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Internal medicine > Endocrine and Metabolic Diseases > Flashcards

Endocrine and Metabolic Diseases Flashcards

1
Q

What is the most common cause of Hyperthyroidism (80%), and what is the pathophysilogy?

A

Graves disease (diffuse toxic goiter).

An autoimmune disorder; Thyroid stimulating immunoglobulin (IgG) antibody binds to TSH receptors on the surface of thyroid cells, and triggers synthesis of excess thyroid hormone.

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2
Q

What does Graves disease typically show on radioiodine scan?

A

Diffuse uptake, because every thyroid cell is hyperfunctioning.

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3
Q

What is the 2nd most common cause of Hyperthyroidism (15%)? What is the pathophysiology?

A

Plummer disease (multinodular toxic goiter).

Hyperfunctioning areas that produce high T4 and T3 levels, thereby decreasing TSH. As a result, the rest of the thyroid is not functioning -> atrophy.

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4
Q

What does Plummer disease (multinodular toxic goiter) typically show on radioiodine scan?

A

Patchy uptake

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5
Q

Name 4 other causes of Hyperthyroidism

A
  1. Toxic thyroid adenoma (single nodule)
  2. Hashimoto thyroiditis and subacute (granulomatous) thyroiditis - causes transient hyperthyroidism)
  3. Postpartum thyroiditis
  4. Excessive doses of levothyroxine
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6
Q

Clinical Sx of hyperthyroidism

A 
Nervousness
Insomnia 
Tremor 
Irritability 
Hyperactivity 
Sweating 
Heat intolerance
Weight loss, incr. appetite
Diarrhea
Palpitations 
Muscle weakness
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7
Q

Clinical signs of hyperthyroidism

A
  1. Thyroid gland:
    - Graves: diffusely enlarged (symmetric), nontender thyroid, bruit may be present.
  • Subacute thyroiditis: tender, diffusely enlarged gland (with a viral illness)
  • Plummer: bumpy, irregular and asymmetric (if multinodularity)
  1. Extrathyroidal:
    - Proptosis, due to edema in the extraocular muscles + retroorbital tissue
    - Arrhytmias, elevated BP
    - Brisk DTR, tremor
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8
Q

Diagnosis of hyperthyroidism

A

Test TSH and T4. Most important. TSH should be low and T4 should be elevated.

Radioactive T3 uptake can be donw if you want to differentiate between elevations in thyroidhormones due to increased TBG from true hyperthyroidism (due to an actual increase in free T4.)

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9
Q

Treatment-types of hyperthyroidism

A
  1. Pharmacologic
    - Methimazole and PTU
    (inhibit thyroid hormone synthesis and conversion of T4 to T3). (side effect Agranulocytosis)
  • B-blockers
    (for acute/uncomfortable sx)
  • Sodium ipodate or iopanoic acid
  • Fast acting, appropriate for acute mx of severe hyperthyroidism that is not responding to conventional therapy.
  1. Radioiodine 131
    - Destroys thyroid follicular cells
    - Main complication is hypothyroidism
  2. Surgical - subtotal thyroidectomy
    - Effective, but many get permanent hypothyroidism etc.
    - Watch for clinical sx of hypocalcemia, due to parathyroid inflammation or accidental removal.
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10
Q

Most serious side effect of Thionamides (Methimazole and PTU)

A

Agranulocytosis

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11
Q

Which tx is contraindicated in pregnancy?

A

Radioiodine 131 (due to risk of cretinism).

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12
Q

What is typical “side-effects” of subtotal thyroidectomy

A
  1. Permanent hypothyroidism
  2. Recurrence of hyperthyroidism
  3. Recurrent laryngeal nerve palsy
  4. Permanent hypoparathyroidism
  5. Hypocalcemia (parathyroid)
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13
Q

In immediate control of adrenergic symptoms of hyperthyroidism, you give:

A

B- blockers

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14
Q

What do you give to nonpregnant patients with Graves?

A

a) Methimazole + B-blocker
b) Stop B-blocker after 4-8w (when Methimazole starts to work)
c) Continue methimazole for 1-2y. Measure TS-IgG at 12m. If absent, discontinue therapy.

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15
Q

What do you give to pregnant patients with Graves?

A

a) Endocrinology consult indicated before starting tx

b) PTU is preffered! (Pregnant = Ptu)

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16
Q

Which patients may benefit by Radioactive iodine?

A
  1. Elderly patients
  2. Patients with a solitary toxic nodule
  3. Patients with Graves disease in whom therapy with antithyroid drugs fails.
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17
Q

What is thyroid storm?

Sx?

A

Rare, life-threatening complication of thyrotoxicosis characterized by an acute exacerbation of the manifestation of hyperthyroidism.(mortality rate up to 20%)

Sx: Marked fever, tachycardia, agitation, psychosis, confusion, diarrhea, vomiting, nausea

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18
Q

What can cause a thyroid storm?

A

Precipitating factors such as infection, diabetic ketoacidosis, stress (e.g surgery, trauma, illness, childbirth)

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19
Q

Treatment of a thyroid storm

A
  1. IV fluids
  2. Cooling blankets
  3. Glucose
  4. PTU every 2h
  5. Iodine to inhibit thyroid hormone release.
  6. B-blockers for control of HR
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20
Q

Most common cause of Primary hypothyroidism? (95%) Pathophysiology?

A

Hashimoto disease (chronic thyroiditis) - failure of the thyroid to produce sufficient thyroid hormone.

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21
Q

Second most common cause of Primary hypothyroidism? + examples

A

Iatrogenic. Results from prior tx of hyperthyroidism, including:

  • Radioiodine therapy
  • Thyroidectomy
  • Medications (e.g lithium)
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22
Q

What is secondary hypothyroidism?

A

Due to pituitary disease, i.e., deficiency of TSH

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23
Q

What is tertiary hypothyroidism?

A

Due to hypothalamic disease, ie., def. of TRH.

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24
Q

What are typical findings of secondary and tertiary hypothyroidism?

A

Both are associated with a LOW free T4 and a LOW TSH level.

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25
Q

Clinical sx of hypothyroidism

A 
Fatigue
Weakness
Lethargy
Heavy menstrual periods
Cold intolerance
Constipation
Slow mentation, low concentration
Muscle weakness, arthralgia
Depression
Diminished hearing
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26
Q

Clinical Signs of hypothyroidism

A

Dry skin, coarse hair, thickened, puffy features
Hoarseness
Nonpitting edema
Carpal tunnel syndrome
Slow relaxation of DTR
Loss of lateral portion of eyebrows
Bradycardia
Goiter (Hashimoto disease - goiter is rubbery, nontender and even nodular)
History of URI and fever (subacute thyroiditis)

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27
Q

Diagnosis of hypothyroidism

A
  1. HIGH TSH level - most sensitive indicator of hypothyroidism
  2. Low TSH level (secondary hypothyroidism)
  3. Low free T4 level in patients with clinically overt hypothyroidism. Free T4 may be normal in subclinical cases.
  4. Increased antimicrosomal antibodies (Hashimoto thyroiditis)
    Also:
    - Elevated LDL and decreased HDL levels
    - Anemia - mild normocytic anemia is the most common
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28
Q

Treatment of hypothyroidism

A

Levothyroxine (T4)

  • Effect evident in 2-4 weeks, highly effective in achieving euthyroid-state.
  • Tx is continued indefinitely.
  • Monitor TSH level
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29
Q

Thyroiditis - Types

A
  1. Subacute (viral) thyroiditis
  2. Subacute lymphocytic thyroiditis
  3. Chronic lymphocytic thyroiditis
  4. Fibrous thyroiditis
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30
Q

Subacute (viral) thyroiditis (subacute granulomatous thyroiditis):

A

Usually follows a viral illness; assoc. with HLA-B35

  • Prodromal phase of a few weeks (fever, flu-like illness)
  • Can cause transient hyperthyroidism due to leakage of hormone from inflamed thyroid gland. This is followed by a euthyroid state and then a hypothyroid state (as hormones are depleted)
  • Painful, tender thyroid gland(may be enlarged).

Dx:

  • Radioiodine uptake is low because thyroid follicular cells are damaged and cannot trap iodine.
  • Low TSH level secondary to suppression by increased T4 and T3 levels; high erythrocyte sedimentation rate (ESR)

Tx:
Use NSAIDS if mild, steroid if severe, usually resolves within a couple of months.

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31
Q

Subacute lymphocytic thyroiditis

A

Painles, silent thyroiditis.
a) A transient thyrotoxic phase of 2-5months may be followed by a hypothyroid phase. The last phase is usually self-limited and may be the only manifestation (if the hyperthyroid phase is brief).

b) Low radioactive iodine uptake - differentiates it from Graves disease during thyrotoxic phase.
3. Similar to subacute (viral) thyroiditis, only without the pain and tenderness of the thyroid gland.

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32
Q

Chronic lymphocytic thyroiditis (Hashimoto thyroiditis, lymphocytic thyroiditis)

A
  1. Most common cause of autoimmune thyroid disorder, more common in women.
  2. Causes:
    a) Genetic component - family history is common
    b) Antithyroid antibodies are present in the majority of patients
  3. Clinical:
    - Goiter most common feature
    - Slow decline in thyroid function is common. Hypothyroidism is present in 20% of cases when first diagnosed but often occurs later in disease.
  4. Dx:
    - Thyroid function studies are normal (unless hypothyroidism is present)
    - Antithyroid antibodies: antiperoxidase antibodies (present in 90% of patients), antithyroglobulin antibodies (present in 50%).
    - Irregular distribution of 131I-thyroid scan - not required for diagnosis.
  5. Treatment: thyroid hormone (to achieve euthyroid state)
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33
Q

Fibrous thyroiditis (Riedel thyroiditis)

A

Fibrous tissue replaces thyroid tissue, leading to a firm thyroid.

  • Surgery may be necessary if complications occur.
  • Patient may be hypothyroid as well, in which case thyroid hormone should be prescribed.
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34
Q

Thyroid nodules - Characteristics

A

Cancer is found in 4-10% of nodules investigated.
- A solitary nodule can be either thyroid cancer or a benign adenoma.
Palpate for a nodule, may be a multinodular condition with only one palpable node. Must be at least 1cm.

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35
Q

What characteristics is typical for malignancy in a thyroid nodule?

A
  1. If the nodule is fixed in place and no movement occurs on swallowing
  2. Unusually firm consistency or irregularity of the nodule
  3. If the nodule is solitary
  4. History of radiation therapy to the neck
  5. History of rapid development
  6. Vocal cord paralysis (recurrent laryngeal nerve paralysis)
  7. Cervical adenopathy
  8. Elevated serum calcitonin
  9. Family history of thyroid cancer
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36
Q

Diagnosis of thyroid nodule

A
  1. Fine-needle aspiration
    - Test of choice for initial evaluation of a thyroid nodule (95% specificity and sensitivity)
  2. Thyroid scan (radioactive iodine)
    - It is performed if the FNA biopsy isintermediate (se figur 4-3). It gives representation of the distribution of radioactive iodine in the gland - useful in identifying whether thyroid nodules show decreased (“cold”) or increased (“hot”) accumulation of radioactive iodine compared with normal, paranodal tissue. When lesions are “cold” on scan, thyroid lobectomy is reccomended.
  3. Thyroid USG
    a) Differentiates a solid from a cystic nodule; most cancers are solid.
    b) Can identify nodules 1-3 mm in diameter
    c) Cystic masses larger than 4cm in diameter are not malignant
    d) Cannot distinguish between benign and malignant.
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37
Q

Risk factors for Thyroid cancer

A
  1. Head and neck radiation (during childhood)
  2. Gardner syndrome and Cowden syndrome for papillary cancer
  3. MEN type II for medullary cancer
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38
Q

Types of Thyroid cancer

A
  1. Papillary carcinoma
    - 70-80% of all thyroid cancers
    - Least aggressive thyroid cancer - slow growth, slow spreading with good prognosis
    - Most important risk factor is a history of radiation in head/neck.
    - Spreads via lymphatics in neck, frequently metastasis in cervical lymph nodes, distant metastasis is rare.
    - Positive iodine uptake
  2. Follicular carcinoma
    - Accounts for 15% of all thyroid cancers, avidly absorbs iodine.
    - Prognosis worse than for papillary cancer, spreads early via a hematogenous route, metastasis in 20%.
    - May be assoc. with iodine def.
    - One variant is the “Hurtle cell” carcinoma - characteristic cells containabundant cytoplasm, tightly packed mitochondria, and oval nuclei with prominent nucleoli. These tumors are radioiodine resistant.
  3. Medullary carcinoma
    - 2-3% of all thyroid cancers
    - One third assoc. with MEN II
    - Arises from the parafollicular cells (C cells) - produces Calcitonin
  4. Anaplastic carcinoma
    - 5% of all thyroid cancers
    - Highly malignant
    - May arise from a longstanding follicular or papillary thyroid carcinoma
    - Prognosis - death typically occurs within a few months.
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39
Q

Which thyroid cancer produces Calcitonin?

A

Medullary carcinoma

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40
Q

How do you treat Papillary carcinoma?

A

a. Lobectomy with isthmusectomy
b. Total thyroidectomy if tumor is > 3cm, tumor is bilateral, tumor is advanced, or distant metastases are present.
c. Adjuvant treatment: TSH suppression therapy; radioiodine therapy for larger tumors.

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41
Q

How do you treat Follicular carcinoma?

A

Total thyroidectomy with postoperative iodine ablation.

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42
Q

How do you treat Medullary carcinoma?

A

Total thyroidectomy, Modified radical neck dissection is also indicated when there is lymph node involvement.

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43
Q

How do you treat Anaplastic carcinoma?

A

Chemo and radiation therapy may slightly improve survival, otherwise Palliative.

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44
Q

Pituitary adenomas in general

A

Account for 10% of intracranial neoplasms.
- Almost all are benign
Gives “parasellar” signs and symptoms.
- Size: Microadenoma (diameter < 10 mm), macroadenoma (diameter > 10mm)

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45
Q

Clinical features of pituitary adenoma

A

Hormonal effects occur due to hypersecretion of one or more of the following hormones:

  1. Prolactin - hyperprolactinemia
  2. GH - results in acromegaly or gigantism
  3. ACTH - Cshing disease
  4. TSH - hyperthyroidism

Can also occur HYPOpituitarism - if compression of hypothalamic-pituitary stalk; GH-def, hypogonadotropic hypogonadism are the most common symptoms.

Mass effect: Headache, visual defects such as bitemporal hemianopsia

TX: Transsphenoidal surgery + radiation therapy and medical therapy.

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46
Q

Most common cause of hyperprolactinemia?

A

Prolactinoma (is also the most common type of pituitary adenoma 40%)

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47
Q

Other causes of hyperprolactinemia?

A
  1. Medications (psychiatric, h2-blockers, metoclopramide, verapamil, estrogen)
  2. Pregnancy
  3. Renal failure
  4. Suprasellar mass lesion
  5. Hypothyroidism
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48
Q

Sx of hyperprolactinemia in men vs women?

A

Men:
- Hypogonadism, decr libido, infertility, impotence, galactorrhea, gynecomastia, parasellar signs (visual field defects, headache)

Women:
a) Premenopausal:
Menstrual irregularities, oligomenorrhea, amenorrhea, anovulation, infertility, decr libido, dyspareunia, vaginal dryness, risk of osteoporosis, galactorrea

b) Postmenaupausal:
Parasellar signs and symptoms.

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49
Q

Treatment of hyperprolactinemia?

A
  1. Treat underlying cause
  2. If prolactinoma: treat with BROMOCRIPTINE (a dopamine agonist that secondarily diminishes the production). Continue tx for 2y, then attempt cessation. CABERGOLINE may be better tolerated, and is often first-line.
  3. Consider surgical intervention if symptoms progress despite appropriate medical therapy.
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50
Q

Acromegaly - in general

A

Acromegaly is broadening of the skeleton, which results from excess secretion of pituitary GH AFTER epiphyseal closure (if before -> gigantism).

51
Q

What is the most common cause of acromegaly?

A

It is almost always caused by a GH-secreting pituitary adenoma (represents 10% of pituitary adenomas)

52
Q

Clinical features of Acromegaly

A
  1. Growth promotion
    - Soft tissue and skeleton overgrowth
    - Coarsening of facial features
    - Abnormally large hand and foot size
    - Organomegaly
    - Arthralgia
    - Hypertrophic cardiomyopathy
    - Enlarged jaw (macrognathia)
  2. Metabolic disturbances
    - Glucose intoleranceand DM in 10-25% of patients
    - Hyperhidrosis
  3. Parasellar manifestations
    - Headache
    - Superior growth leads to compression of the optic chiasm, which results in visual loss (bitemporal hemianopsia)
    - Lateral growth leads to cavernous sinus compression
    - Inferior growth leads to sphenoid sinus invasion
    - HTN, sleep apnea
53
Q

How to diagnose Acromegaly?

A
  1. IGF-1 aka Somatomedin C -should be significantly elevated
  2. Oral glucose supression test - glucose load fails to suppress GH
  3. MRI of the pituitary
54
Q

Treatment of Acromegaly?

A
  1. Transsphenoidal resection of pituitary adenoma - treatment of choice
  2. Radiation therapy if IGF-1 levels stay elevated after surgery
  3. Octreotide or other somatostatin analog to suppress GH secretion
55
Q

Craniopharyngioma

A

Tumors of the suprasellar region arising from embryologic remnants of Rathke pouch.

  • Pituitaryadenoma is most common
  • Results in visual field defects due to compression of the optic chiasm and may also cause headaches, papilledema and changes in mentation.
  • Diagnosed by brain MRI
  • May cause hyperprolactinemia, diabetes insipidus or panhypopituitarism.
56
Q

Hypopituitarism - General characteristics

A
  1. All or some of the hormones released from the anterior pituitary may be absent.
  2. Loss of hormones is unpredictable, but LH, FSH and GH are usually lost before TSH and ACTH.
  3. Clinical manifestations depend on which hormones are lost.
57
Q

Most common cause of hypopituitarism?

A

Hypothalamic or pituitary tumor is the most common cause.

58
Q

Diagnosis of hypopituitarism

A
  1. Low levels of target hormones with low or normal levels of trophic hormones (it is the suppression of the trophic hormone that is important).
  2. MRI of the brain (may miss microadenomas)
59
Q

Treatment of hypopituitarism

A
  1. Replacement of appropriate hormones

2. Women who want to concieve should be referred to an endocronologist.

60
Q

Diabetes Insipidus - the two forms

A
  1. Central DI = most common. Due to low ADH secretion by posterior pituitary
  2. Nephrogenic DI - ADH secretion is normal but tubules cannot respond to ADH.
61
Q

Causes of Central DI

A
  1. Idiopathic (50%)
  2. Trauma (surgery, head trauma)
  3. Other destructive processes, involving hypothalamus, including tumors, sarcoidosis, tuberculosis, syphilis etc.
62
Q

Causes of Nephrogenic DI

A

The most common cause in adults in chronic lithium use.

63
Q

Clinical findings of DI

A
  1. Polyuria
  2. Thirst and polydipsia
  3. Hypernatremia, usually mild
64
Q

Diagnosis of DI

A
  1. Urine - low specific gravity and low osmolality
  2. Plasma osmolality - elevated
  3. A water deprivation test, the measure urine osmolality every hour. When rine osmolality is stable, inject 2g desmopressin, then measure urine osmolality 1h later.
  4. ADH level - low in central DI, elevated or normal in nephrogenic DI
65
Q

Treatment of Central DI

A
  1. Desmopressin (DDAVP) = primary therapy
  2. Chlorpropamide increases ADH secretion and enhances the effect of ADH
  3. Treat underlying cause
66
Q

Treatment of Nephrogenic DI

A
  1. Treat with sodium restriction and thiazide d iuretics
67
Q

Syndrome of inappropriate secretion of antidiuretic hormone - Pathophysiology

A

Excess ADH is secreted from the posterior pituitary or an ectopic source. Elevated levels leads to water retention and excretion of concentrated urine. Leads to two major effects: hyponatremia and volume expansion.
BUT! Edema is NOT seen because natriuresis occurs despite hyponatremia.

68
Q

SIADH - Reasons for natriuresis? (3)

A
  1. Volume expansion causes an increase in atrial natriuretic peptide (increases urine sodium excretion)
  2. Volume expansion leads to a decrease in proximal tubular sodium absorption.
  3. The renin-angiotensin-aldosteron system is inhibited
69
Q

SIADH - Causes (6)

A
  1. Neoplasms or lymhoma/leukemia
  2. CNS disorders (stroke, head trauma, infection)
  3. Pulmonary disorders (pneumonia, tuberculosis)
  4. Medication (vincristine, ssris, oxytocin, morphine, desmopressin)
  5. Postoperative state (anasthesia, pain)
70
Q

SIADH - Clinical (acute vs chronic)

A
  1. Acute hyponatremia
    - Sx are secondary to brain swelling (osmotic water shifts, leading to incr. ICF volume)
    a) Lethargy
    b) Seizures, coma, death if untreated
  2. Chronic hyponatremia
    a) May be asymptomatic
    b) Anorexia, nausea, vomiting
    c) CNS symptoms are less common because chronic loss of sodium and potassium from brain cells decrease brain edema (due to secondary water shifts from ICF to ECF)
71
Q

SIADH - Diagnosis

A
  1. SIADH is a diagnosis of exclusion. The following help support the dx:
    - Hyponatremia and concentrated urine (plasma osmolality270 mmol/kg)
    - Low serum uric acid level
    - Low BUN and Creatinine
    - Normal thyroid and adrenal function, as well as renal, cardiac and liver function
    - Measurement of plasma and urine ADH level
    - Absence of significant hypervolemia
72
Q

SIADH - Treatment

A
  1. Correct underlying cause
  2. For asymptomatic: fluid retention can be enough (+/- normal saline + loop diuretic, lithium carbonate or demeclocycline are other options - they inhibit effect of ADH in kidney)
  3. For symptomatic pts:
    - Restrict water intake
    - Give isotonic saline. Hypertonic saline in severe cases

! Do NOT raise serum sodium too quickly. Rapid flux of water into the ECF can result in central pontine myelinolysis (demyelination syndrom may result) . Replacement should not exceed 0.5 mEq/L per hour. !

73
Q

What can happen if you raise serum sodium too quickly?

A

Central Pontine Myelinolysis

74
Q

Causes of hypoparathyroidism

A
  1. Head and neck account for majority of cases (thyroidectomy, parathyroidectomy, radical surgery for head and neck malignancies). Nonsurgical hypoparathyroidism is rare
75
Q

Clinical features of hypoparathyroidism

A
  1. Cardiac arrhytmias
  2. Rickets/osteomalacia
  3. Increased neurumuscular irritability due to hypocalcemia
    - Tetany
    - Hyperactive DTR
    - Chvostek sign
    - Trousseau sign
    - Grand mal seizures
  4. Basal ganglia calcifications
  5. Prolonged QT-interval on ECG - hypocalcemia should always be in the differential of a prolonged QT-interval.
  6. Cataracts
76
Q

Diagnosing hypoparathyroidism

A
  1. Low serum calcium
  2. High serum phosphate
  3. Serum PTH inappropriately low
  4. Low urine cAMP
77
Q

Treating hypoparathyroidism

A
  1. IV calcium gluconate in severe cases
  2. Oral calcium in mild to moderate cases
  3. Note that both vitamin D and calcium replacement can increase urinary calcium excretion, precipitating kidney stones. Therefore, administer with caution to avoid hypercalciuria (goal is serum calcium 8.0-8.5 mg/dl)
78
Q

Hyperparathyroidism - General

A

One or more glands produce inappropriately high amounts of PTH relative to the serum calcium level.
- Most common cause of hypercalcemia in outpatient setting.

79
Q

Causes of hyperparathyroidism (3)

A
  1. Adenoma (80% of cases) - usually involve a single gland
  2. Hyperplasia (15-20%) - all four glands usually affected
  3. Carcinoma (< 1% of cases)
80
Q

Hyperparathyroidism - Clinical features

A

“Stones, bones, groans, psychiatric overtones”

  1. Stones
    a) Nephrolithiasis
    b) Nephrocalcinosis
  2. Bones
    a) Bone aches and pains
    b) Osteitis fibrosa cystica (“brown tumors”) - predisposes patient to pathologic fractures
  3. Groans
    a) Muscle pain and weakness
    b) Pancreatitis
    c) Peptic ulcer disease
    d) Gout
    e) Constipation
  4. Psychiatric overtones
    - Depression, fatigue, anorexia, sleep disturbances, anxiety.
  5. Other:
    a) Polydipsia, polyuria
    b) HTN, shortened QT-interval
    c) Weight loss
81
Q

Diagnosing hyperparathyroidism

A
  1. Hypercalcemia
  2. PTH- levels elevated to serum calcium
  3. Hypophosphatemia
  4. Hypercalciuria
  5. Urine cAMP elevated
  6. Chloride/Phosphorus ratio of > 33 is diagnostic of primary hyperparathyroidism (33:1-rule)
  • Radiographs: subperiosteal bone resorption, osteopenia
82
Q

Treatment of hyperparathyroidism

A
  1. Surgery is the only definitive treatment, but not all patients require it. If the patient is over 50, and is asymptomatic, surgery may not be needed.
    a) Primary hyperparathyroidism due to hyperplasia - all four glands are removed. (a small amount of parathyroid tissue isplaced in the forearm muscle, so that you dont need reexploration of the neck if hyperplasia recurs postoperatively.
    b) Primary hyperparathyroidism due to adenoma - Surgical removal is curative
    c) Primary hyperparathyroidism due to carcinoma - remove the tumor, ipsilateral thyroid lobe, and all enlarged lymph nodes.
  2. Medical - encourage fluids. Give diuretics (furosemide) to enhance calcium excretion if hypercalcemia is severe(Do not give Thiazide diuretics!)
83
Q

Cushing syndrome vs Cushing disease- General

A
  1. Cushing SYNDROME results from excessive levels of glucocorticoids (cortisol is the principal glucocorticoid) due to any cause.
  2. Cushing DISEASE results from pituitary Cushing syndrome (pituitary adenoma)
84
Q

Causes of cushing syndrome

A
  1. Iatrogenic = Most common cause, and is due to prescribed prednisone or other steroids.
  2. ACTH-secreting adenoma of the pituitary(cushing disease) = 2nd most common.
  3. Adrenal adenomas and carcinomas (10-15%)
  4. Ectopic ACTH production (10-15%)
    - ACTH secreting tumor stimulates the cortisol release from the adrenal glands without the normal negative feedback loop
    - More than two-thirds are small cell carcinomas of the lung. Bronchial carcinoid and thymoma may be the cause.
85
Q

Cushing syndrome - Clinical

A
  1. Change in appearance (Central obesity, hirsutism, moon facies, “buffalo hump”, purple striae om abdomen, lanugo hair, acne, easy bruising
  2. HTN
  3. Decreased glucose tolerance (diabetes)
  4. Hypogonadism - menstrual irregularity and infertility
  5. Masculinization in females (androgen excess - only seen in ACTH-dependent forms
  6. Musculoskeletal - proximal muscle wasting and weakness, osteoporosis, aseptic necrosis of femoral head may occur
  7. Psychiatric disturbances - depression and mania
  8. Increased likelihood of infection(impaired immunity)
86
Q

Diagnosing Cushing syndrome

A
  1. Initial screening
    a) An overnight (low-dose) dexamethasone supression test is the initial screening test. Give the patient 1 mg of dexamethasone at 11pm. Measure the serum cortisol level at 8pm.
    - If serum cortisol < 5, cushing syndrome can be
    excluded
    - If serum cortisol is > 5, and often > 10, the patient
    has Cushing syndrome. Order a high dose
    dexamethasone supression test to determine the
    cause (cushing disease vs.adrenal tumor
    vs.ectopic ACTH tumor)

b) The 24h urinary free cortisol level is another excellent screening test, values greater than four times normal are rare except in Cushing syndrome.

  1. ACTH level - once you establish a diagnosis of Cushing syndrome, measure the ACTH level.
    - If it is LOW - likely an adrenal tumor or hyperplasia, not a pituitary disease or an ectopic ACTH-producing tumor
  2. High-dose dexamethasone suppression test
    a) In Cushing disease, the result is a decrease in cortisol levels.
    b) If cortisol suppression does NOT occur and plasma ACTH levels are high, an ectopic ACTH-producing tumor is likely the diagnosis.
  3. CRH stimulation test - CRH is administered I.v
    a) If ACTH/cortisol levels increase, then cushing disease is the diagnosis
    b) If ACTH/cortisol levels do not increase(“no response”), then the patient has either ectopic ACTH secretion or an adrenal tumor
  4. Imaging test -CT or MRI

(se “table 4-2 s.185)

87
Q

Treatment of Cushing syndrome

A
  1. Iatrogenic - tapering of glucocorticoid
  2. Pituitary cushing syndrome: surgery (transsphenoidal ablation of pituitary adenoma)
  3. Adrenal adenoma or carcinoma: surgery
88
Q

Pheochromocytoma - General

A

Rare tumors that produce, store and secrete catecholamines. 90% found in adrenal MEDULLA.

  • May be fatal if undiagnosed
  • Arise from the chromaffin cells of the adrenal medulla, or from the sympathetic ganglia if extra-adrenal.
89
Q

Clinical features of pheochromocytoma

A
  1. HTN - persistently high, with episodes of severe HTN
  2. Severe pounding headache
  3. Inappropriate severe sweating
  4. Tachycardia
  5. Palpitations, with sudden severe HTN
  6. Anxiety
  7. Feeling of impending doom
  8. Labs: hyperglycemia, hyperlipidemia, hypokalemia
90
Q

Diagnosing pheochromocytoma

A
  1. Urine screen, test for presence of:
    - Metanephrine
    - Vanillylmandelic acid, homovanillic acid, normetanephrine
  2. Plasma metanephrines have been proposed by some as superior to rine.
  3. Urine/serum epinephrine and norepinephrine levels - if the epinephrine level is elevated, the tumor must be adrenal or near the adrenal gland, because nonadrenal tumors cannot methylate norepinephrine to epinephrine.
  4. Tumor localization tests - CT, MRI
91
Q

Treating pheochromocytoma

A
  1. Surgical tumor resection with early ligation of venous drainage is treatment of choice. Pts. should be tx with a-blockade (typically phenoxybenzamine) for 10-14 days prior to surgery as well as B-blockade (propranolol) for 2-3 days prior to surgery. The a-blockade is used to control BP, and the B-blockade is used to decrease tachycardia.
92
Q

Primary hyperaldosteronism

A

Excessive production of aldosteron by the adrenal glands independent of any regulation by the renin-angiotensin system. Excessive mineralcorticoids increase the activity of the Na/K - pump in the cortical collecting tubules.

a) Sodium retention, causing ECF volume expansion and HTN
b) Potassium loss - results in hypokalemia

Excess aldosterone also increases the secretion of hydrogen ions into the lumen of the medullary collecting tubules, results in metabolic alkalosis.

93
Q

Causes of primary hyperaldrosteronism

A
  1. Adrenal adenoma = most common (Conn-syndrome)
  2. Adrenal hyperplasia- almost always bilateral
  3. Adrenal carcinoma (in < 1% of cases)
94
Q

Hyperaldosteronism - clinical features (4)

A
  1. HTN
  2. Headache, fatigue, weakness
  3. Polydipsia, nocturnal polyuria
  4. Absence of peripheral edema
95
Q

Diagnosing primary hyperaldosteronism

A

If plasma aldosterone-to-renin ratio is > 30 - evaluate further.
For definite diagnosis, one of the two tests:
1. Saline infusion test
- Infusion of saline will decrease aldosterone levels in normal patients, but not in those with primary aldosteronism
- If aldosterone levels are < 8,5ng/dL after saline, primary aldosteronism may be ruled out.

  1. Oral sodium loading
    - The pt is given a high salt diet for 3 days. High urine aldosterone in the setting of high urine sodium confirms the diagnosis.
96
Q

Treating primary hyperaldosteronism

A
  1. For adenoma- surgical resection
  2. For bilateral hyperplasia
    a) Spironolactone inhibits the action of aldosterone
    b) Surgery is not indicated
97
Q

Adrenal insufficiency - Causes

A
  1. Primary adrenal insuff = Addison disease
    a) Idiopathic - autoimmune = most common
    b) Infectious diseases - tuberculosis, fungal inf.
    c) Iatrogenic - f.eks, a bilateral adrenalectomy
    d) Metastatic disease
  2. Secondary adrenal insuff
    a) Patients on long term steroid-therapy = Most common
    b) Hypopituitarysm (rare)
  3. Tertiary adrenal insuff - hypothalamic disease
98
Q

Clinical features of Adrenal insufficiency

A
  1. Lack of cortisol
    a) GI-symptoms - anorexia, nausea, vomiting, vague abd.pain, weight loss
    b) Mental symptoms - lethargy, confusion,psychosis
    c) Hypoglycemia - Cortisol is a gluconeogenic hormone
    d) Hyperpigmentation
    - low cortisol stimulates ACTH and MSH secretion
  2. Low aldosteron
    - Sodium loss, causing hyponatremia and hypovolemia, which may lead to hypotension, decr. cardiac output, decr. renal perfusion, weakness, shock, syncope AND hyperkalemia (due to retention of potassium
99
Q

Diagnosing Adrenal Insufficiency

A
  1. Decreased plasma cortisol level
  2. Plasma ACTH level - if low, this implies a secondary adrenal insufficiency
  3. Standard ACTH test
    - This is a definitive test for primary adrenal insufficiency; give an IV infusion of synthetic ACTH, and measure plasma cortisol at the end of the infusion.
    - In primary adrenal insuff, cortisol does not increase sufficiently.
    - In secondary adrenal insuff, cortisol fails to respond to ACTH infusion, as in primary adrenal insufficiency.

4.MRI of pituitary/hypothalamus

100
Q

Treating Adrenal insufficiency

A
  1. Primary: daily oral glucocorticoid (hydrocortisone or prednisone) and daily fludrocortisone (mineralcorticoid)
  2. Secondary: same as in primary, exept that mineralcorticoid replacement is not necessary.
101
Q

Congenital adrenal hyeprplasia - General

A
  1. Autosomal recessive disease

2. Ninety percent of the cases are due to 21-hydroxylase deficiency (11-hydroxylase is the next most common cause)

102
Q

Congenital adrenal hyperplasia - Clinical

A
  1. Decreased cortisol and aldosterone production are the main events. Increased ACTH secretion (due to the lack of neg. feedback) causes adrenal hyperplasia
  2. As precursors of cortisol and aldosterone build up, they are shunted toward the synthesis of androgens, causing cirilization.
  3. Virilizing features:
    - Female infants - born with ambigous genitalia but normal female ovaries and uterus
    - Male infants - no genital abnormalities
  4. Salt wasting form
    a) Emesis, dehydration, hypotension and shock
    b) Hyponatremia and hyperkalemia - due to lack of aldosterone
    c) Hypoglycemia - due to lack of cortisol
103
Q

Diagnosing CAH

A

High levels of 17-hydroxyprogesterone in the serum

104
Q

Treating CAH

A
  1. Medically: use cortisol and mineralocorticoid; this shunts off the xcess ACTH secretion (via neg.feedback).
  2. Surgically - early correction of female genital abnormalities is generally recommended.
105
Q

Diabetes Mellitus - General/Classification

A
  1. DM1 - ca 5% of all
    - Severe deficiency of insulin. Patients require insulin to live.
    - Onset typically before 20
    - Not related to obesity
  2. DM2 - 90% or more of all
    - Insulin levels normal to high, diminishes over years
    - Insulin resistance (due to obesity)
    - Often goes undiagnosed for years
  3. Impaired glucose tolerance
    - Fasting glucose between 110-125mg/dl or a 2-hour postprandial glucose between 140-199 mg/dL
    - One percent to five percent annual increase in risk of developing type 2 DM.
    - Increased risk for cardiovascular disease
106
Q

Pathogenesis of DM1 and 2

A

DM1:

  • Autoimmune disease - destruction of B-cells
  • Overt DM1 does not appear until about 90% are destroyed.

DM2:

  • Obesity - incr. fatty acids -> muscles more insulin resistant -> reducing glucose uptake. Therefore, obesity exacerbates insulin resistance.
  • Genetics
  • Age (Insulin production decreases with age)
107
Q

Which test-association is typical in Type 1 DM but not in type 2?

A

HLA-DQ/DR

108
Q

Diagnosing DM

A
  1. Fasting plasma glucose = preferred test for screening
    - If between 100 and 126 mg/dL, perform a 75g OGTT or recheck fasting glucose
  2. Random plasma glucose - criteria for DM: glucose > 200mg/dL in a person with diabetic symptoms
  3. 2h-postprandial glucose level - criteria for DM: glucose > 200 mg/dL after administration of the equivalent of a 75g glucose load .
  4. HbA1c - criteria for DM: A1c > 6.5%
109
Q

Treating DM

A
  1. Diet and excercise
  2. Oral hypoglycemic drugs
    a) Use these in type II diabeteic patients when conservative therapy fails.
    b) Start with one agent (Metformin is best initial drug therapy) If monotherapy fails, use two agents from different classes in combination.
    c) Metformin blocks gluconeogenesis. It is contraindicated in patients with renal failure

d) Other oral hypoglycemics include:
- Sulfonylureas
- Thiazilodinediones
- Alpha glucosidase inhibitors
- Incretins
- Pramlintide
- Repaglinide/nateglinide

110
Q

Most common macrovascular complications of DM

A
  1. Accelerated atherosclerosis -> MI, Stroke, CHF –> keep a lowered BP.
    (Risk of CAD is 2-4x higher in diabetics)
    - Most common cause of death in diabetic patients
    - Silent MI are common
    - Cerebral strokes are common
111
Q

Most common microvascular complications of DM

A
  1. Diapetic nephropathy = most important cause of ESRD.
    a) Nodular glomerular sclerosis (Kimmelstiel-Wilson syndrome) - hyaline deposition in one area of glomerulus = pathognomif for DM
    b) Diffuse glomerular sclerosis
    c) Isolated glomerular basement membrane thickening
    ! If microalbuminuria is present, strict glycemic control is critical!
    - HTN increases the risk of progression of diabetic nephropathy to ESRD. Control BP aggressively.
    - Initiate ACE inhibitors or ARB immediately. These agents are proven to decrease the rate of progression of nephropathy.
    - Microalbuminuria is the screening test.
  2. Diabetic retinopathy
    - Annual screening reccomended
    - Can lead to blindness, laserphotocoagulation is tx
    - Fundoscopic examination shows hemorrhages, exudates, microaneurysms, and venous dilation.
  3. Diabetic neuropathy
    - Usually affects sensory nerves in a “stocking/glove” pattern. Usually begins in feet, later involves hands. Numbness and parasthesias are common
    - Ulcer formation - charcot joints.
    - Painful diabetic neuropathy - tx: gabapentin, TCA, pregabalin
    - CN complications - secondary to nerve infarction (most commonly involves CN III, but also CN VI and IV.
  • Mononeuropathies (s.199)
  • Autonomic neuropathy (s.199)
  • Diabetic foot
112
Q

Diabetic ketoacidosis - General

A

DKA is an acute, life-threatening medical emergency that can occur in both type I and type II diabetic patiens (most common in type 1).

  • This occurs secondary to insulin deficiency and glucagons excess, both of which contribute to accelerated severe hyperglycemia and accelerated ketogenesis.
  • Severe hyperglycemia leads to an osmotic diuresis, which causes dehydration and volume depletion.
  • Consequences of DKA include hyperglycemia, ketonemia, metabolic acidosis and volume depletion.
113
Q

Precipitating factors of DKA

A

Any type of stress/illness, such as infection, trauma, MI, stroke, surgery, sepsis, GI bleeding.
- Inadequate administration of insulin

114
Q

Clinical features of DKA

A
  1. Nausea, vomiting
  2. Kussmaul respiration - rapid, deep breathing
  3. Abdominal pain that may mimic acute abdomen - often with guarding and rigidity
  4. Fruity (acetone) breath odor
  5. Marked dehydration, orthostatic hypotension, tachycardia - volume depletion is always present
  6. Polydipsia, polyuria, polyphagia, weakness
  7. Altered consciousness, drowsiness, frank coma
  8. Symptoms usually occur rapidly, typically in less than 24h.
115
Q

Diagnosing DKA

A
  1. Hyperglycemia; serum glucose typically > 450 mg/dL and < 850 mg/dL
  2. Metabolic acidosis; Blood pH < 7..3 and serum HCO3 < 15 MEQ/L
  3. Ketonemia and ketonuria

!Ketonemia and acidosis are required for the diagnosis of DKA!

116
Q

Treating DKA

A
  1. Insulin - but be certain that the patient is not hypokalemic before giving insulin.
    - Give a priming dose of 0.1 units/kg of regular insulin, followed by an infusion of 0.1 units/kg per hour. Continue insulin until metabolic acidosis is corrected, then begin to decrease insulin.
  2. Fluid replacement (normal saline)
    - Give immediately after diagnosing
    - Add 5% glucose once the blood glucose reaches 250 mg/dL to prevent hypoglycemia.
  3. Replace potassium prophylactically with IV fluids
    - Initiate within 1-2h of starting insulin
    - Monitor potassium, magnesium and phosphate levels very closely and replace as necessary.
117
Q

Hypoglycemia - general

A

The primary organ at risk in hypoglycemia is the brain.

  • Unlike other tissues, the brain cannot use free fatty acids as an energy source.
  • Hypoglycemia is really due to an imbalance between glucagon and insulin
118
Q

Hypoglycemia - Causes

A
  1. Drug-induced (insulin)
  2. Factitious hypoglycemia (check C-peptide - the C-peptide will be low)
  3. Insulinoma
  4. Ethanol ingestion
  5. Postoperative complication after gastric surgery
  6. Reactive hypoglycemia
  7. Adrenal insufficiency
  8. Liver failure
119
Q

Hypoglycemia - Symptoms

A

Sweating, tremors, increased BP, anxiety, palpitations, irritability, behavioural changes, weakness, drowsiness, headache, confusion, convulsions, coma and even death.

120
Q

Diagnosing hypoglycemia

A
  1. Blood glucose below 50
  2. Whipple triad
  3. Lab test - C peptide, serum insulin
121
Q

Insulinoma - general

A
  1. Insulin-producing tumor arising from the B-cells of the pancreas
  2. Associated with MEN 1 syndrome
  3. Usually benign (in up to 90% of the cases)
122
Q

Clinical features of Insulinoma

A

Hypoglycemia (Diaphoresis, palpitations, tremors, high blood pressure, anxiety, headache, visual disturbances, confusion,seizures, coma)

123
Q

Zollinger Ellison Syndrome (Gastrinoma)

A

A pancreatic islet cell tumor that secretes high gastrin, which leads to profound gastric acid hypersecretion, resulting in ulcers.

  • 60% are malignant, 20% associated with MEN 1.
124
Q

Glucagonoma

A

A glucagon-producing tumor located in the pancreas
- Clinical manifestation include necrotizing migratory erythema (usually below the waist), glossitis, stomatitis, DM, hyperglycemia.
Tx: surgical resection.

Internal medicine (16 decks)

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