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UWorld CA and Derm Flashcards

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USMLE® Step 1 flashcards
1
Q

What are the roles of topo 1 and topo 2?

A

Topo1 - single strnaded nicks to relieve negative supercoilingTopo 2 - transient double stranded breaks in DNA to relieve positive and negative supercoiling.

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2
Q

What is the mech of Etoposide and podophyllin? What are they used it?

A

Both imhibit topo 2s ability tos eal double stranded breaks it induces -> cell death. Etoposide - testituclar and small cell lung CAPodophyllin - genital warts.

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3
Q

ERB-B2 - what is another name for this? Where is it seen?What targets this?

A

HER2-Neu - member of epidermal growth factor receptor - overexpressed in 30% of breast CA as well as adnoCa of ovary, stomach, lung, saliva. Transmembrane glycoprotein w/ tyrosine kinase activity.This is targed by trastuzumab. (atni-HER-2) - monoclonal Ab.

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4
Q

What is the problem in xoerderma pigmentosum? Molecular namesInheritance?

A

UVA causes Thymine dimers - Lack of UV ENDONUCELASE REPAIR. AR (it’s enzymatic)

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5
Q

What passes through the jugular foramen?

A

CN 9, 10, 11, Jugular vein

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6
Q

Damage to CN10 (uvula) - points to which side?

A

Points to the opposite side (normal)Tongue points to the side of damage.

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7
Q

Rb - how is EF2 released?

A

Phosphorylation of Rb leads to activity.Allows G1 to S phase to occur. Resting (G0) are in hypophosphorylated form. (active)When it is hyperphosphorylated (inactive) by Cyclin D, E, CDK4 etc., releases E2F. Think of Rb as a mall cop with no donuts (active), snooping around on the job holding onto his Taser (EF2). When it is hyperphosphorylated w/ donuts, it becomes inactive, and drops its Taser (inactive).. allows cell cycle to begin! Teenager theft.

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8
Q

What is the p27 protein?

A

Cell cycle inhibitor. Acts during G1 to inhibit CDk. Normal tissue contain high levels of p27 (inhibiting)Maligant tissue contain very low levels of p27.

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9
Q

How does methotrexate work?

A

Structurally similar to folic acid. Competitively inhibits the enzyme dihydrofolate reductase, which catalyzes THF synth. Causes intermediate DHF polyglutamate to accumulate.

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10
Q

What makes LN malignant?Pleomorphism, abundant mitotic features, nuclear change, admixture?

A

None of these. What makes it malignant is monoclonal

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11
Q

Giant tumor cells? What do you think?

A

Anaplastic tumor. pleomorphic cell w/ large hyperchromatic nuclei growing in disoganized fashion - no resemblance to tissue of organ.

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12
Q

How has lung cancer prevalence changed in women?

A

Lung Cancer incidence and mortality has INC over the last four years - number 1 killer and number 2 presence.

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13
Q

What is Cladribine - why is it special and what is it used for?

A

Purine analogu - resistant to degradation of adenosine deaminse - is able to reach high intracellular concentration adn be incoroproated into DNA -> Srand breaks.Penetrates the CNS. D.O.C. for hair y cell leukemia.

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14
Q

Cisplatin - what does it do? What is it used for? How do you limit tox?

A

Cisplatin - “crosslink DNA” - platinum containing compound - forms reactive oxygen species that form DNA crosslinks. Testicular, bladder, ovary, lung CA. Nephrotoxicity. - ATN and acoustic nerve damage. Must use AGGRESSIVE hydration and AMIFOSTINE (free-radical scavenging agent) +Also chloride diuresis (IV normal saline) - cisplatin stays in nonreactive state w/ higher chloride conce.

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15
Q

Pt w/ tingling in hands and feet. What is this? What systemic chemo drug could this be? What is mech of drug?

A

Peripheral neuropathy - Vinca alkaloids (esp. VINCRISTINE) - prevent separation of chromosomes during M phase - inhibit B tubuiln. - inhibit polymerase.used esp. for solid tumors, leukemias, lymphomasOPPOSITE OF paclitaxel - hyperstabilize M phase.

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16
Q

Imaging and histo of pilocystic astrocytoma? Location?

A

Most common = usu occur in cerebellum - sometimes cerebral ehmispheres.Appear as mass PLUSS a cyst. Histo - rosenthal fibers. Good prognosis. Medulloblastoma - 2nd most common - HUIGHLY MALIGNANT (sheets of small blue cells w? hyperhcromatic nuclei) - poor prognosis. Ependymomas - rosettes + hydrocephalus.

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17
Q

What are the effects of oral contraceptive smutliparity and breast feeding on risk for ovarian CA?

A

all 3 reduce risk.

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18
Q

Whhat is MDR1 and what does it do?

A

MDR1 - multidrug resistance 1 gene - codes of P-glycoprotein - a transmembrane ATP dependent EFFLUX PUMP w/ broad specificity for hydrophobic compounds. Reduces influx of drug and can INC efflux.

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19
Q

Explain the process of UVA DNA dmg and repair

A

UVA causes colvanet bonds between adjacent thymine residues - UV specific endonucleases MAKE NICKS AT damaged sites. These are later EXCSIED by E’3 EXONUCLEASE activity of DNA polymerase. which also synthesizes DNA in the place of damged DNA (2 for 1)

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20
Q

Hist description of GBM.

A

Psuedopalisading NECORISS and possible hemorrhage.

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21
Q

How to prevent fever, painful mouth ulcers and pnacytopenia in methotrexate? What are these signs/symptoms caused by? How to prevent tox of Cyclophoshamide? Doxorubicin/ ANthracycline?Cisplatin

A

Folinic acid. These signs are caused by death in rapidly dividing cells (GI and bone marrow) - apthous ulcers and pancytopenia are classic. Cyclophoshamide - Mesna (binds acrolein - toxic) -> prevents hemorrhagic cystitis. Doxorubicin/anthracycline - DexrazoxaneCisplatin - Amifostine

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22
Q

What can be used to treat nausea and vomiting found in chemo

A

Ondansetron

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23
Q

What can be used to stimulate granulocytes in pt w/ neutropenia?

A

FIlgrastim - G(granulocyte)-CSF analog

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24
Q

How does radiation work against CA? What is the graph associated w/ radiation dose?

A

Radiation - 1.) induces DNA dmg -> double stranded breaks and 2.) formation of oxygen free radicals.Curve firs plataues based on radiation, then sharply DEC cell survival.

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25
Q

What are the 2 predominant drivers of angiogenesis?

A

Fibroblast growth factor (FGF) and VEGF.

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26
Q

What does epidermal growth factor stim?

A

Mitogenic influence on epithelial cells, hepatocytes, and fibroblasts - does not appear to directly stimulate anigogenesis (FGF, and VEGF)

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27
Q

What is somatomedin C?

A

IGF1. stimualtes cell growth. does not directly stimulate anigogenesis.

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28
Q

How do you calculate numbe rneeded to harm?

A

NNH = 1/Attributable risk.So first calculate adverse event rate in treatment group.Adverse event rate in placebo group.Subtract those.Then 1/answer.

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29
Q

Basic description of what Bcl2 does?

A

Bcl2 -> inhibits apoptosis (keeps cytochrome C inside of cell.So overexpression of Bcl1 -> inhibits apoptosis and survival of tumor cells. Bcl2 is: 18Ig heavy: 14

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30
Q

What is c-myc found in? What ARE the roles of mycs?

A

c-myc - Burkits.Mycs are TRANSCRIPTION ACTIVATORS. (nuclear phosphoprotein) conrol cell prolif, differnetiation and apoptosis

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31
Q

Hemorrhagic cystitis after chemo. What should have been given toa bvoid this condition?

A

This is from cyclophosphamide - should have given Mesna - binds acrolein

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32
Q

Ondansetron - mech - used for?

A

Inhibits serotonin receptors (5-HT3) - used to treat nausea and vomiting after chemo. Most 5HT3 loated peripherally in presympatic terminals of vagus GI. Represented centrally in chemoreceptor trigger zone.

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33
Q

What degrades 6MP?

A

Xanthine oxidase

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34
Q

Vimentin found in?

A

Intermeidate filament - present in mesenchymal

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35
Q

HER2/neu oncogene - what is it? How does it activate/lead to CA?

A

Transmembrane glycoprotein w/ intracellular tyrosine kinase activity.

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36
Q

What is the most common indolent nonhodgkin lymphoma in adults. AKA DOES NOT PROGRESS WITH TIME. What is cytology?

A

Follicular LNA - waxing and waning LAN. Bcl2 in Follicula

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37
Q

Which thymidylate drugs can be overcome w/ folate. Cannot be?

A

Methotrexate - can be overcome w/ folate sup5FU - cannot - it affects downstream of FU.

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38
Q

How can you distinguish small cell lung CA w/ staining?

A

Of neuroendocrine origin - express neuroendocrine markers and contain neurosecretory granules.

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39
Q

What are 5 Tumor promoters?

A

Rasn-MUCERBTGFasisabl

40
Q

What are 7 tumor suppressors

A

p53DCCRBAPCNF1BRCAWT1

41
Q

What is the mech of BRCA?

A

Tumor suppressor. Functions in gene/DNA repair and regulation of cell cycle. Mutation INC risk of breast and ovarian CA.

42
Q

Familiarl sarcomas of the breast, brain, adrenal crotex?

A

Li Fraumeni - AD inheritance of P53 mutation.

43
Q

What cause peau d’orange?

A

Pitting edema caused when neoplastic cells plug dermal LYMPHATIC channels. Can get discoloration (pale pink to deep red/brown to purple)

44
Q

Back pain not relieved by position change or rest?

A

Neoplastic. W/ urinary urgency, nocturia, frequency> HGIHLY SUGGESTIVE OF PROSTATE CA W/ METS.

45
Q

WHY do you get hyperpigmentation in HPA axis defect?

A

Any HIGH LEVELS OF ACTH. Seen w/ cushings syndrome, ACTH directly stimulates melanotropin.Also seen in Addisons - adrenal insufficiency leads to INC ACTH (MSH is a by product of ACTH production from POMC). So In both Cushing and Addisons.

46
Q

How are pro-CA changed into carginogens?

A

Via p450 - w/ p450 MONOOXYGENASE (MICROSOMAL MONOOXYGENASE)

47
Q

Apocrine vs Eccrine?

A

Apocrine - dermis of breast areolae/mamillary ducts, axillae, genital. Innervated by adrenergic of sympathetic. Eccrine (merocrine) - present in skin throughout body - except areas like lips and glands of penis. Holocrine (sebaceous - scalp skin)

48
Q

Melanomas are embryologically drived from?Neural crestNeuroectodermSurface ectoderm?

A

Neural crest. Surface ectoderm = epidermis, mammary glands, lens of eye, adenohypophysis.BUT the melanocytes (not really epidermis) are from NEURAL CREST)

49
Q

What should you supplement in disease w/ loss of neutral aromatic AA in urine/gut?

A

hartnup disease - renal and gut absoprtion of tryptophan is defective.Tryptophan is a precursor to Niacin,( AKA Nicotininc Acid)Serotonin and melatonin.Results in Niacin deficiency.May present w/ erythamatous, pruiritic skin (pellagra like) lesions and loose stool.

50
Q

Pneumocystis infection - if this is in an immunocompromised individual, which immunity is knocked out?

A

Pneumocystis - from T cell def. Would not see in agammaglobulinemia.However, recurrent otitis media, chronic diarrhea + pnuemocystic = SCID.

51
Q

Candida skin test reacts which 2 cell types? (be specific)

A

M! + CD4+ T cell (also CD8 T and NK)

52
Q

peripheral blood smear - giant cytoplasmic granules in N! and M! albino + nystagmus. What is this?

A

Chediak higashi - N! phagosome LYSOSOME fusion defect. May also ahve receurrent infection. AR

53
Q

Telomerase prosses what enzyme activity? What cells have it? What does nucleotides does it add to 3’ end?

A

REVERSE TRANSRITPASE (RNA depednent DNA polyemrase) - seen in stem cells and CA cells. Adds TTAGGG repeats.

54
Q

Oxidase positive, nonlactose fermenting bacteria in burn victim. What is it and what to treat w?

A

Pseudomonas - tx w/ Cefepime (4th gen), Also Ceftazidime (3rd gen), Pip Tazo, Ciprofloxacin, Imipenem, Amikacin, Gentamicin, Tobramycin. NOT CEFTRIAXONE! (3rd gen) - good for Strep penumo, S pyogenes, H flu, Klebsiella, E Coli - but POOR against Pseudomonas.

55
Q

PKU inheritance?

A

AR.

56
Q

What is the mech of Terbinafine?

A

Terbinafine - squalene epoxidase BLOCKER. - Treats dermatophytosis. Blocks Squalene epoxide and thus Lanosterol formation.

57
Q

Wha t are the viral independent (dont require viral phosphrylating enzymes) drugs?

A

Cidofovir, Tenofovir.Viral dependent nucleosides: acyclovir, valacyclovir, famciclovir, GANCiclovirCell dependent nucleosides (Zidovudine, Lamivudine)

58
Q

What are processes that give you xanthelasma (foamy macrophages) - can deposit in eyes etc.

A

Hyperlipidemia/cholesterolemia states - cholestatic conditions can cause this - primary biliary cirrhosis, etc

59
Q

Cough, coryza, conjunctivitis, koplic spots precede?

A

Maculopapular skin rash.

60
Q

What do PABA containing sunscreends protect against?

A

UBV only! UBV is the major cause of burns (UVBAD) and skin damage. Have no sign affect on UVA.

61
Q

What nucleotides are at the 5’ end of tRNA?

A

CCA - recognition sequence for proteins - binds Amino Acids.

62
Q

Measles - what can you give to benefit recovery?

A

VitA

63
Q

With what organs do you see graft-vs- host?How does this manifest?

A

Tranplsnat of organs rich in lymphocytes, liver, bones, etc. 1 week after - attack on skin, liver, intestines. These 3 are often attacked.

64
Q

What is the first thing to do when suspecting child abuse?

A

Call Child Protective Services - even before talking to parents.

65
Q

Actinic keratosis - description and histo - what is it a precursor to?

A

Actinic keratoses - small scaly erythematous lesions in sun eposed areas - may show hyperkeratosis and parakeratosis - May lead to SQUAMOUS cell CA.

66
Q

What are the local cutaneous effects of long time topica corticosteroid tx?

A

Atrophy/thinning of dermis - assoc w/ loss of dermal colalgen, cracking, tightening of skin, telangiectasia,s ecchymoses.

67
Q

What are age related changes seen to dermis and epidermis?

A

Epidermis - thinningDermis - reduction of subQ fat, blood vessels, hair follicles, sweat/sebacoeus glands) - loss of SubQ tissue -> tskin becomes atrophic and more vunlerable to damage (wrinking).

68
Q

What ist he mech of Isopropanol, ethanol in disinfection?Chlorhexidine?Hydrogen peroxide?Iodine?

A

Isopropanol - Disruption of cell membranes, denatures proteins. (nonsporicidal)CHlorhexidine - disrupts cell membrane, COAG of cytoplasm (nonsporicidal)H2O2 - free radicals (sporicidal)Iodine - halogenation of protiens/nucleic acid (sporicidal)

69
Q

Niacin def leads to? Be descriptive.

A

Dermatitis, diarrhea, dementia (pellagra)

70
Q

Coinlike lesions that appear they are stuck on and can be peeled off? Velvety/granular texure.

A

Seborrheic keratosis.

71
Q

What ist he rapid plasma reagin test? (RPR)

A

Serum mixed w/ cardiolipin choletserol, lecithin.Aggregation/flocculation - demostrates cardiolipin Ab to serum. Detects ab to cells that are DESTROYED by T pallidum (syphilis) - It does not actually test for syphilis directly.

72
Q

What is the histo of urticaria?Esp from drug induced allergy?

A

IgE ab sensitzationSuperficial DERMAL edem and lymphatic channel dilation.NOT EPIDERMAL.

73
Q

When are nafcillin, methicil, oxacillin used? What are tehy?

A

Penicillinase reistant penicillin -work agains S. aureus but not RMSA> Nafcillin used to treat skin and soft tissue infections (folliculitis etc)

74
Q

Most common cause of hair loss in males and females?

A

Androgenetic alopecia - demonstrates polygenic inheritance w/ variable penetrance.

75
Q

Common treatments for psoriasis?

A

Calciprotriene, Calcitriol, Tacalcitol - Vitamin D analogs - bind to VitD receptor (NUCLEAR TRANSCRIPTION FACTOR) and inhibit keratinocyte proliferation.

76
Q

Febrile, maculopapular rash that BEGINS ON FACE and spreads to trunk. Think what 2 things?

A

Rubeola (measles) and rubella (german measles)Postauricular LNA -> rubella

77
Q

Acanthosis nigricans - caused by?

A

Inuslin resistant states (DM, acromegaly, obesity)And GI malignancies.

78
Q

5 y.o w/ skin rash related to consumption of foods. what is this?

A

NOT CELIAC AND DERMATITIS HERPETIFORMIS - Gluten enteropathy usu presents in 4th or 5th decade of life. This is ATOPIC DERMATITIS - ingestions of foods or envt irritiants - assoc w/ eeczema and asthma. INTENSE PRURITUS is a hallmark of atopic dermatitis - diagnosis cannot be made w/o it.

79
Q

POison Ivy - what type of HSR is this?

A

T4 HSR. T lymphocte mediated.

80
Q

Chronic lymphedema seen in mastectomy pt is a risk for?

A

Cutaneous ANGIOSARCOMA. Known as Stewart Treves syndrome. Axillary LN dissection is clacssic predisposing procedure although any chronic Lymphedema can do this.

81
Q

After zoster in older patient, what is most likely to occur?

A

Localzied dermatomal pain - “potser herpetic neuralgia” Described as stabbing and can last for several months.Affects 10% of pt w/ epsidoes of herpes zoster, it affects more than 75% of pt OLDER THAN 70!Basically older you are more likely you are to get pain.

82
Q

Describe actinic keratosis?AK is labeled in such a way to make you concerned for future?

A

Erythematous papules w/ central scale due to HYPERKERATOSIS - sandpaper like texutre - lesions are small at first, but may enlarge and become elvated.Develop often in excess sun exposure - regarded as PREMALIGNANT condition of CA in situ but less than 1% evolve into squamous cell CA>

83
Q

Splice site mutations often results in?

A

Larger protein w/ altered function but PRESERVED immune reaction.

84
Q

Recurrent skin blistering w/ elevated total plasma porphyrins. What is defect what is this?

A

Porphyria cutanea tarda (most common) - photosensitivity in porphyria - can cause AB PAIN.

85
Q

Erroneous tRNA-AA binding. What happens?

A

Improper AA is incorporated into chain.Once AA binds to tRNA via aminoacyl tRNA synthetase there is no correction.

86
Q

INC stratum spinosum. DEC stratum granulosum. + Acanthosis w/ parakeratotic scaling. (Nuclei still in stratum corneum) What is htis?

A

Psoriasis.

87
Q

When do you have DEC production of melanin, and when do you have DEC melanocytes?

A

DEC production - albinism (normal melanocyte count) - tyrosine kinase def. DEC melanocyte - vitiligo - autoimmune destruction.

88
Q

Difference between Tuberculoid and Lepromatous Leprosy?

A

Tuberculoid - High cell mediated - CD4 (Th1)Lepromatous - low cell mediated - CD4(Th2)SO BOTH ARE CD4 mediated - one is just higher inr esponse. CD4 Th1 activates a stronger MACROPHAGE response. Lepromin skin tests is positive in pt w/ TUBERCULOID leprosy - as they exhibit a strong CD4+ TH1 cell mediated responses.

89
Q

What is peau d’orange caused by? What is inverted nipple caused by?

A

Lymphatic drainage is impeded can get pitting etc. =- peau d’orangeInverted nipple can be caused by CA infiltrating and descrotying suspensory Cooper ligaments.

90
Q

Blisteres w/ oral involvement.

A

PEMPHIGOUS VULGARISBullous does not have oral mucosa involvement.

91
Q

Before giving isotretinoin to female on OCP must?

A

Test for pregnancy.Sexually active females are advised to use TWO FORMS of contraception and have monthly pregnancy tets.

92
Q

What size are ecchymoses? Do they blanch?

A

Ecchymoses - largest bruise - over 1cm. Do not blanch under pressure - unlike telangiectasias. They do not blanch because the RBC are no logner contained within vasculature.

93
Q

Eczematous dermatitis (contact dermatitis) - oozing - what are common histo findings?

A

Spongiosis. Example was mascara to eye - can lead to weeping, encrusted lesions - while wet - prone to bacterial superinfection - Characterized by epidermal accumulation of edematous fluid in intercellular spaces (SPONGIOSIS) - intercellular bridges become even more distinct - appear “spongy” EDEMA can even tear desmosomes apart.

94
Q

Histo of excessive..:AcanthosisLichen planus

A

Acanthosis - INC spinosum (psoriasis)Lichen planus - INC granulosum.

95
Q

What do P bodies do? Where are hey lcoated?

A

P bodies - in cytoplasmP body - play a role in translational repression and mRNA decay. contain exonucleases and decapping - “mRNA QUALITY CONTROL and microRNA silencing” - Also a storage of mRNA - can ue used later.

96
Q

BRAF mutation. What is it? Found in ? Hence hwat is treatment?

A

BRAF is a protein kinase.Seen in Melanoma. Tx w/ BRAF kinase inhibitor (Vemurafenib)

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