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KMK Pharm > Systemic Pharm > Flashcards

Systemic Pharm Flashcards

1
Q

Common side effects of oral antibiotics

A

Nausea, vomiting, bloating, decreasing appetite, diarrhea.

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2
Q

2 classes of cell wall inhibitors

A
  1. Peptidoglycan/mucopeptide - Bacitracin
  2. Transpeptidase inhibitor (B lactam) -Penicillins, cephalosporins

Peptidoglycan are the building blocks, transpeptidase is the enzyme that cross links the peptidoglycan.

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3
Q

2 combo medications involving bacitracin

A

Polysporin- polymyxin B + Bacitracin

Neosporin- Neomycin + polymyxin B + Bacitracin

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4
Q

2 types of penicillins and their coverage

A

Amoxicillin
Pro: BROAD SPEC!!!!
Con: Bacterial resistance unless combined with clavulonic acid –> Augmentin)

Dicloxacillin
Pro: resistance against penicillinase (enzyme that breaks down transpeptidase inhibitors)
Con: (gram +) not broad

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5
Q

Difference between penicillin and cephalosporins

A

Penicillin has a 5 member beta lactam ring

cephalosporins have a 6 member ring

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6
Q

3 generations of cephalosporins and their coverage

A

1st gen: Gram +, Cephalexin
2nd gen: Gram + and -
3rd gen: Gram + and -, Cephriaxone

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7
Q

When the patient should have IV ceftriaxone

A

Gen 3 cephalosporin (gram + and -)

-Gonococcal conjunctivitis or orbital cellulitis

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8
Q

30S subunit drug categories

A

Aminoglycosides: Gentamycin, tobramycin

Tetracyclines: Doxycycline, minocycline

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9
Q

Aminoglycoside coverage

A

Gram + and -

Used to be first line therapy before fluroquinolones came out. Can still be fortified to be stronger.

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10
Q

Tobradex

A

Tobramycin (aminoglycoside) + dexamethasone

-Rx for staph marginal keratitis and K infiltrates

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11
Q

When can you prescribe doxycycline

A
  • Meibomianitis and acne rosacea. Alters the configuration of oil glands.
  • Chlamydial
  • After RCE to prevent recurrence
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12
Q

What drugs should you take on an empty stomach?

A

PAT an empty stomach:
Penicillin
Azithromycin
Tetracyclines (Except doxy- eliminated by liver–> feces, not the kidney)

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13
Q

Tetracycline contraindications

A

Pregnancy
Children
Side effects include- IIH, teeth discoloration, bone growth retardation.

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14
Q

Minocycline may cause

A

A blue sclera and pigmented cysts on the conj

not a small mino…… big blue shark with cysts!

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15
Q

Blockers of protein synthesis at the 50S ribosomal subunit (affective against gram positive and negative)

A
  • Macrolides- Erythromycin, azithromycin, clarithromycin
  • Other- Linezolid, clindamycin (these REVERSIBLY bind to the 50S subunit)
  • Chloramphenicol
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16
Q

Adverse effects of topical chloramphenicol

A

Fatal aplastic anemia (bone marrow replaced– less RBC production)

Optic neuritis

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17
Q

When to prescribe oral azithromycin

A 
Chlamydial infections (trachoma or inclusion) 
Single 1 gram dose, take on empty stomach
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18
Q

Ointment prescribed for prophylaxis of gonococcal ophthalmia neonatorum (in place of silver nitrate)

A

Erythromycin ointment

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19
Q

How folic acid is made in bacterial cells

A 
PABA
Synthase enzyme (targeted by sulfonamides) 
Dihydrofolic acid 
Reductase (targeted by trimethoprim) 
Tetra acid
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20
Q

Drugs that Treat Marrow Poorly

A

Trimethoprim
Methotrexate
Pyrimethamine (can be used to tx histo along with sulfadiazine)

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21
Q

Bactrim combo

A

Sulfamethoxazole + Trimethoprim

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22
Q

2 drugs used to tx histo

A

sulfadiazine and pyrimethamine

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23
Q

Side effects of oral sulfonamides

A

Myopic shift
SJS
Kernicterus (bilirubin accumulation in infants)

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24
Q

SJS

A

Fever, lesions of the skin and mucous membranes that result in sloughing of the skin over 10% or less or the body surface area.

85% of cases involve the conj.

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25
Q

MOA of sulfonamides vs trimethoprim/pyrimethamine

A

Sulfonamides- Inbibit the first stage in folic acid synthesis, dihydropteroate synthase

Trimethoprim/pyrimethamine- Inhibit the second stage in folic acid synthesis, dihydrofolate reductase

26
Q

Oral FluoroquinoLONES can

A

Hurt the attachments to your BONES (Tendinitis)

27
Q

Contraindications of oral fluoroquinolones

A

Pregnancy, children under 18 due to damage to cartilage formation and inhibited bone growth.

28
Q

What 4 medications you should think of for treating TB

A

RIPE cheese- caseous necrosis and phlyctenules.

  1. Rifampin
  2. Isoniazid
  3. Pyrazinamide (not on test)
  4. Ethambutol
29
Q

Rifampin

  • MOA
  • Side effects
A

Binds to RNA polymerase and prevents RNA synthesis.

RIFle to the liver–> hepatotoxicity
rifamPINK- pink/orange tears and urine

30
Q

Isoniazid MOA and side effects

A

Prevents cell wall synthesis by inhibiting mycolic acid synthesis.

Hepatotoxicity, similar to Rifampin.
Optic neuritis, similar to ethambutol.

31
Q

Ethambutol MOA and common SE

A

Inhibits the synthesis of the mycobacterial cell wall by inhibiting arabinosyl transferase.

May cause bilateral, retrobulbar optic neuritis. Ex: Pt comes in with 20/200 vision OU.

32
Q

Drug for the flu

A

Oseltamivir (Tamiflu)

Inhibits influenza A and B viral neuraminidase- prevents the spread of the virus.

33
Q

Zidovudine

A 
HIV therapy (usually want to use 3 meds) 
Inhibits reverse transcriptase (NRTI- nucleoside reverse transcriptase inhibitor)

Adverse effects: BM suppression, lactic acidosis, muscle breakdown.

34
Q

Ribavirin

A 
Hepatitis C therapy (use in combo with other drugs like interferon) 
-iNhibits viral RNA polymerase. 
-Conjunctivitis is the most common ocular side effects. Other side effects include: RIBAViriN 
Retinal detachment 
Ischemia (CWS) 
Bleeding (hemes) 
Arterial and venous occlusions 
optic Neuritis
35
Q

All herpes medications act the same. What is the MOA

A

Inhibit DNA polymerase.

36
Q

Difference between Zirgan (ganclyclovir) and Viroptic (triflurodine)

A

Zirgan/Gancyclovir: 5x per day, BAK

Viroptic/Triflurodine: 9x per day, thimerosal.

37
Q

DNA polymerase inhibitor for tx of herpes administered via IV

A

Foscarnet (Foscavir)

-May cause nephrotoxicity and seizures

38
Q

Difference between fungal cells and human cells

A

Ergosterol is in their cell membranes- cholesterol in ours. Most anti fungal drugs target ergosterol.

39
Q

Antifungal polyene macrolides

  • 3 drugs
  • MOA
A

Binds to ergosterol and forms pore.

Amphotercin B (borad spectrum)
Natamycin (only ophthalmic anti-fungal)
Nystatin

40
Q

Antifungal azole drugs

  • 3
  • MOA
A

Ketoconazole, fluconazole, miconazole

Inhibits ergosterol synthesis

41
Q

Antifungal drug that inhibits fungal mitosis by interfering with microtubule formation

A

Griseofulvin (greasy microtubules)

42
Q

2 antiparasitics prescribed for the treatment of toxo

A

Sulfadiazine

Pyrimethamine

43
Q

2 MOA of chloroquine

A
  1. Build up of heme- a breakdown product of hemoglobin within red blood cells- this is toxic to the parasite responsible for malaria.
  2. Inhibits phospholipase A2, similar to steroids.
44
Q

How does chloroquine cause bulls eye maculopathy

A

Chloroquine binds to melanin with RPE cells causing localized RPE damage and subsequent migration of RPE cells to the other nuclear and outer plexiform layers. The initial sign of bulls eye is RPE mottling within the macula.

45
Q

Lindane

  • MOA
  • Tx
A

Lipophilic structure absorbed through exoskeleton of insects–> death

Treatment of lice (with shampoo) and scabies (with lotion)

Shampoo tx can cause conjunctivitis when applied to the eyelashes.

46
Q

Role of leukotrienes

A

Synthesized by the enzyme lipoxygenase, bind receptors in the nose and bronchi–> Rhinitis and bronchoconstriciton.

47
Q

The dosage of concern for maculopathy is ___ mg/kg/day of chloroquine and ___mg/kg/day of hydroxy

A

2.3

5

48
Q

Systemic effects of oral steroids

A

Diabetes, insulin resistance, increase in BG, weight gain, fat redistribution, immune suppression, osteoporosis, HTN, and poor wound healing.

49
Q

Aspirin
MOA
Indications
adverse effects

A

Irreversible Cox 1 and 2 inhibitors

Anti-fever, anti pain, anti inflammatory, reduces risk of recurrent HA.

GI effects, anti platelet (bleeding), Reye’s syndrome in children with viral infection.

50
Q

Buckets

A

Bucket 1: Cholinergic agonists
Bucket 2: Cholinergic antagonists
-Anti anxiety, anti psychotics, anti depressants, anti histamine.
Bucket 3: Adrenergic agonists and dopamine
Bucket 4: Adrenergic antagonists

51
Q

3 drugs that cause pigmentary retinopathy

A

Clorpromizine (anti psychotics)
Thioridazine (anti psychotics)
Indomethacin

52
Q

Contraindications in NSAIDs (not aspirin)

A

Contra in patients with history of CAD or stroke, unlike aspirin.
These do not cause Reyes syndrome, like aspirin does.

53
Q

Indomethacin side effects

A

Whorl Keratopahty and retinal pigmentary changes

54
Q

Celecoxib

  • MOA
  • adverse effects
A

Selective cox 2 inhibitor, spree the cox 1 pathway, which helps protect the gastric mucosa.

Adverse effects- Conjunctivitis, blurry vision, SJS

55
Q 
Adrenergic agonists: 
Alpha 2
Beta 1 and 2 (non selective) 
Beta 2 
Nonspecific alpha and beta
A

Alpha 2- Clonidine

Beta 1 and 2 (non selective) - isoproterenol

Beta 2 - Salmeterol (long lasting) , albuterol, levalbuterol, terbutaline, metaproterenol.

Nonspecific- Sudafed

56
Q

Dopamine Agonists

A

Bromocriptine
ADHD drugs (methylphenidate, dextroamphetamine)
Parkinson’s disease (amantadine)

57
Q

Adrenergic antagonists

  1. Alpha 1 antagonists
  2. Non selective beta antagonists
  3. Beta 1 specific antagonists
A
  1. Tamsulosin, Terasozin, Prazosin
  2. Labetolol, propranolol
  3. Atenolol, metoprolol
58
Q

H1 and H2 receptors. where are they located and activation leads to what?

A

H1: Located in smooth muscles of bronchi, blood vessels, and intestines. Causes itching, vasodilation, increased vascular permeability.

H2: Located in gastric parietal cells, heart, pulmonary blood vessels, and immune system. causes itching, vasodilation, mucous discharge and gastric secretion.

H1 receptor is primarily in the eye.
H2 receptor antagonists are used for GI.

59
Q

First generation antihistamines, oral

A

Promethazine
DiPHENhydramine
ChlorPHENhydramine
BromPHENhydramine

May cause sedation due to CNS penetration. Mydriasis, Dry eyes, and dry mouth. Anticholinergic effects.

60
Q

What makes second gen H1 receptor blockers different from first gen

A

Second gen are less lipid soluble–> less CNS penetration and less side effects

KMK Pharm (2 decks)

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