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Review / Wrong Answers > 6/14 UWorld > Flashcards

6/14 UWorld Flashcards

1
Q

MOA of Cladribine

A
  • Sketchy:
    • caveman clad in bear skin
  • Cytotoxic purine analog (–> purine stone hammer)
    • Is resistant to adenosine deaminase, enzyme that normally degrades purine analogs
  • Can incorporate into DNA causing
    • DNA breaks
    • Inhibition of DNA synthesis and repair by inhibiting DNA polymerase alpha and beta
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2
Q

MOA of Cytarabine

A

Sketchy = saber tooth tiger

Pyrimidine analog

Inhbitis DNA pol alpha and beta

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3
Q

MOA of Gemcitibine

A

Sketchy = geods with gems inside

Cytotoxic pyrimidine analog - inhibits DNA polymerase, blocking DNA synthesis and repair

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4
Q

What are the alkylating agent anti-neoplastics?

A

Cyclophosphamide - cyclops

Busulfan - beautiful sirens

Nitrosoureas - centaurs (“-mustine” - mustang)

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5
Q

MOA, uses, and adverse effects of Cyclophosphamide

A
  • Mechanism of action:
    • Works by attaching an alkyl group to the guanine base of DNA at the #7 nitrogen atom
    • This leads to intra- and inter-strand cross-links
    • Cell division halts and the cell undergoes apoptosis
    • This is cell cycle NON-specific
  • Uses:
    • Hematologic and solid malignancies (e.g. leukemias and lymphomas, breast cancer, ovarian cancer

Immunosuppressive (e.g. nephrotic syndrome, nephritic syndrome, vasculitis, autoimmune hemolytic anemia)

  • Adverse effects
    • Myelosuppression (leading to cytopenias)
    • Hemorrhagic cystitis
      • Cyclophosphamide is metabolized by the kidney into a molecule that is toxic to uroepithelial cells if in contact with the cells for too long
    • Increased risk for bladder cancer (high grade transitional cell carcinoma)
    • Hyponatremia due to SIADH
    • Toxic to ovaries and testes
      • Can cause infertility and premature menopause
      • Can cause decrease in sperm count and irreversible azoospermia
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6
Q

How do you prevent hemorrhagic cystitis from use of Cyclophosphamide

A
  • Prevent with aggressive hydration and co-administration with 2-mercaptoethanesulfonate (MESNA), which will bind and inactivate the toxic metabolite
    • Sketchy = protective maze around cystitis fountain
    • Cyclophosphamide is metabolized by the kidney into a molecule that is toxic to uroepithelial cells if in contact with the cells for too long
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7
Q

MOA, uses, and adverse effects of Busulfan

A
  • Mechanism of action
    • Alkylating agent that forms DNA intra-strand cross-links, preventing DNA replication and leading to apoptosis
  • Uses:
    • Used as a conditioning agent prior to bone marrow transplant – aka significantly depletes the bone marrow
  • Adverse effects:
    • Lung toxicity (e.g. acute lung injury, interstitial fibrosis, alveolar hemorrhage)
    • Skin darkening (“busulfan tan”)
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8
Q

Names of Nitrosoureas

A
  • Drugs:
    • “-mustine**” suffix (e.g. **Carmustine, Lomustine)
      • à centaur is a mustang horse
    • Streptozotocin
      • à striped zebra centaur
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9
Q

MOA, uses, and adverse effects of nitrosoureas

A
  • Uses:
    • Brain tumors (e.g. glioblastoma multiforme)
    • Are highly lipophilic so can cross the BBB
  • Adverse effects:
    • Neurotoxicity (e.g. convulsions, dizziness, atazia)
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10
Q

Describe the correlation betweeen azathioprine and Allopurinol

A

Azathioprine and 6-MP are metabolized by xanthine oxidase

So they will have increased toxicity if given with Allopurinol (which inhibits xanthine oxidase, thus preventing the breakdown of AZA/6-MP)

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11
Q

MOA, uses, and adverse effects of platinum analogs (Cisplatin, Carboplatin

A
  • MOA:
    • Cross-links DNA
  • Uses:
    • Solid malignancies: Testicular, bladder, ovary, and lung carcnioma
  • Adverse effects:
    • Neurotoxoity
      • Ototoxicity
      • Peripheral neuropathy
    • Nephrotoxicity
    • Immunosuppression
    • Myelosuppresion
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12
Q

What drug can be used to protect against Cisplatin-induced nephrotoxicity, and what is it’s MOA?

A
  • Amifostine
    • Sketchy = amethyst
  • Mechanism of action
    • Is an organic thiophosphate
    • Can bind to and detoxify the reactive metabolites (free radicals) of Cisplatin
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13
Q

MOA, uses, and adverse effects of Bleomycin

A
  • Mechanism of action
    • Antitumor antibiotic
    • Small peptide with a DNA binding region on one end and an iron binding region on the other end
    • After binding to DNA, it chelates metal ions, producing a pseudo-enzyme that reacts with O2 to produce superoxide and hydroxide free radicals that cleave DNA
    • Free radicals leads to single and double-stranded breaks of DNA
    • Is cell cycle specific – cells become arrested in G2
      • = Galleon (GII)
  • Uses:
    • Hematologic and solid malignancies (e.g. Hodgkin and Non-Hodgkin lymphoma, germ cell tumors, squamous cell carcinoma of the skin, cervix, and vulva
  • Adverse effects:
    • Pulmonary toxicity
    • Skin toxicity (e.g. rash, exfoliation, hyperpigmentation, atrophic striae)
    • Stomatitis and mucositis
    • Alopecia
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14
Q

What drugs are part of the Anthracyline family and what is their MOA

A
  • Sketchy = Santa Anthracycline
  • Drugs:
    • “-rubicin**” suffix (e.g. **Doxorubicin, Daunorubicin)
  • Mechanism of action:
    • Antitumor antibiotic
    • Promote the generation of oxygen free-radical through an iron-dependent reductive process
    • Also bind to DNA through intercalation – are planar molecules that can fit themselves between base pairs of DNA – leading to blocking of DNA and RNA synthesis
  • Uses:
    • Broad range of solid and hematologic malignancies
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15
Q

Adverse effects of anthracyclines

Drug used to prevent adverse effect

A
  • Cardiotoxicity secondary to buildup of free radicals in cardiac myocytes
    • Presents as dilated cardiomyopathy with symptoms presenting months after drug is stopped
    • Dexrazoxane is an iron chelator that prevents anthracycline-induced cardiotoxicity
      • = chelating/clinging the heart sack
      • = is on the deck (dex-) with a razor (-razoxane)
  • Myelosuppression
  • Stomatitis and mucositis
  • Alopecia
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16
Q

MOA, uses, and adverse effects of Actinomycin D

A
  • Sketchy = artifact-inomycin (doll artifact)
  • Mechanism of action:
    • Is an antitumor antibiotic
    • Intercalates into DNA, blocking DNA and RNA synthesis
  • Uses:
    • Numerous pediatric malignancies (e.g. Wilms tumor, Ewing sarcoma, rhabdomyosarcoma)
  • Adverse effects:
    • Alopecia
    • Myelosuppression
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17
Q

MOA of Etoposide and Teniposide + what part of the cell cycle they work on?

A
  • Mechanism of action
    • Topoisomerase II inhibitors (double stranded breaks to relieve supercoiling)
    • Prevent the re-ligation of double strand breaks induced by topoisomerase II
  • Cycle specific
    • Inhibit DNA synthesis, arresting cells in the S phase
    • Also block the G2 phase (double check and repair) of the cell cycle in cells that happen to make it past the S phase
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18
Q

MOA, uses, and adverse effects of Topotecan and Irniotecan

A
  • Mechanism of action
    • Topoisomerase I inhibitors (single stranded nicks to relieve supercoiling)
  • Uses:
    • Topotecan
      • Ovarian cancer and small cell lung cancer
    • Irinotecan
      • Colon cancer
  • Adverse effects:
    • Myelosuppression
    • Severe diarrhea
      • = loose bird stool
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19
Q

MOA, cell cycle, and adverse effects of Vincristine and Vinblastine

A
  • Mechanism of action
    • Cytotoxic vinca alkaloid
    • Inhibit microtubule production and mitotic spindle assembly
    • This arrests the cell in metaphase and cell division is brought to a halt
  • Cell cycle specific
    • Block mitosis – M phase
  • Uses:
    • Hematologic and solid malignancies (e.g. leukemias, lymphomas, pediatric tumors, breast cancer, and germ cell cancer
  • Adverse effects:
    • Neurotoxicity (e.g. peripheral sensory neuropathy)
    • Autonomic dysfunction (e.g. paralytic ileus, constipation)
      • = plunger
    • Alopecia
      • = bald monkey
    • Myelosuppression (especially Vinblastine)
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20
Q

MOA of Taxanes

A

Hyerstabilize microtubules in M phase so mitotic spindle cannot break down

21
Q

MOA, uses, and adverse effects of Imatinib

A
  • Sketchy = serious guy IMITATING the king
  • Mechanism of action
    • Small molecule tyrosine kinase inhibitor
  • Uses:
    • Chronic myeloid leukemia (increased levels of mature granulocytes: basophils, eosinophils, neutrophils)
    • Imatinib blocks the tyrosine kinase domain in the BCR/ACL fusion protein (mutation in CML)
    • Most common cause of CML is t(9;22) = Philadelphia chromosome
    • Also blocks c-kit tyrosine kinase (in GIST – gastrointestinal stromal tumor)
      • à congress kit box
      • à crab buttons on belly of the guy holding congress kit
  • Adverse effects:
    • Fluid retention (ankle and periorbital edema)
22
Q

MOA, uses, and adverse effects of Erlotinib

A
  • = british Earl Geoffrey
  • Mechanism of action
    • Small molecule tyrosine kinase inhibitor
    • Blocks the epidermal growth factor receptor (EGFR) tyrosine kinase
  • Uses:
    • EGFR is overexpressed in a number of tumors (e.g. non-small cell lung cancer (NSCLC), pancreatic cancer)
  • Adverse effects:
    • Papulopustular acneiform rash
    • Diarrhea
23
Q

MOA, uses, and adverse effects of Sunitinib and Sorafenib

A
  • = rising sun and soaring eagle
  • Mechanism of action
    • Small molecule tyrosine kinase inhibitor
    • Inhibits multiple receptor tyrosine kinases, including vascular endothelial growth factor, VEGFR (angiogenic growth factor)
  • Uses:
    • Renal cell carcinoma
    • Gastrointestinal stromal tumor
    • Hepatocellular carcinoma
  • Adverse effects:
    • Hyperkeratosis and skin rash
    • Increased risk of hemorrhage
24
Q

MOA and uses of Vemurafenib

A
  • = venom of snake drawing
  • Mechanism of action
    • Small molecule tyrosine kinase inhibitor
    • Inhibits B-Raf kinase (B-Raf activates singaling pathways drive melanocyte proliferation)
      • = B. Fra (Ben Franklin signature) written on drawing
    • BRAF mutation V600e (valine à glutamic acid) seen in 40-60% of patients with melanoma
      • You can kind of get this from the name of the drug:
        • V600e (Ve) mutated (mu) B-Raf (raf) inhibitor (nib)
  • Uses
    • Malignant melanoma
25
Q

MOA, uses, and adverse effects of Rituximab

A
  • MOA:
    • Antibody against CD20 (on B-cells)
    • Is chimeric
  • Uses:
    • Non-Hodgkin lymphoma, CLL, rheumatoid arthritis, immunosuppression
  • Adverse effects:
    • Immunosuppression and increased risk of infection
    • Higher risk of progressive multifocal leukoencephalopathy (PML) due to reactivation of JC virus
    • IV infusion reaction:
      • Constellation of symptoms occurring within first hour (e.g. HA, fever, rash, pruritus, dyspnea, hypotension)
      • Occurs due to antibody-antigen interaction, resulting in cytokine release
        • Managed with antihistamines, acetaminophen, or NSAIDs
    • Delayed onset poisoning – only occurs in chimeric drugs
      • Serum sickness occurring in 7-14 days (e.g. fever, rash, arthralgia) – due to Type III hypersensitivity reaction
      • Serum sickness occurs due to patient’s body attacking the non-human parts of the drug since it is chimeric
26
Q

MOA, uses, and adverse effects of Cetuximab

A
  • Tusk of elephant
  • MOA:
    • Antibody against EGFR (tyrosine kinase receptor)
      • à GiRaFe pattern on elephant blanket
    • Chimeric
  • Uses:
    • Solid tumors (colorectal cancer)
  • Adverse effects:
    • Papulopustular acneiform rash (due to abundance of EGFR in the skin)
      • à red spots on giraffes
    • IV infusion reaction:
      • Constellation of symptoms occurring within first hour (e.g. HA, fever, rash, pruritus, dyspnea, hypotension)
        • à red angel statue – swollen cherub with ivy
      • Occurs due to antibody-antigen interaction, resulting in cytokine release
        • Managed with antihistamines, acetaminophen, or NSAIDs
    • Delayed onset poisoning – only occurs in chimeric drugs
      • Serum sickness occurring in 7-14 days (e.g. fever, rash, arthralgia) – due to Type III hypersensitivity reaction
        • à delayed onset poisoning
      • Serum sickness occurs due to patient’s body attacking the non-human parts of the drug since it is chimeric
27
Q

MOA, uses, and adverse effects of Bevacizumab

A
  • Beverage lady
  • MOA:
    • Antibody against VEGF
    • Inhibits angiogenesis
  • Uses:
    • Metastastic tumors
    • Wet macular degeneration
  • Adverse effects
    • Hemorrhage
    • Blodd clots
    • Impaired wound healing
28
Q

MOA, uses, and adverse effects of Alemtuzumab

A
  • = alms of the beggar
  • Mechanism of action
    • Is an IgG antibody that binds to CD52 (found on normal and malignant B- and T-cells)
    • Binding to CD52 leads to a direct cytotoxic effect, through complement fixation and antibody dependent cell-mediated cytotoxicity
  • Uses:
    • Chronic lymphocytic leukemia (CLL)
      • = chronic (old/frayed) tapestry with antibody archers and T-knights
  • Adverse effects:
    • Bone marrow suppression
    • Infections
    • Emergence of autoimmune disorders
29
Q

MOA, uses, and adverse effect of Trastuzumab

A
  • = tapestry weaver
  • Mechanism of action
    • Antitumor monoclonal antibody
    • Binds to epidermal growth factor receptor 2 (e.g. HER2)
    • HER2 is a receptor tyrosine kinase
  • Uses:
    • HER2+ breast cancer
  • Adverse effects
    • Cardiotoxicity (e.g. decreased LVEF, heart failure)
      • = unraveling heart at end of the tapestry
30
Q

What is serum sickness?

A

Type II HSR

  • Serum sickness occurs due to patient’s body attacking the the non-human parts of the drug since it is chimeric
  • Occurring in 7-14 days (e.g. fever, rash, arthralgia)
31
Q

Diseases associated with Berry aneurysm

A

Ehlers Danlos syndrome

Autosomal dominant polycystic kidney disease

32
Q

Describe cluster HA (duration, location, features, associated sx, treatment)

A

15 min – 3 hours

Repetitive (often occur daily at the same time)

Unilateral, non-throbbing heading

Excruciating pain, usually perioribital

Associated with lacrimation, rhinorrhea, and Horner syndrome (ptosis and miosis, not anhidrosis)

Treatment: 100% O2, sumatriptan

33
Q

Describe tension HA (duration, location, features, associated sx, treatment)

A

Usually 4 – 6 hours

Bilateral headache with constant, steady pain

Usually in frontal or occipital lobe

No throbbing, no photophobia, no phonophobia, no aura

Treatment: NSAIDs, Acetaminophen

34
Q

Describe migraine HA (duration, location, features, associated sx, treatment)

A

Usually 4 – 72 hours

Unilateral pulsing, throbbing headache

Associated with nausea, photophobia, phonophobia, and aura

Treatment: Triptans

35
Q

Describe the MOA of Triptans

A

Mechanism of action:

Selective agonists of 5HT-1B and 5HT-1D receptors located on meningeal vessels, trigeminal nerve, and brainstem

Activation of these receptors on vessels causes vasoconstriction of cerebral and meningeal vessels (this will attenuate inflammation and decrease the stretch at pain receptors)

Activation of receptors directly on trigeminal nerve will prevent the release of vasoactive peptides, thus preventing vasodilation in the first place

Activation of receptor in brainstem can inhibit pain pathways

36
Q

Tumors associated with von Hippel Lindau

A
  • Hemangioblastoma
  • Angiomatosis
  • Bilateral renal cell carcinoma
  • Pheochromocytoma

THINK: HIPA

  • Hemangioblastoma, Inreased risk for RCC, Pheochromocytoma, Angiomatosis
37
Q

Tumor marker for astrocytes

A

GFAP+

38
Q

Describe the blood supply of the brainstem (medial and lateral of midbrain, pons, and medulla

A
  • Midbrain:
    • Medial - posterior cerebral
    • Lateral - posterior cerebral
  • Pons:
    • Medial - Basilar
    • Lateral - Anterior inferior cerebellar artery (AICA)
  • Medullar:
    • Medial - anterior spinal (ASA)
    • Lateral - Posterior inferior cerebellar artery (PICA)
39
Q

What is the mechanism of Hepcidin sequestering iron

A

Hepcidin influences body iron storage through its interaction with ferroportin, a transmembrane protein responsible for transferring intracellular iron to the circulation

Upon binding Hepcidin, ferroportin is internalized and degraded, decreased intestinal iron absorption and inhibiting the release of iron by macrophages

40
Q

What are the 4 midline structures and associated lesion presentations in the brainstem

A

Motor pathway - contralateral weakness

Medial lemniscus - contralateral proprioception/vibration deficit

Medial longitidinal fasciculus - ipsilateral internuclear ophthalmoplegia

Motor nuclues and nerve - ipsilateral CN motor loss (3, 4, 6, 12)

41
Q

What are the 4 lateral structures and associated lesion presentations of the brainstem?

A

Spinocerebellar - ipsilateral ataxia

Spinothalamic - contralateral pain and temp

Sensory V - ipsilateral pain and temp of the face

Sympathetic - ipsilateral Horner’s

42
Q

Mechanism of Desmopressin treatment in bleeding disorders

A

Increases release of Factor VIII (treats Hemophilia A) and vWF (treats von Willebrand disease)

43
Q

MOA of Flutamide

A

Testosterone receptor inhibitor

Inhibits androgen receptor binding

Used for prostate cancer (b/c cancer is testosterone-dependent)

44
Q

Equation for volume of distribution

A

Vd = (amount of drug in body) / (plasma drug concentration)

45
Q

Equation for drug clearance

A
  • CL = (rate of elimination of drug) / (plasma drug concentration)
  • CL = Vd x Ke (elimination constant)
    • Ke = 0.7 / (half-life of drug)
46
Q

Equation for loading dose

A
  • LD = (concentration at steady state) x (volume of distribution)
    • Concentration at steady state (Css) = desired concentration
47
Q

Equation for maintenance dose

A
  • MD = Css x Clearance
48
Q

Important number to remember for half life

A
  • The time required to change the amount of drug in the body by ½ during elimination
  • In first-order kinetics, a drug infused at a constant rate takes 4 half-lives to reach 94% of steady state
  • Half life = (0.7 x Vd) / CL
    • In first order kinetics

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