Can someone help with these?
11. 39-year-old man with 1-week of red spots on shins, joint pain and fatigue. PE shows purpura over lower extremities. Liver palpated 4 cm below costal margin. Labs: WBC 10,000, AST 142, ALT 154, hepatitis C virus RNA positive, anti-hepatitis C virus antibody positive, cryoglobulins positive, C4 120 (N=350-600), urine protein 4+, urine RBC numerous. Hypersensitivity reaction?
- Type III (immune complex-mediated)
Sounds like Henoch-Schnolein purpura to me. They just left out the word "palpable" to make it more difficult. HSP causes Ag/Ab complexes that deposit in tissues so Type III.
26. 50-year-old woman with COPD comes with 3 months of progressive shortness of breath. Physical shows JVD, loud pulmonary component of S2. Pulmonary function tests show FEV1:FVC ratio of 20% and decreased diffusing capacity for carbon monoxide. Which is decreased in pulmonary vascular smooth muscle?
- Endothelial nitric oxide synthase production
Hypoxic vasoconstriction is a unique feature of the lung where it shunts blood away from areas with poor ventilation to go for the "good alveoli" instead of vasodilating vessels to increase flow (as seen in other organs during an ischemic event). So NO synthesis will decrease.
39. 50-year-old man with pulmonary embolus. Treated with intravenous heparin. 24 hours later, warfarin added. Day 2, partial thromboplastin time is 52 seconds (control 26 sec), and prothrombin time is 12 seconds (control 12.1 sec; INR = 1). Best explanation for normal prothrombin time and INR?
- Long half-life of factor II (prothrombin) (?)
When you start a patient on anticoagulants like Warfarin, you usually start Heparin too to avoid the hypercoagulable state induced by warfarin (Warfarin knocks out protein C & S as well, and protein C's half life is only 14 hours, longer than most of the other coag factors (except Factor VII), so you gotta give heparin to avoid this hypercoagulable state). Heparins effect is on ATIII which is endogenously present in our vessels so its effect is immediate, shown as the elevated PTT. But the PT/INR is still normal because the half life of PT (Factor II) is 60 hours, longest of them all so it takes time to actually increase the PT.
33. Researching new cancer drug, effective at killing rapidly dividing cells, in mice caused profound myelosuppression. In patients, most appropriate to follow which when at risk for infectious complications?
- Neutrophil counts
When we talk about drugs that cause bone marrow suppression (Clozapine, Carbamazepine, PTU/Methimazole, Colchicine), we're mostly worried about neutropenia, leading to infections.
26. 64-year-old with non-Hodgkin lymphoma and 3-day history of abdominal pain and nausea. T 99.7F, HR 100, bp 130/80. Abdominal exam tenderness of flanks and lower quadrants. BUN 34 and creatinine 3.8. CT shows bilateral hydronephrosis and lymphadenopathy compressing ureters. Tx to improve renal function?
- Bilateral stents in the ureters
I got this right, but I wasn't too sure about it when I was choosing that answer. I figured why not just do something about the LAD, but it wasn't a choice, lol. So I figured the stents would be the next best option.
Thank you!