Explanation:

Diabetic ulcers typically develop at pressure points, and the heel is a favorite location. The patient has evidence of neuropathy, and the correlation with the trauma inflicted by the new shoes is classic. Ischemic ulcers, whether due to arteriosclerosis or embolization are typically seen at the tip of the toes, as far away from the heart as one can get.

Explanation:

This patient has hypercalcaemia with a borderline low phosphate concentration but an inappropriately normal parathyroid hormone (PTH) concentration.
This suggests hyperparathyroidism, which is a relatively common disorder amongst elderly females.
The story of the breast lump in this case is endeavouring to throw the candidate.
Vitamin D excess would be expected to cause an elevated phosphate.

Explanation:

HbA1C is a test that measures the amount of glycosylated hemoglobin in your blood. The test gives a good estimate of how well diabetes is being managed over time. In particular over the past 3 months, since that is the life span of the red blood cell that contains the hemoglobin molecule.
This test measures blood sugar control over an extended period in people with diabetes. In general, the higher your HbA1C value, the higher the risk that you will develop complications from diabetes (eye disease, kidney disease. nerve damage, heart disease, and stroke). This is especially true if your HbA1C remains elevated on more than one occasion. Most physicians will consider HbA1C less than 7 as an indicator of good diabetic control. Unlike a diary, the HbA1C value does not lie.

Explanation:

Women older than 65 years of age who have low serum TSH levels, indicating physiologic hyperthyroidism, are at increased risk for new hip and vertebral fractures. Use of thyroid hormone itself does not increase the risk of fracture if TSH levels are normal.

Explanation:

Cushing´s syndrome is one of the secondary causes of hypertension. Therefore the blood pressure would be high. Along with Cushing´s, the other causes include Hyperaldosteronism, Aortic coarctation, Pheochromocytoma and Stenosis of renal artery. Remember the mnemonic C.H.A.P.S. for these 5 causes of secondary hypertension.

Explanation:

Explanation:

Thyroxine is the hormone of choice for replacement therapy. It has a half life of seven days, and any alteration in dose is not reflected for four to six weeks. Therefore, it is very unlikely that she will develop signs and symptoms of hypothyroidism. She will not be given the medication either through the nasogastric tube or intravenously, nor does she require a preoperative loading dose.

Explanation:

A pheochromocytoma is a catecholamine secreting tumor of chromaffin cells typically located in the adrenals. It causes persistent or paroxysmal hypertension. Common symptoms and signs are paroxysms of tachycardia, diaphoresis, postural hypotension, tachypnea, cold and clammy skin, severe headache, angina, palpitations, nausea, vomiting, epigastric pain, visual disturbances, dyspnea, paresthesias, constipation, and a sense of impending doom. Diagnosis is by measuring catecholamine products in blood or urine. Imaging tests, especially CT or MRI, help localize tumors. Treatment involves removal of the tumor when possible. Drug therapy for control of BP includes alpha-blockade possibly combined with beta blockade. Ectopic amylase production by lung, ovary, pancreas, and colon malignancies; pheochromocytoma; thymoma; multiple myeloma (increased salivary amylase); and breast cancer (increased pancreatic amylase) are miscellaneous causes of hyperamylasemia.

Explanation:

Aldosterone, a hormone produced and secreted by the adrenal glands, signals the kidneys to excrete less sodium and more potassium. Hyperaldosteronism can be caused by a tumor (usually a noncancerous adenoma) in the adrenal gland (a Condition called Conn´s syndrome), although sometimes both glands are Involved and are overactive. Sometimes hyperaldosteronism is a response to certain diseases, such as very high blood pressure (hypertension) or narrowing of one of the arteries to the kidneys. A doctor who suspects hyperaldosteronism first tests the levels of sodium and potassium in the blood. The doctor may also measure aldosterone levels. If they are high, spironolactone, a drug that blocks the actlon of aldosterone, may be given to see if the levels of sodium and potassium return to normal. In Conn´s syndrome, the levels of renin are also very low.

Explanation:

The condition described in the question stem is very common among diabetics, and is due to atrophy of lumbricals and interosseus muscles secondary to diabetic neuropathy. Another finding that may be seen is the presence of corns and callosities on the dorsal surface of the feet overlying the protuberant interphalangeal joints. All of these degenerative changes add to the diabetic´s foot disease, predisposing for sores that heal poorly in the poorly vascularized diabetic foot, often leading to gangrene and requiring amputation of the distal toot. Flexor digitorum longus is an extrinsic muscle of the foot that flexes the distal phalanges of the lateral four toes and assists in plantar flexion of the foot. Peroneus longus is an extrinsic muscle of the foot that plantar-flexes and everts the 4 foot. Tibialis anterior is an extrinsic muscle of the foot that dorsi flexes and inverts the foot.

Explanation:

Cystic fibrosis is not associated with goiters. All of the other conditions can result in goiters.

Explanation:

A high-fiber diet has not been shown to increase the bone density in osteoporosis. Hormone replacement therapy can slow the progression of osteoporosis even greater than five years postmenopause. Adding progestins can decrease the incidence of endometrial hyperplasia. Slow-release fluoride has been approved by the FDA- alendronate -to inhibit osteoclastic activity and reduce the progression of osteoporosis. Calcium carbonate and vitamin D are both important nutrients for stronger bone formation. Elderly patients should also be exposed to sunlight to get enough vitamin D. Calcitonin works by directly inhibiting osteoclast activity via the calcitonin receptor. It directly induces inhibition of osteoclastic bone resorption by affecting actin cytoskeleton which is needed for the osteoclastic activity.

Explanation:

Hypothyroid patients should be treated with thyroid hormone replacement. Surgical thyroidectomy and radioactive thyroid treatment will potentiate the problem. Stimulation with thyroid stimulating hormone will not be effective in patients that have depleted thyroxine stores. Hypothyroidism does not correct spontaneously

Explanation:

This patient presents with steroid psychosis secondary to excess cortisol level from Cushing´s syndrome. Hypercortisolism can have features of “buffalo hump,” lipomatosis, hirsutism, ecchymosis, and hypertension. A 24-hour urine cortisol level (B) would be a useful screening tool. An oral glucose tolerance test (A) would tell us nothing except that the patient has diabetes. Cushing´s syndrome can cause diabetes. If one suspects hypertensive encephalopathy exclusively a CT of the brain (C) would be useful to rule out hemorrhage. Lupus patients can also present with cerebral psychosis, but none of the other features would be present. An ANA level (D) would be ordered if one suspects lupus. An elevated aldosterone level (E) is present in Conn´s syndrome. This would present with hypertension, hypernatremia, and hypokalemia. None of the other features would be present.

Explanation:

This woman has excess cortisol levels in the body. Cushing´s disease is the most common cause, and it occurs from a pituitary adenoma which secretes ACTH which in turn stimulates cortisol from the adrenal glands. Chronic cortisol elevation causes the above physical findings as well as moon facies and buffalo hump. Elevated thyroid-stimulating hormone (A) is seen in hypothyroid-patients who have hormone cause delayed reflexes and myxedema. Elevated aldosterone levels (C) cause hypokalemia and hypertension. Primary hyperaldosteronism is due to adrenocortical adenoma or hyperplasia. Elevated vasopressin levels (D) are seen in syndrome of inappropriate ADH, and causes volume expansion and hyponatremia. Melatonin (E) is produced by the pineal gland and regulates circadium rhythm. It is usually elevated at night.

Explanation:

This patient has Addison´s disease. The apical scarring on chest radiography suggests old tuberculosis, which used to cause granulomatous infiltration of the adrenals in some individuals. Such infiltration can produce Addison´s. The radiographic findings and many of the patient´s symptoms are not consistent with adenocarcinoma of the lung. Hypothyroidism would not present with such a constellation of symptoms. The clinical pattern is not suggestive of sepsis or candida infection.

Explanation:

The diagnosis here may be Cushing´s syndrome. This is supported by the weight gain, high BMI, hypertension, menstrual irregularities and glycosuria.
There is a possibility that this vignette describes polycystic ovary syndrome (PCOS), but a single testosterone reading would add little information to the suspected diagnosis. However raised urinary cortisol is a relatively sensitive marker of Cushing´s.
A random aldosterone level tells you little, and an Hb_Alc is not an accepted screening tool, even for diabetes.
The history does not suggest prolactinoma, which may present with vague symptomatology, galactorrhoea and menstrual irregularities.

Explanation:

The use of bicarbonate in DKA is controversial.
However, most authorities agree that a bicarbonate infusion may be used in subjects with a severe metabolic acidosis (pH less than 7).

Explanation:

The symptoms of hypoglycemia rarely develop until the level of sugar in the blood falls below 60 milligrams per deciliter of blood. Some people develop symptoms at slightly higher levels, especially when blood sugar levels fall quickly, and some do not develop symptoms until the sugar levels in their blood are much lower.
The body first responds to a fall in the level of sugar in the blood by releasing epinephrine from the adrenal glands. Epinephrine stimulates the release of sugar from body stores but also causes symptoms similar to those of an anxiety attack: sweating, nervousness, shaking, faintness, palpitations, tingling sensation; around the mouth and hunger.
More severe hypoglycemia reduces the sugar supply to the brain, causing dizziness, fatigue, weakness, headaches, inability to concentrate, confusion, inappropriate behavior that can be mistaken for drunkenness, slurred speech, blurred vision, seizures, and coma. Severe and prolonged hypoglycemia may permanently damage the brain. Symptoms can begin slowly or suddenly, progressing from mild discomfort to severe confusion or panic within minutes.

Explanation:

The patient is presenting with signs of septic shock from pyelonephritis, including nausea, confusion, chills, fever, flank pain, and cloudy urine. The hemorrhagic extremity lesions are most likely a sign of septicemia and toxemia. Immediate treatment with intravenous antibiotics is necessary to prevent cardiopulmonary collapse and death.

Explanation:

Explanation:

Primary hyperparathyroidism is one of the most common causes of hypercalcemia and should be considered in any individual with an elevated calcium level. A single parathyroid adenoma is the underlying pathology in 85% of cases.
The symptoms have become known as “moans, groans, stones, and bones with psychic overtones”. They include feelings of weakness and fatigue, depression, or aches and painful bones, renal stones, abdominal groans, and psychic moans. With more severe disease, a person may have a loss of appetite, nausea, vomiting, constipation, confusion or impaired thinking and memory, and increased thirst and urination. Patients may have thinning of the bones without symptoms, but with risk of fractures. Elevated parathyroid hormone (PTH) levels in the setting of hypercalcemia establish the diagnosis of hyperparathyroidism

Explanation:

Abnormal morphology (shape) and motility can prevent the sperm from reaching the egg. The sperm need motility to be able to swim well and survive for a number of hours n the female reproductive tract. If they do meet, abnormal-looking sperm might be incapable of fertilization. The motility of this man´s sperm i.e. poor and therefore he is unlikely to be able to be fertile. In addition, infertility specialists have stated that 1 million motile sperm is the minimum amount of sperm associated with a reasonable chance of pregnancy success at intrauterine insemination. However in-vitro fertilization IVF can be used to treat Infertility due to his oligospermia. The procedure would involve controlled ovarian hyperstimulation, oocyte retrieval, and fertilization with, sperm, embryo culture, and embryo transfer. Impotence is defined as an inability to achieve and/or maintain an erection.

Explanation:

Explanation:

Subacute thyroiditis is usually secondary to a viral infection. The thyroid is moderately enlarged and tender with a decrease in the radioactive iodine uptake. Analgesics are given for the pain and fever, and this disease resolves on its own over time. Preformed thyroid hormones are released from the follicles. Struma ovarii is thyroid tissue located in ovarian dermoid tumors and teratomas which autonomously secrete thyroid hormone. Thyrotoxicosis factitia is caused by ingestion of excessive amounts of exogenous thyroid hormones. This can also be caused by consumptions of ground beef contaminated with bovine thyroid gland. Grave´s disease is the most common cause of thyrotoxicosis. It is an autoimmune disorder. The radioactive iodine uptake is increased and the thyroid gland is enlarged. Autonomous toxic adenomas of the thyroid can be single or multiple. There is increase in the radioactive iodine uptake and negative anti-thyroid antibodies in the plasma.

Explanation:

Obesity produces a relative insulin resistance and hyperinsulinemia, at least early in the development of diabetes. Facial edema (A) is not associated with obesity nor are hyperthyroidism (C), Addison´s disease (D), or hypernatremia (E).

Explanation:

The patient probably has a medullary carcinoma of the thyroid gland. These tumors are derived from the calcitonin secreting neuroendocrine C cells of the thyroid gland. Hurthle cells are altered thyroid follicular cells with very eosinophilic cytoplasm. A parathyroid tumor composed of either chief cells or oxyphil cells might secrete parathyroid hormone but not calcitonin. Thyroid glandular epithelial cells can secrete triiodothyronine and thyroxine but not calcitonin.

Explanation:

Counterregulatory hormones increase hepatic glucose production and decrease utilization in nonhepatic tissues. Glucagon, secreted by pancreatic alpha cells, is the primary counter regulatory hormone. Epinephrine and norepinephrine, released from the adrenal medulla and sympathetic nervous system, are critical in the absence of glucagon. Cortisol and growth hormone play an important role during periods of prolonged fasting or sustained hypoglycemia. Somatomedins, also known as insulin like growth factors, are important in growth stimulation.

Explanation:

Pseudohypoparathyroidism is inherited as an X-linked dominant with variable penetrance. Osteomalacia is not hereditary. Hemophilia is X-linked recessive. Classical gout, if it has any hereditary component, is multifactorial. Hyperparathyroidism is not known to be genetically linked.

Explanation:

Euthyroid goiters are not associated with choriocarcinoma, an invasive cancer originating in placental tissue, but can be seen in all of the other conditions.

Explanation:

Gastrointestinal bleeding is not increased in morbidly obese individuals, but all of the other conditions are.

Explanation:

Explanation:

Explanation:

This patient obviously has diabetes mellitus and the diagnosis should be confirmed with either a fasting plasma glucose above 7 mmol/l or a random plasma glucose above 11.1 mmol/l.

Explanation:

The most appropriate initial treatment of this amiodarone induced hyperthyroidism would be carbimazole. Despite stopping the amiodarone thyrotoxicosis may persist for many months and so additional treatment is often required. Two types of amiodarone induced hyperthyroidism recognized. The first being a consequence of iodine overload contained within the amiodarone of which the above is a typical example and the second type is due to an acute thyroiditis with thyroid cell destruction and increased parameters of inflammation. The former is best treated with carbimazole, the latter with prednisolone.

Explanation:

This man has significant hyperglycaemia and symptoms of catabolism weight loss, thirst, polyuria, etc. In this case the consensus recommends moving straight to insulin therapy, both for rapid control of glucose levels with symptom resolution, and because type I diabetes cannot be excluded in this case. Depending on circumstances, oral medications can be added later insulin even withdrawn in some cases.

Explanation:

This young woman probably has an autoimmune hypothyroidism and now presents with features typical of acute hypoadrenalism. The biochemistry os also supportive with low sodium, low glucose and elevated potassium. The diagnosis may be confirmed with inadequate cortisol response in the short synacthen test. A random cortisol concentration is not adequate to diagnose hypoadrenalism.

Explanation:

Metformin has been shown to increase the rate of conception in PCOS through improved insulin sensitivity. Ethinyloestradiol and cyproterone acetate combine to form Dianette the oral contraceptive. Spironolactone is used for hirsuitism but is teratogenic. Glibenclamide is not used in PCOS.

Explanation:

This young woman has a slightly elevated thyroxine (T4) and an elevated thyroid stimulating hormone (TSH). The most probable explanation is poor compliance. This also explains the slightly high prolactin concentration too; a consequence of reduced dopaminergic tone on the lactotrophs. The typical scenario is that the patients take their medication in the days before the clinic.

Explanation:

It is important to know the relative potencies of the glucocorticoids. Dexamethasone for instance is roughly 30 times more potent than hydrocortisone.

Explanation:

Pregnancy and the oral contraceptive pill (OCP) both increase transferrin level. Iron is carried in the blood bound to transferrin Fe2+ (ferrous iron) is oxidised to Fe3+ (ferric iron) by caeruloplasmin to bind to transferrin which is about one third saturated with iron. The saturation of transferrin (plasma iron concentration/TIBC X 100) is used as a measure of iron stores. A value below 16% is indicative of iron deficiency. The transferrin level and the TIBC rise in iron deficiency. Pregnancy and the OCP both increase transferrin levels; whereas transferrin and TIBC fall in iron overload, percentage saturation is increased in haemochromatosis.

Explanation:

Superior extension of the tumour can lead to compression of firstly the optic apparatus and later the hypothalamus.
Lateral extension of the tumour with compression or invasion of the cavernous sinus can compromise third fourth or sixth cranial nerve function, manifest as diplopia in 5 to 15 % of pituitary tumour patients.
The optic chiasm lies 5-10mm above the diaphragm sellae and anterior to the stalk.
Adenomas larger than 1.5cm frequently have suprasellar extension and a magnetic resonance imaging (MRI) scan will show compression and upward displacement of the optic chiasm.

Explanation:

The likelihood that this patient has significant thyroid disease is very low given the minimal elevation of TSH, normal clinical examination, and concomitant pneumonia. The elevated TSH level is likely due to her illness rather than to any underlying psychiatric condition. Even if she had a palpable thyroid, her risk of hypothyroidism would be on the order of 5%. A TSH level ≥ 20 U/mL in an acutely ill patient reflects true hypothyroidism only about 49% of the time. It is likely that this patient has sick euthyroid syndrome and that follow-up thyroid testing after discharge when she has recovered is appropriate and is very likely to be normal. Free T4, rT3, and TSH levels would be appropriate for subsequent evaluation if the patient´s laboratory values did not return to normal after resolution of the pneumonia.

Explanation:

In primary hyperparathyroidism, hypercalcemia is the result of excessive PTH secretion by one or more abnormal, enlarged parathyroid glands. Laboratory findings in most patients with primary hyperparathyroidism reflect the mild clinical presentation of the disorder. The serum calcium level is often 1 mg/dL or more above the upper limits of normal. Bone radiographs may show the classic changes of subperiosteal bone resorption in the occasional patient with hyperparathyroidism, but in most cases they are normal or may show osteopenia. Osteocalcin is an osteroblast specific protein. It is a marker of increased skeletal turnover, and it is usually not indicated clinically. The development of highly sensitive and specific assays for intact, largely active PTH has simplified the assessment of parathyroid activity. Bone densitometry is a test to determine-the degree of osteoporosis.

Explanation:

The more severe and long-standing is the diabetes, the worse the neuropathy. Distal symmetrical diabetic polyneuropathy is the most common because of its refractoriness to therapy. Diabetic third nerve palsy, proximal neuropathies, compression neuropathy (carpal tunnel syndrome), and autonomic neuropathies can also occur in long-standing diabetes. Diabetic proximal motor neuropathy is vascular in origin because the blood vessels that supply the motor nerves become damaged and result in progressive nerve ischemia. The Diabetes Control and Complications Trial Research Group showed that intensive treatment with insulin injections delays onset and slows progression of diabetic neuropathy, retinopathy, and nephropathy. Very little can be done to restore sensation, but foot ulcers.
Osteomyelitis and Charcot joints can be prevented by having a physician check the foot every six months and by keeping the toenails clipped and cleaned. Symptoms of pain caused by neuropathy can sometimes be alleviated by adjusting the doses of amitriptyline, phenytoin, desipramine, and topical capsaicin. Topical capsaicin works by inhibiting substance P in the superficial nerve fibers and diminishing the sensation of tenderness.

Explanation:

During chronic total parenteral nutrition, deficiencies in trace elements may manifest. Deficiency in zinc can produce a rash; poor wound healing, alopecia, and taste and smell disturbances. Copper deficiency may manifest as an iron-unresponsive anemia or pancytopenia. Manganese deficiency may present with weight loss, altered hair pigmentation, and low serum triglycerides. Symptoms of magnesium deficiency include: hyperexcitability, dizziness, muscle weakness and fatigue.

Explanation:

The distinctive cell balls described are broken off papillary clusters, and are considered pathognomic of papillary carcinoma of the thyroid. This is the most common form of thyroid carcinoma. It tends to present in the third to fifth decades of life and shows a modest female predominance. Despite its propensity for local lymphatic intrusion (which may cause multifocality of tumor in the thyroid or cervical lymph node metastases) the tumor generally has an excellent prognosis with 90% of the patients having 20 year survival. It is typically associated with a history of radiation to the neck. Pretibial myxedema is associated with Graves´s disease, the most common form of hyperthyroidism. Weight gain is associated with hypothyroidism. If anything, the patient´s cancer would likely lead to weight loss. Cold intolerance is also associated with hypothyroidism. Heat intolerance is seen with hyperthyroidism, as in patients with Grave´s disease.

Explanation:

Ovarian cancer does not produce hirsutism. However, hirsutism is a common component of polycystic ovaries, congenital adrenal hyperplasia, Cushing´s syndrome, and minoxidil.

Explanation:

This patient is likely undergoing menopause. Drenching night sweats and daytime sweating (“hot flashes”) are very common, as are occasional mood changes. A patient with a systemic infection, such as miliary tuberculosis, AIDS, or subacute bacterial endocarditis, would be likely to have some anorexia, weight loss, true fevers, and other manifestations of the constitutional illness. Hyperthyroidism is not associated with such pronounced sweating.

Explanation:

Explanation:

Maternal iodine deficiency is responsible for cretinism. Plumbism is lead intoxication. Wilson´s disease is a genetic abnormality of ceruloplasmin which results in abnormal copper metabolism. Cystic fibrosis and maternal anemia also are not related to cretinism.

Explanation:

This patient has low calcium which could be due to either Vitamin D deficiency or hypoparathyroidism.
The most likely cause in a young patient who has otherwise been quite well with normal renal function would therefore be hypoparathyroidism. Urine calcium concentrations are useful in familial hypercalciuric hypocalcaemia (as opposed to the more common familial hypocalciuric hypercalcaemia).

Explanation:

TSH has been recognized as an exquisitely sensitive indicator of thyroid status. A normal TSH result suggests adequate thyroid hormone replacement and euthyroidism. Similarly elevated TSH with normal thyroid hormone concentrations would suggest poor compliance and suppressed TSH with normal high T4 suggests over-replacement.

Explanation:

This patient is likely to have anaplastic carcinoma of the thyroid with compression/ infiltration of the trachea. This is unlikely to be a multinodular goiter as this would be unlikely to compress the trachea unless retrosternal and the description is more compatible with a thyroid malignancy. Medullary thyroid cancer is associated most often with MEN II and would be particularly unusual. Again follicular would be unlikely to produce such marked infiltrative features in such a short period of time. Typically patients with follicular disease would present with a nodule and/or LAP.

Explanation:

Thyrotoxicosis with a high 24-hours radioactive iodine uptake (RAIU) is caused by Graves´ disease, toxic multinodular goiter, a solitary hot nodule, a TSH-secreting pituitary tumor, molar pregnancy, and choriocarcinoma. Thyrotoxicosis with a low 24-hour RAIU may be the result of subacute thyroiditis, sporadic silent thyroiditis, postpartum lymphocyctic thyroiditis, radiation-induced thyroiditis, iodine-induced thyroiditis, thyrotoxicosis factita, metastatic follicular thyroid cancer, and struma ovarii.

Explanation:

A pheochromocytoma is a catecholamine secreting tumor of chromaffin cells typically located in the adrenals. It causes persistent or paroxysmal hypertension.
Common symptoms and signs are paroxysms of tachycardia, diaphoresis, postural hypotension, tachypnea, cold and clammy skin, severe headache, angina, palpitations, nausea, vomiting, epigastric pain, visual disturbances, dyspnea, paresthesias, constipation, and a sense of impending doom. Diagnosis is by measuring catecholamine products in blood or urine. Imaging tests, especially CT or MRI, help localize tumors. Treatment involves removal of the, tumor when possible. Drug therapy for control of BP includes alpha-blockade, possibly combined with β-blockade. Ectopic amylase production by lung, ovary, pancreas, and colon malignancies; pheochromocytoma; thymoma; multiple myeloma (increased salivary amylase); and breast cancer (increased pancreatic amylase) are miscellaneous causes of hyperamylasemia.

Explanation:

Hypocalcemia is not associated with ingestion of Aminophylline. It can be a manifestation of magnesium deficiency (A) pancreatitis (B), hypoparathyroidism (C), and acute rhabdomyolysis (D).

Explanation:

Chronic high dose corticosteroid ingestion does not cause hyperthyroidism, but diabetes mellitus, osteoporosis, thrush, and cataracts are all potential side effects of steroid treatment.

Explanation:

Explanation:

Acetaminophen does not affect the glucose tolerance test. Nicotine and caffeine can produce apparent hyperglycemia during a glucose tolerance test, while ethanol and aspirin can produce low glucose levels.

Explanation:

First degree heart block is not associated with hypocalcemia. The electrocardiographic finding that is associated with hypocalcemia is a prolonged QT interval. Tetany, seizures, bronchospasm, and paresthesias all are manifestations of hypocalcemia.

Explanation:

This lady has eunatraemia, hypertonicity (high serum osmolality) inappropriately dilute urine) which is consistent with Diabetes insipidus. Of the drugs listed Lithium would be the most likely cause a nephrogenic DI.

Explanation:

Beta blockers and spironolactone need to be discontinued prior to measuring aldosterone and renin concentrations. Beta-blockers cause elevation of the renin concentrations and hence produce a spuriously low PRA: Aldosterone ratio. ACE inhibitors on the other hand may actually improve the sensitivity of the test.

Explanation:

Generally, if patients are not using insulin, sulphonylureas or glinides (Repaglinide or Netaglinide), then the consensus does not recommend self-monitoring of blood glucose levels. With respect to insulin titration however, self monitored blood glucose results play a crucial part in appropriate dose adjustment. The consensus recommends a target of between 3.9 and 7.2 mmol/l for fasting and pre-prandial glucose levels. If fasting levels are in range yet the HbA1c is elevated, post-prandial monitoring is recommended, aiming for glucose levels of less than 10 mmol/l

Explanation:

Explanation:

This patient has uncontrolled glycaemia despite the current dose of Insulin glargine, oral hypoglycaemic therapy and dietary intervention. Rosiglitazone is already contraindicated because of the history of heart failure and the use of insulin. The current basal insulin regime of the insulin analogue detemir is failing to control his glycaemia; however the current dose is inadequate. Current practice would favour increasing the dose of detemir aiming for a fasting (pre-breakfast) BM of <7.0. Only once fasting readings of this level are achieved, (with a sub optimal HbA1c), would one think of adding a prandial insulin. The caveat would be nocturnal hypoglycaemia, in which case a chance the insulin regime would be warranted, however this was not mentioned in the vignette.

Explanation:

This patient is likely to have secondary hypoadrenalism following his pituitary surgery or his radiotherapy. Hypopituitarism may develop indolently after radiotherapy and patients should be monitored closely for this potential complication. He requires hydrocortisone replacement therapy at a physiological dose – 10 mg/5 mg/5 mg, mimicking the diurnal cortisol profile. This diagnosis should not be missed as the consequences may be catastrophic. Hydrocortisone replacement is an urgent measure which may be life-saving, testosterone and thyroxine replacement should then be considered.

Explanation:

In the treatment of CAH the lowest dose of glucocorticoid that suppresses (not totally) adrenal androgens, whilst maintaining normal growth and weight gain, is the optimum dose of glucocorticoid replacement. Renin activity levels can be used to monitor adequacy of mineralocorticoid and sodium replacement. Hydrocortisone has a relatively short half life and must therefore be administered twice daily, whilst the preferred mode of glucocorticoid replacement in children is hydrocortisone as it minimises growth suppression. Over treatment with mineralocorticoids leads to hypertension, suppressed plasma rennin activity and possibly growth retardation.

Explanation:

Metoclopramide acts as a dopamine antagonist. Dopamine inhibits the release of prolactin from the anterior pituitary gland. Therefore, metoclopramide can predispose to hyperprolactinaemia and consequent galactorrhoea.

Explanation:

The most likely diagnosis is steroid induced hypogonadism. Body builders may be involved in the illicit use of anabolic and androgenic steroids. These results are consistent with ongoing use of androgens. The hypogonadism if persistent may be treated with human chorionic gonadotropin. In the event of a non-functioning pituitary tumour, the testosterone would be low together with the LH and FSH, and an MRI of the pituitary would not miss this diagnosis. The GH axis would also be likely to be suppressed, and a low IGF-1 would result. In the event of androgen insensitivity, the patient may appear phenotypically female. One would expect a low testosterone in isolated gonadotrophin deficiency. Kallman´s syndrome results in hypogonadotrophic hypogonadism. A teratoma is unlikely to cause hypogonadotrophic hypogonadism.

Explanation:

MAS are capillary aneurysms. Haemorrhages are collections of exudated lipid and protein. C is correct; multiple CWS are a pre-proliferative sign. Haemorrhages (or HEs) close to the fovea represent a risk of macular oedema and are therefore sight threatening Laser destroys ischaemic but viable retina to reduce the secretion of angiogenic growth factors and allow new vesel regresion, it is not applied directly to new vessels as this would cause bleeding.

Explanation:

This is a tough question as a number of answers are possible. This young asthmatic has a hypokalaemic hypertension and I´m assuming that his hypertension is sustained. This would therefore suggest a secondary cause which may be either hyperaldosteronism or pseudohyperaldosteronism. A rare CAH 11-beta hydroxysteroid dehydrogenase (11-BHSD) deficiency) may be responsible for hypokalaemic hypertension and the presentation is variable ranging from birth to adulthood but typically birth. Bartter´s syndrome is not associated with hypertension. Conn´s syndrome is usually found in middle aged patients and would be unusual in a patient of this age but even so is probably the best answer here. Liquorice ingestion could again fit this picture but would again be somewhat unusual in this patient. Salbutamol may cause hypokalaemia particularly when given via nebuliser or particularly IV but should not produce hypertension.

Explanation:

This patient is likely to have Cushing´s syndrome. It is a difficult choice between an overnight dexamethasone suppression test and the urine free cortisol estimation but on balance, the simplest test would be urine free cortisol assessment. In the dexamethasone suppression test 25-30 micrograms/kg is used (maximum 2mg), so the amount suggested in this question is too small. 9 am cortisol and adrenocorticotropic hormone (ACTH) concentrations will not confirm the diagnosis. A short Synacthen test is used to confirm hypoadrenalism.

Explanation:

This patient is likely to be insulin resistant; however there is evidence of heart failure and fluid overload, so use of thiazolinediones (Rosiglitazone or Pioglitazone) are absolutely contraindicated. These drugs promote fluid retention by means of an action on the collecting ducts of the kidney so promoting sodium and water retention. The only appropriate action therefore is to stop Rosiglitazone, substituting this with the insulin secretagogue gliclazide which will hopefully improve his glycaemic control.

Explanation:

This patient has fairly good glucose control with the exception of her 11 AM glucose measurement. These pre-lunch sugars reflect her morning regular insulin dose. AM regular insulin will peak in 2 to 4 hours, which should coincide with the increased serum glucose that occurs after eating and digesting breakfast. Increasing AM regular insulin would therefore be helpful in decreasing her 11 AM blood sugars.
Patients with type I diabetes do not respond well to oral medications. This is because the mechanism for their poor glucose control is different from that found in type II diabetes. Type I patients have no problem with insulin resistance and no ability to increase their own insulin production; therefore, conventional oral diabetes medication will not be effective.
Because our patient´s 4 pm sugars are fairly well controlled, adjusting her pre-breakfast NPH is incorrect. The 4 PM glucose measurements are a reflection of the patient´s morning NPH insulin dose. Remembering that the peak action of NPH insulin is 6 to 12 hours after administration should help one remember that the NPH in the morning will help the patient control the glucose surge that occurs after lunchtime. We risk hypoglycemia by increasing the NPH at this time.
Increasing pre-dinner regular insulin is incorrect. Our patient´s 9 PM sugars are a reflection of pre-dinner regular insulin doses. Although our patient does have elevated glucose on Sunday, the remainder of her blood sugars at 9 PM is excellent. This isolated hyperglycemic episode might be caused by a dietary indiscretion on Sunday night. Further history would likely clarity.
Making no changes at this time is not appropriate because our patient is a young woman with long history of diabetes. Good glucose control in this patient may prevent or delay the complications of diabetes, including blindness and kidney disease. Our goal should be to mimic the blood sugars of a patient not effected by diabetes.

Explanation:

This patient is thyrotoxic; however, as the non-suppressed thyroid- stimulating hormone (TSH) suggests that this is due to excessive TSH production by the pituitary gland, the possibility of a thyrotroph adenoma must be pursued.
In primary hyperthyroidism the TSH should always be suppressed by negative feedback, which is not the case here. TSH-omas are indeed very rare, but the giveaway would be the normal or elevated TSH with thyrotoxicosis.

Explanation:

Explanation:

Hypothyroidism is thyroid hormone deficiency. It is diagnosed by clinical features such as a typical facies, hoarse slow speech, and dry skin, and by low levels of thyroid hormones. Management includes treatment of the underlying cause and administration of thyroxine.

Explanation:

A patient who is compliant with his diet and his insulin, tests his blood as directed, and still has glucose levels that are out of control is the best candidate for implantation of an insulin pump that would provide continuous administration of insulin. Use of the pump is neither necessary nor medically appropriate in any of the other types of patients.

Explanation:

Insulin resistance may result from prereceptor, receptor, or postreceptor abnormalities. In diabetics with full-blown resistance, prereceptor resistance to insulin antibodies is present (A). Obesity the most common cause of insulin resistance, a postreceptor defect, with failure to activate tyrosine kinase, is present (B). Leprechaunism is associated with mutations in the insulin receptor (E). Several syndromes have been associated with acanthosis nigricans. In the type A syndrome affecting young women with reproductive abnormalities, mutations of the insulin receptor have been described. In type B women, insulin resistance results from blocking antibodies to the insulin receptor (D). A rare disorder, pineal hyperplasia syndrome, is associated with insulin resistance (C).

Explanation:

While Hand-Schuller-Christian disease (A), Letterer-Siwe disease (B), and eosinophilic granuloma (C) are all subtypes of Langerhand´s cell histiocytosis, the classical triad of Hand-Schuller- Christian disease is skull lesions, diabetes insipidus, and exopthalmus. Letterer-Siwe disease can also present this way; however, it occurs predominantly in males. Eosinophilic granulomas can occur in men and women, as well as children; however, typically the skull lesions are unifocal. Waldenstrom´s macroglobulinemia (D) and cryoglobulinemia (E) do not present in this way.

Explanation:

Drugs and medications used in the treatment of diabetes may produce hypoglycemia, particularly if “tight” control is undertaken. Propranolol decreases the glycogenolytic response to epinephrine and blunts awareness of hypoglycemia due to epinephrine release. Diabetic persons are more likely than those of the general population to develop polyglandular autoimmune deficiency, with its associated adrenal insufficiency. Hypoglycemia results from high levels of circulating insulin antibodies. Renal disease produces hypoglycemia through decreased clearance of drugs, anorexia associated with renal failure, and through reduced gluconeogenesis. The Smogi phenomenon refers to rebound hyperglycemia following an episode of hypoglycemia due to counter-regulatory release. Changing exercise patterns resulting in a haphazard fashion may precipitate hypoglycemia.

Explanation:

Development of diabetic ketoacidosis results from the combination of insulin deficiency and excessive secretion of counterregulatory hormones. The most important of these is glucagon. Other counterreulatory hormones are catecholamines, growth hormone, and cortisol. Prolactin, vasopressin, thyrotropin, and luteinizing hormone are not counterregulatory hormones.

Explanation:

Metformin is a biguanide used as an oral antidiabetic agent. One of its main advantages over some other oral agents is that it does not cause hypoglycemia. Lactic acidosis, while rare, can occur in patients with renal impairment. In contrast to most other agents for the control of elevated glucose, which often cause weight gain, metformin reduces insulin levels and more frequently has a weight maintaining or even a weight loss effect. Gastrointestinal distress is a common side effect of metformin, particularly early in therapy,

Explanation:

Methimazole is an antithyroid drug similar to propylthiouracil (PTU) used to treat hyperthyroidism. Methimazole inhibits the formation of thyroid hormone by interfering with the incorporation of iodine into tyrosyl residues of thyroglobulin (Tg) and by inhibiting the coupling of iodotyrosyl residues to form iodothyronines. These effects are accomplished by inhibiting the enzyme thyroid peroxidase. When Graves disease is treated with methimazole or PTU, the concentration of thyroid stimulating immunoglobulins in the circulation often decreases, suggesting an immunosuppressive effect. The incidence of agranulocytosis is approximately 1:500. It is recommended that patients immediately report the development of sore throat or fever. Discontinuation of methimazole and administration of recombinant human granulocyte colony stimulating factor may increase recovery. Inhibition of the activity of peptic transferase is part of the mechanism of action of chloramphenicol, which is an antibicterial agent. Inhibition of the production of the vitamin K-dependent clotting factors is the mechanism of action of warfarin. This agent would be detrimental to the patient.

Explanation:

Ten to twenty percent of patients with Crohn disease and ulcerative colitis develop an arthritis that resembles ankylosing spondylitis. Similar arthropathies are seen in psoriasis or Reiter syndrome (arthritis, urethritis, conjunctivitis, and rash following chlamydial infection), as well as related syndromes seen following Shigella, Salmonella, or Yersinia enterocolitis. The other answers are distracters.

Explanation:

Although the lead in might make you think that this patient could gain access to thyroxine and so a diagnosis of factitious hyperthyroidism possible, in practice this is extremely unlikely. A strong family history of thyrotoxicosis is typical for Graves´ disease and the absence of goitre with the absence of TPO antibodies (found in 80% Graves cases) again is compatible with a diagnosis of Graves.

Explanation:

This patient who has typical type 2 diabetes , which should initially be treated with diet and lifestyle advice, appropriate dietary advice and exercise programme to endeavour to achievce weight loss. He should receive at least three months of this intervention before re-assessing and considering pharmacological intervention if the lifestyle approaches are not succeeding. If this is the case then the drug of choice would be metformin.

Explanation:

The metabolic syndrome is becoming hugely important as a cluster of features associated with increased cardiovascular and diabetes risk. The condition is defined by various criteria the latest of which is global definition for the IDF as central obesity (>=94cm for men, >=8 cm for women) plus any two of the following:

• Hypertriglyceridaemia >1.7 mmol/1
• Low HDL concentration <1.03 mmol/l male, <1.29 mmol/l female
• BP > or = 130/85 mmHg, or on treatment for hypertension
• Fasting glucose > or = 5.6 mmol/l, or known to have type 2 diabetes. Thus, in our patient´s case the elevated fasting glucose of 6.3 mmol fulfills this diagnostic criterion. The BMI is not a function of the diagnostic criteria as the waist circumference appears to be a far more powerful predictor of risk.

Explanation:

The history and confirmed polyuria are suspicious of diabetes insipidus which is not uncommon after head injury. This can be confirmed with a water deprivation test where failure of urine concentration would be expected. MRI of the pituitary and hypothalamus may show no abnormality but would be undertaken after the diagnosis of DI is confirmed. Similarly anterior hormone assessment would also be undertaken after the diagnosis is confirmed. A therapeutic trial of DDAVP is only appropriate if the diagnosis of DI is confirmed as primary polydipsia can also be a feature of trauma and in these circumstances DDAVP may precipitate hyponatraemia. Autoantibodies to ADH neurones are irrelevant.

Explanation:

The question of increased cardiovascular risk for sulfonylureas (SUs) was raised after the university group diabetes programme (UGDP) stud conducted during the 1970s. The consensus authors state however that the question ha: since been answered by the UK prospective diabetes study (UKPDS) and ADVANCE studies, where no cardiovascular risk signal was seen for SUs. Whilst SUs are well known to have a rapid onset of glucose lowering effect, their side effects of hypoglycaemia and weight gain are well own.

Explanation:

This man´s HbA1c is high at 9.1%, he has a low high density lipoprotein (HDL) cholesterol, is losing weight, and has a history of microalbuminuria. The two established therapy options at this stage, as stated in the consensus are to either add a sulfonylurea (SU) or insulin. Given his need for greatly improved metabolic control, insulin is the better option here. The guidelines recommend starting with either morning or evening long acting insulin, or with bedtime intermediate acting insulin.

Explanation:

Thin man has a co-incidentally detected pituitary macroadenoma. The small elevation in prolactin probably reflects stalk compression and does not indicate that this is a prolactinoma. In macroprolactinomas, the prolactin concentration is greater than 2000 mU/L. In this man´s case, with no visual field defects and the tumour being distant from the chiasm, the most appropriate treatment would be observation with serial scanning to assess for any change in size that would then merit surgical intervention. However, this man who is eupituitary may never encounter any growth in this co-incidentally detected non-functional pituitary tumor.

Explanation:

The diagnosis of acromegaly is confirmed with a failure of GH Suppression during an oral glucose tolerance test. Though a Pituitary adenoma may be present it is not diagnostic of acromegaly.

Explanation:

The approximate equivalent glucocorticoid action of prednisolone to hydrocortisone is 4:1. Hence the equivalent dose for 20 mg of hydrocortisone is roughly 5 mg per day of prednisolone. For other glucocorticoid dose conversions try this online glucocorticoid dose calculator.

Explanation:

Primary HPT can be divided pathologically into adenoma, hyperplasia, and carcinoma. Adenomas clearly are the most prevalent entity representing 80-85% of cases. Hyperplasia is the second most common diagnosis constituting 15% of cases. Carcinoma represents <1% of total cases. Double adenoma has been found in approximately 5% of the time, and complicates the clinical distinction between adenoma and hyperplasia. Histologically, normal parathyroid tissue shows a cell to fat ratio of 1:1. Hypercellular parathyroid tissue is typified by the loss of the normal amount of fat. In primary hyperparathryroidism there is usually hypercalciuria. Secondary hyperparathyroidism may progress to tertiary but primary does not.

Explanation:

In the treatment of CAH the lowest dose of glucocorticoid that suppresses (not totally) Adrenal androgens, whilst maintaining normal growth and weight gain. Renin activity levels can be used to monitor adequacy of mineralocorticoid and sodium replacement. Hydrocortisone has a relatively short half-life and must therefore be administered twice daily, whilst the preferred mode of glucocorticoid replacement in children is hydrocortisone as it minimises growth suppression. Over treatment with mineralocorticoids leads to hypertension, suppressed plasma rennin activity and possibly growth retardation.

Explanation:

Insulin acts via cell surface receptors. Insulin binding to its receptor results in receptor autophosphorylation on tyrosine residues and the tyrosine phosphorylation of insulin receptor substrates (IRS1, IRS-2 and IRS-3) by the insulin receptor tyrosine kinase. Insulin is synthesised in the beta cells of the Islets of Langerhans not the alpha cells.

Explanation:

Patients who have been on chronic daily oral therapy with prednisone must be tapered slowly, often over many months. Abrupt cessation or very rapid tapering over a short period of time can result in Addisonian crisis. If alternate day use is desired, it must be achieved slowly. An agent such as methotrexate is not substituted for prednisone. It is sometimes given to appropriate patients, such as those with rheumatoid arthritis or lupus, as a remittive agent that has so-called “steroid-sparing” attributes, but it is not used in general as a single-drug therapy, substituting for prednisone.

Explanation:

A picture such as this in a diabetic individual is very likely to be thrush, i.e., candida, which usually responds to ketoconazole. None of the other choices is appropriate.