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Endocrinology_UW Flashcards

1
Q

What is gastroparesis?

A

Delayed gastric emptying.

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2
Q

Diabetic autonomic neuropathy occurs in ?% of patients and how can it manifest?

A

Greater than 50% of patients with longstanding type 1 or 2 DM. Can manifest as esophageal motility (dysphagia), gastric emptying (gastroparesis) or intestinal function (diarrhea, constipation)

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3
Q

What are the symptoms of diabetic gastroparesis?

A

Anorexia, vomiting, nausea, early satiety, postprandial fullness and imparied glycemic control (low blood sugar levels with insulin administration prior to meals).

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4
Q

What meds are useful in managing diabetic gastroparesis?

A

Prokinetic agents such as metoclopramide (has both prokinetic and antiemetic), erythrmocyin, cisapride.

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5
Q

A patient with acute, severe illness with abnormal thryoid tests has what condition? It is due to?

A

Sick Euthyroid syndrome due to caloric deprivation and increased production of cytokine levels. **side note: thyroid function testing not usually done in such patients unless there is clinical suspicion of actual underlying thryoid disease.

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6
Q

What is the most common thyroid hormone pattern in such patients?

A

Remember “low T3 syndrome.” Fall in total and T3 levels, normal T4 and TSH levels. *Side note: decreased T3 due to less peripheral conversion of T4 to T3. If non-thyroidal illness continues then serum T4 and TSH also decrease.

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7
Q

Primary hyperaldosteronism is usually due to?

A

Adenoma or bilateral adrenal hyperplasia

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8
Q

What is the preferred treatment for 1) unilateral adrenal adenoma and 2) bilateral adrenal hyperplasia?

A

1) surgery 2) medical therapy with aldosterone antagonists (eg. Spironolactone, eplerenone)

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9
Q

What is eplerenone?

A

It is a very selective mineralocorticoid (aldosterone) antagonist with a very low affinity for progesterone or androgen receptors and therefore has fewer endocrine side effects compared to spironolactone.

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10
Q

What kind of side effects does spironolactone have

A

it is a progesterone and androgen receptor antagonist and can cause decreased libido, gynecomastia in men and breast tenderness and menstrual irreguaries in women.

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11
Q

Primary hypogonadism vs secondary hypogonadism - testosterone/sperm count and LH/FSH levels?

A

Primary: low testosterone and/or sperm count, above-normal LH and FSH. Secondary (which is central): low testosterone and/or sperm count, low or normal LH and FSH

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12
Q

When patients have elevated serum prolactin, serum testosterone

A

MRI of the pituitary

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13
Q

What is D5W? What it is it used to treat?

A

Hypotonic solution. Used to treat hypernatremia rather than hyponatremia

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14
Q

What are bisphosphonates used to treat?

A

Hypercalcemia, osteoporosis prevention, and adjunctive treatment for certain malignancies.

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15
Q

What is dexamethasone?

A

Glucocorticoid used to treat autoimmune, inflammatory and allergic conditions, and cerebral edema.

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16
Q

Asymptomatic patients or those with mild symptoms of SIADH is treated with?

A

Fluid restriction and or oral salt tablets.

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17
Q

Patients with severe symptoms of SIADH is treated with?

A

Hypertonic (3%) saline

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18
Q

What are the findings of SIADH?

A

Elevated urine omsolality. >100mOsm/kg and urine sodium >40mEq/L. Serum osmolality

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19
Q

What physical findings are found in hyperthryoid patients?

A

Goiter, hypertension, tremors involvings hands/feet, hyperreflexia, proximal muscle weakness, lid lad, afib

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20
Q

What should be suspected in stuporous patients with rapid breathing and a hx of weight loss, polydipsia, and polyuria.

A

diabetic ketoacidosis

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21
Q

Tests done for suspicion of DKA?

A

First fingerstick glucose, then chemistry, ABG, CBC

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22
Q

Aldosterone levels are low/normal/high in 1) central adrenal insufficiency 2) primary adrenal insufficiency?

A

1) central (secondary AI) levels are normal 2) primary: levels are low

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23
Q

Chronic supraphysiologic doses of glucocorticoids cause what kind of adrenal insufficiency? What do lab studies show?

A

Central (or secondary adrenal insufficiency). Lab studies show low ACTH and coristol levels and relatively normal aldosterone levels.

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24
Q

What do lab studies show for primary adrenal insufficiency?

A

Low cortisol, high ACTH, low aldosterone (therefore sodium wasting and hyponatremia, hyperkalemia).

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25
Q

Example of isotonic fluid?

A

0.9% saline

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26
Q

Example of hypotonic fluid?

A

5% dextrose preferred over 0.45% saline.

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27
Q

What is the preferred tx for hypovolemic hypernatremia?

A

IV normal saline (0.9%) - isonotic fluid

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28
Q

What is the preferred tx for euvolemic hypernatremia?

A

5% dextrose preferred over 0.45% saline.

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29
Q

What are the components of MEN type 2A

A

Medullary carcinoma of the thyroid, primary hyperparathyroidism, and pheochromocyoma

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30
Q

What is the recommended screening test for suspected MEN 2 syndromes?

A

Genetic testing (RET proto-oncogene germline mutation). More sensitive than the biochemical measurement (serum calcitonin)

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31
Q

What is the biohemical testing to dx pheochromocytoma?

A

24-hour urine for metanephrines and free catechoalmines or plasma free metanephrines to diagnose pheochromocytoma.

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32
Q

Components of MEN2B?

A

Medullary thyroid cancer, pheochromocytoma, other such as mucosal and intestinal neuromas and marfanoid habitus.

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33
Q

Components of MEN1?

A

Primary hyperparathyroidism (>90%), enteropancreatic tumors (60%-70%), pituitary tumors (10-20%)

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34
Q

What is the function of Vit D as it relates to calcium and phosphate ions?

A

Vit D increases dietary calcium and phosphate absorption, increases bone resoprtion that increases calcium and phosphate ions

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35
Q

Chronic GI disease like steathorrhea, celiac disease can cause vit D deficiency. Patients then usually develop?

A

Hypocalcemia, low phosphorus and elevated PTH (secondary hyperparathyroidism). Patients can be asymptomatic or develop bone pain/tenderness, muscle weakness or cramps, gait abnormalities.

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36
Q

What is doxazosin?

A

Alpha blocker. Used to treat high blood pressure and also BPH

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37
Q

What should be considered before the start of sildanefil?

A

1) contraindicated in patients being treated with nitrates and those hypersensitive to sildanefil 2) used with caution in patients with conditions predisposed to priapism 3) concurrent use of drugs that interfere with sildanefil metabolism (erythrmomycin, cimetidine) 4) combination with alpha blocker (liek doxazosin) - need to give drugs with at least 4 hour interval to reduce risk of hyotension.

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38
Q

What is the main tx for most patients with prolactinoma?

A

Dopamine agonists such as bromocriptine or cabergoline (newer drug with lower side effects). Same tx for micro prolactinoma (smaller than 10mm) or macroprloactinoma. Leads to normalization of prolactin levels and also reduction in tumor size.

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39
Q

What are examples of dopaminergic agents?

A

Bromocriptine and cabergoline

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40
Q

Elevated levels of which androgen are specifically seen in patients with androgen producing adrenal tumors?

A

Dehydroepiandrosterone-sulftate (DHEA-S)

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41
Q

What are the risk factors for diabetic foot ulcers?

A

Diabetic neuropathy, previous foot ulceration, vascular disease, and foot deformity. Diabetic neuropathy is the most important contributing factor and found in >80% of patients with ulcers.

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42
Q

What test assess patient’s risk of foot ulcers?

A

Monofilament testing => test for pressure sensation using a 10g monofilament (placed on plantar surface at right angle with increasing pressure until filament buckles).

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43
Q

What is virilization?

A

Development of male physical characteristics (muscle bulk, body hair, deep voice) in a female or precociously in a boy, typically due to excess androgen production.

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44
Q

Rapidly developing hyperandrogenism with virilzation is highly suggestive of?

A

Androgen secreting neoplasm of the ovary or adrenal glands.

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45
Q

Testing for what levels is helpful in delineating site of excess androgen production?

A

Testosterone and DHEA-S. High levels of testosterone with normal levels of DHEA-S suggests ovarian source of androgens. High levels of DHEA-s with normal testosterone levels suggests adrenal source.

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46
Q

Untreated hyperthryoid patients are at risk for developing?

A

Rapid bone loss due to increased osteoclastic activity in the bone cells and also for cardiac tachyarrhythmias, including afibrillation.

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47
Q

Increased thryoid hormone levels with suppressed TSH levels, selective radioactie iodine scan suggests dx of?

A

Toxic adenoma. Toxic adenoma presents with symptoms suggestive of thyroid toxicosis.

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48
Q

What is hypercalcemia of immobilization?

A

Unclear underlying mechanism but likely due to increased osteoclastic bone resorption. Risk is increased in immobilized patients with high bone turnover(young individuals, older individuals with paget’s disease). Onset of hypercalcemia depends on the balance between the magnitude of bone turover and renal calcium excretion but th emedian onset is around 4 weeks after immobilization.

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49
Q

What is used to reduce hypercalcemia and prevent osteopenia in immobilized patients?

A

Bisphosphonate therapy and hydration.

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50
Q

What is the preferred initial screening test for primary hyperaldosteronism

A

Plasma aldosterone concentration/plasma renin activity. Ratio of greater than 20 with plasma aldosterone >10ng/dL suggests primary hyperaldosteronism.

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51
Q

What tests can confirm diagnosis of primary hyperaldosteronism?

A

Adrenal suppression testing which usually involves salt loading and inability to suppress aldosterone.

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52
Q

What is the most sensitive test to distinguish between adrenal adenoma and bilateral adrenal hyperplasia in patients without discrete unilateral adrenal mass on imaging?

A

Adrenal venous sampling

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53
Q

What is the immediate treatment of choice for patients with symptomatic moderate (12-14mg/dL) or severe hypercalcemia (>14mg/dL)?

A

IV saline hydration. It helps restore intravascular volume and promotes urinary calcium excretion.

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54
Q

What other treatments are used for hypercalciemia?

A

Calicotonin reduces serum calcium concentration within 4-6 hours and should be administered with IV saline. Bisphosphonates are recommended for long-term management in addition to tx of underlying cause.

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55
Q

What are the symptoms of significant hyperalcemia?

A

Polyuria, polydipsia, nausea, vomiting and constipation

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56
Q

Hypercalcemia of malignancy can be due to what?

A

Increased tumor production of PTH-rP (90% of malignancy induced hyperalcemia), osteolytic metastasis with local cytokine production (IL-6 levels, IL-3, Rank-L, TNF-alpha, macrophage inflammatory factor 1-a), increased tumor production of 1,25 dihydroxyvitamin D, or ectopic PTH production.

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57
Q

What are the PTH levels like in hypercalcemia of malignancy?

A

Low/suppressed

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58
Q

How are serum calcium levels in hypercalcemia of malignancy vs. primary hyperparathyroidism?

A

Generally much higher >13mg/dL.

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59
Q

What happens to total body K+ stores in DKA?

A

depletion of K+ body stores due to osmotic diuresis even though serum K+ level may be elevated.

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60
Q

KNOW THE CLINICAL PRESENTATION OF DKA

A

Metabolic acidosis, polyuria, dehydration, decreased level of consciousness, and diffuse abdominal pain

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61
Q

What a patient presents with hypokalemia, alkalosis and normotension, what should be suspected? What test can be used/measured to distinguish the etiologies?

A

Surreptitious vomiting, Diuretic abuse, Bartter sydnrome and gitelman’s syndrome. Urine chloride concentration. All etiologies besides vomiting has high chloride concnetration.

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62
Q

How does vitamin D deficiency affect intestinal calcium, phosphorus absorption and PTH?

A

Leads to decreased intestinal absorption of calcium and phosphorus with resultant secondary hyperparathyroidism. Typical labs are hypophosphotemia, hypocalcemia, and elevated alkaline phosphatase.

63
Q

What is the most common cause of death in patients with acromegaly?

A

Cardiovascular, accounting for 38-62% of deaths

64
Q

Patients with primary hyperaldosteronism typically present with what? Also, what are their renin levels like?

A

Mild hypernatremia, hypokalemia, metabolic alkalosis and low renin levels.

65
Q

Generally, every 1% increase in HbA1c corresponds with what increase in the mean plasma glucose level?

A

35mg/dL

66
Q

Paget’s disease is characterized by what kind of bone problem? Also, what levels are high?

A

Chracterized by abnormal bone remodeling - initially localied excess osteoclastic bone resoprtion followed by disorganized bone formation by osteoblasts => chaotic mosic pattern of lamellar bone and woven bone. Isolated elevated levels of alkaline phosphatase

67
Q

Paget’s disease patients are mostly symptomatic or asyptomatic?

A

Asymptomatic

68
Q

What are the possible manifestations of paget’s disease?

A

Headaches, increased head size, hearing loss, compression of cranial nerves, spinal cord, or spinal nerve roots, bone pain, spinal stenosis, bowing deformities with increased fracture risk.

69
Q

Lab data for Paget’s disease show?

A

Elevated alk phosphatase but normal calcium, phosphorus and other liver enzymes (like GGT)

70
Q

How are symptomatic patients with Paget’s disease treated? How are asymptomatic patients treated?

A

Oral or IV aminobisphosphonates. Asymptomatic pateints involving non-weight bearing bones generally do not require treatment.

71
Q

What is the MOA for bisphosphonates?

A

Inhibit osteoclasts to suppress bone turnover and are the preferred therapy for Paget’s disease. Clinical response (decrease in bone pain) often seen before decrease in Alk Phos

72
Q

Hypocalcemia in alcoholics can be caused by decreased levels of which electrolyte?

A

Hypomagnesemia => causes hypocalcemia.

73
Q

How does hypomagnesemia cause hypocalcemia?

A

Etiology of hypomagnesemia in alcohlics is multifactorial - urinary losses, malnutrition, acute pancreatitis, and diarrhea. Hypomagnesemia causes resistance to PTH as well as decreases PTH secretion.

74
Q

Hypoparathyroidism induced by low magnesium is not associated with elevated what levels unlike other causes hypoparathyroidism

A

Phosphorus levels. Remember that PTH decreases phosphate resabsorption in proximal convoluted tubule. Therefore decreased PTH generally leads to increased phosphorus levels.

75
Q

What is the most common type of neuropathy found in diabetics?

A

Symmetric distal sensorimotor polyneuropathy - characterized by classic “stocking glove” pattern of sensory loss. Diabetics can also have monomeuropathies of cranial and peripheral nerves.

76
Q

What drug has been shown to have a beneficial effect on slowing the progression fo diabetic neuropathy?

A

Addition of ACE inhibitors to tx regime.

77
Q

Serum calcium concentration decreases by ? for every 1g/dL decrease in serum albumin

A

serum calcium concentration decreases by 0.8mg/dL for every 1g/dL decrease in serum albumin

78
Q

Developmemt of nephropathy is preceded by development of?

A

Excess protein secretion, the initial syages of which is called microalbuminuria

79
Q

What is considered generally acepted screening method for microalbuminuria?

A

Spot urine collection and timed urine collection for measurement of urine microalbumin/creatinine ratio.

80
Q

What is the screening for diabetes recommendation?

A

Sustained blood pressure > 135/80mmHg (USPSTF) and may also be considered in all patients over age 45 (ADA)

81
Q

What is the preferred treatment for most patients with Graves’ disease? What are the contraindications to this therapy?

A

Radioactive iodine therapy. Contraindications = pregnancy and severe opthalmopathy.

82
Q

What is the most common side effect of radioiodine therapy?

A

Hypothyroidism. Occurs from the destruction of thyroid follicles by radioactive iodine. But hypothyoridism is easily treated by levothyroxine therapy.

83
Q

What is cosyntropin?

A

Synthetic ACTH analogue

84
Q

What is the best initial screening test for patients with suspected adrenal insufficiency? What result rules out primary adrenocortical insufficiency (Addison’s disease)

A

Early morning cortisol, ACTH and cosyntropic (analogue of ACTH) stimulatio. Increase in serum cortisol (>20 microg/dL 30-60 minutes after the administrtation of 250 micrograms of cosyntropin) virtually rules out primary adrenocortical insufficiency)

85
Q

What is the most characteristic physical finding of chronic adrenal insufficiency?

A

Increased hyperpigmentation

86
Q

Patients with PCOS are at increased risk for developing?

A

Insulin resistance and T2DM

87
Q

What is the preferred method of screening for glucose intolerance and T2DM?

A

75g 2 hour oral glucose tolerance test (OGTT). If this is not feasible, fasting blood glucose and glycated hemoglobin can be obtained but these are not as sensitive in detecting glucose intolerance.

88
Q

What additional metabolic abnormalities can hypothyroidism cause?

A

Hyperlipidemia, hyponatremia (due to decreased free water clearance) and asymptomatic elevations of creatinine kinase and serue transaminases (ALT and AST). Most patients have hypercholesterolemia alone (due to decreased LDL surface receptors/and or decreased LDL receptor activity) or conbined with hypertriglyceridemia (due to decrased lipoprotein lipase activity).

89
Q

Patients with hypothryoidism tht start oral estrogen (OCPs or estrogen replacement therapy) have an increased need for?

A

Levothryoxine beause oral estrogen leads to decreased clearance of thyroxine binding globulin (TBG) => leading to elevated TBG levels. Therefore patients need increased dose to saturate the increased number of TBG binding sites.

90
Q

What are the drugs of choice for diabetic neuropathy? What symptoms can they worsen, however?

A

Tricyclic antidepressants such as amitryptiline, desipramine, nortriptyline. Urinary symptoms (cystopathy) and orthostatic hypotension (due to cardiovascular autonomic neuropathy).

91
Q

What are alternative drugs used to treat diabetic neuropathy

A

Gapabentin, NSAIDS (but watch for renal dysfunction)

92
Q

Systolic hypertension in thryotoxicosis is caused by what?

A

Hyperdynamic circulation from Increased mycoardial contractility and heart rate

93
Q

Patients with Hashimoto’s thyroiditis is at increased risk for what kind of cancer?

A

Lymphoma

94
Q

In contrast to patients with primary adrenal insufficiency, adrenal insufficiency due to hypopituitarism is not a/w? why?

A

Hypoaldosteronism. This is because aldosterone secretion from the adrenal glands is ACTCH-independent and primary regulared by renin-angtiotension axis. Therefore serum K is normal.

95
Q

What is hypopituitarism characterized by?

A

Glucocorticoid deficiency, hypogonadism, and hypothryoidism.

96
Q

The clinical manifestations of vit D toxicity are mainly due to what condition? What are the manifestations?

A

Hypercalcemia. Characteristic features of hypercalcemia - constipation, abdominal pain, polydipsia and polyuria.

97
Q

What are potassium stores like for patients with HHS or DKA? Why?

A

HHS and DKA patients can have elevated serum potassium levels but depleted potassium stores due to excessive urinary loss caused by glucosuria induced osmotic diuresis.

98
Q

What should always be considered in patients with unexplained elevation of serum creatinine kinase concentration and myopathy?

A

Hypothyroidism.

99
Q

What is the most sensitive test to diagnose hypothyroidism?

A

TSH levels.

100
Q

Best initial test for patients with suspected hyperthyroidism

A

TSH levels.

101
Q

If TSH is low and free plasma T4 is high, what is the diagnosis? If the diagnosis is confirmed, what test should then be done?

A

Clinical hyperthyroidism. 24 hour thyroid radioiodine uptake and scae to differentiate Grave’s hypertheyoridism from other causes.

102
Q

What drug tx is used for symptomatic relief untl the underlying cause of hyperthyroidism is identified?

A

Propanolol

103
Q

What are the most common causes of thyrotoxicosis with reduced uptake of radioiodine?

A

1) Subacute lymphocytic thyroiditis (painless). Usually seen in post partum. 2) subacute granulomatous thyroiditis 3) levothyroxine overdose 4) iodine-indied thyrotoxicosis.

104
Q

What test can distinguish between central and nephrogenic diabetes insipidus?

A

Water depriviation test

105
Q

What test can definitively rule out primary polydipsia

A

Water deprivation test

106
Q

What results of the water deprivation test show central diabetes insipidus?

A

If urine osmolality increases by at least 50% following desmopressin administration. Nephrogenic diabetes show no to little change.

107
Q

Factiious thryotoxicosis has what levels for the following? TSH, RAIU, T3/T4, RAIU, serum thryoglobulin

A

Low TSH, high T3 or T4 or both depending on what is being taken, RAIU, low serum thyroglobulin (diagnostic)

108
Q

During metaboilc acidosis during DKA, is the patient typically hypo or hyperkalemic and why?

A

Hyperkalemic. Body potassium reserves are depleted due to increased GI losses and osmotic diuresis. 1) extracellular shift of potassium in exchange to hydrogen ion 2) imparied inulin dependent cell entry of the potassium ion. Early potassium supplementatoin is very important i the treatment of patients with DKA.

109
Q

What cell is the principal source of testosterone?

A

Leydig cells

110
Q

In Leydig cell tumors, what production is increased? This leads to inhibition of what?

A

Estrogen production is increased. Leydig cells can make estrogen due to increased aromatase expression. This leads to inhibition of FSH and LH.

111
Q

What level of prolactin is virtually diagnositc of a prolactinoma

A

> 200ng/mL (serum levels of prolactin generally correlate with the size of the prolactinoma)

112
Q

Function of thyrotropin releasing hormone (from hypothalamus)

A

Stimulates release of TSH AND proalctin

113
Q

What is the most common pituitary tumor?

A

Prolactinoma

114
Q

What is the most beneficial therapy to reduce the progression of diabetic nephropathy?

A

Strict bp control. Treat towards target BP of 130/80mm Hg. This primary intervention slows the decline in GFR once azotemia develops.

115
Q

Thyroid stimulating hormone secreting pituitary adenoma is characterized by what kind of levels of TSH and thyroid hormone?

A

Central hyperthyroidism with elevated thryoid hormone and normal/elevated TSH.

116
Q

What kind of symptoms is it associated with?

A

Sx due to mass effect, including headache, visual field defects and impaired function of surrounding pituitary tissue.

117
Q

What is the most important step in the management of non-ketotic hyperglycemic coma

A

Fluid replacement with normal saline and then replaced with 0.45% saline.

118
Q

When treating patients with pheochromocytoma, what drugs are preferred to decrease the blood pressure

A

alpha-blockers are preferred. DO NOT GIVE BETA-BLOCKERS FIRST. Will cause hypertensive crisis. Give alpha-blocker, followed by beta blocker. Blocking beta-receptors leads to unopposed stimulation of vascular alpha-receptors by circulating catecholamines.

119
Q

How do glucocorticoids help blunt hyperthyroid symptoms?

A

It decreaeses the peripheral conversion of T4 to T3 (biologically active thyroid hormone)

120
Q

What are the three main tx options for Graves’ disease?

A

1) Radioactive iodine 2) antithryoid drugs (propylthiouracil, methimazole) and 3) thryoidectomy

121
Q

Which hyperthyroid tx is a/w potential development/worsening of Graves opthalmopathy

A

radioactive iodine. In first few days after RAI, the destroyed thyroid cells release excess thyroid hormone => temporariiy worsens the hyperthyroid state. Pretreatment with glucocorticoids prevents worsening of disease.

122
Q

What is the most common type of thyroid cancer? What are the risk factors?

A

Papillary carcinoma of the thyroid is the most common thryoid malignancy. Risk factors = family history,exposure to radiation during childhood.

123
Q

What is recommended for patients with asymptomatic primary hyeprparathyroid patients?

A

Parathyroidectomy for patients with asymptomatic PH and at least one of the following 1) serum calcium >=1mg/dL above upper limit of normal 2) young age

124
Q

Diagnosis of hyperosmolar hyperglycemic state is diagnosed by?

A

High serum glucose levels (>600mg/dl), plasma osmolality (>320mOsm/L) and absent ketonemia.

125
Q

Unlike osteoporosis, patients with osteomalacia complain of?

A

Bone pain and muscle weakness

126
Q

What are the x ray findings for osteomalacia

A

Decreased bone density with thinning of cortex and pseudofractures (looser zones)

127
Q

For patients with osteomalacia what are the levels for 1) calcium 2) phosphate 3) serum PTH 4) 25-OH vit D levels 5) Alk phos

A

1) low to normal 2) low 3) high 4) low 5) elevated.

128
Q

What are the main substrates of gluconeogenesis

A

1) gluconeogenic amino acids (alanine, glutamine for example) 2) lactate (from anaerobic glycolysis) and 3) glycerol-3-phosphate (from triacyleglycerol in adipose).

129
Q

What is alanine converted to in gluconeogenesis

A

Pyruvate. Lactate is also converted to pyruvate.

130
Q

In respiratory alkalosis, what happens to ionized calcium? Why?

A

Respiratory alkalosis (this can happen in PE) => dissociation of H+ from albumin thereby freeing up albumin to bind to calcium => leads to drop in ionized serum calcium levels.

131
Q

What suggests agranulocytosis in a patient taking anti-thyroid drugs?

A

Fever and sore throat.

132
Q

What is the current recommendation of actio when patient complains of fever and sore throat after starting anti-thyroid meds?

A

Discontinue drug asap and measure WBC count. Total of less than 1000 / cubic mm warrants permanent discontinuation of the drug.

133
Q

Histopathologically, what is needed to differentiate follicular cancers from follicular adenomas?

A

Invasion of blood vessels and capsule.

134
Q

generalized resistance to thyroid hormone is chharacterized by what kind of 1) T4 / T3 levels and 2) TSH levels? Patients have features of what kind of thyroidism?

A

1) high T4/T3 levels 2)normal to mildly elevated TSH levels. Patients generally have features of hypothyroidism despite elevated free thryoid hormones.

135
Q

What effect does PTH have on phosphate?

A

Decreases reabsorption of phosphate in proximat convoluted tubule / i.e. increases excretion of phosphates.

136
Q

What is the most common cause of hypercalcemia in the ambulatory setting?

A

Primary hyperparathyroidism.

137
Q

Hypercalcemia due to primary hyperparathyroidism is a/w what levels of serum PTH and phosphorums?

A

Serum PTH is elevated or inappropriately low. Hypercalcemia in primary hyperparathyroidism does not significantly suppress PTH secretion from the autonomously functioning adenomatous or hyperplastic parathyroid glands. Serum phosphorus may be low or normal.

138
Q

What antibodies are present in patients with Hashimoto’s thyroiditis?

A

Anti-thryoid peroxidase and anti-thyroglobulin antibodies.

139
Q

What urine and plasma osmolality is diagnostic of SIADH in suspected patients?

A

Low plasma osmolality (100-150 mOsm/Kg) in suspected patients is diagnostic.

140
Q

What is the preferred screening test for acromegaly?

A

o IGF-1 is the preferred screening test for acromegaly and not growth hormone levels due to wide fluctiations in ciriculating levels.

141
Q

What is the most sensitive dynamic test for acromegaly

A

Measurement of NON-SUPPRESSIBLE growth hormone levels following an oral glucose load. Typically performed after IGF-1 levels are measured.

142
Q

Classic triad for pheochromocytoma?

A

Diaphoresis, headache and tachycardia.

143
Q

What is a thyroid storm?

A

Life threatening thyrotoxicosis triggered by a a specific event (thryoid or non-thyroid surgery, trauma, infection, iodine contrast, childbirth).

144
Q

What do patients present with in a thyroid storm?

A

Tachycardia, hypertension, arrhythmias, high fever, tremor, altered mentation and lid lag.

145
Q

What is the recommendation for statins for diabetic patients age 40-75 WRT lipid levels.

A

Receive statin treatment regardless of baseline lipid levels. Dose intensity depends on overall risk of cardiac events.

146
Q

What is the screening test for primary hyperaldosteronism?

A

Early morning plasma aldosterone / plasma renin ratio > 20 and plasma aldosterone >15ng/dL

147
Q

Propotosis in Graves results from?

A

Increased retor-orbital tissue volume. Direct result of anti-TSH receptor autoantibodies.

148
Q

What are the essential measures in the management of DKA

A

Steps 1 and 2 most important and appropriate initial management! 1) Restoration of intravascular volume: using 0.9% (normal) saline 2) Correction of hyperglycemia: using IV regular insulin 3) Correction of electrolyte imbalances. Potassium correction is essential.

149
Q

High dose dexamethasone suppression test is used to distinguish between?

A

Cushing’s disease and ectopic ACTH production.

150
Q

Cushing’s syndrome due to ectopic ACTH production is characterized by?

A

Rapid onset of symtpoms, hypokalemic alkalosis, pigmentation and hypertension. Serum cortisol and urine cortisol levels are not suppressed following administration of high dose dexamethasone test.

151
Q

Polyuria in nonhospitalized patients can be due to?

A

Primary polydipsia (used to be known as psychogenic polydipsia) or diabetes insipidus.

152
Q

What is primary polydipsia due to? What are plasma and urine osmolality levels and serum sodium levels like?

A

Due to Increased water intake. Urine osmolality

153
Q

Serum sodium of >145mEq.L with dilute urine excludes

A

primary polydipsia

Medicine Shelf (11 decks)

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