Mix10 Flashcards

1
Q

What cardiovascular sequallae do you need to be concerned about in a chronic renal failure who presents with chest pain on lying down?

A

Uremic pericarditis. Elevated BUN >60 can cause inflammation of visceral and parietal pericardium. Pt may complain of pleuritic chest pain that is worse in supine position. Can be heard as a “high freq squeeking/friction rub” at LSB when Pt leans forward.

Initiation of dialysis is recommended for most patients for symptom resolution. But since most cases are accompanied by pericardial effusion, you need to rule out cardiac tamponade.

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2
Q

Why do you have increased risk of bladder cancer with cyclophosphamide?

A

Cyclophosphamide is an alkylating agent used as an immunosuppressant in SLE, vasculitis, and certain cancers. Cyclophosphamide has a lot of different effects that can include acute hemorrhagic cystitis, bladder CA, and myelosuppression.

Hemorrhagic cystitis and bladder CA are due to production of acrolein (bladder toxic metabolite of cyclophosphamide)

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3
Q

What’s the typical treatment for cryptococcal meningoencephalitis?

A

Induction therapy with 2 wks of IV amphotericin B and flucytosine followed by fluconazole for consolidation and maintenance therapy.

** Serial LP may need to be done to reduce intracranial pressure.

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4
Q

If a patient presents with loud P2 heart sound, holosystolic murmur at lower L sternal border, elevated JVP, peripheral edema, ascites, and hepatomegaly then what would be the primary cause of this constellation of symptoms?

A

Cor pulmonale - R HF from pulmonary HTN (most often due to COPD). May have exertional syncope from decreased CO, and may have exertional angina from increased myocardial O2 demand.

Holosystolic murmur at LSB = tricuspid regurg

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5
Q

What CXR and ECG findings are pathognomonic for pulmonary hypertension?

A

CXR = enlarged central pulmonary arteries and loss of retrosternal air space due to RVH.

ECG = R axis deviation, R BBB, RVH, and RA enlargement.

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6
Q

What’s the progression of ECG changes found in hyperkalemia?

A

Peaked T wave&raquo_space; short QT interval&raquo_space; QRS widening&raquo_space; sine wave with V-fib.

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7
Q

How may NSAIDs cause hyperkalemia?

A

Impaired local prostaglandin synth&raquo_space; reduced renin and aldosterone secretion.

** remember that aldosterone R causes potassium wasting in exchange for Na reabsorption.

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8
Q

How often should you get Td vaccination?

A

Every 10 years after the initial Tdap vaccination, and also with each pregnancy.

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9
Q

What’s the screening guidelines for Pap smears?

A

Every 3 years from age 21-65 (or if they do Pap smear + HPV testing then it’s every 5 years from 30-65).

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10
Q

What’s the initial management of suspected sciatica?

A

NSAIDs and APAP. Most Pt will experience spontaneous resolution, no need for MRI (doesn’t change treatment) or surgical decompression.

Sciatica = lumbosacral radiculopathy due to compression of nerve root by herniated disc.

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11
Q

What is fomepizole used for?

A

Ethylene glycol toxicity. Fomepizole (or ethanol) inhibits alcohol dehydrogenase and prevents breakdown of ethylene glycol into toxic products such as glycolic acid and oxalic acid.

  • Glycolic acid - injures renal tubules
    Oxalic acid - binds Ca2+&raquo_space; hypocalcemia and Ca oxalate deposition in the kidneys. Causes AKI and metabolic AG acidosis

Should also give sodium bicarb to alleviate metabolic acidosis as well as hemodialysis if severe acidosis or end organ damage is present.

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12
Q

What are the treatment options for chronic prostatitis/chronic pelvic pain syndrome?

A

Chronic prostatitis = noninfectious chronic prostate inflammation and is a Dx of exclusion. Characterized by irritative voiding Sx (frequency, urgency, hesitancy), perineal/genital pain, and pain on ejaculation.

Rx = Abx (fluoroquinolones), alpha blockers (tamsulosin), and 5-alpha reductase inhibitors (finasteride).

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13
Q

What’s the difference between beta thalassemia minor vs thalassemia major?

A

Beta thal minor = due to defect in one B-Hb gene. Causes mild microcytic anemia. Beta thal major = both B-Hb genes affected. Characterized by severe anemia and transfusion dependence at an early age.

** These conditions present as a microcyctic anemia nonresponsive to Fe supplementation. Mut results in reduced Hb synth&raquo_space; hypochromic microcytic anemia

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14
Q

Would EPO depletion result in microcytic/normocytic/macrocytic anemia?

A

Normocytic

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15
Q

What lab findings would support a diagnosis of rheumatoid arthritis (what Ab are present)?

A

Positive anti-CCP Ab (diagnostic testing)
High IgM Rheumatoid Factor

** High ESR and CRP correlate with disease activity

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16
Q

If a 40 year old woman presents with easy fatigability and loss of energy, bilateral joint swelling in hands worse in the morning, then what tis the most likely Dx?

A

Rheumatoid arthritis. Insidious onset, morning stiffness lasting several hours, improves with activity, small joints of hand affected (MCP, PIP, MTP)

17
Q

In the case of septic shock would you have increased or decreased afterload?

A

Septic shock = distributive shock. You would have decreased systemic vascular resistance (cardiac afterload) due to overall peripheral vasodilation.

You would also have decreased (or low normal) pulmonary capillary wedge pressure due to capillary leakage&raquo_space; decreased preload.

You would have mixed venous oxygen saturation due to hyperdynamic circulation in lungs. CO is increased in response to decreased SVR to maintain peripheral tissue perfusion, but tissues aren’t able to adequately extract O2&raquo_space; lactic acidosis from tissue hypoperfusion.

18
Q

How would Epo, ESR, and serum iron levels change for polycythemia vera?

A

LOW Epo, LOW ESR, Low Serum Iron.

** Normally Epo is released by kidneys and liver as a response to tissue hypoxia. Epo then drives activation of Jak2 tyrosine kinase to differentiate late myelocytes into RBC. In PV, RBC production is driven by constitutively active Jak2 rather than by tissue hypoxia.

  • In PV, there is a higher relative [ ] of erythrocytes to circulating plasma proteins so you have a low ESR.

Serum iron levels are low due to increased hematopoiesis and utilization of iron.

19
Q

What’s the first diagnostic step in evaluating an undiagnosed pleural effusion (MRI, XRay, diuretics, bronch, thoracentesis, echo, etc.?)

A

Diagnostic thoracentesis is the preliminary investigation of choice in management of pleural effusion except in cases of classic signs + sx of CHF (pedal edema, fluid overload, crackles) where a trial of diuretic is warranted.

20
Q

What type of diuretic would you use in the case of calcium oxalate ureteral stones?

A

Thiazides. Recurrent Ca2+ stones likely due to idiopathic hypercalciuria. Treat with increased fluid intake, reduced Na+ consumption and protein restriction, and thiazides. Thiazides cause a mild volume depletion&raquo_space; compensatory rise in Na+ and water reabsorption with increased passive reabsorption of Ca2+. Lowering urinary [ ] of Ca2+ reduces its precipitation as insoluble Ca2+ salt.

21
Q

What’s the initial treatment for suspected polymyositis?

A

Prednisone. Initial remission can be induced with glucocorticoids. Most people also get a glucocorticoid sparing agent like methotrexate and azathioprine.

** Since polymyositis can present after a paraneoplastic syndrome, Pt should also have age appropriate Ca2+ screening.

22
Q

What’s the initial drug of choice in treating rheumatoid arthritis?

A

Want to use DMARD (disease modifying antirheumatic drugs) with Methotrexate being the preferred treatment. Should start them as early as possible in course of disease.

NSAIDs and glucocorticoids (prednisone) can be used for initial temporary relief while waiting for DMARDs to kick in.

DMARD = nonbiolic agents like MTX, hydroxychloroquine, sulfasalazine, leflunoamide, and azathioprine.

Biologics = Etanercept, infliximab, adalimumab, tocilizumab, rituximab.

** Pt who don’t respond after 6 mo of DMARD should use step up to biologics.

23
Q

What’s the first therapeutic measure in a case of suspected temporal/giant cell arteritis with visual disturbances (anterior ischemic optic neuropathy)?

A

HIGH DOSE GLUCOCORTICOIDS (prednisone)

Don’t wait for temporal artery biopsy to confirm Dx. Start prednisone immediately to reduce progression of visual Sx.

24
Q

How do loop diuretics promote H+ loss?

A

Loop diuretics (furosemide) inhibit Na-K-2Cl in loop of Henle&raquo_space; increased loss of Na+ in urine. Increased sodium delivery to distal tubule&raquo_space; elevated H+ and K+ secretion in urine.

Loop diuretics also cause volume contraction and increased aldo levels&raquo_space; further H+ loss in urine.

25
Q

What paraneoplastic syndromes are associated with SCLC?

A

^ ACTH production and SIADH

26
Q

What are 3 classes of medications that commonly cause acute urinary incontinence in the elderly?

A
  1. Alpha adrenergic antagonists (urethral relaxation)
  2. Anticholinergics, opiates, CCB (urinary retention/overflow)
  3. Diuretics (excess urine production)