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Internal Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is the pathophysiology of Graves Disease

A

Autoimmune disorder in which IgG antibody binds to the TSH receptor and triggers synthesis of excess thyroid hormone

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2
Q

What does a radioiodide scan show in Graves Disease?

A

Diffuse uptake because every thyroid cell is hyperfunctioning

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3
Q

What is Plummer Disease

A

AKA Toxic Multinodular Goiter. It’s when there are discrete areas of hyperfunctioning thyroid gland.

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4
Q

What does a radioiodide scan show in Plummer Disease?

A

Patchy uptake

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5
Q

What are 2 causes of transient hyperthyroidism?

A

Hashimoto’s Thyroiditis, Subacute (Granulomatous) Thyroiditis

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6
Q

What are the three signs of hyperthyroidism that are specific to Grave’s Disease?

A
  • Exophthalmos
  • Pretibial Myxedema
  • Thyroid Bruit
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7
Q

What do you find on exam in subacute thyroiditis?

A

An exquisitely tender, diffusely enlarged gland with a viral illness.

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8
Q

What is the mechanism of the development of exophthalmos?

A

There is edema of the extraocular muscles and retro-orbital tissues.

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9
Q

What is the mechanism of the development of pretibial myxedema?

A

Edema over the tibial surface due to the accumulation of mucopolysaccharides in the dermis.

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10
Q

What situations cause an increase in TBG?

A
  • Pregnancy
  • Liver disease
  • OCP use
  • Aspirin
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11
Q

For patients on thyroid medication, what should you monitor and why?

A

You should monitor the leukocyte count because they can cause agranulocytosis.

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12
Q

What are the shared side effects of Methimazole and PTU?

A

-Rash, agranulocytosis, hepatotoxicity, arthralgias

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13
Q

What is the MOA of PTU?

A

Inhibits thyroid hormone synthesis and inhibits the peripheral conversion of T4 to T3.

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14
Q

What is the MOA of Methimazole?

A

Inhibits thyroid hormone synthesis

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15
Q

What are some complications of thyroid surgery?

A
  • Permanent hypothyroidism
  • Accidental hypoparathyroidism (look for hypocalcemia)
  • Recurrent laryngeal nerve palsy
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16
Q

How do you treat pregnant patients with Graves Disease?

A

PTU

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17
Q

What are some precipitants of thyroid storm?

A
  • Stress (trauma, surgery, childbirth, illness)
  • Infection
  • DKA
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18
Q

What are the clinical manifestations of thyroid storm?

A
  • Marked fever
  • Tachycardia
  • GI upset (N/V/D)
  • Agitation or psychosis
  • Confusion
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19
Q

How do you treat thyroid storm?

A
  • Supportive: IV fluids, cooling blankets, glucose
  • PTU every 2 hours
  • Beta blockers to control heart rate
  • Dex to impair peripheral generation of T3 from T4 and to provide adrenal support.
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20
Q

What are patients with hashimotos at increased risk for?

A

-Increased risk for thyroid carcinoma and thyroid lymphoma

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21
Q

What are the risk factors for thyroid cancer?

A
  • Head and neck radiation
  • Gardner Syndrome and Cowden syndrome for papillary cancer
  • MEN type II for medullary cancer
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22
Q

What is the most important risk factor for papillary carcinoma?

A

History of radiation to the head and neck

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23
Q

Which thyroid cancer has the best prognosis?

A

Papillary carcinoma

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24
Q

How does papillary carcinoma spread?

A

via the lymphatics. Distant mets are rare.

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25
Q

What is the prognosis for Follicular Carcinoma

A

Has a worse prognosis than papillary carcinoma. It spreads early via hematogenous spread and there may be distant mets in up to 20% of cases.

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26
Q

How do you diagnose follicular carcinoma?

A

You MUST doe a fine needle biopsy because tumor extension through the tumor capsule or vascular invasion distinguishes it from a benign adenoma.

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27
Q

What is Hurthle Cell Carcinoma?

A

Variant of follicular carcinoma. It has characteristic cells containing abundant cytoplasm, tightly packed mitochondria, and oval nuclei with prominent nucleoli. These tumors do not take up iodine.

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28
Q

If you have a patient with medullary carcinoma, what should you also screen for and why?

A

Screen for pheochromocytoma because 1/3 of medullary carcinomas are associated with MEN II.

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29
Q

What cells do medullary carcinoma arise from?

A

Parafollicular C Cells.

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30
Q

What do parafollicular C cells produce?

A

Calcitonin, therefore you expect it to be high in medullary carcinoma.

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31
Q

What is the prognosis of anaplastic carcinoma?

A

It is the worst. Death typically occurs within a few months. Mortality is usually due to invasion of adjacent organs (trachea, neck vessels etc).

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32
Q

What are some exam findings that suggest malignancy of the thyroid?

A
  • Fixed nodule, no movement on swallowing
  • Firm consistency or irregular
  • Solitary nodule
  • Hx of radiation to the neck
  • Hx of rapid development
  • Vocal cord paralysis (recurrent laryngeal nerve paralysis)
  • Cervical adenopathy
  • Elevated serum calcitonin
  • Fam hx of thyroid cancer.
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33
Q

What is the initial test of choice for evaluation of a thyroid nodule?

A

-Fine Needle Aspiration

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34
Q

Which cancer is FNA not reliable for?

A

Follicular. You need surgery because histology does not differentiate between benign and malignant follicular cells.

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35
Q

When do you perform a thyroid scan after FNA?

A

If the FNA is indeterminate or if patients have a low TSH since they are more likely to have a hyperfunctioning nodule.

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36
Q

Which nodules are more likely to be malignant?

A

Cold, meaning they are hypofunctional and don’t have as much uptake.

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37
Q

What is the cause of subacute thyroiditis and what HLA is it associated with?

A
  • Usually follows a viral illness

- Associated with HLA-B35

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38
Q

Describe the clinical course of subacute thyroiditis

A
  • Prodrome for about 2 weeks with fever or flu-like illness
  • May have transient hyperthyroidism due to leakage of hormone from an inflamed thyroid gland. This is followed by a euthyroid state, then a hypothyroid state as hormones are depleted
  • Painful tender thyroid gland that may or may not be enlarged.
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39
Q

How do you diagnose subacute thyroiditis?

A
  • Radioiodine uptake is low
  • Low TSH secondary to suppression with T3/T4
  • High ESR
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40
Q

What is the treatment for subacute thyroidits?

A

NSAIDs and aspirin. May use corticosteroids if more severe pain. Pt usually resolves within a few months to a year.

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41
Q

Describe the pathology of Fibrous Thyroiditis/Reidel Thyroiditis?

A

There is fibrous tissue deposition that replaces normal thyroid tissue, leading to a FIRM thyroid. Patients may be hypothyroid.

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42
Q

What is the difference between subacute viral thyroiditis and subacute lymphocytic thyroiditis?

A

Subacute lymphocytic thyroiditis does NOT have pain or tenderness of the thyroid gland.

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43
Q

Descibe the clinical course of subacute lymphocytic thyroiditis

A

There is a transient thyrotoxic phase of 2-5 months that may be followed by a hypothyroid phase. The hypothyroid phase is usually self limited and may be the only manifestation of the disease.

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44
Q

Describe the clinical manifestations of Hashimoto’s Disease.

A
  • Goiter, most common feature

- Slow decline in thyroid function

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45
Q

How do you make the diagnosis of Hashimoto’s

A
  • May be hypothyroid
  • Antiperoxidase antibodies
  • Antithyroglobulin antibodies
  • Antimicrosomal antibodies
  • Irregular distribution of iodine on the thyroid scan
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46
Q

Treatment of Hashimoto’s

A

Thyroid hormone to achieve a euthyroid state

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47
Q

What are the two most common causes of hypothyroidism?

A
  • hashimoto’s thyroiditis

- Iatrogenic hypothyroidism (radiation, thyroidectomy, medications like lithium or amiodarone)

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48
Q

What lab values are seen in secondary or tertiary hypothyroidism, with respect to TSH and T4

A

Both TSH and T4 levels would be low

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49
Q

Would you expect LDL to be elevated or low with hypothyroidism? What about HDL?

A

Elevated LDL

Low HDL

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50
Q

What is a myxedema coma?

A

A rare condition that presents with a depressed state of consciousness, profound hypothermia and respiratory depression.

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51
Q

How do you treat myxedema coma?

A

Supportive care, IV fluids, IV thyroxine, and hydrocortisone, maintain BP

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52
Q

What is the most sensitive indicator of hypothyroidism?

A

High TSH

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53
Q

Size of a microadenoma

A

<10 mm

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54
Q

Size of a macroadenoma

A

> 10mm

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55
Q

What is the most common type of a pituitary adenoma?

A

A prolactinoma. Also the most common cause of hyperprolactinemia.

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56
Q

What are some causes of hyperprolactinemia?

A
  • Pituitary adenoma
  • Medications
  • Pregnancy
  • Renal failure
  • Suprasellar mass lesion
  • Hypothyroidism
  • Idiopathic
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57
Q

What are some medications that can cause hyperprolactinemia?

A
  • Antipsychotic medications like risperidone
  • H2 blockers
  • metoclopramide
  • verapamil
  • estrogen
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58
Q

What are some signs and symptoms of hyperprolactinemia in men?

A
  • Decreased libido
  • Hypogonadotropic hypogonadism
  • Infertility
  • Impotence
  • Galactorrhea or gynecomastia
  • Visual field defects and headaches
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59
Q

What are some signs and symptoms of hyperprolactinemia in women?

A
  • Premenopausal menstrual irregularities
  • Anovulation and infertility
  • Decreased libido
  • Dyspareunia or vaginal dryness
  • Osteoporosis
  • Galactorrhea
  • Visual field defects and headaches
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60
Q

Why does hyperprolactinemia cause hypogonadism?

A

Elevated levels of prolactin inhibit secretion of GnRH and therefore there is less release of LH and FSH and inhibiting production of testosterone and estrogen.

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61
Q

Describe the workup for hyperprolactinemia symptoms

A
  • Get a prolactin level
  • Pregnancy Test
  • TSH level (elevated TRH can cause prolactin release)
  • MRI or CT
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62
Q

What is the medical treatment for prolactinomas?

A

Bromocriptine or cabergoline. Both are dopamine agonists. Remember that dopamine inhibits prolactin release.

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63
Q

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

A

Cardiovascular disease (cardiomegaly)

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64
Q

What are the growth findings seen in acromegaly?

A
  • Enlarged hands and feet
  • Enlarged jaw
  • Visceral enlargement/organomegaly
  • Arthralgia
  • Hypertrophic cardiomyopathy
  • Coarsening of facial features
  • Thickening of soft tissue and skeleton
65
Q

What are the metabolic disturbances seen in acromegaly?

A
  • Glucose intolerance/DM

- Hyperhidrosis

66
Q

How do you workup acromegaly?

A
  • Get an IGF-1 (Somatomedin C) which should be elevated
  • Do a glucose suppression test (normally glucose should suppress GH, with an adenoma it won’t)
  • Do an MRI of the pituitary
67
Q

In addition to surgical resection or radiotherapy, what medical therapy is available for acromegaly?

A

Octreotide or another somatostatin analog. These suppress GH secretion.

68
Q

How does a craniopharyngioma form?

A

Tumor arises from the remnants of Rathke’s pouch

69
Q

Clinical features of craniopharyngioma?

A

Varies. Could have visual field defects, DI, panhypopituitarism, hyperprolactinemia.

70
Q

What radiologic finding is associated with craniopharyngioma?

A

Calcifications of the supresellar region

71
Q

List the causes of hypopituitarism

A
  • Tumor
  • Radiation
  • Sheehan syndrome
  • Infiltrative process (sarcoidosis, hemochromatosis)
  • head trauma
  • Cavernous sinus thrombosis
  • Surgery
72
Q

A patient has polyuria and polydipsia. What things are in your differential?

A
  • Diabetes mellitus
  • Diabetes insipidus
  • Diuretic use
  • Primary polydipsia
73
Q

What are some causes of central DI?

A

-Tumor, infiltrative process like sarcoidosis, TB, syphilis, Hand-Shuller-Christian Disease, Eosinophilic granuloma, and encephalitis

74
Q

What is the most common cause of nephrogenic DI in adults?

A

Chronic lithium use

75
Q

What are some other causes of nephrogenic DI in adults?

A

hypercalcemia, pyelonephritis, demeclocycline, congenital mutation in the ADH receptor gene or the aquaporin-2 gene.

76
Q

What are the clinical features of diabetes insipidus?

A
  • Polyuria w/ clear dilute urine
  • Thirst and polydipsia
  • Mild hypernatremia
77
Q

What findings in the urine indicate DI?

A

Low specific gravity and low osmolality

78
Q

What is the serum osmolality in DI

A

High, like 280-310

79
Q

Describe the water deprivation test and the results.

A

You hold fluids and measure urine osmolality every hour. When the urine osmolality is stable, inject 2 g of desmopressin subcutaneously and measure urine osmolality 1 hour later.

In Nephrogenic DI: there will be no response to ADH and there will be no increase in urine osmolality with dehydration.

In Central DI: there will be a response to ADH with an increase in urine osmolality after administration.

With primary polydipsia: there will be an increase in urine osmolality after withholding fluids.

80
Q

What are 2 medications you can give for central DI?

A

DDAVP and chlorpropamide, which increases ADH secretion and enhances the effects of ADH.

81
Q

How do you treat nephrogenic DI?

A

Salt restriction and thiazide diuretics.

82
Q

Describe the pathophysiology of SIADH

A

There is excess secretion of ADH either from the posterior pituitary or an ectopic source. elevated levels lead to water retention and excretion of concentrated urine. This has two major effects, hyponatremia and volume expansion.

83
Q

Why is edema not present in SIADH?

A

Because there is natriuresis (excretion of excess sodium in the urine) despite the hypernatremia. This happens because volume expansion causes the release of atrial natriuretic peptide and also inhibits the renin-aldosterone system.

84
Q

What are the signs and symptoms of acute hypernatremia?

A

These are secondary to brain swelling and include lethargy, somnolence, weakness, seizures, coma or death if left untreated.

85
Q

SIADH is a diagnosis of exclusion. What are some things that can help support the diagnosis?

A
  • Hyponatremia
  • Inappropriately concentrated urine osmolality
  • Low serum uric acid (hypouricemia)
  • Low BUN and Cr
  • Normal thyroid, adrenal, renal, cardiac and liver function
  • Measurement of plasma and urine ADH levels
  • Absence of significant hypervolemia
86
Q

What is the treatment of SIADH for an asymptomatic patient?

A
  • Usually just fluid restriction
  • Can do lithium or demeclocycline because these inhibit ADH at the kidneys but they have side effects
  • Can use normal saline with a loop diuretic
87
Q

What is the treatment of SIADH for symptomatic patients?

A
  • Water restriction

- Isotonic saline, hypertonic saline may be indicated in severe cases.

88
Q

What is a major complication of treatment for SIADH if not done carefully?

A

Central Pontine Myelinolysis can occur if you raise the serum sodium level too quickly.

89
Q

What is the guideline for how quickly you should raise sodium levels?

A

0.5 mEq/L per hour.

90
Q

What is the most common cause of hypoparathyroidism?

A

Head and neck surgery

91
Q

Clinical features of hypoparathyroidism/hypocalcemia

A
  • Cardiac arrhythmias
  • Rickes and osteomalacia
  • Increased neuromuscular irritability
  • -Circumoral numbness
  • -Tetany
  • -Hyperactive DTRs
  • -Chvostek sign
  • -Trousseau sign
  • Grand Mal seizures
  • Basal Ganglia calcifications
  • prolonged QT interval
  • Cataracts
92
Q

What are the lab findings associated with hypoparathyroidism

A
  • Hypocalcemia
  • Low PTH
  • High serum phosphate
  • Low urine cAMP
93
Q

What are the lab findings associated with psueodhypoparathyroidism, or end organ resistance to PTH?

A
  • Hypocalcemia
  • HIGH PTH
  • High serum phosphate
  • Low urinary cAMP
94
Q

Treatment of hypoparathyroidism

A
  • IV Calcium gluconate (or oral)
  • Vitamin D supplementation
  • Be careful when replenishing that you don’t cause Kidney Stones!!
95
Q

What are 3 causes of hyperparathyroidism

A
  • Adenoma
  • Hyperplasia
  • Carcinoma
96
Q

What are the clinical features of hypercalcemia (General)

A
  • Stones
  • Bones
  • Groans
  • Psychiatric overtones
  • Shortened QT Interval
97
Q

What are the “Stones” symptoms of hypercalcemia?

A
  • Nephrolithiasis

- Nephrocalcinosis

98
Q

What are the “Bones” symptoms of hypercalcemia?

A
  • Bone aches and pains

- Osteitis Fibrosa Cystica (Brown Tumor) which predisposes to pathologic fracture

99
Q

What are the “Groans” symptoms of hypercalcemia?

A
  • Muscle pain, weakness
  • Pancreatitis
  • PUD
  • Gout
  • Constipation and abdominal pain
100
Q

What are the “Psychiatric overtones” of hypercalcemia?

A

Anxiety, depression, fatigue, anorexia, lethargy, sleep disturbance

101
Q

What are the lab findings with hyperparathyroidism

A
  • Hypercalcemia
  • Elevated PTH
  • Hypophosphatemia
  • Hypercalciuria
  • High Urine cAMP
  • Chloride: Phosphate ratio of >33
102
Q

What are the radiographic findings of hyperparathyroidism?

A
  • Subperiosteal bone resorption (usually on the radial aspect of the second and third phalanges)
  • Osteopenia
103
Q

Which diuretics should you avoid in hypercalcemia/hyperparathyroidism?

A

THIAZIDES

104
Q

In which part of the adrenal gland are most pheochromocytomas found?

A

The adrenal medulla

105
Q

Pathophysiology of pheochromocytoma

A

Tumor arising from neuroendocrine chromaffin cells of the adrenal medulla or from the sympathetic ganglia if extra-adrenal which produces, stores, and secretes catecholamines.

106
Q

What are the symptoms of pheochromocytoma?

A
  • Pounding HA
  • Paroxysmal severe HTN
  • Sweating
  • Tachycardia
  • Palpitations
  • Apprehension or sense of impending doom
  • Anxiety
  • Hyperglycemia, hyperlipidemia, hypokalemia
107
Q

What is the rule of 10s for pheochromocytoma?

A 
10% familial 
10% malignant 
10% occur in children 
10% extra-adrenal 
10% multiple 
10% bilateral
108
Q

What are you looking for in the urine of someone w/ pheo?

A

VMA, HVA, metanephrines, normetanephrine

109
Q

How do you treat pheo? Including the prep before surgery?

A

Alpha-blocker for 10-14 days before surgery to control BP. Beta-blocker for 2-3 days before surgery to control the tachycardia. Then removal of the tumor during surgery.

110
Q

MEN Type I

A

Parathyroid hyperplasia
Pancreatic adenoma
Pituitary adenoma

111
Q

MEN Type IIA

A

Medullary thyroid cancer
Parathyroid hyperplasia
Pheochromocytoma

112
Q

MEN Type IIB

A

Medullary thyroid cancer
Marfanoid habitus
Mucosal neuromas
Pheochromocytoma

113
Q

MEN Type I is caused by a mutation in?

A

MEN1 gene

114
Q

MEN Type II is caused by a mutation in?

A

The RET protooncogene

115
Q

What is the result of hyperaldosteronism on sodium and potassium and what are the effects of this?

A
  • Hypernatremia leading to ECF volume expansion and HTN

- Potassium loss causing hypokalemia

116
Q

Does hyperaldosteronism cause an acidosis or alkalosis?

A

Metabolic alkalosis because aldosterone promotes the secretion of H+ ions into the lumen of the medullar collecting tubules.

117
Q

What are 3 causes of primary hyperaldosteronism?

A
  • Adrenal adenoma (aka Conn Syndrome), most common
  • Adrenal hyperplasia
  • Adrenal Carcinoma
118
Q

What are the clinical features of hyperaldosteronism?

A
  • Hypertension
  • Fatigue, weakness, headache
  • Polydipsia, nocturnal polyuria
  • Absence of peripheral edema!!!
119
Q

How do you screen for hyperaldosteronism if you suspect it?

A

Look at the plasma aldosterone to renin level. If aldosterone is abnormally elevated in the face of low renin, you should suspect primary hyperaldosteronism. If the ratio of plasma aldosterone: renin is >30, it requires further investigation.

120
Q

Describe the saline infusion test.

A

You infuse saline into the person, and a normal person will have a decrease in aldosterone after saline infusion. If aldosterone decreases to <8.5 ng/dL, you can rule out primary aldosteronism.

121
Q

Describe the oral sodium loading test.

A

The patient is given a high salt diet for 3 days. Serum and urine electrolytes, aldosterone, and creatinine are measured on the third day. High urine aldosterone in the setting of high urine sodium confirms the diagnosis.

122
Q

Describe the adrenal venous sampling test.

A

This is one test in which you can diagnose the CAUSE of the hyperaldosteronism. A high level of aldosterone on one side indicates an adenoma. High levels on both sides indicates bilateral hyperplasia.

123
Q

Describe the renin-aldosterone stimulation test.

A

Recumbency or upright positions are assumed, followed by measurement of serum aldosterone?

124
Q

How do you treat an adenoma?

A

Surgical resection.

125
Q

How do you treat bilateral adrenal hyperplasia?

A

Spironolactone which inhibits the action of aldosterone.

126
Q

What are 4 causes of primary adrenal insufficiency?

A
  • Idiopathic (thought to be autoimmune)
  • Infection
  • Malignancy
  • Iatrogenic
127
Q

What is the cause of secondary adrenal insufficiency? Describe the pathophysiology.

A

Patients on long term steroid therapy-most common cause of secondary adrenal insufficiency today.

When these patients develop a serious illness or undergo trauma, they cannot release an appropriate amount of cortisol because of chronic suppression of CRH and ACTH by the exogenous steroids therefore symptoms of adrenal insufficiency result.

128
Q

What are some of the most common clinical findings associated with adrenal insufficiency?

A
  • Weakness
  • Fatigue
  • Weight loss
  • Hyperpigmentation
  • Anorexia
  • Nausea
  • Postural hypotension (due to hyponatremia and hypocortisolism)
  • Abdominal pain
  • Hypoglycemia
  • Decreased CO, decreased renal perfusion, shock, syncope.
129
Q

Does hyperpigmentation occur in secondary adrenal insufficiency? Explain the reasoning.

A

No. In secondary adrenal insufficiency, ACTH levels are low and therefore cortisol levels are low. If it is primary, just cortisol levels are low and this negative feedback means there will be increased ACTH release along with MSH secretion leading to hyperpigmentation.

130
Q

How do you treat primary adrenal insufficiency?

A

Daily oral glucocorticoid (hydrocortisone or prednisone) and a daily mineralocorticoid (fludrocortisone)

131
Q

How do you treat secondary adrenal insufficiency?

A

Just a daily oral glucocorticoid. You don’t need to replace the mineralocorticoid in secondary disease.

132
Q

Inheritance pattern of CAH

A

Autosomal recessive, 21-hydroxylase deficiency is most common cause; 11-hydroxylase is second most common cause

133
Q

Describe the pathophysiology of CAH.

A

There is a deficiency of an enzyme needed to produce cortisol and aldosterone. Therefore, there is increased ACTH due to the loss of negative feedback and this results in bilateral adrenal hyperplasia. As precursors of cortisol and aldosterone build up, they are shunted toward the synthesis of androgens, causing virilization.

134
Q

If a female baby is born with CAH, what does she look like?

A

She is born with ambiguous EXTERNAL genitalia, but normal female uterus and ovaries.

135
Q

If a male baby is born with CAH, what does he look like?

A

He has no genital abnormalities.

136
Q

What are some symptoms of salt wasting CAH?

A

This is the more severe form of the disease. Emesis, dehydration, hypotension and shock can develop within 2-4 weeks of life. Hyponatremia and hyperkalamia occur due to the lack of aldosterone and there is hypoglycemia due to the lack of cortisol.

137
Q

How do you diagnose CAH?

A

HIgh levels of 17-hydroxyprogesterone in the serum.

138
Q

How do you treat CAH medically?

A

Replete cortisol and aldosterone. This will normalize the feedback loop on ACTH.

139
Q

Pathyphysiology of Insulin Dependent DM

A

-Autoimmune disease where the immune system mediates the destruction of beta-cells. It develops in genetically susceptible individuals who are exposed to an environmental trigger. Overt T1DM doesn’t develop until about 90% of the beta cells are destroyed.

140
Q

If the renin: aldo ratio is <10 what does that indicate?

A

That means that potentially both renin and aldo are high but it is the renin elevation that is causing the aldosterone elevation and this can be caused by renovascular hypertension 2/2 fibromuscular dysplasia in a young woman or atherosclerotic disease in an old man. You can treat this with stenting.

141
Q

If both renin and aldosterone levels are low what could it be?

A

It could be CAH or licorice ingestion.

142
Q

How do you diagnose facticious hypoglycemia?

A

High Insulin levels and low C-peptide

143
Q

If a patient presents with hypoglycemia of unknown cause, what 4 things should you measure?

A
  • C-peptide
  • Plasma insulin levels
  • Anti-insulin antibodies
  • Urine and plasma sulfonylurea levels
144
Q

At what level do symptoms occur in hypoglycemia, and what are those symptoms?

A

40-50. Sweating, tremors, increased BP and pulse, anxiety, palpitations, weakness, drowsiness, headache, AMS, confusion, convulsions, coma or death.

145
Q

What is the acute treatment of hypoglycemia?

A

If the patient can eat, give them sugar containing foods. If the patient cannot eat, give 1/2 to 2 ampules of D50W IV. Repeat D50W as needed but switched to D10W as clinical condition improves and glucose level is approximately >100 mg/dL.

146
Q

What is an insulinoma? What syndrome is it associated with?

A

It is an insulin producing tumor that arises from the beta-cells of the pancreas. It is associated with MEN I syndrome.

147
Q

What are the clinical features of an insulinoma?

A

HYPOGLYCEMIA

148
Q

How do you diagnose an insulinoma?

A

A 72 hour fast. As a person becomes hypoglycemia from fasting, insulin levels should decrease. However, in a person with an insulinoma, the levels will either increase, or stay the same. They may decrease slightly.

149
Q

Define the Whipple Triad

A
  • Hypoglycemic symptoms brought on by fasting
  • Blood glucose <50 during symptomatic attack
  • Glucose administration brings relief of symptoms.
150
Q

How do you distinguish insulinoma from exogenous insulin administration?

A

With an insulinoma both insulin and C-peptide will be high. With exogenous insulin adminstration, insulin will be high but C-peptide will be low.

151
Q

Define Zollinger-Ellison Syndrome

A

This is a pancreatic islet cell tumor that secretes high gastrin which leads to profound gastric acid hypersecretion resulting in ulcers.

152
Q

How do you diagnose Zollinger Ellison?

A

Secretin suppression test. Normally secretin suppresses gastrin secretion. IN patients with ZES, gastrin levels increase substantially after being given secretin.

Fasting gastrin level is also elevated.

153
Q

How do you treat ZES?

A

High dose PPI and surgical resection/debulking.

154
Q

What is a glucagonoma?

A

It is a glucagon producing tumor located in the pancreas.

155
Q

What are the clinical features of glucagonoma?

A

NECROTIZING MIGRATORY ERYTHEMA. Usually occurs below the waist. Also see glossitis, stomatitis, DM, and hyperglycemia. Tx is surgical resection.

156
Q

What is the triad seen in somatostatinoma?

A

-Gallstones, diabetes, and steatorrhea

157
Q

What are the clinical features of a VIPoma?

A

-Watery diarrhea, Hypokalemia, and Achlorhydria because VIP inhibits gastric acid secretion.

158
Q

3 key features of DKA

A
  • Hyperglycemia
  • Serum or urine ketones
  • Metabolic acidosis
159
Q

Are ketones and acidosis present in HHNS?

A

Typically no. If they are it is minimal. Ketogenesis is minimal because a small amount of insulin is released to blunt the counterregulatory hormone release.

Internal Medicine (6 decks)

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