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Therapy Spring 2018 > Exam 1 Leukemias, Drug injury, Anemias, Oncology > Flashcards

Exam 1 Leukemias, Drug injury, Anemias, Oncology Flashcards

1
Q

What 8 drugs are most common in drug injury?

A
  1. Abx
  2. Antineoplastics
  3. CNS
  4. Cardiovascular agents
  5. Anticoagulants
  6. Analgesics
  7. hypoglycemics
  8. Diagnostic agents
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2
Q

Risk factors for drug induced injury 7

A
  1. Age old and young
  2. Pulmonary
  3. Comorbidities
  4. Organ dysfunction
  5. Hx of allergy or sensitivity
  6. Exposure
  7. Genetics
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3
Q

Patient and Disease factors for ADRs 8

A

___

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4
Q

Medication factors for ADR

4

A
  1. Med hx
  2. Med info
  3. Med admin
  4. Med formulation
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5
Q

Establishing causality of ADR

9

A
  1. Prior reports of reaction
  2. Temporal relationship
  3. de challenge
  4. Re challenge ethically not that cool
  5. Diagnostic tests
  6. Dose-response relationship
  7. Alt etiologies
  8. Past hx of response to class or medication
  9. Drug-drug interaction
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6
Q

Naranjo probability classification for ADR?

A
  • 9- highly probable
  • 5-8 probable
  • 1-4 possible
  • 0 doubtful
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7
Q

Liverpool ADR causality chart

A
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8
Q

WHat type of reaction is Acetaminophen induced hepatotoxicity and what labs do you see?

A
  • Type A dose related rxn and you see a large elevation in ALTs
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9
Q

APAP concentrations when looking at APAP OD?

A
  • Levels might be normal or undetectable at time of test
  • Chronic vs. acute exposure?
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10
Q

Tx of APAP OD?

<4 hrs consider?

IV vs. Oral APAP

What is the oral dosing for NAC? WHen can treatment be DCed?

A
  • <4 hrs consider induction of vomitting or NG lavage via activated charcoal
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11
Q

What is the oral dosing for NAC? WHen can treatment be DCed?

IV dosing?

A
  • 140 mg/kg then 70 mg/kg q4hrs x 17 doses
    • DC if Transaminases are normal and APAP undetectable in 36 hours
    • Chronic OD pts should be Tx for at least 24 hrs
  • IV 100 mg/kg load then 50 mg/kg over 4 hrsm then 100 mg/kg over 16 hours
    • Continue until transaminases trend downward
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12
Q

What is the number 1 cause for postmarketing drug withdrawal?

A

Hepatotoxicity

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13
Q

DILI Risk factors

A
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14
Q

How is drug induced hepatic injury categorized?

A
  • Hepatocellular
  • Cholestatic
  • Mixed
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15
Q

WHat usually causes hepatocellular injury and what 2 atributes might you see?

A
  • Hepatoxins usually cause the hepato injury
    • Leakage of aminotransferase enzymes (AST/ALT) from injured liver (liver specific)
    • No evidence of obstruction
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16
Q

Cholestasis?

A

Usually reversible and less morbid

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17
Q

WHat aminotransferase is more specific for liver?

A

ALT

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18
Q

What is an indicator of a cholestatic injury?

A

Significant Alk phos elevation

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19
Q

Hepatocellular injury

Values

A
  • ALT > 2 x ULN and R >=5
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20
Q

Cholestatic Injury Values?

A
  • Alk Phos > 2 x ULN R <=2
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21
Q

Mixed injury Values?

A
  • Alk and ALT > 2 x ULN and R between 2 and 5
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22
Q

Acetaminophen and friends what type of injury is seen? 3 friends

A
  • Nevirapine, valpro, isoniazid
    • Acute hepatocellular injury with elevated ALTs and (+/-) hyperbilli
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23
Q

Drugs and examples of what types of injury they cause to the liver

A
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24
Q

What are the 3 keys to assess causality?

A
  • Temporal Relationship
  • Individuals susceptibility
  • Be diligent in excluding other cuases
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25
Q

Main Tx for DILI?

A
  1. DC the drug
  2. Supportive and symptomatic therapy
  3. Monitor for development of ALF
26
Q

5 possible drug txs for DILI and one other

A
  1. Glucocorticoid if immune mediated
  2. IV Carnitine for Valpro injury
  3. Ursodeoxycholic acid for cholestatic
  4. NAC for non-APAP DILI
  5. Cholestyramine for leflutamide associated DILI
  6. At earliest stages of liver failure- Transplant
27
Q

When should Re-challenging with a DILI drug not be considered?

A
  • Pts with significant elevation in enzymes >5x ULN
  • Pts that have signs of an immunologic reaction
28
Q

How is DIKD usually detected inpatient?

Outpatient?

A

Changes in SCr and BUN

Signs and Symptoms of renal failure

29
Q

What is the mot common DIKD Clinical manifestation?

A

Decline in GFR

  • Increase SCr and BUN
  • Delayed from acute kidney injury
30
Q

Signs and Symptoms of DIKD? 7 all together

A
  • Malaise (Uneasy feeling)
  • Anorexia
  • Vomiting
  • Shortness of Breath
  • Edema
  • HTN
  • Changes in urine output.
31
Q

What SCr changes are you looking for for DIKD

A
  • >0.3 mg/dl within 48 hours
  • >50% increase from baseline in 7 days
32
Q

Tubular Epithelial Damage

Direct Toxicity to tubules epithelial cells found in the urine

Loss of bicarb, glucose, phosphate, urate, potassium, magnesium

What are the 4 agents that have been seen to do this?

A
  • Aminoglycosides, cisplatin, radiocontrast media, amphotericin B
33
Q

Hemodynamic Injury

Drugs causing reduced intraglomerular pressure

Constrict afferent or efferent

Ag II and PGE2 are important in the pathway

What are the 3 drugs?

A
  • NSAIDs
  • ACE-I
  • ARBs
34
Q

Obstructive Nephropathy

Deposition or precipitation in the renal tubules

4 drugs

What is key for this and what would you give people if they were experiencing this.

A
  • Hydration and pH of urine is key for Tx is Acid drug give them bicarb if basic give them ammonium chloride
  • Sulfonamide, Acyclovir, Methotrexate, Triamterene
35
Q

What symptoms are specific for Folate Def or B12 def Anemia?

A

dysphagia, anorexia, weight loss, beefy red tongue.

36
Q

What symptoms are specific for folate?

A

bruising, early graying of hair.

37
Q

B12 specific symptoms?

A

ataxia, paresthesias of hands/feet, forgetfulness, personality changes, dementia, psychoses. (possible cause of dementia in elderly)

38
Q

Fe Def Anemia

What is weird about this?

A

koilonychia (spooning of nails), glossitis, angular stomatitis, achlorhydria, craving for substances low in iron such as clay, ice, or cornstarch. (this effect is known as PICA. We had a young patient who ate the yellow pages, but eating dirt or ice is more common)

Patients have weird cravings

39
Q

Hemolytic Anemias

A

painful crises (especially with sickle cell disease), abdominal pain, hemoglobinuria, jaundice. With chronic hemolysis: cholelithiasis (bilirubin stones); and rarely: angina, syncope, congestive heart failure (high output), leg ulcers.

40
Q

Iron def anemia 5 low labs

One high

A

MCV, MCHC, ferritin, Fe, %sat (TSAT)

HIGH: TIBC

41
Q

What dosage of Fe should patients get when treating iron def

A
  • 150-200 mg/day of elemental iron for at least 6 months.
    • 325 mg TID FeSO4 (20% elemental Fe)
  • Sulfate is the cheapest and best absorbed when not taken with food.
  • SR not good
  • liquid form can stain teeth, dosage errors
42
Q

What are the 4 DIs with Fe?

Food?

A

Acid Blockers, quinolones, tetracyclines, cholestyramine

Tea, coffee, fiber, milk, formula, decrease absorption

43
Q

resasons to use parenteral Fe

A
  • History of malabsorption, renal dialysis, poor adherence to PO
44
Q

Monitoring for a response to Fe Def Tx? For any replacement therapy)

A
  • Increased reticulocytes (3-10 days)
  • Increased Hb/Hct (2-4 wks)
  • Then should see correction of MCV and MCHC after that
  • Opposite order when anemia is appearing
45
Q

What def can cause nerve damage?

A

B12

46
Q

Megaloblastic Anemias

Folate and B12

Elevated?

A

MCV

47
Q

Vit B12 DIs

A

PPI, H2RAs, metformin decreases absorption

48
Q

What might be better at indicating B12 def?

A

methymalonic acid

49
Q

What B12 replacements are for maintenance only?

A

Nasal stuff

50
Q

WHere can you get folate from your diet?

WHat form is absorbed?

What drugs can decrease absorption or utilization?

A

leaft green veggies, fortified bread and cereal, cooking reduces the levels though

Monoglutamated is absorbed

ETOH, phenytoin, phenobarb, carbamazepine, sulfasalazine, OCs, PPIs, H2RAs, methotrexate, TMP-SMZ, folate can reduce phenytoin effects.

51
Q

FOlate dosing?

A

1 mg daily for 2-3 wks

52
Q

High emetic risk How many drugs and what are they?

A
  • NK1 antagonist + 5HT antagonist + dexamethasone + olanzapine
53
Q

Moderate Emetic Risk Regimen

A
  • 5HT antagonist + dexamethasone
    • NK1 antagonist for carboplatin AUC >4 containing regimens
54
Q

Low emetic risk

A

5HT antagonist

Dexamethasone

55
Q

Minimal Emetic Risk

A

None

56
Q

5HT3 Antagonists

4

A

Ondansetron PO/IV Most frequently used

Granisetron (PO/IV/Patch)

Dolasetron PO

Palonosetron

57
Q

NK1 Antagonists

4

A
  • Aprepitant PO
  • Fosapritant IV
  • Rolapitant PO/IV
  • Netupitant PO Combo with palonosetron
58
Q

What drugs are high, mod, low, minimal emetic risk?

COPR

A
  • Cisplatin
  • Oxaliplatin
  • Pacitaxel
  • Retuximab
59
Q

What are the indications for vancomycin in NF

A
  1. Hemodynamically unstable or evidence of sepsis
  2. G (+) Culture
  3. Pneumonia positive with radiography
  4. Skin/soft tissue infection
  5. Clinically suspected serious catheter related infection
  6. Known colonization of MRSA
  7. Sever mucositis if FQ prophylaxis has been given and ceftazidime is employed as empiric therapy
60
Q

WHat are the 3 metabolic abnormalities in TLS?

A

Hyperkalemia, hyperphosphatemia, hypocalemia

61
Q

Rasburicase for TLS

Dosing based on UA and wt.

A
  • UA>=12 or >=100kg —–> 6 mg IV once
  • UA 8-12 or >=100 kg —–> 3 MG IV once
  • UA <=8 ——-> Not indicated
62
Q
A

Therapy Spring 2018 (5 decks)

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