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Involuntary Weight Loss Flashcards

1
Q

Mr. M is a 35 YO male who comes in for evalulation of weight loss. He reports a loss of 35 lb in the last 6 mo. Vitals are normal. He is thin, with temporal wasting and bilateral enlarged cervical lymph nodes.

What are your top diagnoses?

What tests do you order?

A
  • Top Diagnoses: HIV, cancer
  • Tests
    • CBC & differential
    • Complete metabolic profile
    • TSH
    • HIV Ab
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2
Q

Normal CD4 T-cell count = _______

CD4 T-cell count <200 = ________

A

Normal CD4 T-cell count = 450-500

CD4 T-cell count <200 = risk for opportunistic infections (PCP)

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3
Q

For treating HIV:

How many drug classes?

How many drugs?

Why?

A
  • 3 or more drugs
  • > 2 drug classes
  • Stop viral replication
  • Prevent mutations that can lead to resistance
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4
Q

What factors should you consider when selecting the initial drug regimen to treat a patient’s HIV?

A
  • Viral resistance profile
  • Factors to enhance compliance
    • Dosing frequency, pill burden, combination products
    • Tolerable side effects
    • Cost
  • Other Rx: drug-drug interactions
  • Co-morbid conditions
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5
Q

What are some examples of drug combinations for treatment of HIV?

A
  • 2 NRTIs + integrase inhibitor (___-tegravir)
  • 2 NRTIs + PI (____-navir) + booster
  • 2 NRTIs + NNRTI
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6
Q

What are some examples of this drug combination?

2 NRTIs + integrase inhibitor

A

tenofovir + emtricitabine + raltegravir

tenofovir + emtricitabine + dolutegravir

abacavir + lamivudine + dolutegravir

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7
Q

What are some examples of this drug combination?

2 NRTIs + PI + booster

A

tenofovir + emtricitabine + darunavir + ritonavir

tenofovir + emtricitabine + atazanavir + ritonavir

abacavir + lamivudine + darunavir + ritonavir/cobicistat

tenofovir + emtricitabine + lopinavir + ritonavir

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8
Q

What are some examples of this drug combination?

2 NRTIs + NNRTI

A

tenofovir + emtricitabine + efavirenz

tenofovir + emtricitabine + rilpivirine

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9
Q

What is something you would like to know before prescribing abacavir?

A
  • HLA-B*5701 status
  • Associated w/ potentially fatal hypersensitivity rxns
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10
Q

What is something you would like to know before prescribing a protease inhibitor?

A
  • Diabetes
    • PI’s block GLUT4 glucose uptake & can decrease glucose sensing by ß-cells
  • Hyperlipidemia, CV disease
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11
Q

What is something you would like to know before prescribing ritonavir?

A

Ritonavir is a strong inhibitor of CYP3A

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12
Q

Which of the following may be of concern in patients with a history of psychiatric illness?

  • Maraviroc
  • Zidovudine
  • Efavirenz
  • Raltegravir
  • None of the above
A

Efavirenz

  • High incidence of CNS & psychiatric symptoms, possibly for suicide ideation
  • Strong in 1st month, decreases over time
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13
Q

What are the side effects of Maraviroc?

A

hepatic, cardiovascular

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14
Q

What are the side effects of Zidovudine?

A
  • Bone marrow suppression
  • Drug interactions: glucuronyltransferase
  • Myopathy
  • Lactic acidosis, hepatic steatosis
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15
Q

What are the side effects of Raltegravir?

A
  • Myopathy
  • CK elevations
  • Some hypersensitivities
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16
Q

Your patient Mr. M comes back after 2 years of HIV treatment with a 10 lb weight loss & difficulty swallowing. He has missed several of his last appointments. On exam, you see this:

What does he have?

A

Oral Candidiasis

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17
Q

What are each of these?

A
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18
Q

What is the most effective mechanism to prevent opportunistic infections in HIV patients?

A

Inhibit HIV replication

  • Keeps CD4 counts high enough to lessen chance of opportunistic infections
  • Low CD4 counts increase susceptibility to opportunistic infections including fungi
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19
Q

If your HIV patient comes into your office with oral candidiasis, what questions do you have for them? What tests would you like to order?

A

Have you been taking all of your HIV drugs daily?

HIV viral load & CD4 count

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20
Q

What is the most common initial treatment for oral Candida?

A
  • Fluconazole (pill, oral)
  • Clotrimazole (oral troche)
  • Nystatin (oral suspension)
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21
Q

What are some drug interactions to be concerned about when administering fluconazole?

A
  • Fluconazole & other -conazole anti-fungals work by inhibiting fungal P450s
  • They also inhibit human CYP3A & CYP2C9
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22
Q

______ do not have significant CYP interactions

A

NRTIs

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23
Q

_______ ________ are metabolized by CYP3A

A

Protease inhibitors are metabolized by CYP3A

-conazole antifungals can increase PI levels

24
Q

NNRTIs & maraviroc have __________ links

A

CYP3A

  • Maraviroc: CYP3A substrate
  • NNRTIs can inhibit & introduce CYP3A & other CYPs
25
If your patient has *Candida glabrata*, what should you switch them to? (from fluconazole)
* Oral * Itraconazole * Voriconazole * Posaconazole * IV * Caspofungin * Anidulafungin * Micafungin * Amphotericin B (if life-threatening)
26
What do you need to consider if your HIV patient skipped some days of medication & developed oral candidiasis?
May have developed **resistance** secondary to his many missed doses * Check for mutations which preclude resistance to certain medications * Genotype
27
A _55 YO_ otherwise healthy male has lost 20 lb in the last 2 mo. He has had an increase in urination (all day) & feels thirsty all day. He drinks 6-8 glasses of water everyday. He has mild nausea when eating heavy meals & mild tenderness on R calf after recent bike ride. He is noticably more pale than normal. On exam he has unilateral edema & swelling of the R calf. Chemistry reveals Na 130, K 4.9, Glucose 360. On lower extremity ultrasound he has a +R DVT. **What is going on here?**
* Summary: Otherwise healthy & fit individual w/ weight loss & new diagnosis of diabetes & DVT * Loss of \>10% of body weight = _RED FLAG_ * Unilateral swelling & erythema = _RED FLAG_ * Migratory thrombophlebitis = Trousseau syndrome * You're thinking **MALIGNANCY**
28
What is Trousseau syndrome? \*from First Aid\*
* Migratory thrombophlebitis * Redness & tenderness on palpation of extremities * Indication of gastric or pancreatic cancer
29
Your patient experiences increasing band-like epigastric pain. A CT scan of the chest abdomen & pelvis revealed a large head of the pancrease mass encasing the SMA & 4 liver metastases (largest 3cm) were noted. Serum CA 19-9 was 6500. ## Footnote **What test will provide you with the most information?**
Liver metastasis biopsy
30
What is a type of pancreatic cancer associated with flushing & diarrhea?
**Neuroendocrine tumor** \*carcinoid syndrome\*
31
Migratory thrombophlebitis is most commonly seen in which two cancers?
gastric cancer & pancreatic cancer
32
Which of the following are known risk factors for pancreatic cancer? * Lynch Syndrome * Diabetes Mellitus * Peutz Jeghers Syndrome * BRCA Hereditary breast cancer * All of the above
**All of the above**
33
Clinical signs of pancreatic cancer include: * Virchow's node * Sister Mary Joseph's node * Trousseau's sign * Jaundice * All of the above
**All of the above** * Virchow's node * Involvement of L supraclavircular node by metastasis from stomach * Sister Mary Joseph's node * Subcutaneous periumbilical metastasis
34
Treatment administered after surgical resection for pancreatic cancer is called: * Adjuvant treatment * Neoadjuvant treatment * Definitive treatment * Palliative treatment * Alternative treatment
**Adjuvant treatment** * Adjuvant treatment * Surgical intervention meant to cure & prevent metastasis after the definitive treatment * Neoadjuvant treatment * Before the definitive treatment * Definitive treatment * Standard for type of cancer with intention of curing * Palliative treatment * Treatment in incurable * Focus on symptoms * Alternative treatment * Different treatment sought out by patients w/ incurable diseases
35
A drop in CA 19-9 (is/is not) considered a marker for improved survival in pancreatic adenocarcinoma.
**IS**
36
Your patient has Metastatic Pancreatic Adenocarcinoma. What are some options for treatment?
* Proposed treatment: **Folfirinox** chemotherapy * Overall survival = 11.1 mo * **Gemcitabine** in combination w/ nab-paclitaxel is a reasonable alternative * Overall survival = 8.5 mo
37
What are some risk factors for pancreatic adenocarcinoma? \*First Aid\*
* Tobacco use * Chronic pancreatitis (esp \>20 YO) * Diabetes * Age \>50 YO * Jewish & African American males
38
How does pancreatic adenocarcinoma present? \*First Aid\*
* Abdominal pain radiating to back * Weight loss (due to malabsorption & anorexia) * Migratory thrombophlebitis (Trousseau) * Obstructive jaundice w/ palpable, non-tender gallbladder (Courvoisier sign)
39
What are the drugs approved for pancreatic cancer by the National Cancer Institute? (7)
* Paclitaxel (albumin-stabilized) * 5-fluorouracil * Erlotinib * Everolimus * Gemcitabine * Mitomycin C * Sunitinib
40
What are some drug combinations used for pancreatic cancer?
* Gemcitabine + cisplatin * Gemcitabine + oxaliplatin * **Folfirinox** * Leucovorin + 5-FU + irinotecan + oxaliplatin * **OFF** * Oxaliplatin + 5-FU + leucovorin
41
A patient is being treated w/ a combination of drugs for pancreatic cancer. Her recent labs show these serum abnormalities: * Creatinine: 5.5 [0.5-1.2 mg/dL] * BUN: 45 [6-20 mg/dL] * Mg2+: 0.2 [1.5-2.0 mM] Which of these drugs is most likely responsible? * Cisplatin * Gemcitabine * 5-FU * Erlotinib * Paclitaxel
**Cisplatin** * Well-recognized cause of _renal damage_ * Hydration & diuresis decrease risk * _Electrolyte abnormalities_
42
Which of these drugs has a low incidence of renal toxicity & which have lower renal effects but no Mg2+ effects? * Gemcitabine * 5-FU * Erlotinib * Paclitaxel
* Low incidence of renal toxicity * Erlotinib, 5-FU * Lower incidence renal effects (_\<_12%), but not magnesium effects * Gemcitabine, paclitaxel
43
What are two reasons for giving leucovorin in anti-neoplastic therapy?
* Rescue normal cells from methotrexate * Enhance the effectiveness of 5-FU
44
As predicted from their mechanisms of action, which of the following drugs for pancreatic cancer primarily targets the S phase of the cell cycle? * Paclitaxel * Erlotinib * Cisplatin * Gemcitabine * 5-FU
**Gemcitabine, 5-FU**
45
What is the mechanism of action of 5-FU?
S-phase targeting * Pyrimidine analog * FdUMP inhibits thymidylate synthase
46
What is the mechanism of action of Gemcitabine?
S-phase targeting * Dilfuorocytidine analog * Gemcitabine tri-P competes for dCTP for DNA incorporation * Gemcitabine di-P inhibits ribonucleotide reductase
47
What is the mechanism of action of Paclitaxel?
* Late G2 (G2/M) * Enhances assembly & stability of MTs
48
What is the mechanism of action of Cisplatin?
* Cycle-specific phase-non-specific * Platinumb coordination complex * DNA cross-links * Inhibits thioredoxin reductase
49
What is the mechanism of action of Erlotinib?
* Cell cycle arrest (in G1) * Inhibits tyrosine kinase of EGFR, blocking growth promoting signal
50
A patient being treated for pancreatic cancer develops peripheral neuropathy. Which of the following drugs are most likely to cause this adverse effect? * 5-FU * Paclitaxel * Cisplatin * Gemcitabine * Oxaliplatin * Irinotecan
* Peripheral Neuropathy * Paclitaxel, cisplatin, oxaliplatin * 5-FU: rare * Gemcitabine: \<10% (usually mild) * Irinotecan: \<3%
51
What is the advantage of albumin-stabilized paclitaxel nanoparticles vs. paclitaxel?
* **Paclitaxel** * Highly hydrophobic * Traditionally given w/ a detergent (Cremaphor) * Severe hypersensitivity rxns * Poor drug distribution/penetration * **Albumin-stabilized paclitaxel** * No detergent needed * Avoids hypersensitivity rxns * Improved tissue/tumor penetration * Improved anti-tumor effects
52
What is Irinotecan?
* Topoisomerase inhibitor * Blocks re-ligation of DNA strand breaks (during replication) * S-phase
53
What are the most common side effects of Irinotecan?
* Myelosuppresion (98%, dose-limiting) * Alopecia (60%) * Nausea, diarrhea, vomiting, fever
54
What is the mechanism of Protease Inhibitors in treatment of HIV? \*First Aid\*
"-navir" * Assembly of virions depends on HIV-1 protease (pol gene), which cleaves the polypeptide products of HIV mRNA into their functional parts * **Thus, PIs prevent maturation of new viruses**
55
What is the mechanism of NRTIs in the treatment of HIV?
* Competitively inhibit nucleotide binding to reverse transcriptase & terminate the DNA chain (lack a 3' OH group) * Tenofovir is a nucleotide; the others are nucleosides & need to be phosphorylated to be active
56
What is the mechanism of NNRTIs in the treatment of HIV?
* Bind to reverse transcriptase at site different from NRTIs * Do not require phosphorylation to be active or compete w/ nucleotides

Symptoms (17 decks)

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