A nurse assesses a client who has a history of polycystic kidney disease (PKD). Which assessment findings would the nurse expect? (Select all that apply)

Nephrotic syndromeis characterized by massive proteinuria, hypoalbuminemia, and severe edema. The glomerular damage allows large amounts of plasma proteinsto leak into the urine. For patients who still have a normal glomerular filtration rate (GFR), the dietary goal is to replace the lost proteins to maintain oncotic pressureand support cellular repair, while also managing the metabolic complications like hyperlipidemia and fluid retention.

Rationale:

A.Carbohydrate intake does not need to be decreased in nephrotic syndrome unless the patient has comorbid diabetes. In fact, adequate carbohydrate intake is necessary to provide energy and prevent the body from breaking down protein for fuel (the protein-sparing effect). The client’s focus should remain on protein and lipid management rather than simple carbohydrate restriction.

B.While vitamin C is important for general immune health and tissue repair, there is no specific scientific requirement for "increased" intake as a primary treatment for nephrotic syndrome. The condition is defined by protein loss and lipid derangement, not a vitamin deficiency. The dietary teaching must prioritize the macros that are directly affected by the glomerular leaking.

C.The client should increase protein intakeif their GFR is normal to compensate for the massive amounts of albumin lost in the urine. High-quality protein helps rebuild serum protein levels, which is essential for maintaining oncotic pressure and reducing interstitial edema. This statement shows the client understands how to nutritionally offset the primary hallmark of their disease, which is proteinuria.

D.While hyperlipidemia occurs in nephrotic syndrome, the primary diet education for a patient with normal GFR and massive protein loss focuses on protein replacement. Decreasing fat is a secondary goal to manage high cholesterol levels, but it does not address the fundamental issue of hypoalbuminemia. The most direct and essential dietary intervention is the replenishment of protein stores.

Immune thrombocytopenic purpura(ITP) is an acquired bleeding disorder characterized by an isolated low platelet count (thrombocytopenia). The pathophysiology involves autoantibody-mediated destructionof platelets by splenic macrophages. This immune dysregulation can arise spontaneously or be triggered by specific pathogenic infectionsthat induce molecular mimicry, causing the immune system to misidentify platelet glycoproteins as foreign antigens.

Rationale:

A.Primary ITP is a classic cause where the immune system develops autoantibodies against its own platelet antigens. These antibodies, usually IgG, coat the platelets and lead to their premature clearance by the spleen. This results in a significant reduction in circulating platelets, increasing the risk of petechiae, ecchymosis, and mucosal bleeding.

B.Bacterial infections such as Helicobacter pylorihave been scientifically linked to the development of secondary ITP. In many cases, eradicating the infection with antibiotics leads to an increase in the platelet count. The mechanism is thought to involve cross-reactive antibodies that target both the bacteria and the patient's own platelet surfaces.

C.Viral infections like the Epstein Barr virus (EBV) are known triggers for the immune system to malfunction and produce anti-platelet antibodies. This is often seen in pediatric or post-viral cases where the ITP follows an acute infection. The virus disrupts normal immune tolerance, leading to the transient or chronic destruction of the patient's platelets.

D.ITP is not primarily caused by a decrease in platelet production; it is characterized by increased destruction. While some patients may have secondary marrow issues, the defining feature of ITP is the accelerated clearance of healthy platelets from the peripheral circulation. Therefore, stating that a production decrease is the cause misrepresents the autoimmune nature of the disease.

E.Secondary ITP is defined by immune destruction associated with another condition, not inadequate production. Conditions that cause inadequate production fall under the category of bone marrow failure or aplastic anemia. In ITP, the bone marrow is typically normal or shows increased megakaryocytes as it attempts to compensate for the rapid peripheral destruction.