Trisha N. Branan, PharmD, BCCCP

• Clinical Assistant Professor, Department of Clinical & Administrative Pharmacy, University of Georgia College of Pharmacy
• Critical Care Clinical Pharmacist, Athens Regional Medical Center, Athens, Georgia

https://rx.uga.edu/faculty-member/trisha-branan-pharm-d/

Over the past year diabetes symptoms 10 year old generic 17 mg duetact free shipping, she has noticed soreness of her muscles and joints and has had a 4-kg weight loss diabetes medications and side effects order 16 mg duetact with visa. She has pain on deep inspiration diabetic diet glycemic index purchase 16 mg duetact visa, and a friction rub is heard on auscultation of the chest diabetes sweating order generic duetact. Aldosterone Endothelin Erythropoietin Natriuretic peptide Vasopressin 26 A 58-year-old man is found to have mild hypertension blood glucose levels in children cheap duetact 16 mg buy on-line. Blood/serum test for which of the following is most likely to be abnormal in this patient Anti­glomerular basement membrane antibody Antinuclear antibody Anti­neutrophil cytoplasmic autoantibody Anti­streptolysin O C3 nephritic factor Hemoglobin A1c Hepatitis B surface antigen 29 A 19-year-old woman has had a fever and chills accompanied by right flank pain for the past 3 days. Laboratory findings show a serum glucose level of 77 mg/dL and creatinine level of 1 mg/dL. His serum urea nitrogen level increases to 38 mg/dL, and he undergoes hemodialysis for 3 weeks. His condition improves, but the urine output remains greater than 3 L/day for 1 week before the urea nitrogen returns to normal. Acute pyelonephritis Acute tubular injury Malignant nephrosclerosis Membranous nephropathy Renal vein thrombosis 30 A 51-year-old woman has had dysuria and urinary frequency for the past week. On physical examination, her temperature is 38° C, and she has pain on palpation over the left costovertebral angle. Microscopic examination of the urine shows numerous neutrophils, and a urine culture is positive for Escherichia coli. Acute tubular necrosis Crescentic glomerulonephritis Hydronephrosis Necrotizing papillitis Renal calculi 28 A 63-year-old man is in stable condition after an acute myocardial infarction when he became hypotensive for 3 hours before paramedical personnel arrived. Over the next week, the serum urea nitrogen level increases to 48 mg/dL, the serum creatinine level increases to 5 mg/dL, and the urine output decreases. He undergoes hemodialysis for the next 2 weeks and then develops marked polyuria, with urine output 31 A 53-year-old woman has had fever and flank pain for the past 2 days. Laboratory findings show serum urea nitrogen level of 68 mg/dL and creatinine level of 7. Acute tubular injury Chronic glomerulonephritis Hydronephrosis Renal cell carcinoma Renal papillary necrosis 32 A 30-year-old woman has had increasing malaise with nocturia and polyuria for the past year. A renal ultrasound scan shows an enlarged right kidney with pelvic and calyceal enlargement and cortical thinning; the left kidney appears normal. A right-sided nephrectomy is performed, and grossly there are large U-shaped scars at the poles with underlying blunted calyces. Microscopic examination shows inflammatory infiltrates extending from the medulla to the cortex, with tubular destruction and extensive interstitial fibrosis. Which of the following underlying conditions is most likely to produce these findings Polycystic kidney disease Essential hypertension Congestive heart failure Systemic lupus erythematosus Systemic amyloidosis Vesicoureteral reflux 33 A 29-year-old woman has had a fever and sore throat for the past 3 days. Two weeks later, she develops fever and a rash, and notices a slight decrease in urinary output. A Deposition of immune complexes with streptococcal antigens B Formation of antibodies against glomerular basement membrane C Hematogenous dissemination of septic emboli D Hypersensitivity reaction to ampicillin E Renal tubular cell necrosis caused by bacterial toxins 34 A 32-year-old man developed a fever and rash over 3 days. On physical examination, the maculopapular erythematous rash on his trunk has nearly faded away. Urinalysis shows 2+ proteinuria; 1+ hematuria; and no glucose, ketones, or nitrite. Antibiotic ingestion Congestive heart failure Eating poorly cooked ground beef Streptococcal pharyngitis Urinary tract infection 36 A 49-year-old man is found on physical examination to have a blood pressure of 160/110 mm Hg, but no other abnormalities. This effect on urinary output is most likely mediated by the unopposed action of which of the following chemicals Aldosterone Histamine Nitric oxide Prostaglandin Tumor necrosis factor 37 A 28-year-old man is diagnosed with acute myelogenous leukemia (M2), with a total leukocyte count of 45,000/mm3, including 60% blasts. After induction with a multiagent chemotherapy protocol, he has an episode of lower abdominal pain accompanied by passage of red urine. Which of the following additional urinalysis findings is most likely to be reported for this patient She now has bone pain, and a radionuclide scan shows multiple areas of increased uptake in the vertebrae, ribs, pelvis, and right femur. Which of the following abnormal laboratory findings is most likely to be reported for this patient He has had three respiratory tract infections with Streptococcus pneumoniae during the past year. A renal biopsy specimen stained with H&E shows deposits of amorphous pink material within glomeruli, interstitium, and arteries. He has started "seeing spots" before his eyes and experienced periods of mental confusion. Urinalysis shows 1+ proteinuria; 2+ hematuria; and no glucose, ketones, or leukocytes. Her temperature is 37° C, pulse is 90/min, respirations are 18/min, and blood pressure is 90/50 mm Hg. The peripheral blood smear shows schistocytes, and the serum D-dimer level is elevated. This complication develops most commonly after infection with which of the following organisms Candida albicans Clostridium difficile Escherichia coli Proteus mirabilis Staphylococcus aureus 40 A 66-year-old woman has experienced five transient ischemic attacks within a week. On physical examination, the only abnormal finding is a blood pressure of 150/95 mm Hg. The representative high magnification microscopic appearance of the kidneys is shown in the figure. Which of the following renal lesions is most likely to be present in this patient Acute tubular necrosis Fibromuscular dysplasia Hyaline arteriolosclerosis Interstitial nephritis Necrotizing vasculitis 43 Adult patients with bilateral renal cystic disease are found to have defects in renal tubular function. An ultrasound scan shows bilaterally small kidneys with barely visible medullary cysts concentrated at the corticomedullary junction. An abdominal ultrasound shows enlarged kidneys with the representative gross appearance shown in the figure. An ultrasound scan shows bilaterally enlarged echogenic kidneys and a markedly decreased amniotic fluid index. At autopsy, there are deformations resulting from marked oligohydramnios, including flattening of the facies, varus deformities of the feet, and marked pulmonary hypoplasia. Microscopic examination of the liver shows multiple epithelium-lined cysts and a proliferation of bile ducts. Autosomal dominant polycystic kidney disease Autosomal recessive polycystic kidney disease Medullary sponge kidney Multicystic renal dysplasia Urethral atresia 46 A 31-year-old woman experiences abdominal pain 1 week after noticing blood in her urine. Urinalysis shows 2+ hematuria, 1+ proteinuria, hypercalciuria, and no glucose or ketones. She is advised to increase her daily intake of fluids, and her condition improves. Which of the following renal cystic diseases is most likely to be associated with these findings On physical examination, he has a 2-cm nonhealing ulceration on the ball of his right foot. The lesion is well circumscribed and cystic with a thin wall and focal hemorrhage. Acute pyelonephritis Acute tubular injury Diabetic nephropathy Hydronephrosis Simple renal cyst Renal cell carcinoma Urothelial carcinoma Kidney 321 dominal palpation. Acute tubular injury Malignant nephrosclerosis Papillary necrosis Renal cell carcinoma Staghorn calculus 50 A 24-year-old man has severe lower abdominal pain that radiates to the groin. Calcium oxalate Cystine Magnesium ammonium phosphate Mucoprotein Uric acid 53 A 55-year-old man has had back pain and has passed dark-colored urine for the past month. Which of the following substances is most likely to be increased in the blood of this man Cortisol Globlulins Erythropoeitin Renin Vasopressin 51 A 28-year-old, previously healthy man suddenly develops severe abdominal pain and begins passing red urine. Acute bacterial cystitis Diabetes mellitus Idiopathic hypercalciuria Primary hyperparathyroidism Secondary gout 52 A 54-year-old woman has had recurrent urinary tract infections for the past 15 years. For the past 4 days, she has had a burning pain on urination and urinary frequency. There is marked tenderness on deep pressure over the right costovertebral angle and on deep ab- 54 A 60-year-old man has a feeling of fullness in his abdomen and a 5-kg weight loss over the past 6 months. A right-sided nephrectomy is performed, and gross examination reveals that the mass has invaded the renal vein. A mutation involving which of the following genes is most likely to be found in this family A neoplasm is most likely to have arisen in which of the following urinary tract locations in this man Bladder dome Calyx Penile urethra Renal cortex Urachus Ureter 57 A 4-year-old girl has complained of abdominal pain for the past month. On physical examination, she is febrile, and palpation of the abdomen shows a tender mass on the right side. A rightsided nephrectomy is performed; the gross appearance of the mass is shown in the figure. Urothelial carcinoma is likely to be unilateral, with sufficient reserve renal function in the remaining kidney to prevent azotemia. Type I hypersensitivity may play a role in drug-induced acute interstitial nephritis. Mesangial cells have a phagocytic function, but they also can elaborate inflammatory mediators, cytokines, and matrix. Proliferation of mesangial cells may be induced by injury, particularly immune complex deposition. Parietal epithelial cells line the Bowman capsule and may proliferate with severe glomerular injury to produce crescents. Endothelial cells are most likely to be damaged with thrombotic microangiopathies. Injuries that cause effacement, retraction, detachment, and vacuolization allow protein, principally albumin, to escape into Bowman space. The remaining listed options do not participate in this epithelial protein filtration barrier. Some cases of membranous nephropathy are associated with hepatitis B virus infection, but the immune complex deposition is granular, not linear. The lack of immune deposits excludes anti­glomerular basement membrane disease (Goodpasture syndrome). Quantitative serum immunoglobulins are not helpful because the important consideration is the pattern of immune deposits in the kidney. Hyperplastic arteriolosclerosis can lead to focal hemorrhages and necrosis, but without a granulomatous component, and the blood pressure is usually quite high. Membranous nephropathy is most likely to produce nephrotic syndrome without crescents. Diffuse basement membrane thickening, in the absence of proliferative changes, and granular deposits of IgG and C3 are typical of this condition. It is caused by antibody targeting M-type phospholipase A2 receptor antigen, the deposition of immune complexes on the basement membrane, and complement activation. In 75% of patients with membranous nephropathy, the cause of immune complex deposition is unknown. Antibodies that react with basement membrane give rise to a linear immunofluorescence pattern, as in Goodpasture syndrome. There also is no evidence of cytokine-mediated or T cell­mediated damage in this disease. The most likely cause of foot process fusion is a primary injury to visceral epithelial cells caused by T cell­derived cytokines. Acute cellular renal transplant rejection is mediated by T cell injury with tubulitis. IgA nephropathy with mesangial IgA deposition and consequent glomerular injury causes recurrent gross or microscopic hematuria and, far less commonly, nephrotic syndrome. Immune complex deposition in membranous nephropathy can cause nephrotic syndrome, but is less common in children than in adults and is not steroid responsive. Certain verocytotoxinproducing Escherichia coli strains can cause hemolytic uremic syndrome by injury to capillary endothelium. In contrast, corticosteroidresponsive nephrotic syndrome in children is typically caused by minimal change disease (lipoid nephrosis) that is not associated with any glomerular change seen under the light microscope. A diabetic patient with nephrotic syndrome is likely to have nodular glomerulosclerosis or diffuse thickening of the basement membrane. About 75% of cases are idiopathic and due to autoantibodies reacting against podocyte antigens; but some cases follow infections. Multiple myeloma can be complicated by systemic amyloidosis, which can involve the kidney. Recurrent urinary tract infections are typically caused by bacterial organisms and can cause chronic pyelonephritis. Nephrolithiasis may lead to interstitial nephritis, but it does not cause glomerular injury. Specialized extracellular areas overlying the glomerular basement membrane between adjacent foot processes of podocytes are called slit diaphragms, and these exert control over glomerular permeability. Anti­glomerular basement membrane antibodies are responsible for Goodpasture syndrome. Inherited defects in basement membrane collagen cause Alport syndrome, also characterized by hematuria, but other congenital abnormalities, such as deafness, are often present, and nephrotic syndrome is uncommon. There is fusion of podocyte foot processes, which can be seen only by electron microscopy. This fusion leads to selective proteinuria of low molecular weight proteins (albumin). Membranous nephropathy is often accompanied by proteinuria but less likely hematuria, and is characterized by thickening of only the basement membrane and small electron-dense deposits. IgA nephropathy is a form of glomerulonephritis that does not produce tubular epithelial changes. Nodular and diffuse glomerulosclerosis are typical changes in diabetic nephropathy that can occur following loss of pancreatic islet beta cells. Toxic injuries are most likely to damage tubular cells, leading to acute tubular necrosis. Nephrotic syndrome is not present, and mesangial IgA deposition is characteristic. IgA nephropathy occurs with increased frequency in patients with celiac disease and liver disease. With progressive glomerular injury and sclerosis, both kidneys become smaller, and their surfaces become granular. Regardless of the initiating cause, these "end-stage" kidneys appear morphologically identical. They have sclerotic glomeruli, thickened arteries, and chronic inflammation of interstitium.

Diseases

• Panthophobia
• Piebaldism
• Gougerot Blum syndrome
• Laryngocele
• Diabetic neuropathy
• Mental retardation short stature ocular and articular anomalies
• Krause Kivlin syndrome
• Waardenburg syndrome type 1
• Fanconi anemia type 3
• Agnathia

Consumption of coagulation factors Defects in platelet aggregation Increased vascular fragility Reduced production of platelets Toxic injury to the endothelium 47 A 37-year-old woman has noted an excessively heavy menstrual flow each of the past 6 months diabetes insipidus usmle discount duetact 17 mg without a prescription. She also has noticed increasing numbers of pinpoint hemorrhages on her lower extremities in the past month diabetes symptoms eating cheap duetact 16 mg on line. On admission to the hospital diabetes prevention program youth purchase duetact with visa, she has melena and after a transfusion of platelets diabetic diet 2000 calorie meal plan cheap 16 mg duetact fast delivery, her platelet count does not increase diabetes type 2 oatmeal duetact 16 mg cheap. A Abnormal production of platelets by megakaryocytes B Defective platelet-endothelial interactions C Destruction of antibody-coated platelets by the spleen D Excessive loss of platelets in menstrual blood E Suppression of pluripotent stem cell division 48 A 9-year-old boy has developed prominent bruises on his extremities over the past week. Which of the following abnormalities is most likely to cause his hemorrhagic diathesis Two weeks after initiation of this therapy, she has a sudden change in mental status and experiences difficulty speaking and swallowing. Which of the following pharmacologic agents used as an anticoagulant in this patient is most likely to have caused these findings Acetylsalicylic acid (aspirin) Heparin Tissue plasminogen activator Urokinase Warfarin Which of the following is the most likely potential consequence of this disease Bone marrow failure from aplasia Excessive bleeding after oral surgery Increasing difficulty with joint mobility Myeloproliferative disorder Recurrent deep venous thrombosis 50 A 56-year-old woman suffers the sudden onset of headache and photophobia, and her condition worsens for the next 2 days. Autoimmune hemolytic anemia -Thalassemia major Disseminated intravascular coagulation Idiopathic thrombocytopenic purpura Paroxysmal nocturnal hemoglobinuria Thrombotic thrombocytopenic purpura 53 A 42-year-old woman has had nosebleeds, easy bruising, and increased bleeding with her menstrual periods for the past 4 months. On physical examination, her temperature is 37° C, pulse is 88/min, and blood pressure is 90/60 mm Hg. Disseminated intravascular coagulation Hemophilia B Immune thrombocytopenic purpura Metastatic breast carcinoma Thrombotic thrombocytopenic purpura Vitamin K deficiency Von Willebrand disease 51 A 44-year-old woman has experienced malaise with nausea and vomiting for 3 months. An abnormal result of which of the following laboratory studies of hemostatic function is most likely to be reported Fibrin split products Immunoassay for plasma von Willebrand factor Platelet aggregation Platelet count Prothrombin time 54 A clinical study is performed involving adult patients diagnosed with microangiopathic hemolytic anemia. A subgroup of patients who had fever or diarrhea preceding the initial diagnosis of anemia were excluded. Which of the following conditions were the patients with this deficiency most likely to have Physical examination shows multiple bruises ranging in color from red to blue to purple on her arms and legs. Disseminated intravascular coagulation Glanzmann thrombasthenia Immune thrombocytopenic purpura Vitamin C deficiency Von Willebrand disease 56 A 12-year-old boy has had worsening problems with joint mobility involving his arms and legs, particularly his knees and ankles, for the past 6 years. Laboratory studies show that prothrombin time is 12 seconds, and partial thromboplastin time is 52 seconds. After addition of an equivalent aliquot of normal plasma, the partial thromboplastin time is 30 seconds. Autosomal dominant Autosomal recessive Confined placental mosaicism Germline mutation X-linked recessive 60 A 25-year-old man involved in a motorcycle accident incurs a laceration to his thigh. The bleeding is stabilized en route to the hospital, but on arrival he is noted to have orthostatic hypotension and his hematocrit is 21%. As the first unit is nearly finished transfusing, he becomes febrile and hypotensive. Which of the following complications of transfusion has most likely occurred in this man A Donor antibodies were directed against his granulocytes B Donor blood was contaminated with hepatitis C virus C Fluid overload led to congestive heart failure D Mislabeled specimens were processed in the laboratory E Foreign T lymphocytes attacked his tissues 61 A 72-year-old woman undergoes laparotomy for ruptured diverticulitis. As the 5th unit is being transfused, she develops sudden severe dyspnea and begins coughing up large quantities of frothy sputum. She is most likely to have developed a transfusion reaction to which of the following components of the donor blood product Albumin Fibrinogen Granulocytes Platelets Red blood cells 57 An 11-year-old child has a history of easy bruising. At age 9 years, he experienced hemorrhaging around the pharynx that produced acute airway obstruction. Family history indicates that other male relatives have similar bleeding problems. Which of the following manifestations of this illness is most likely to ensue without therapy Conjunctival petechiae Hemarthroses Hemolysis Hemochromatosis Splenomegaly 58 A 15-year-old girl has a history of easy bruising and hemorrhages. On physical examination, she displays joint deformity and has decreased mobility of the ankles, knees, and wrists. Antiphospholipid syndrome Hemophilia B Idiopathic thrombocytopenic purpura Thrombotic thrombocytopenic purpura Von Willebrand disease 62 A study of transfusion reactions reveals that some patients experienced an increase in body temperature that was greater than 1°C, accompanied by chills and hypotension. Cryoprecipitate Fresh frozen plasma Granulocytes Platelets Red blood cells 59 A 16-year-old girl has had frequent nosebleeds since childhood. Petechiae and ecchymoses can result from increased vascular fragility, a consequence of nutritional deficiency. Metastatic disease does not directly affect hemostasis, although extensive marrow metastases could diminish platelet production. Acute blood loss does not give rise to iron deficiency if iron stores and diet are adequate. Schistocytes suggest a microangiopathic hemolytic anemia, which can accompany shock or sepsis. Thalassemias with abnormal -globin or -globin chains are associated with hypochromic microcytic anemias. Iron deficiency affects the heme portion of hemoglobin, leading to hypochromia and to microcytosis. Porphyrias may affect the production of porphyrin rings and may lead to hemolytic anemia along with abdominal pain, neurologic problems, or skin findings. An aplastic marrow is very hypocellular and unable to respond to anemia; it is associated with pancytopenia. Iron deficiency impairs the ability of the marrow to mount a significant and sustained reticulocytosis. Iron deficiency anemia is typically microcytic and hypochromic, but could be partially masked here by reticulocytosis, which would not be as marked if iron were not available, but his diet is supplying needed iron. Infiltrative disorders, such as metastases in the marrow, would impair the ability to mount a reticulocytosis of this degree. Hemolysis is often accompanied by reticulocytosis if the marrow is intact and the iron is not lost. This disease is most common in individuals of African and eastern Arabian descent. Vascular occlusions in the lungs are often accompanied by infection and lead to "acute chest syndrome. The cell membranes of reversibly sickled cells are abnormally "sticky," and they adhere to capillary endothelium, especially in lungs. Chronic tissue hypoxia does occur in sickle cell anemia, but it produces insidious impairment of function in organs such as heart, kidneys, and lungs. Defects in the alternative pathway of complement activation predispose to infection with encapsulated bacteria, such as Haemophilus influenzae and Streptococcus pneumoniae. Autoantibodies to alveolar basement membrane can be part of Goodpasture syndrome, which also affects kidneys. Iron deficiency does not occur in hemolytic anemias because the iron that is released from hemolyzed cells is reused. Splenectomy is beneficial because the spherocytes are no longer detained by the spleen. A complete lack of -globin chains precludes formation of hemoglobins A1, A2, and F. Inheritance of three abnormal -globin chains leads to hemoglobin H disease, with tetramers of chains; survival to adulthood is possible. In this condition, there is a severe reduction in the synthesis of -globin chains without impairment of -globin synthesis. The free, unpaired -globin chains form aggregates that precipitate within normoblasts and cause them to undergo apoptosis. The severe anemia triggers erythropoietin synthesis, which expands the erythropoietic marrow. In comparison, the hemolytic anemia is mild in -thalassemia minor, and there is very little ineffective erythropoiesis. There is decreased -globin chain formation, with increased hemoglobin A2 and F to compensate. There is ineffective erythropoiesis and increased erythropoietin to drive increased iron absorption, leading to iron overload. Iron deposited in endocrine tissues can lead to gonadal, pituitary, thyroid, islet cell, and adrenal failure. Secondary hypersplenism can result from the splenomegaly, with sequestration of platelets and leukocytes. The abnormal ankyrin gene leads to hereditary spherocytosis and a mild hemolytic anemia with splenomegaly, but not to iron overload. In glucose-6-phosphate dehydrogenase deficiency, sensitivity to oxidizing agents causes a hemolytic anemia, but this usually is not ongoing. The impaired splenic function and resultant inability to clear bacteria from the bloodstream can occur early in childhood, leading to risk for infection with encapsulated bacterial organisms. Immunodeficiency results from lack of splenic function, not from lack of immunoglobulins. However, the therapeutic response to hydroxyurea often precedes the increase in hemoglobin F levels. Because hemoglobin F levels remain high through the first 5 to 6 months of life, patients with sickle cell anemia typically do not manifest the disease during infancy. Because both -globin chains are affected, no hemoglobin A1 is produced, and A2 levels are never high. Globin synthesis overall is not going to increase, and globin synthesis must be balanced to produce normal hemoglobin. The hemolysis associated with sickling promotes erythropoiesis, but the concentration of hemoglobin S is not changed. Hydroxyurea does not significantly shift the oxygen dissociation curve or change the oxygen affinity of the various hemoglobins. In contrast to -thalassemia major, there is usually a mild anemia without major organ dysfunction with -thalassemia minor. Anemia of chronic disease may mimic iron deficiency and thalassemia minor with respect to hypochromia and microcytosis; however, anemia of chronic disease is associated with an increase in the serum concentration of ferritin. Mutations in the -globin chain can give rise to hemoglobinopathies such as sickle cell anemia. Patients with factor V (Leiden) and prothrombin G20210A mutations can present with thromboses, but there is no anemia or leukopenia. The lack of this enzyme subjects hemoglobin to damage by oxidants, including drugs such as primaquine, sulfonamides, nitrofurantoin, phenacetin, and aspirin (in large doses). The "bite cells" result from the attempts of overeager splenic macrophages to pluck out the Heinz bodies, adding an element of extravascular hemolysis. Heterozygotes with -thalassemia (1 or 2 abnormal genes out of 4 total -globin genes) have no major problems, but in cases of -thalassemia major, perinatal death is the rule. Likewise, -thalassemia minor and sickle cell trait are conditions usually with no major problems and no relation to drug usage. Some autoimmune hemolytic anemias can be drug related, but the hemolysis is predominantly extravascular. The inclusions damage the cell membrane directly, giving rise to intravascular hemolysis. Because the introns are usually involved, the flanking exons remain, and some normal splicing can occur, so that some -globin chain synthesis can occur, but not sufficient for adequate hemoglobin production. The other listed mutations lead to a block in translation, with no functional -globin chain synthesis, typical for 0 thalassemia. These include proteins that protect cells from lysis by spontaneously activated complement. Defects in platelet function are believed to be responsible for venous thrombosis. Infections such as mononucleosis and Mycoplasma are associated with cold autoimmune hemolytic anemia (with an elevated cold agglutinin titer). With an increase in temperature within core internal organs, the IgM is dissociated from the cell, leaving behind C3b. Sickle cell anemia is not likely to be found in the population groups in the countries noted, and persons with this disease are not likely to be playing rugby. Splenic sequestration is a feature of hemolytic anemias due to membrane defects and antibodies. IgG is typically involved in warm antibody hemolytic anemia, which is chronic and is not triggered by cold. Raynaud phenomenon occurs in exposed, colder areas of the body, such as the fingers and toes. Chemotherapy can suppress bone marrow production, but more likely all cell lines, and without an immune component. Non-Hodgkin lymphomas do not often involve colon, but this might account for gastrointestinal bleeding with features of iron deficiency and microcytosis. They are more resistant to malaria, particularly the most malignant form caused by P. The malarial parasite has difficulty completing its life cycle, even in cells with moderate amounts of hemoglobin S, as found in heterozygotes, giving a selective advantage to such persons living in endemic areas for falciparum malaria. Cryptococcus neoformans can cause granulomatous disease in immunocompromised individuals. Autoimmune hemolytic anemias can be a feature of autoimmune diseases, such as systemic lupus erythematosus in this woman. Most of the hemolysis is extravascular in the spleen, but some can be intravascular. The reticulocyte count is typically increased (polychromasia) with hemolysis, and serum haptoglobin is diminished. An elevated D-dimer suggests a microangiopathic hemolytic anemia, but she has no schistocytes on the peripheral blood smear. Her mild macrocytosis indicates increased reticulocytosis, not vitamin B12 deficiency, and hemolysis is not part of pernicious anemia. Increased serum ferritin is typical for anemia of chronic disease (mild increase) or hemochromatosis (marked increase). A fetalmaternal hemorrhage in utero or at the time of delivery in a previous pregnancy (or with previous transfusion of incompatible blood) can sensitize the mother, resulting in production of irregular IgG antibodies. In subsequent pregnancies, these antibodies (in contrast to the naturally occurring IgM antibodies) can cross the placenta to attach to fetal cells, leading to hemolysis. The bite of the Anopheles mosquito introduces sporozoites, which travel to the liver to reproduce. Babesiosis is far less common than malaria, is endemic to the northeastern United States, and does not produce episodic fevers.

In cirrohosis due to primary sclerosing cholangitis diabetes test negative buy generic duetact 16 mg online, there is characteristic beading of intra- and extrahepatic bile ducts due to irregular strictures and dilatation diabetes mellitus type 1 definition order duetact 16 mg free shipping. Microscopically diabetes diet cookbook discount 16 mg duetact with amex, the features of intra- and extrahepatic cholestasis correspond to primary and secondary biliary cirrhosis respectively discussed on page 599 blood sugar scale buy duetact 16 mg low cost. The inflammatory infiltrate too extends beyond the portal tracts into surrounding hepatic parenchyma diabetes xpert course duetact 17 mg buy online. Cholangitis, sterile or pyogenic, with accumulation of polymorphs around the bile ducts. The fibrous septa contain prominent lymphoid infiltrate and proliferated bile ducts. Clinical features of the three types of biliary cirrhosis are variable: Primary biliary cirrhosis may remain asymptomatic for months to years. The patients present with persistent pruritus, dark urine, pale stools, steatorrhoea, jaundice and skin pigmentation. The earliest laboratory finding is a markedly elevated serum alkaline phosphatase level. Death usually results from hepatic failure, variceal bleeding, intercurrent infections and concomitant development of cancers of liver and breast. The patients of primary sclerosing cholangitis may remain asymptomatic or may show features of cholestatic jaundice (raised alkaline phosphatase, pruritus, fatigue). Primary Biliary Cirrhosis Possibly autoimmune; association with other autoimmune diseases Middle-aged women Male: Female = 1:9 Alkaline phosphatase Conjugated bilirubin Autoantibodies present Chronic destructive; cholangitis of intrahepatic bile ducts Secondary Biliary Cirrhosis Extrahepatic biliary obstruction; biliary atresia Any age and either sex Alkaline phosphatase Conjugated bilirubin Bile stasis in bile ducts, and sterile or pyogenic cholangitis Primary Sclerosing Cholangitis Possibly autoimmune; association with inflammatory bowel disease Middle age Male: Female = 2:1 Alkaline phosphatase Conjugated bilirubin Hypergammaglobulinaemia Fibrosing cholangitis with periductal fibrosis 627 Feature 1. Pathologic changes the contrasting features of three main types of intrahepatic disorders leading to biliary cirrhosis are summarised in Table 21. The condition is characterised by a triad of features- micronodular pigment cirrhosis, diabetes mellitus and skin pigmentation. Males predominate and manifest earlier since women have physiologic iron loss delaying the effects of excessive accumulation of iron. A general discussion of iron metabolism and iron excess states is given on page 41. Normally, the body iron content is 3-4 gm which is maintained in such a way that intestinal mucosal absorption of iron is equal to its loss. In haemochromatosis, however, this amount goes up to 4 mg/day or more, as evidenced by elevated serum iron (normal about 125 g/dl) and increased serum transferrin saturation (normal 30%). In idiopathic or hereditary haemochromatosis, the primary mechanism of disease appears to be the genetic basis in which the defect may either lie at the intestinal mucosal level causing excessive iron absorption, or at the post- absorption excretion level leading to excessive accumulation of iron. The excess iron in primary haemochromatosis is deposited mainly in the cytoplasm of parenchymal cells of organs such as the liver, pancreas, spleen, heart and endocrine glands. The last-named phenomenon is observed in Bantu siderosis affecting South African Bantu tribals who consume large quantities of home-brew prepared in iron vessels. Cases of secondary haemochromatosis have increased iron storage within the reticuloendothelial system and liver. Excessive deposition of iron in organs and tissues is ferritin and haemosiderin, both of which appear as golden-yellow pigment granules in the cytoplasm of affected parenchymal cells and haemosiderin stains positively with Prussian blue reaction. The organs most frequently affected are the liver and pancreas, and to a lesser extent, the heart, endocrine glands, skin, synovium and testis. Initially, the clinical manifestations are referable to liver involvement such as jaundice and hepatomegaly (hepatic form) but later progressive neuropsychiatric changes and Kayser-Fleischer rings in the cornea appear. Excess copper so absorbed through the stomach and duodenum is transported to the liver where it is incorporated into 2-globulin to form ceruloplasmin, which is excreted by the liver via bile normally. However, increased copper in the kidney does not produce any serious renal dysfunction. However, serum copper levels are of no diagnostic help and may vary from low-to-normal-to-high depend- ing upon the stage of disease. The liver shows varying grades of changes that include fatty change, acute and chronic active hepatitis, submassive liver necrosis and macronodular cirrhosis. Cirrhosis in -1-Antitrypsin Deficiency Alpha-1-antitrypsin deficiency is an autosomal codominant condition in which the homozygous state produces liver disease (cirrhosis), pulmonary disease (emphysema), or both (page 479). The patients may present with respiratory disease due to the development of emphysema, or may develop liver dysfunction, or both. In adolescence, the condition may evolve into hepatitis or cirrhosis which is usually well compensated. Pulmonary changes in 1-antitrypsin deficiency in the form of emphysema are described in Chapter 17. The hepatic changes vary according to the age at which the deficiency becomes apparent. Cardiac Cirrhosis Cardiac cirrhosis is an uncommon complication of severe right-sided congestive heart failure of long-standing duration (page 99). The patients generally have enlarged and tender liver with mild liver dysfunction. Thus, the picture resembles acute alcoholic hepatitis but without the fatty change and with greatly impaired regeneration. There is marked increase in hepatic copper since the milk consumed by such infants is often boiled and stored in copper vessels in India. The condition may run a variable natural history rangingfrom indolent to severe rapid course. This form of hepatitis has prominent autoimmune etiology is supported by immunologic abnormalities and a few other characteristic diagnostic criteria as under: 1. Exclusion of chronic hepatitis of other known etiologies (viral, toxic, genetic etc). Autoimmune hepatitis is morphologically indistinguishable from chronic hepatitis of viral etiology. There are features of burnt out chronic autoimmune hepatitis accompanied with cirrhosis. The condition is seen more commonly in affluent western socieities, has a strong association with obesity, dyslipidaemia and type 2 diabetes mellitus. Pateints are generally asymptomatic and are diagnosed by routine biochemical tests. The condition is a form of chronic hepatitis after known causes have been excluded. Cryptogenic Cirrhosis Finally, when all the known etiologic types of cirrhosis have been excluded, there remain patients with cirrhosis in whom the cause is unknown. These cases are grouped under a waste-basket diagnosis of cryptogenic cirrhosis (crypto = concealed). One of the types associated with increased portal fibrosis without definite cirrhosis is seen in idiopathic (primary) portal hypertension with splenomegaly, reported from India and Japan. The type common in India, particularly in young males, is related to chronic arsenic ingestion in drinking water and intake of orthodox medicines. It could also be due to portal vein thrombosis leading to intimal sclerosis of portal vein branches. Another variant is congenital hepatic fibrosis seen in polycystic disease of the liver. Grossly, the liver is small, fibrous and shows prominent fibrous septa on both external as well as on cut surface forming irregular islands in the liver. These include weakness, fatiguability, weight loss, anorexia, muscle wasting, and low-grade fever due to hepatocellular necrosis or some latent infection. Progressive hepatic failure and its manifestations as described already (page 602). Infections are more frequent in patients with cirrhosis due to impaired phagocytic activity of reticuloendothelial system. Haematologic derangements such as bleeding disorders and anaemia due to impaired hepatic synthesis of coagulation factors and hypoalbuminaemia are present. In males these consist of feminisation such as gynaecomastia, changes in pubic hair pattern, testicular atrophy and impotence, whereas in cirrhotic women amenorrhoea is a frequent abnormality. The ultimate causes of death are hepatic coma, massive gastrointestinal haemorrhage from oesophageal varices (complication of portal hypertension), intercurrent infections, hepatorenal syndrome and development of hepatocellular carcinoma. Measurement of these pressures helps in localising the site of obstruction and classifying the portal hypertension. Based on the site of obstruction to portal venous blood flow, portal hypertension is categorised into 3 main types-intrahepatic, posthepatic and prehepatic (Table 21. Rare cases of idiopathic portal hypertension showing non-cirrhotic portal fibrosis are encountered as discussed above. Congestive heart failure Constrictive pericarditis Hepatic veno-occlusive disease Budd-Chiari syndrome C. Portal vein thrombosis Neoplastic obstruction of portal vein Myelofibrosis Congenital absence of portal vein 1. Other less frequent intrahepatic causes are metastatic tumours, non-cirrhotic nodular regenerative conditions, hepatic venous obstruction (Budd-Chiari syndrome), veno-occlusive disease, schistosomiasis, diffuse granulomatous diseases and extensive fatty change. This is uncommon and results from obstruction to the blood flow through hepatic vein into inferior vena cava. The causes are neoplastic occlusion and thrombosis of the hepatic vein or of the inferior vena cava (including Budd-Chiari syndrome). Blockage of portal flow before portal blood reaches the hepatic sinusoids results in prehepatic portal hypertension. Such conditions are thrombosis and neoplastic obstruction of the portal vein before it ramifies in the liver, myelofibrosis, and congenital absence of portal vein. Irrespective of the mechanisms involved in the pathogenesis of portal hypertension, there are 4 major clinical consequences-ascites, varices (collateral channels or portosystemic shunts), splenomegaly and hepatic encephalopathy. Ascites is the accumulation of excessive volume of fluid within the peritoneal cavity. Presence of neutrophils is suggestive of secondary infection and red blood cells in ascitic fluid points to disseminated intraabdominal cancer. However, some cases of ascites may develop serious complication of spontaneous bacterial peritonitis characterised by sponateneous infection of the ascitic fluid without any intrabdminal infection. The ascites becomes clinically detectable when more than 500 ml of fluid has accumulated in the peritoneal cavity. There is hypoalbuminaemia from impaired hepatic synthesis of plasma proteins including albumin, as well as from loss of albumin from the blood plasma into the peritoneal cavity. In cirrhosis, there is increased aldosterone secretion by the adrenal gland, probably due to reduced renal blood flow, and impaired hepatic metabolism and excretion of aldosterone. Reduced renal blood flow and excessive release of antidiuretic hormone results in renal retention of sodium and water and impaired renal excretion. Portal venous pressure is not directly related to ascites formation but portal hypertension in combination with other factors contributes to the formation and localisation of the fluid retention in the peritoneal cavity. Obstruction of hepatic vein such as in Budd-Chiari syndrome and increased intrasinusoidal pressure found in cirrhotic patients stimulates hepatic lymph formation that oozes through the surface of the liver. As a result of rise in portal venous pressure and obstruction in the portal circulation within or outside the liver, the blood tends to bypass the liver and return to the heart by development of porto-systemic collateral channels (or shunts or varices). The enlargement of the spleen in prolonged portal hypertension is called congestive splenomegaly (page 387). The spleen is larger in young people and in macronodular cirrhosis than in micronodular cirrhosis. Porto-systemic venous shunting may result in a complex metabolic and organic syndrome of the brain characterised by disturbed consciousness, neurologic signs and flapping tremors. Hepatic encephalopathy is particularly associated with advanced hepatocellular disease such as in cirrhosis. Primary hepatic tumours may arise from hepatic cells, bile duct epithelium, or mesodermal structures (Table 21. These cysts are mainly of 3 types-congenital, simple (nonparasitic) and hydatid (Echinococcus) cysts. They are usually small (less than 1 cm in diameter) and are lined by biliary epithelium. Malignant Hepatocellular (liver cell) carcinoma Hepatoblastoma (Embryoma) Cholangiocarcinoma Combined hepatocellular and cholangiocarcinoma Cystadenocarcinoma Angiosarcoma Embryonal sarcoma Benign A. Mesodermal tumours Haemangioma numerous ducts, warranting the designation of congenital hepatic fibrosis. Simple cysts are solitary non-parasitic cysts seen more frequently in middleaged women. Histologically, the cyst wall is composed of compact fibrous tissue and is lined by low columnar to cuboid epithelium and occasionally by squamous lining. On cut section, many of the tumours have varying degree of infarction and haemorrhage. Histologically, liver cell adenomas are composed of sheets and cords of hepatocytes which may be normal-looking or may show slight variation in size and shape but no mitoses. The hepatocytes in adenomas contain greater amount of glycogen than the surrounding liver cells and may sometimes show fatty change. Numerous blood vessels are generally present in the tumour which may be thrombosed. Thrombosis leads to infarction and may result in rupture with intraperitoneal haemorrhage. Bile Duct Adenoma (Cholangioma) Intrahepatic or extrahepatic bile duct adenoma is a rare benign tumour. Grossly, haemangiomas appear as solitary or multiple, circumscribed, red-purple lesions, commonly subcapsular and varying from a few millimetres to a few centimetres in diameter. They are commonly cavernous type giving the sectioned surface a spongy appearance. Histologically, haemangioma of the liver shows characteristic large, cavernous, blood-filled spaces, lined by a single layer of endothelium and separated by connective tissue. An important mycotoxin, aflatoxin B1, produced by a mould Aspergillus flavus, can contaminate poorly stored wheat grains or groundnuts, especially in developing countries.

On physical examination diabetes 1 and 2 order duetact overnight, she is afebrile and normotensive diabetes prevention cdc purchase duetact 17 mg with mastercard, and her heart rate is irregular managing diabetes complications buy 16 mg duetact overnight delivery. A radiograph of the left hand shows focal expansion by a cystic lesion of the third proximal phalanx metabolic disorder high triglycerides discount duetact online. A technicium radionuclide scan shows a 1-cm area of increased uptake in the right lateral neck blood sugar will not go down 17 mg duetact buy mastercard. Laboratory testing for glucose and insulin levels and autoantibody formation is performed on a periodic basis. A cohort of the subjects who are 8 to 22 years old has no overt clinical illnesses and no hyperglycemia; however, autoantibodies to glutamic acid decarboxylase are present. Which of the following pancreatic abnormalities is most likely to be found in this cohort of study subjects Acinar acute inflammation and necrosis Acinar fibrosis and fatty replacement Islet amyloid deposition Islet hyperplasia Insulitis Normal islets in a fibrous stroma 32 A 68-year-old man has experienced increasing malaise for 3 years. Which of the following endocrine glandular lesions has developed secondary to the underlying disease in this patient Adrenal atrophy Islet cell hyperplasia Multinodular goiter Parathyroid hyperplasia Pituitary microadenoma 36 A 23-year-old woman has a routine health status examination. She is most likely to have a mutation in a gene encoding for which of the following On physical examination, there is a 2-cm nodule in the right lobe of the thyroid gland. A fine-needle aspiration biopsy is performed, and microscopic examination of the specimen shows cells consistent with a follicular neoplasm. Which of the following laboratory tests should be performed on this patient in the immediate postoperative period On physical examination, she is hypotensive and tachycardic with deep, rapid, labored respirations. Urinalysis shows 4+ glucosuria and 4+ ketonuria levels, but no protein, blood, or nitrite. Which of the following maternal diseases is the most likely cause for the observed findings in this infant Cystic fibrosis Diabetes mellitus, type 2 Gestational diabetes Maturity onset diabetes of the young Pancreatic neuroendocrine tumor 43 A 52-year-old man has been concerned about a gradual weight gain over the past 30 years. On physical examination, he has decreased sensation to pinprick and light touch over the lower extremities. Based on these findings, which of the following complications is most likely to occur in this man Gangrene Hypoglycemic coma Ketoacidosis Mucormycosis Pancreatitis Systemic amyloidosis 40 A clinical study is conducted in patients diagnosed with either type 1 or type 2 diabetes mellitus. Persons with either type develop complications of accelerated and advanced atherosclerosis. Which of the following features common to patients with either type 1 or type 2 diabetes mellitus is most likely to be found by this study Which of the following laboratory studies is most likely to afford the best method of monitoring disease control in this man Cholesterol, total Fasting plasma glucose Glycosylated hemoglobin Microalbuminuria Random plasma glucose Serum fructosamine 44 A 45-year-old woman has had angina pectoris, polyuria, and polydipsia for the past 5 years. Which of the following is the most likely mechanism leading to the disease causing her findings Chronic pancreatitis Glucokinase gene mutation Insulin resistance Systemic amyloidosis T-cell mediated B-cell destruction 42 A 50-year-old man has had a nonhealing ulcer on the bottom of his foot for 2 months. Chloride ion channel abnormality Chromosome 21 trisomy Glucokinase gene mutation Peripheral insulin resistance Loss of T-cell tolerance 45 A 50-year-old man has a 35-year history of diabetes mellitus. He now has problems with sexual function, including difficulty attaining an erection. He also is plagued by mild but recurrent low-volume diarrhea and difficulty with urination. These problems are most likely to originate from which of the following mechanisms of cellular injury A Cross-linking of extracellular matrix proteins B Production of vascular endothelial growth factor C Abnormal transforming growth factor-beta signaling D Increased endothelial procoagulant activity E Nonenzymatic glycosylation F Polyol-induced susceptibility to oxidative stress 46 A 74-year-old woman is admitted to the hospital in an obtunded condition. Her temperature is 37° C, pulse is 95/ min, respirations are 22/min, and blood pressure is 90/60 mm Hg. The next day, a fasting blood glucose is 120 mg/dL, followed by a value of 122 mg/ dL on the following day. She is given an oral glucose tolerance test, and her blood glucose is 240 mg/dL 2 hours after receiving the standard 75-g glucose dose. Each time, she has a prodrome of lightheadedness followed by a brief loss of consciousness. After each episode, she awakens and on examination has no loss of motor or sensory function. Physical examination after the current episode shows that she is afebrile, with a pulse of 72/min, respirations of 17/min, and blood pressure of 120/80 mm Hg. Which of the following pancreatic disorders is most likely to be present in this patient Acute necrotizing pancreatitis Adenocarcinoma Cystic fibrosis Neuroendocrine tumor Pseudocyst 48 A family is followed longitudinally for two generations. Treatment with insulin 50 A 43-year-old man from Stockholm, Sweden, has had low-volume watery diarrhea for the past 3 months. On physical examination, he is afebrile; on palpation, there is no abdominal tenderness and no masses. Three months later, repeat endoscopy shows that the ulcerations are still present. Which of the following analytes is most likely to be increased in his in serum or plasma He has cutaneous striae over the lower abdomen and ecchymoses scattered over the extremities. Laboratory findings show fasting plasma glucose level of 200 mg/dL, serum Na+ of 150 mmol/L, and serum K+ of 3. Administration of low and high doses of dexamethasone fails to suppress the plasma cortisol level and excretion of urinary 17-hydroxycorticosteroids. Adenohypophyseal adenoma Adrenal cortical adenoma Extra-adrenal pheochromocytoma Small cell carcinoma of the lung Thyroid medullary carcinoma the Endocrine System 379 52 A 43-year-old woman has had absent menstrual cycles along with increasing weakness and weight gain over the past 5 months. A radiograph of the spine shows decreased bone density with a compression fracture at T9. Which of the following radiographic findings is most likely to be present in this patient Physical examination shows muscle wasting and 4/5 motor strength in all extremities. A chest radiograph shows a 6-cm perihilar mass on the right and prominent hilar lymphadenopathy. Amyloidosis Ectopic corticotropin syndrome Meningococcemia Metastatic carcinoma Pituitary adenoma 54 A 28-year-old, otherwise healthy man has had headaches for the past 2 weeks. Physical examination yields no remarkable findings except for a blood pressure of 174/116 mm Hg. A right adrenalectomy is done; the figure shows the gross appearance of the specimen. Which of the following laboratory findings in his blood was most likely reported in this patient before surgery Hyperglycemia Hyperkalemia Hyponatremia Low corticotropin level Low insulin level Low renin level 55 A 40-year-old woman has experienced increasingly frequent episodes of weakness accompanied by numbness and tingling in her hands and feet for the past year. Which of the following radiologic findings is most likely to be present in this woman Laboratory studies include a serum cortisol level of 3 g/mL at 8:00 am with a serum corticotropin level of 65 pg/mL. Type 2 diabetes mellitus Classic polyarteritis nodosa Hashimoto thyroiditis Systemic lupus erythematosus Ulcerative colitis 56 A 5-year-boy has developed features that suggest puberty over the past 6 months. On physical examination, the boy has secondary sex characteristics, including pubic hair and enlargement of the penis. Which of the following morphologic features is most likely to be seen in his adrenal glands Cortical atrophy Cortical hyperplasia Cortical nodule Medullary atrophy Medullary hyperplasia Medullary nodule 57 A female infant is born at term to a 41-year-old Yupik woman after an uncomplicated pregnancy. Which of the following enzyme deficiencies is most likely to be present in this infant Aromatase 11-Hydroxylase 21-Hydroxylase 17-Hydroxylase Oxidase 61 A 44-year-old woman has become increasingly listless and weak and has had chronic diarrhea and a 5-kg weight loss over the past 7 months. She also notices that her skin seems darker, although she rarely goes outside because she is too tired for outdoor activities. Adenohypophyseal adenoma Autoimmune destruction of the adrenals Pancreatic neuroendocrine tumor Metastatic carcinoma with lung primary Neisseria meningitidis infection of the adrenals Sarcoidosis of the lung and adrenals 58 A 19-year-old, previously healthy woman collapsed after complaining of a mild sore throat the previous day. Imaging studies show her adrenal glands are enlarged, and there are extensive bilateral cortical hemorrhages. Cytomegalovirus Histoplasma capsulatum Mycobacterium tuberculosis Neisseria meningitidis Streptococcus pneumoniae 62 A 37-year-old woman states that, although most of the time she feels fine, she has had episodes of palpitations, tachycardia, tremor, diaphoresis, and headache over the past 3 months. When her symptoms are worse, her blood pressure is measured in the range of 155/90 mm Hg. She collapses suddenly one day and is brought to the hospital, where her ventricular fibrillation is converted successfully to sinus rhythm. On postoperative day 2, she becomes somnolent and develops severe nausea and vomiting. Blood cultures are negative, and laboratory studies now show Na+ of 128 mmol/L, K+ of 4. Which of the following morphologic findings in the adrenal gland cortex is most likely to be present in this patient Adenoma Atrophy Carcinoma Caseating granulomas Hemorrhagic necrosis Nodular hyperplasia 63 A 25-year-old woman gives birth to a term infant following an uncomplicated pregnancy. On physical examination, the newborn is found to have an enlarged abdomen, but there are no other abnormal findings except for slightly elevated blood pressure. An abdominal ultrasound scan shows a right retroperitoneal mass in the adrenal gland. An increase in which of the following substances is most likely to be associated with the lesion in this neonate There are no neurologic abnormalities and no visual defects; however, he has an enlarged thyroid. A total thyroidectomy is performed, and on sectioning, the thyroid has multiple tumor nodules in both lobes. Microscopically, the thyroid nodules are composed of nests of neoplastic cells separated by amyloidrich stroma. Which of the following morphologic findings in the adrenal glands is most likely to be present in this patient Bilateral 4-cm medullary masses Bilateral cortical atrophy Bilateral cortical nodular hyperplasia Solitary caseating granuloma Solitary 1-cm cortical mass with contralateral cortical atrophy F Solitary 12-cm hemorrhagic cortical mass the Endocrine System 381 serum calcium concentration returned to normal. Adrenal pheochromocytoma Endometrial carcinoma Pituitary adenoma Pulmonary small cell anaplastic carcinoma Thyroid medullary carcinoma 65 A 26-year-old man developed sudden severe abdominal pain. During surgery, four enlarged parathyroid glands were found and excised, with reimplantation of one half of one gland. After the surgery, his 66 A 10-year-old boy has been bothered by frequent headaches for the past 5 months. In addition to her galactorrhea and infertility, this patient also may have decreased libido, and her amenorrhea is secondary to the excessive prolactin secretion. Microadenomas might not have pressure effects on surrounding structures such as optic chiasm, but they can be discovered because of their hormonal effects. In adults with closed epiphyses, gigantism does not occur, but acromegaly of soft tissues does. Chief cells in the parathyroids produce parathormone that increases serum calcium. Because the hypothalamus is unaffected, corticotropin-releasing hormone would still be present. She does not have diabetes insipidus from lack of antidiuretic hormone, because the posterior pituitary is less likely to be involved. Instead, the increase in soft tissue mass manifests as increasing shoe or glove size, carpal tunnel syndrome, and coarse facial features. This woman probably has an abnormal glucose tolerance test result, but this does not indicate the underlying cause of diabetes mellitus, which in this case is secondary to acromegaly. Functional pituitary tumors can be detected clinically before they become large enough to cause pressure symptoms such as visual disturbances. Cushing syndrome from an adrenal cortical neoplasm producing cortisol could be accompanied by glucose intolerance, hypertension, and truncal obesity, but there is no overall increase in soft tissues. There is failure of resorption of free water in the renal collecting tubules-hence the increased dilute urine with higher serum osmolality and hypernatremia. Corticotropin stimulates the adrenal glands, mainly with the effect of increasing cortisol secretion. Prolactin and melatonin deficiencies have no identifiable specific clinical effects in men. Although the increased pressure can lead to reduction in pituitary tissue through compression atrophy, there is typically adequate functional anterior pituitary to prevent hypopituitarism. This herniation can cause a "stalk section" effect, however, with loss of prolactin inhibition and hyperprolactinemia. A craniopharyngioma is a destructive tumor mass that is usually seen at a younger age. Hemochromatosis can interfere with organ function, including hypopituitarism; onset usually occurs later in women than in men (in the 60s in women compared with the 40s in men), owing to differences in physiologic iron losses. Prader-Willi syndrome is an example of genomic imprinting with hypothalamic dysfunction seen in prepubertal boys. If she had Sheehan syndrome after her pregnancy, she would have manifested hypopituitarism within months, not years. The laboratory findings in this patient suggest adrenal insufficiency, and her inability to breastfeed is caused by lack of prolactin; loss of menstrual cycles suggests that 9 A Craniopharyngiomas are uncommon, usually suprasellar neoplasms; they are typically found in young individuals. They are thought to arise from embryologic remnants of the Rathke pouch in the region of the pituitary. These are aggressive neoplasms that infiltrate and destroy surrounding tissues, making complete excision difficult. Despite their aggressive behavior, they are composed of benign-appearing squamoid or primitive tooth structures. The increase in prolactin occurs as a "stalk section" effect, and the hypernatremia results from diabetes insipidus caused by destruction of the hypothalamus, posterior pituitary, or both. Prolactinomas, similar to pituitary adenomas, can enlarge the sella when they are macroadenomas, but are not typically suprasellar or destructive of surrounding structures. There are increased catecholamine levels, and the -blocker propranolol will help prevent emergent death from cardiac failure. The fever and ancillary findings here go beyond what would be expected with an acute infection. Antiribonucleoprotein antibodies are seen in some collagen vascular diseases, such as mixed connective tissue disease. The transient hyperthyroidism results from inflammatory destruction of the thyroid follicles and release of thyroid hormone. The released colloid acts as a foreign body, producing florid granulomatous inflammation in the thyroid. Hashimoto thyroiditis can enlarge the thyroid transiently, but there is usually no pain or hyperthyroidism. Thyroid neoplasms are not typically associated with signs and symptoms of inflammation and are rarely functional. A toxic multinodular goiter likewise produces no signs of inflammation, and does not reverse functionality.

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