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Hyperventilation leads to respiratory alkalosis, causing symptoms like dizziness, paresthesia, or tetany due to decreased carbon dioxide levels. It does not cause renal colic, which involves severe, spasmodic flank pain typically from ureteral obstruction. This makes hyperventilation an incorrect cause for the patient’s acute pain presentation.

Urinary tract infections may cause dysuria, frequency, or suprapubic discomfort but rarely produce the severe, colicky flank pain characteristic of renal colic. While infections can coexist with stones, the primary presentation of acute, severe pain points to nephrolithiasis, making this a less likely primary cause.

Trauma can cause renal pain or hematuria but typically presents with a history of injury and signs like bruising or hemodynamic instability. Renal colic’s hallmark is spontaneous, severe pain without trauma history, making trauma an unlikely cause for this patient’s acute presentation.

Release of inflammatory mediators drives inflammation, not angiogenesis. Pathological angiogenesis is excessive or abnormal vessel growth, often in diseases like cancer, so this is incorrect for the term.

New vessel formation in response to injury is physiological angiogenesis, not pathological. Pathological angiogenesis involves abnormal, excessive growth, so this is incorrect for the described process.

Inhibition of vessel formation is anti-angiogenic, not pathological angiogenesis. Excessive vessel growth defines the pathological state, so this is incorrect for the term.

Weight loss helps GERD by reducing abdominal pressure, but calcium channel blockers can worsen reflux by relaxing the lower esophageal sphincter. This makes the regimen counterproductive, as it does not effectively reduce acid exposure, rendering it an incorrect treatment choice.

Surgical correction of the pylorus addresses gastric outlet issues, not GERD, which involves lower esophageal sphincter dysfunction. Procedures like fundoplication target GERD, but surgery is reserved for severe cases, making this an incorrect primary treatment regimen.

Antacids provide temporary relief but do not suppress acid production long-term. Avoiding exacerbating positions and soft diets help, but they are less effective without stronger acid suppression, making this regimen less comprehensive than proton pump inhibitors for managing GERD.

Polycythemia involves an increased erythrocyte count, not a decrease. A low erythrocyte count causes anemia, leading to fatigue or hypoxia, not the neurological symptoms like headaches or dizziness seen in polycythemia, making this an incorrect cause.

Tissue destruction by macrophages is not a primary feature of polycythemia. It may occur in inflammatory conditions, but polycythemia’s neurological symptoms stem from blood flow changes, not macrophage activity, making this an incorrect cause.

Hypoxia occurs in conditions with inadequate oxygen delivery, like anemia or lung disease. Polycythemia increases oxygen-carrying capacity but causes symptoms due to viscous blood flow, not hypoxia, making this an incorrect primary cause.

Retching is the involuntary attempt to vomit, involving abdominal muscle contractions without expelling stomach contents. The patient is actively expelling contents, which defines vomiting, not just the effort of retching, making this an incorrect term for documentation.

Expectorate refers to coughing up and spitting out mucus or sputum from the respiratory tract. The patient is expelling stomach contents, not respiratory secretions, making expectorate an incorrect term for this gastrointestinal event.

Regurgitation is the passive return of undigested food or liquid from the stomach or esophagus, often without force. The forceful expulsion of stomach contents described indicates vomiting, not regurgitation, making this an incorrect documentation term.

Hemorrhagic stroke often causes headache and severe neurological deficits, not just sudden weakness. Ischemic stroke, from a clot, fits Isky’s sudden focal symptoms, so this is incorrect.

Transient ischemic attack resolves quickly, unlike Isky’s ongoing symptoms. Ischemic stroke causes persistent deficits, matching her presentation, so this is incorrect for the stroke type.

Subarachnoid hemorrhage typically involves severe headache, not focal weakness. Ischemic stroke aligns with Isky’s sudden, unilateral symptoms, so this is incorrect for her condition.

Inward-pointing feet, or pigeon-toed appearance, describe intoeing, often due to metatarsus adductus or tibial torsion. Genu varum involves the knees angling outward, causing a bowed leg appearance, not foot positioning, making this an incorrect description.

Knees angling inward, causing a knock-kneed appearance, describes genu valgum, not genu varum. These are opposite deformities, with genu varum involving outward knee angulation, making this an incorrect description of the condition.

Hyperextension of the knee joint, causing excessive leg straightening, describes genu recurvatum, not genu varum. Genu varum involves lateral knee angulation, not hyperextension, making this an incorrect description of the condition.

Immune thrombocytopenic purpura (ITP) causes isolated thrombocytopenia due to autoimmune platelet destruction, leading to bleeding like petechiae. However, it does not typically cause prolonged PT/aPTT, elevated D-dimer, or DVT, making it inconsistent with Lorretta’s multi-system coagulopathy.

Thrombotic thrombocytopenic purpura (TTP) involves microangiopathic hemolytic anemia, thrombocytopenia, and organ damage but typically presents with neurological or renal symptoms, not prolonged PT/aPTT or DVT. Lorretta’s coagulopathy and DVT history better align with another condition, making TTP incorrect.

Hemophilia, a genetic clotting factor deficiency, causes prolonged aPTT but not thrombocytopenia, elevated D-dimer, or DVT. It primarily affects males and causes joint or muscle bleeds, not diffuse bleeding like Lorretta’s, making this an incorrect diagnosis.

Extending red blood cell lifespan is not a goal in polycythemia vera, where excessive red cell production increases blood viscosity. Treatment aims to reduce cell mass, not prolong cell life, as this would worsen hyperviscosity, making this an incorrect goal.

Reducing the mean size of red blood cells is irrelevant, as polycythemia vera involves increased red cell count, not size. Treatment focuses on lowering hematocrit to decrease viscosity, not altering cell dimensions, making this an incorrect treatment goal.

Controlling hypertension is a secondary concern in polycythemia vera, often resulting from increased blood volume. While managed, the primary goal is reducing blood viscosity to prevent complications, as hypertension is a symptom, not the root cause, making this incorrect.