67
Q

Antianginal therapy-> β-blockers + Nitrates

A

Blood Pressure ↓

Myocardial O2 consumption ↓↓

68
Q

Antianginal therapy-> Nitrates

A 
Blood Pressure↓
Contractility ↑
Ejection time↓
End-Diastolic volume↓
Heart rate↑
Myocardial O2 consumption↓
69
Q

Antianginal therapy-> β-blockers

A 
Blood Pressure↓
Contractility ↓
Ejection time↑
End-Diastolic volume -
Heart rate↓
Myocardial O2 consumption↓
70
Q

Tx for a flare of her Crohn’s disease in pregnant

A

Antibodies against tumor necrosis factor (TNF) α -> infliximab

71
Q

increased risk using infliximab

A

tuberculosis reactivation, patients should get a purified protein derivative (PPD) test

72
Q

purine analogue and inhibits purine nucleotide synthesis and metabolism

A

6-mercaptopurine

73
Q

inhibits dihydrofolate reductase. It also inhibits purine synthesis and decreases the production of inflammatory cytokines

A

Methotrexate (MTX)

74
Q

Tx elevated intracranial pressure (ICP) ICP ≥ 20 mm

A

mannitol -> causes osmotic diuresis and increased urine output
** may cause (or worsen) pulmonary edema (due to rapid increase i the vascular hydrostatic pressure)

75
Q

Tx for SIADH

A

Demeclocycline is an ADH antagonist

76
Q

Tx for DI

A

Desmopressin is a synthetic version of ADH and can be used to treat central diabetes insipidus (DI).

77
Q

first-line therapy for patients that present with decompensated heart failure

A

Furosemide -> loop diuretic

78
Q

should not be used in cases of elevated ICP

A

Glucocorticoids->unless the elevation is due to malignancy

79
Q

Contraindications Mannitol

A
  • Anuria

- Heart failure

80
Q

Contraindications -> Spironolactone

A
  • Addison disease (chronic adrenal insufficiency)

- Hyperkalemia

81
Q

Contraindications -> Thiazide diuretics

A

Gout (thiazides reduce the clearance of uric acid since they compete for the same transporter)
Hypokalemia
Hypotension
Sulfa allergy

82
Q

Contraindications ->Loop diuretics

A 
Hyperuricemia
Sulfa allergies (ethacrynic acid is the only loop diuretic that can be used in a patient with a sulfa allergy)
83
Q

Contraindications >Acetazolamide

A

Sulfa allergy

Nephrolithiasis (acetazolamide promotes calcium phosphate stone formation)

84
Q

chronic graft-versus-host disease (GVHD)

A

Skin is the most commonly affected organ in chronic GVHD, and skin findings are usually classified as lichen planus-like or sclerotic.

85
Q

prophylactic agent for the prevention of chronic GVHD

A

methotrexate + leucovorin
*Administering leucovorin (folinic acid) along with methotrexate can reduce the likelihood and severity of methotrexate adverse effects

STEP1 (19 decks)

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