Mix7

Question 1

What are the early vs late renal changes seen in diabetic nephropathy?

Answer 1

Early changes = glomerular hyperfiltration

Late change = mesangial expansion, thickening of GBM, glomerular scleroris

Question 2

What are the extradermal manifestations of systemic sclerosis?

Answer 2

Systemic sclerosis = connective tissue thickening due to fibroblast dysfunction.

Cutaneous features include thickening of the skin with dermal sclerosis and valvular dysfunction (Raynaud).

Extradermal manifestations include esophageal dysmotility, interstitial lung disease, and HTN.

Anti Top 1 (anti Scl70) = serologic marker

Question 3

Anti smooth muscle Ab is found primarily in which disease?

Answer 3

Autoimmune hepatitis.

Question 4

Hypoxemia can be associated with reduced inspired O2 tension, hypoventilation, diffusion limitation, V/Q mismatch or shunting. Which of these causes of hypoxemia would be supported by normal A-a gradient and low pH?

Answer 4

Hypoventilation is associated with a normal A-a gradient and a respiratory acidosis (high PaCO2 and high PaO2).

PAO2 = (.21 x [760-47]) - (PaO2/0.8)

A-a gradient = PAO2 (calculated) - PaO2 (given)

Normal A-a gradient < 15

Question 5

Would persistent diarrhea cause you become alkalotic or acidotic?

Answer 5

Acidotic. Diarrhea results in bicarb loss&raquo_space; non AG metabolic acidosis.

• All types of rental tubular acidosis (RTA) also cause a non AG metabolic acidosis.

Question 6

Would primary hyperaldosteronism cause a metabolic acidosis or alkalosis?

Answer 6

Metabolic alkalosis. Aldosterone causes H+ and K+ excretion.

Patients also normally develop HTN, expanded ECF, and hypokalemia. Urine chloride is normally > 20 mEq/L (no stimulus for renal NaCl reabsorption)

Question 7

How does treatment of mild tinea corporis differ from a severe infection?

Answer 7

Mild = topical antifungals (terbinafine, clotrimazole)

Severe = oral systemic therapy
terbinafine, fluconazole, itraconazole

Question 8

What antibiotic regimen is used to treat H influenzae?

Answer 8

Need IV Abx = Ceftriaxone + Vanc

** Presents as fever, sore throat, drooling, airway obstruction (stridor, dyspnea), pooled oropharynx secretions.

Can be rapidly progressive/life threatening.

Question 9

If a patient has HOCM where is the best place to hear that murmur?

Answer 9

Can hear systolic murmur of HOCM along lower L sternal border.

** Pt present with exertional angina, dyspnea, dizziness, and presyncope/syncope.

Can have systolic anterior motion of the mitral valve.

Question 10

Would iron deficiency cause microcytic, normocytic, or macrocytic anemia?

Answer 10

Microcytic

Question 11

In the case of tumor lysis syndrome, what effects would chemo have on serum levels of K, Ca, and PO4?

Answer 11

Hyper K and Hyper PO4.

HYPO Ca (PO4 binds and precipitates Ca2+&raquo_space; reduced intravascular levels).

The Hyper K and hypo Ca2+ is one reason why you have cardiac arrhythmias with tumor lysis syndrome.

Question 12

What is the cause of levido reticularis?

Answer 12

Arterial cholesterol embolism showering smaller arterioles.

Question 13

If a patient comes in with QRS prolongation, high temp, seizures, and dilated pupils after a medication overdose then what was the most likely medication and what should be offered as an initial therapy?

Answer 13

Medication is most likely a TCA. Overdose is treated with Na Bicarb.

TCA decreases myocardial conduction velocity&raquo_space; QRS prolongation + risk of ven arrhythmia. This is because TCA causes HYPOkalemia. BUT major cause of mortality in TCA overdose is TCA induced hypotension. Need to make sure their airway is secure. Na Bicarb increases systolic BP, narrows QRS complex and decreases likelihood of ven arrhythmia.

Question 14

If a patient presented with ECG changes of peaked T waves followed by PR and QRS interval prolongation, then what medication should you give immediately?

Answer 14

This is a state of HYPERkalemia. Give calcium gluconate to stabilize the membrane.

Question 15

Explain the mechanism of heparin induced thrombocytopenia:

Answer 15

In HIT heparin induces conformational change to surface protein of a platelet (platelet factor 4 - PF4) which results in exposure of neoantigen. Immune system makes IgG against neoantigen&raquo_space; coats surface of platelets with IgG and forms complexes (heparin-PF4-HIT Ab).

Reticuloendothelial system (RES) [spleen] removes these Ab coated platelets&raquo_space; mild/moderate thrombocytopenia.

HIT Ab also activates platelets&raquo_space; platelet aggregation and release of procoag factors&raquo_space; ^ risk of thrombus.

If HIT is suspected, DC all heparin products and use a diff anticoag (argotroban, fondaparinux, etc)

Question 16

How does treatment of HIT differ if you have renal vs hepatic dysfunction?

Answer 16

For patients with normal renal and hepatic dysfunction, argotroban (reversible direct thrombin inhibitor) is used.

If renal dysfunction is present, use argatroban (metabolized hepatically). If hepatic damage is present, use fondaparinux (inhibits Xa)

Question 17

If a patient presents with diffuse telangiectasias, recurrent epistaxis, and widespread AVMs, then what is the most likely Dx?

Answer 17

Hereditary Telangiectasia (osler weber rendu syndrome). Autosomal dominant d/o.

AVM in the lungs can shunt blood from the R to the L side of the heart&raquo_space; chronic hypoxia and reactive polycythemia. Pulmonary AVM can cause massive sometimes fatal hemoptysis.

Question 18

Why are exertional dyspnea and fatigue the most common symptoms of MR?

Answer 18

MR causes decreased CO and ^ LA pressure/dilation.