Myasthenia Gravis and Other Neuromuscular Disorders MCQs

Drugs that may exacerbate myasthenia gravis and potentiate the action of nondepolarizing muscle relaxants are: Antibiotics Aminoglycosides e.g Streptomycin Tetracyclines Quinolones e.g ciprofloxacin Macrolides e.g erythromycin Non-depolarizing muscle relaxants e.g d-Tubocurarine Beta-blockers like propranolol, atenolol, metoprolol Local anaesthetics Botulinum toxin Quinine derivatives like quinine, quinidine, chloroquine, mefloquine Magnesium Penicillamine

VIPomas [vasoactive intestinal peptide (VIP) originate in amine precursor uptake and decarboxylation (APUD) cells of the gastroenteropancreatic endocrine system and in adrenal or extra-adrenal neurogenic sites. Features of VIP syndrome include watery diarrhea (100%), hypochlorhydria (70% in adults), hyperglycemia (20-50% in adults), hypercalcemia (20-50% in adults), flushing (20% in adults) and hypokalemia due to diarrhea. Initial treatment is directed toward correcting volume and electrolyte abnormalities by using potassium chloride and sodium bicarbonate. Octreotide controls diarrhea in 80% of cases. Glucocorticoids reduce symptoms in 50% of patients with VIPoma. Reference: Harrison's Principles of Internal Medicine, 21 st Ed, Ch: 84 Pg: 665

Weight loss, tenesmus and a recent change in bowel habit all point towards an underlying diagnosis of colorectal cancer. Onset of symptoms in later life and a relatively short duration (that is, weeks rather than years) also point towards a 'biological' cause rather than irritable bowel syndrome. The passage of mucus per rectum is a normal physiological function and not indicative of underlying pathology. The symptoms are not suggestive of malabsorption. Diverticulitis and inflammatory bowel disease are both potential diagnoses but given the duration of symptoms less likely than a colonic neoplasm. Reference: Harrison's Principles of Internal Medicine, 21 st Ed, CH: 81, Pg: 639

This is a case of Crohn’s disease . Remission of Crohn's disease may be achieved by the use of steroids, elemental diet, surgery or infliximab. Mesalazine may maintain remission if induction has been achieved by surgery and if an 8-week course of metronidazole is administered. It has many side effects. In other scenarios, the most useful drug to maintain long term remission is azathioprine . Steroids (prednisolone) are only used for induction of remission. They are not appropriate for long term maintenance therapy. Cyclosporine is used in severe cases of ulcerative colitis refractory to steroid therapy. Reference: Harrison's Principles of Internal Medicine, 21 st Ed, Ch: 326 Pg: 2488

The diagnosis here is giardiasis, caused by Giardia lamblia. Giardia has been reported as a cause of chronic diarrhea.Most patients respond to oral metronidazole 250-400 mg three times daily for five days. Reference : Harrison's Principles of Internal Medicine, 21 st ed, Ch: 229, Pg: 1765

The current recommendations are early aggressive therapy to reduce joint deformity using combination therapy. Methotrexate is the cornerstone in treatment of RA and combination therapy should be built with Methotrexate as the base. The accepted combinations include Methotrexate plus HCQ plus Sulfasalazine Methotrexate with biologicals Methotrexate with Leflunomide Combination therapy involves starting the treatment with Methotrexate and to rapidly step up to the desired combination in 3-6 months. Reference: Harrison's Principles of Internal Medicine, 21st ed, Ch: 358, Pg: 2761-2764

This question deals with the clinical features of Cobalamine deficncy. Haematological abnormalities like macrocytic anemia will not be seen in 40% of patients with Subacute combined degeneration. In cobalamine deficiency, there will be blocade of steps that require cobalamine as cofactor and hence homocysteine and methyl manioc acid will be accumulated. In patients with pernicious anemia, the management is parenteral cyanocobalamine. But in food cobalamine malabsorption, the patients can absorb free cobalamine and hence oral supplementation is enough, at the dose of 1000mcg/day. The haematological abnormalities completely respond to cobalamine replacement. But the neurologoical manifestations tend to be permanent in about 50% patients. Reference: Harrison's Principles of Internal Medicine, 21 st ed, ch:446, Pg: 3496

This is a case of celiac disease . The following antibodies are found- Antibodies against tissue transglutaminase IgA Antiendomysial antibodies Deamidated anti-gliadin antibodies. Serum IgA levels are measured to detect false-negative results from IgA deficiency. Deamidated anti-gliadin IgG antibodies or tissue transglutaminase IgG antibodies are detectable and diagnostic in IgA-deficient patients. Small intestinal biopsy is the confirmatory test . Biopsies typically show characteristic villus blunting, crypt hyperplasia, and inflammation, including increased intraepithelial lymphocytes. Reference: Harrison's Principles of Internal Medicine, 21 st ed, Ch: 318, Pg: 2251 - 2253