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Flashcards in Derm and Hematology Deck (126)
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1
Q

two types of anti-inflammatory agents for the skin

A

topical corticosteroids and tar compounds

2
Q

variation on steroid transdermal absorption based on region

A

high: face, scalp, armpits, groind
medium: chest, back, abdomen
low: hand, feet, arms, legs

3
Q

low potency topical steroid

intermiediate

high

highest

A

triamcinolone

hydrocortisone

desoximetasone

clobetasol

4
Q

what skin conditions are coal tar used for

issues

A

psoriasis, lichenified dermatitis for anti-itch effect

messy, can be irritating

5
Q

three ingredients of triple abx ointment

A

neomycin, bacitracin, polymyxin

6
Q

what is mupirocin used for

atabax

A

gram + (impetigo)

also impetigo

7
Q

typical topical azoles

A

miconazole

clotrimazole

8
Q

ciclopirox is good for what

A

in lotion its good for tinea

in nail polish its good for onychomycosis

9
Q

what is oral terbinifine used for

how long is the treatment

what must be monitored

A

onychomycosis

3-6mo

can be liver toxic

10
Q

types of drugs used for acne

A

retinoids

benzoyl peroxide

azelaic acid

ABx

11
Q

what are retinoids made of

what are they used for

A

vitamin A derivatives

acne and psoriasis

12
Q

general guidelines for retinoid use in acne

A

8-12 weeks to max benefit

may make acne look worse to start

avoid mucous membranes and eyes

use sunscreen after treatment ↑risk of skin cancer

13
Q

100% necessity for retinoid therapy

A

must be on oral contraceptives because they cause birth defects

14
Q

ADRs related to isoretinoin

A

chapped lips

dry skin

nose bleeds

dry eyes

15
Q

action of bezoyl peroxide for acne

what is it tpically paired with

A

opening skin pores with some intrinsic antibiotic effect

clindamycin or erythromycin

16
Q

what is the mode of action of azelaic acid

common side effect

A

antibacterial and may ↓test conversion ot DHT

erythema and dryness

17
Q

Abx for acne treatment

A

systemic: tetracycline or erythromycin
topical: clindamycin, erythromycin, metronidazole

18
Q

anti itching drugs

A

steroids

doxepin

pramoxine

19
Q

doxepin is a what?

what is its method of action

ADRs?

A

tricyclic antidepressant

not sure, possible antihistamine effect

drowsiness, exacerbate narrow angle glaucoma

20
Q

pramoxine for dermal itching

A

topical anesthetic, not going to fix the issue!

can be used with hydrocortisone

may cause burning

21
Q

psoriasis defined

females <>=males?

symptoms

A

chronic relapsing skin disorder

no bias

itching, joint inflammation, depression

22
Q

wht causes psoriasis

A

rapid turnover of skin cells

23
Q

psoriasis treatment options

A

high potency topical steroids and tar

acitretin

tazarotene

calcipotriene

24
Q

ADRs of acitretin

A

no blood donation, requires 3 years to clear system

no alcohol (liver toxic)

25
Q

ADRs with tazarotene

A

<20% of body surface is treated

can be teratogenic

also photosensitizing

26
Q

ADRs with calcipotriene

A

hypercalcemia, but rare

27
Q

general causes of anemia

A

nutritional deficiency (folate, iron, B12)

EPO ↓ (CKD)

hemolysis (genetic, drug induced, autoimmune)

bone marrow suppression (drugs, cancer, aplastic anemia)

28
Q

typical causes of iron deficient anemia

A

poor diet

increased need

chronch blood loss

29
Q

treatment for iron deficient anemia

A

ferrous sulfate

ferrous glucaonate

IM or IV iron

30
Q

compliance issues with iron supplements

A

GI upset very common

black stools

might need a creative dosing schedule

31
Q

what is the role of vitamin C in iron therapy

A

500mg taken with iron sulfate can help absorption

32
Q

what is the last resort for iron deficient anemia

why should you refer

A

parenteral

anaphylaxsis risk warrants refereal

33
Q

chronic hemochromatosis can come from what

A

iron toxicity leading to organ failure

34
Q

iron toxicity in pediatrics can becaused by how many pills

what is the risk

A

>10

neocrotizing enteritis

35
Q

when should iron supplements be avoided

A

men with normal diets

non-menstruating women with normal diets

36
Q

causes of vitamin b 12 deficient anemia

A

diet deficient

loss of intrisic factor

37
Q

why is dietary deficiency of vitamin B 12 rare

A

small daily needs with large stores

38
Q

what might cause loss of intrinsic factor leading to anemia

A

pernicious anemia, gastric surgery, gastric atophy

39
Q

what causes pernicious anemia

DX by what

treatment consideration

A

intrinsic factor autoantibodes that ↓folate absorption

megaloblastic anemia and progressively declining neurologic function

treating the folate ↓ will fix anemia but not the the neuro issues

40
Q

usual treatment for Vit B 12 deficienct

A

IM injections daily, then weekly, then monthly

OR massive oral doses

41
Q

what is folate used for

what will low folate do to a fetus

A

essential cofactor for AAs, purines, DNA

↑ risk for ancephaly and spina bifida

42
Q

folate deficiency is caused by what

A

diet (↓ fruits and veg)

↓absorption (sprue, drugs)

↑increased need (pregnancy, hemolytic anemia)

43
Q

important safety rule regarding folate and B12 for anemia

A

NEVER prescribe folate for megaloblastic anemia UNLESS you are sure the patient’s B-12 level is normal

44
Q

EPO toxicity issues

A

increase viscosity can cause HTN or DVT

↑risk of CVA or MI with chronic don’t come

can ↓cancer surviability

45
Q

describe the chemical process of a clot

A

fibrinogen is convered to thrombin by prothombin and then is converted to fibrin

plasmin starts to break the clot down into d-dimer and spllit fiborin products

46
Q

natural anticoagulants

A

antithrombin III

protein s and c

47
Q

what accelerates the action of antithrombin III

A

heparin

48
Q

most common genetic cause of hypercoagulability

what does it do

A

abnormal factor V (Leiden)

factor V Leiden cannot be inactivated by protein C

49
Q

most common presentation of thrombosis

A

MI, ischemic stroke, DVT

50
Q

treatment of an acute thrombic event

A

thrombolysis

anticoagulation

thrombectomy

51
Q

anticoagulation strategies

A

block platelet function

inhibit thrombin directly

inhibit thrombin indirectly (vit K or ↑antithrombin III)

inhibit factor X

52
Q

antiplatelet approaches for anticoagulation

A

block prostaglandin

inhibit ADP pathway

block IIb/IIIa platelet receptors

53
Q

antiprostaglandin approach to anticoagulation

A

asipirin to prevent CVD

can cause GI bleeds

54
Q

Anti-ADP approach to anticoagulation

drugs

primary use

side effects

A

plavix

adjunct to stent, used chronically to prevent MI or CVA

nausea, diarrhea, leukopenia

55
Q

what is action of coumadin drugs

why is it still used today

A

interferes with the action of Vitamin K in clot formation

cheap, welll understood, reversible

56
Q

how long does it take for warfarin to have an effect

how should it be monitored

A

8-12 hours with no loading dose

prothrombin time ratio (INR)

57
Q

what two things will cause megaloblastic anemia

A

vit B and folic acid deficiency

58
Q

what is the target INR for warfarin

A

2-3.5

59
Q

ADRs with coumadin

A

hemorrhage

fetotoxic

multiple drug interactions

dietary restrictions

60
Q

what should be done when prescribing warfarin or with a patient who is on warfarin

A

check for drug interactions

61
Q

what is the action of heparin

A

enhances the action of antithrombin III (inhibits activation of factor X)

62
Q

two types of heparin

A

unfractionated and LMW

63
Q

what is the choke point between the intrinsic and extrinsic pathways for clotting

A

factor x or thrombin

64
Q

how is heparin therapy monitored

what is the goal

A

activated protamine titration (PTT)

goal is 2-2.5 x control

65
Q

indications for heparin use

A

prophylaxis (surgery, ICU)

theraputic (DVT, PE)

66
Q

Heparin Toxicity

A

hemorrhage

thrombocytopenia

osteopenia

67
Q

heparin induced thrombocytopenia type II

what is the reactive measure for this

A

Two types, Type II is an immunte related drop in platelets that leads to thombosis

immediately stop thrombin and start something else

68
Q

why does HIT cause thrombosis with thrombocytopenia

A

because all the platelets are being take up by clots

69
Q

what is the advantage of LMW heparin

A

↓risk of thrombocytopenia or osteopenia

usually no monitoring needed

can be used at home

70
Q

LMW heparin preparations

A

enoxaprin (lovenox)

71
Q

when can a patient be switched from lovenox to warfarin

A

INR > 2 for two consecutive days

72
Q

what is the advantage of arixta over lovenox

A

daily dosing

better at DVT prevention with equal prevention of thrombosis

73
Q

common treatment for the prevention of MI

A

clipidogrel (plavix) + aspirin (↑risk for GI bleeds, but relatively small)

74
Q

what is dabigatran (predexa) used for

what is the advantage over other drugs

issues

A

thombin inhibitor

better at preventing stroke and afib, no monitoring

non-reversible, more GI upset, expense

75
Q

two factor X inhibitors

A

rivaroxaban (xarelto) and apixaban(eliquis)

76
Q

what is the advange to factor X inhibitors in anticoagulation

what are the drawbacks

A

oral, no monitoring, no diet restriction

expensive, not easily reverible

77
Q

treatment strategy for an acute thrombus

A

thombolysis

anticoagulation

thrombectomy

78
Q

rules for thrombolytic therapy

A

sooner is better

its not always effective

can cause hemorrhage

79
Q

what is the action of thrombolytic drugs

A

activates plasminogen to become plasmin

80
Q

indications for thrombolytics

A

DVT, PE, ischemic stroke, clotted shunts/catheters

81
Q

examples of thromblytic agents

what is their universal method of adminstration

A

streptokinase, urokinase, etc

all given IV

82
Q

what is the cheapest thrombolytic drug

A

streptokinase

83
Q

contraindications for thrombolytics

A

<10days post op

serious GI bleed

HTN (diastolic >110)

pregnant

84
Q

reversal agents for fibrinolytics (streptokinase)

A

aminocaproic acid (amicar)

85
Q

what is used to reverse heparin

A

protamine sulfate

86
Q

three methods for reversing warfarin

A

vitamin K, FFP, prothrombin concentrats

87
Q

what is the risk with treatment for refludan

A

since it comes from leechs it can cause an allergic reaction

88
Q

multistep theory of oncogensis

A

there must be an activated oncogene and a deactivated or overwhelmed tumor suppressor gene

89
Q

driver mutations

A

oncogenic mutations that drive the cancer process, tend to be the same in the same types of cancer

90
Q

hitchhiker mutation

A

mutations found in cancerous cells that don’t necessarily contribute to the disease

91
Q

four pillars of cancer treatment

A

surgery

chemo

radiation

immunetherapy

92
Q

what types of cells are most susceptible to cytotoxic chemo

A

rapidly dividing cells

93
Q

what is the rationale of chemotherapy in cancer treatment

A

because cancer cells are genetically fragile and rapidly dividing they are susceptble to chemo, allowing therapy to kill the tumor without killing the patient

94
Q

weaknesses on cancer cells that can be exploited by chemo

A

outgrows blood supply

decreased ability to repair themselves

multiple mutations

most cancers have unique antigens

95
Q

factors affecting prognosis of cancer

A

cancer type

differentiation

staging at Dx

age

quality of medical care

96
Q

how does a clinician know when to stop chemotreatment

A

Biochemical markers (HCG, CEA, PSA)

clinical markers (palpable nodes, imaging)

97
Q

how can cancer cells develop resistance to treatment

what can be done to prevent this

A

genetic mutations continue after malignant transformation

use the correct amount of the correct drug

98
Q

what is the action of alkylating agents

three examples

what are three ADRs

A

damages the DNA in dividing cells

cyclophosphamide, ifosfamide

nausea, germ cell destructon, bone marrow suppression

99
Q

types of antimetabolite chemo drugs

A

folic acid analogs (methotrexate)

purine analogs (mercaptopurine)

pyrimidine (flurouracil)

100
Q

typical ADR of methotrexate

A

bone marrow suppression, mucosal ulcers, hepatotoxic

101
Q

what is the action of antibiotic chemo

one example

Three ADRs

A

disrupt DNA

dactinomycin

bone marrow suppression, cardiac toxicicity (adriamycin), pulmonary toxicity (blenoxane)

102
Q

action of microtubule inhibitors

ADRs

A

interrupts mitotic spindle

bone marrow suppression, hypersensitivity

103
Q

common uses for tyrosine kinase inhibitors

ADRs

A

leukemia, lung cancer, renal cell carcinoma

drug interactions, bone marrow suppression

104
Q

what is the action of topoisomerase

commonly used for what?

ADR

A

blocks enzyme for DNA supercoiling

lung, ovarian, colorectal

bone marrow suppression

105
Q

two types of platinum corrdination complexes used in chemo

ADRs

A

cisplatin, carboplatin

severe nausea, ototoxicity

106
Q

how is predinosne used in chemo

A

acute leukemia and lymphoma

107
Q

how is tamoxifen used in chemo

A

reduced risk of breast cancer recurrenct

108
Q

how is letrozole or armidex used in chemo

A

anti aromatases, used to prevent breast cancer

109
Q

how is estrogen used in chemo

A

prostate cancer

110
Q

how is lupron used in chemo

A

down regulation of FSH receptors produces low androgen levesl

111
Q

how is dexamethasone used in chemo

A

anti emesis, blocks hypersentivity reactions

112
Q

what is the advantage of immune therapy

A

it has targeted treatment against specific mutations in cancer cells that uses that patients own immune system

113
Q

specific tactics of immune cancer therapy

A

prevent evasion of apoptosis

increased immune response

monoclonal antibodes against specific targets

114
Q

what is the use of PD-1 blockade in cancer patients

A

allow cytotoxic t cells to recognize cancer cells and kil them

115
Q

what is the advantage of PD-1 blockade

A

20-25 durable response rate, especially useful in difficult to treat cancers (renal cell, melanoma)

116
Q

what is the action of interferon therapy in cancer treatment

notable ADRs

A

stimulation of NK cells

neuropsyciatric

117
Q

describe in vitro immune enhancement

A

in cancers with a specific antigen, lymphocytes can be cultured with that antigen and reinfused to target those cells

118
Q

what is the issue with in vitro lymphcyte training

A

it doesn’t add much to life span an costs a lot

119
Q

describe lymphocyte gene therapy

A

lymphocytes are removed and exposed to a retrovirus that will force expression of CD19nreceptors (b cells)

reinfused T cells will then go kill b cells (used for B cell leukemia/lymphoma)

120
Q

what is the most important determinant of cancer biology

A

cancer genomics, not organ of origin

121
Q

what is HER2 therapy for breast cancer

A

monoclonal antibodies (herceptin) with or without (herceptin + mertansine) will attack cells with mutated human endothelial growth receptor, improving prognosis for HER2 cancer

122
Q

ADRs related to HER2 therapy

A

cardiac toxicity, especially between trastuzumab and doxorubicin

123
Q

describe VEGF therayo for cancer therapy

A

inhibits the BRAF gene, improves outcomes in melanoma, colon, lung cancer

124
Q

why is prevention of bone marrow suppression important to chemotherapy

A

better bone marrow function increased tolerance to additional chemotherapy

125
Q

how is EPO used in cancer treatment

A

helps prevent anemia in the presence of bone marrow suppression

126
Q

what is the action of granulocyte colony stimulating factors

one notable ADR

A

helps prevent neutropenia

can cause bone pain