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MCQ stands for Multiple Choice Questions sometimes called as Objective type questions. Here we discuss the Old Question Papers, High Yield Points and Strategies with respect to the Indian Medical Post Graduate PG Entrance Exams like AIIMS,AIPG, JIPMER, CMC Vellore, PGI Chandigarh, UPSC, TNPSC, State PG Exams like Tamil Nadu PG (TN PG), Delhi PG, UPPG, Tamilnadu PG (TNPG), Karnataka PG, MAHE, COMED-K etc.

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Wednesday, January 07, 2009

Difference between acute pyelonephritis and Uncomplicated UTI are all except

Question 90
Difference between acute pyelonephritis and Uncomplicated UTI are all except
a.       Loss of Concentrating ability
b.      Presence of White blood casts
c.       Presence of Antibody against Tamm-Horsfall proteins of tubules
d.      Bacterial colony Count more than 108
Answer
d. Bacterial colony Count more than 108
Reference:
Harrison 16th Edition Page 1717
Journal reference : 
a.       P. LARSSON, A. FASTH, U. JODAL, A. SOHL ÅKERLUND, C. SVANBORG EDÉN (1978) : URINARY TRACT INFECTIONS CAUSED BY PROTEUS MIRABILIS IN CHILDREN The Antibody Response to O and H Antigens and Tamm-Horsfall Protein and Bacterial Adherence to Uro-epithelium . Acta Paediatrica 67 (5), 591–596. doi:10.1111/j.1651-2227.1978.tb17807.x
b.      Kidney International (1976) 9, 23–29; doi:10.1038/ki.1976.3. Experimental pyelonephritis: The effect of chronic active pyelonephritis on renal function. Thomas E Miller1, David Layzell1 and Elaine Stewart1
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Discussion
Normal urine is sterile.  UTI can therefore be diagnosed if a single viable gram negative bacterium inhabits the urinary tract (kidney, ureters, bladder).  In reality, the bacteria causing UTI multiply in log phase growth in normal urine, and most people with urinary tract infection have 104-106 bacteria/ml.  The acute number will depend on the urine flow rate, characteristics of the urine, the duration of infection, etc.  The problem in diagnosis is that of contamination arising from voided specimens passing through the non-sterile distal urethra.  For this reason, clinicians use the criteria of 105 bacteria/ml of “clean catch” urine to diagnose UTI.  At this level, < 1% of the represent contaminants.  At counts of 1000-10,000/ml, there is a 50/50 chance the result represents contamination.  Such a count may represent true infection, but to be sure a second culture showing the same organism might be more convincing.  The second criteria for diagnosing UTI is the presence of pyuria (> 5 WBC/HPF) on the urinalysis.
Explanation
a.       A severe loss of urine concentrating capacity was demonstrable when the maximum urinary osmolality of a group of cases with pyelonephritis was compared with controls. Concentrating capacity decreased sharply over the first month but further loss over an eight-month period was minimal.
b.      Presence of White blood casts is Pathognomic for Pyelonephritis
c.       Presence of Antibody against Tamm-Horsfall proteins of tubules . "An increase in antibody levels against O antigen and Tamm-Horsfall protein was noted only in patients with acute pyelonephritis indicating that antibody determinations can be useful in differentiating between upper and lower urinary tract infection caused by Proteus in similarity to those caused by E. coli"
d.      Bacterial colony Count more than 108
Comments : This is what the Journal Says : Sera from seven girls with acute symptomatic pyelonephritis and nine children with acute symptomatic cystitis caused by Proteus mirabilis were analysed for antibodies against the bacterial O and H1 antigens and the Tamm-Horsfall protein. An increase in antibody levels against O antigen and Tamm-Horsfall protein was noted only in patients with acute pyelonephritis indicating that antibody determinations can be useful in differentiating between upper and lower urinary tract infection caused by Proteus in similarity to those caused by E. coli. In contrast no difference in adhesive ability was noted comparing Proteus strains causing acute pyelonephritis or cystitis.
Remarks
If you have a better TEXTBOOK, reference, please send a mail to bruno@nellaimedicos.com

Thymoma commonly presents with Myasthenia Gravis

Question 89
Thymoma commonly presents with
a.       Myasthenia Gravis
b.      ??
c.       ??
d.       ??
Answer
a. Myasthenia Gravis
Reference
Harrison 16th Edition Page
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Myasthenia gravis (MG) is an acquired autoimmune disorder characterized clinically by weakness of skeletal muscles and fatigability on exertion. Thomas Willis reported the first clinical description in 1672.
The antibodies in MG are directed toward the acetylcholine receptor (AChR) at the neuromuscular junction (NMJ) of skeletal muscles.
Explanation
The exact mechanism of loss of immunologic tolerance to AChR, a self antigen, is not understood. MG can be considered a B cell–mediated disease, as antibodies (a B cell product) against AChR are responsible for the disease. However, the importance of T cells in pathogenesis of MG is becoming increasingly apparent. The thymus is the central organ in T cell–mediated immunity, and thymic abnormalities such as thymic hyperplasia or thymoma are well recognized in myasthenic patients.
Comments
Since this question is often repeated, every one attempted it in a jiffy that they could not even recollect the other choices afterwards
Tips
Ä     MG is idiopathic in most patients.
Ä     Penicillamine is known to induce various autoimmune disorders, including MG.

Most common islet cell tumour in MEN 1 is Gastrinoma

Question 88
Most common islet cell tumour in MEN 1 is
a.       Gastrinoma
b.      Insulinoma
c.       Glucagonoma
d.      Somatostatinoma
Answer
a. Gastrinoma
Reference
Schwartz 7th Edition Page 1686
Sabiston 15th Edition Page 685
Harrison 16th Edition Page 2231
Robbins 5th Edition Page 1170
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Neoplasia of the pancreatic islets is the second most common manifestation of MEN 1 and tends to occur in parallel with hyperparathyroidism. Increased pancreatic islet cell hormones include pancreatic polypeptide (75 to 85%), gastrin [60%; Zollinger-Ellison syndrome (ZES)], insulin (25 to 35%), vasoactive intestinal peptide (VIP) (3 to 5%; Verner-Morrison or watery diarrhea syndrome), glucagon (5 to 10%), and somatostatin (1 to 5%). The tumors rarely produce adrenocorticotropin (ACTH), corticotropin-releasing hormone (CRH), growth hormone-releasing hormone (GHRH), calcitonin gene products, neurotensin, gastric inhibitory peptide, and others. Many of the tumors produce more than one peptide. The pancreatic neoplasms differ from the other components of MEN 1 in that approximately one-third of the tumors display malignant features, including hepatic metastases (Chap. 93).
Explanation
Of the choices given, the most Common Pancreatic Tumour in MEN I is Gastrinoma.
Comments
Multiple Endocrine Neoplasia (MEN) Syndromes

Type

MEN 1

MEN 2

Mixed Syndromes

MEN 2A
MEN 2B
Name
   Wermer’s Syndrome
   Sipple’s Syndrome
Gene
11q 11-13
RET
Parathyroid
Parathyroid hyperplasia or adenoma
Parathyroid hyperplasia or adenoma
Familial pheochromocytoma and islet cell tumor
von Hippel-Lindau syndrome, pheochromocytoma, and islet cell tumor
Neurofibromatosis with features of MEN 1 or 2
Myxomas, spotty pigmentation, and generalized endocrine overactivity in a single family
Pancreas
Islet cell hyperplasia, adenoma, or carcinoma
Pituitary
Pituitary hyperplasia or adenoma
Thyroid
C Cell Hyperplasia
Medullary Thyroid Carcinoma
MTC
Adrenal
Rarely Cortical Involvement
Pheochromocytoma
Pheochromocytoma
Others
Other less common manifestations: foregut carcinoid, , subcutaneous or visceral lipomas, dermal angiofibromas or collagenomas
Cutaneous lichen amyloidosis
Hirschsprung disease
Familial Medullary Thyroid Carcinoma
Mucosal and gastrointestinal neuromas
Marfanoid features
Tips
This is one of the most repeated topics for AIPG. There will be 2 to 3 questions every year
MEN
Ä     Pancreatic islet cell tumors are diagnosed by identification of a characteristic clinical syndrome, hormonal assays with or without provocative stimuli, or radiographic techniques. One approach involves annual screening of people at risk with measurement of basal and meal-stimulated levels of pancreatic polypeptide to identify the tumors as early as possible; the rationale of this screening strategy is the concept that surgical removal of islet cell tumors at an early stage will be curative. Other approaches to screening include measurement of serum gastrin and pancreatic polypeptide levels every 2 to 3 years, with the rationale that pancreatic neoplasms will be detected at a later stage but can be managed medically, if possible, or by surgery. High-resolution, early-phase computed tomography (CT) scanning provides the best noninvasive technique for identification of these tumors, but intraoperative ultrasonography is the most sensitive method for detection of small tumors.
Ä     ZES is caused by excessive gastrin production and occurs in more than half of MEN 1 patients with pancreatic islet cell tumors. Clinical features include increased gastric acid production, recurrent peptic ulcers, diarrhea, and esophagitis. The ulcer diathesis is refractory to conservative therapy such as antacids. The diagnosis is made by finding increased gastric acid secretion, elevated basal gastrin levels in serum [generally >115 pmol/L (200 pg/mL)], and an exaggerated response of serum gastrin to either secretin or calcium. Other causes of elevated serum gastrin levels, such as achlorhydria, treatment with H2 receptor antagonists or omeprazole, retained gastric antrum, small-bowel resection, gastric outlet obstruction, and hypercalcemia, should be excluded. Gastrin-producing carcinoid-like tumors are frequently present in the duodenal wall.
Ä     Insulinoma causes hypoglycemia in about one-third of MEN 1 patients with pancreatic islet cell tumors. The tumors may be benign or malignant (25%). The diagnosis can be established by documenting hypoglycemia during a short fast with simultaneous inappropriate elevation of serum insulin and C-peptide levels. More commonly, it is necessary to subject the patient to a supervised 72-h fast to provoke hypoglycemia. Large insulinomas may be identified by CT scanning; small tumors not detected by radiographic techniques may be localized by selective arteriographic injection of calcium into each of the arteries that supply the pancreas and sampling the hepatic vein for insulin to determine the anatomic region containing the tumor. Intraoperative ultrasonography can also be used to localize these tumors, but preoperative calcium injection data are helpful in guiding the subtotal pancreatectomy if multiple or no abnormalities are detected by intraoperative ultrasonography.
Ä     Glucagonoma in occasional MEN 1 patients causes a syndrome of hyperglycemia, skin rash (necrolytic migratory erythema), anorexia, glossitis, anemia, depression, diarrhea, and venous thrombosis. In about half of these patients the plasma glucagon level is high, leading to its designation as the glucagonoma syndrome, although elevation of plasma glucagon level in MEN 1 patients is not necessarily associated with these symptoms. The glucagonoma syndrome may represent a complex interaction between glucagon overproduction and the nutritional status of the patient.
Ä     The Verner-Morrison or watery diarrhea syndrome consists of watery diarrhea, hypokalemia, hypochlorhydria, and metabolic acidosis. The diarrhea can be voluminous and is almost always found in association with an islet cell tumor, prompting use of the term pancreatic cholera. However, the syndrome is not restricted to pancreatic islet tumors and has been observed with carcinoids or other tumors. This syndrome is believed to be due to overproduction of VIP, although plasma VIP levels may not be elevated. Hypercalcemia may be induced by the effects of VIP on bone as well as by hyperparathyroidism.

Conn’s Syndrome is Adrenal Adenoma

Question 87
Conn’s Syndrome is 
a.       Adrenal hyperplasia
b.      Adrenal carcinoma
c.       Adrenal adenoma
d.      None of the above
Answer
c. Adrenal Adenoma.
Reference:
Harrison 16th Edition Page 2138
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In the original case of excessive and inappropriate aldosterone production, the disease was the result of an aldosterone-producing adrenal adenoma (Conn's syndrome). Most cases involve a unilateral adenoma, which is usually small and may occur on either side.
Explanation
Self Explanatory. Though Hyperaldosteronism can be due to many causes, an aldosterone producing adrenal adenoma is called as Conn’s Disease
Comments
Rarely, primary aldosteronism is due to an adrenal carcinoma. Aldosteronism is twice as common in women as in men, usually occurs between the ages of 30 and 50, and is present in approximately 1% of unselected hypertensive patients. However, the prevalence may be as high as 10%, depending on the criteria and study population. Most of this difference is not secondary to the prevalence of patients with an aldosteronoma but rather because of the inclusion of those with bilateral hyperplasia.
In many patients with clinical and biochemical features of primary aldosteronism, a solitary adenoma is not found at surgery. Instead, these patients have bilateral cortical nodular hyperplasia. In the literature, this disease is also termed idiopathic hyperaldosteronism, and/or nodular hyperplasia. The cause is unknown
Tips
High blood pressure (hypertension) is the main, and often the only, symptom.
Other symptoms may occur because high aldosterone levels in the blood act on the kidney to increase the loss of the mineral potassium in the urine. This in turn may lead to a fall in blood potassium, resulting in tiredness, muscle weakness and passing of large volumes of urine (polyuria), especially at night (nocturia). However, these symptoms are also found in many other conditions (for example, diabetes mellitus or hypercalcaemia) and do not, by themselves, establish a diagnosis of Conn's syndrome. Also, many patients with proven Conn's syndrome do not have a low blood potassium level.

Cushing’s disease presents with

Question 86
Cushing’s disease presents with
a.       Increased ACTH, Increased Cortisol
b.      Decreased ACTH and Decreased Cortisol
c.       Increased ACTH and Decreased Cortisol
d.      Increased Catecholamines
Answer
a. Increased ACTH and Increased Cortisol
Reference
Harrison 16th Edition Page 2135
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Cushing's syndrome (also called hypercortisolism or hyperadrenocorticism) is an endocrine disorder caused by high levels of cortisol in the blood from a variety of causes, including primary pituitary adenoma (known as Cushing's disease), primary adrenal hyperplasia or neoplasia, ectopic ACTH production (e.g., from a small cell lung cancer), and iatrogenic (steroid use).
Explanation
Self Explanatory
Comments
Cushing's disease was described by American physician, surgeon and endocrinologist Harvey Cushing (1869-1939) and reported by him in 1932.
Tips
Question about the earliest manifestation of Cushings was asked in 2004

A 24 year old female presents with palpable Purpura and with rashes all over trunk limbs buttocks and paid abdomen

Question 85
A 24 year old female presents with palpable Purpura and with rashes all over trunk limbs buttocks and paid abdomen. The most probable diagnosis is
a.       Meningococceimia
b.      HSP
c.       ??
d.      ??
Answer
b. HSP
Reference
Harrison 16th Edition Page 2010
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Henoch-Schonlein purpura, also referred to as anaphylactoid purpura, is a distinct systemic vasculitis syndrome that is characterized by palpable purpura (most commonly distributed over the buttocks and lower extremities), arthralgias, gastrointestinal signs and symptoms, and glomerulonephritis. It is a small vessel vasculitis.
Henoch-Schonlein purpura is usually seen in children; most patients range in age from 4 to 7 years; however, the disease may also be seen in infants and adults. It is not a rare disease; in one series it accounted for between 5 and 24 admissions per year at a pediatric hospital. The male-to-female ratio is 1.5:1. A seasonal variation with a peak incidence in spring has been noted
Explanation
Self Explanatory
Comments TREATMENT
The prognosis of Henoch-Schonlein purpura is excellent. Most patients recover completely, and some do not require therapy. Treatment is similar for adults and children. When glucocorticoid therapy is required, prednisone in doses of 1 mg/kg per day and tapered according to clinical response has been shown to be useful in decreasing tissue edema, arthralgias, and abdominal discomfort; however, it has not proven beneficial in the treatment of skin or renal disease and does not appear to shorten the duration of active disease or lessen the chance of recurrence. Patients with rapidly progressive glomerulonephritis have been anecdotally reported to benefit from intensive plasma exchange combined with immunosuppressive drugs.
Tips :
Ä     Renal failure is the most common cause of death in the rare patient who dies of Henoch-Schonlein purpura.
Ä     Myocardial involvement can occur in adults but is rare in children.
Ä     Routine laboratory studies generally show a mild leukocytosis, a normal platelet count, and occasionally eosinophilia. Serum complement components are normal, and IgA levels are elevated in about one-half of patients.

What will be the appropriate investigation for a 40 female with jaundice and spherocytosis

Question 84
What will be the appropriate investigation  for a 40 female with jaundice and spherocytosis
a.       Osmotic fragility
b.      Coomb's test
c.       Electrophoresis
d.      ??
Answer
b. Coomb’s Test
Reference
Harrison 16th Edition Page 609
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 Hereditary spherocytosis must be distinguished primarily from the spherocytic hemolytic anemias associated with RBC antibodies. The family history of anemia and/or splenectomy is helpful, when present.
Explanation
The diagnosis of immune spherocytosis is usually readily established by a positive direct Coombs test
Comments
Spherocytes are also seen in association with hemolysis induced by splenomegaly in patients with cirrhosis, in clostridial infections, and in certain snake envenomations (due to the action of phospholipases on the membrane). A few spherocytes are seen in the course of a wide variety of hemolytic disorders, particularly glucose-6-phosphate dehydrogenase (G6PD) deficiency
Tips
Many Questions in AIIMS Papers have something called as NESTROF Test. It is nothing but “Naked Eye Single Tube Redcell Osmotic Fragility Test”

A drug used in the treatment of CML is Imatinib Mesylate Gleevec ST1571

Question 83
A drug used in the treatment of CML is – imatinb CML
a.       Imatinib Mesylate
b.      Gleevee
c.       ST1571
d.      All of the above
Answer
d. All of the above
Reference
Harrison 16th Edition Page 639
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Allogeneic Stem Cell Transplant (SCT) is the only curative therapy for CML and, when feasible, is the treatment of choice. However, it is complicated by a high early mortality rate owing to the transplant procedure.
Outcome of SCT depends on multiple factors including:
(1) the patient (i.e., age and phase of disease);
(2) the type of donor [i.e., syngeneic (monozygotic twins) or HLA-compatible allogeneic, related or unrelated];
(3) the preparative regimen;
(4) GVHD; and
(5) posttransplantation treatment
Explanation
Ä     Imatinib is a drug used to treat certain types of cancer. It is currently marketed by Novartis as Gleevec (USA) or Glivec (Europe/Australia) as its mesylate salt, imatinib mesilate (INN). It was originally coded during development as CGP57148B or STI-571 (these terms are used in early preclinical publications). It is used in treating chronic myelogenous leukemia (CML), gastrointestinal stromal tumors (GISTs) and a number of other malignancies.
Ä     It is the first member of a new class of agents that act by inhibiting particular tyrosine kinase enzymes, instead of non-specifically inhibiting rapidly dividing cells.
Comments
Some students felt that Infliximab was one of the choices
Tips
Ä     Infliximab is a “chimeric monoclonal antibody” (“chimeric” refers to the use of both mouse (murine) and human components of the drug i.e. murine binding VK and VH domains and human constant Fc domains)
Ä     The drug blocks the action of TNFα (tumour necrosis factor alpha) by binding to it and preventing it from signaling the receptors for TNFα on the surface of cells. (TNFα is one of the key cytokines that triggers and sustains the inflammation response.)
Ä     Infliximab is used in the treatment of
o       psoriasis,
o       pediatric Crohn's disease,
o       ankylosing spondylitis,
o       psoriatic arthritis,
o       rheumatoid arthritis,
o       ulcerative colitis.
Ä     Infliximab  is administered by intravenous infusion, typically at 6-8 week intervals.

One of the Causative organisms for Crohn's disease is Mycobacterium paratuberculosis

Question 82
One of the Causative organisms for Crohn's disease is
a.       Mycobacterium paratuberculosis
b.      Chlyamidia
c.       ??
d.      ??
Answer
a. Mycobacterium paratuberculosis
Reference
Harrison 16th Edition Page 1777
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Crohn disease is an idiopathic, chronic inflammatory disorder of the bowel that involves any region of the alimentary tract from the mouth to the anus.
Explanation
IBD may have an as yet undefined infectious etiology. Three specific agents have received the greatest attention, Mycobacterium paratuberculosis, Paramyxovirus, and Helicobacter species. The immune response to a specific organism could be expressed differently, depending upon the individual's genetic background. Although M. paratuberculosis had initially been identified in CD patients, further studies have not confirmed a disease association. In addition, antimycobacterial agents have not been effective in treating CD. A role for the measles virus or paramyxoviruses in the development of CD has been suggested based on an increase in the incidence of CD in England that paralleled use of the measles vaccine. However, studies in the United States have not substantiated this finding. In an animal model of IBD, Helicobacter hepaticus has been implicated as a trigger for the inflammatory response; evidence in people is lacking
Comments
Although there are many similarities between ulcerative colitis and Crohn disease, there are also major differences in the clinical course and distribution of the disease in the gastrointestinal tract. The inflammatory process tends to be eccentric and segmental, often with skip areas (i.e., normal regions of bowel between inflamed areas). Whereas inflammation in ulcerative colitis is limited to the mucosa (except in toxic megacolon), gastrointestinal involvement in Crohn disease is transmural. Among children with Crohn disease, the initial presentation most commonly involves ileum and colon (i.e., ileocolitis) but may involve the small bowel alone in about 40% (50% of children have terminal ileitis alone) or colon alone in about 10% (granulomatous colitis). Crohn disease may rarely present in the first years of life. As with ulcerative colitis, Crohn disease tends to have a bimodal age distribution with the first peak beginning in the late teens.
Tips
Several factors have been suggested in causation of crohns disease:
Ä     Genetic - in up to 20% of patients with Crohn's disease there is another family member affected by Crohn's or ulcerative colitis.
Ä     Low intake of fibre from fruit and vegetables has been associated with the development of Crohn's
Ä     Immune mechanisms - may be a down-regulating of the normal mucosal immune response in Crohn's

Which of the following is not true for Hereditary Hemochromatosis – Desferroxamine not treatment of choice

Question 81
Which of the following is not true for Hereditary Hemochromatosis
a.       Gonadal failure is seen
b.      Desferroxamine is the treatment of choice
c.       Arthropathy is seen
d.      Skin pigmentation is seen
Answer
b. Desferroxamine is the treatment of choice
Reference
Harrison 16th Edition Page 2302
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Hemochromatosis is a common disorder of iron storage in which an appropriate increase in intestinal iron absorption results in deposition of excessive amounts of iron in parenchymal cells with eventual tissue damage and impaired function of organs, especially the liver, pancreas, heart, joints, and pituitary. The disease was termed hemochromatosis and the iron-storage pigment was called hemosiderin because it was believed that the pigment was derived from the blood. The terms hemosiderosis and siderosis are often used to describe the presence of stainable iron in tissues, but tissue iron must be quantified to assess body iron status  Hemochromatosis implies potentially severe progressive iron overload leading to fibrosis and organ failure.
Explanation
Ä     Cirrhosis of the liver, diabetes mellitus, arthritis, cardiomyopathy, and hypogonadotrophic hypogonadism are common manifestations.
Ä     The therapy of hemochromatosis involves removal of the excess body iron and supportive treatment of damaged organs. Iron removal is best begun by weekly or twice-weekly phlebotomy of 500 mL. Although there is an initial modest decline in the volume of packed red blood cells to about 35 mL/dL, the level stabilizes after several weeks. The plasma transferrin saturation remains increased until the available iron stores are depleted. In contrast, the plasma ferritin concentration falls progressively, reflecting the gradual decrease in body iron stores. Since one 500-mL unit of blood contains 200 to 250 mg iron and about 25 g iron should be removed, weekly phlebotomy may be required for 1 or 2 years. When the transferrin saturation and ferritin level become normal, phlebotomies are performed at appropriate intervals to maintain levels within the normal range. The measurements promptly become abnormal with iron reaccumulation. Usually one phlebotomy every 3 months will suffice.
Ä     Chelating agents such as deferoxamine, when given parenterally, remove 10 to 20 mg iron per day, which is much less than that mobilized by once-weekly phlebotomy. Phlebotomy is also less expensive, more convenient, and safer for most patients. However, chelating agents are indicated when anemia or hypoproteinemia is severe enough to preclude phlebotomy. Subcutaneous infusion of deferoxamine using a portable pump is the most effective means of administration.
Comments
The management of hepatic failure, cardiac failure, and diabetes mellitus is similar to conventional therapy for these conditions. Loss of libido and change in secondary sex characteristics are partially relieved by parenteral testosterone or gonadotropin therapy
Tips
Ä     Hereditary or genetic hemochromatosis: This disorder is most often caused by inheritance of a mutant HFE gene, which is tightly linked to the HLA-A locus on chromosome 6p. The genetic disease can be recognized during its early stages when iron overload and organ damage are minimal. At this stage the disease is best referred to as early or precirrhotic hemochromatosis.
Ä     Secondary iron overload: Tissue injury usually occurs secondary to an iron-loading anemia such as thalassemia or sideroblastic anemia, in which increased erythropoiesis is ineffective. In the acquired iron-loading disorders, massive iron deposits in parenchymal tissues can lead to the same clinical and pathologic features as in hemochromatosis