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1. AA my internal medicine > 3. Endocrinology > Flashcards

3. Endocrinology Flashcards

1
Q

Causes of hyperthyroidism?

A
  • Graves disease (diffuse toxic goiter): the most common cause 80%.
  • Plummer disease (multinodular toxic goiter): 15%.
  • Toxic thyroid adenoma (single nodule): 2%.
  • Hashimoto thyroiditis and subacute (granulomatous) thyroditis: (both can cause transient hyperthyroidism).
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2
Q

Graves disease is ?

A
  • An autoimmune disorder: A thyroid-stimulating immunoglobulin (IgG) anti- body binds to the TSH receptors on the surface of thyroid cells and triggers the synthesis of excess thyroid hormone.
  • Seen most often in younger women.
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3
Q

Plummer disease is ?

A
  • Characterized by hyperfunctioning areas that produce high T4 and T3 levels, thereby decreasing TSH levels. As a result, the rest of the thyroid is not functioning (atrophy due to decreased TSH).
  • More common in elderly patients, and more common in women than men.
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4
Q

What are the signs/symptoms of hyperthyroidism specific to Graves’s disease?

A
  • Exophthalmos (is a bulging of the eye anteriorly out of the orbit.).
  • Pretibial myxedema.
  • Thyroid bruit.
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5
Q

Symptoms of hyperthyroidism?

A

a. Nervousness, insomnia, irritability
b. Hand tremor, hyperactivity, tremulousness
c. Excessive sweating, heat intolerance
d. Weight loss despite increased appetite
e. Diarrhea
f. Palpitations (duetotachyarrhythmias)
g. Muscle weakness

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6
Q

Signs of hyperthyroidism extra-thyroidal (eyes) ?

A
  • Proptosis, due to edema of the extraocular muscles and retro-orbital tissue, is a hallmark of Graves disease.
  • Irritation and excessive tearing are common due to corneal exposure.
  • Lid retraction may be the only sign in milder disease
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7
Q

Signs of hyperthyroidism extra-thyroidal (CV)?

A
  • Arrhythmias (Sinus tachycardia, atrial fibrillation, and premature ventricular contractions).
  • Elevated BP
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8
Q

Signs of hyperthyroidism extra-thyroidal (Skin changes) ?

A
  • Warm and moist.

- Pretibial myxedema (edema over tibial surface due to dermal accumulation of mucopolysaccharides).

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9
Q

Signs of hyperthyroidism extra-thyroidal (neurologic) ?

A
  • Brisk Deep tendon reflexes.

- Tremors.

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10
Q

Diagnosis of hyperthyroidism?

A
  1. Serum TSH level (LOW)—initial test of choice.
  2. T4 should be elevated.
  3. Testing the T3 level is usually unnecessary but may be helpful if TSH level is low and free T4 is not elevated, because excess T3 alone can cause hyperthyroidism.
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11
Q

What is the treatment for patients with Graves’ disease?

A
  • nonpregnant:
  • Start methimazole (in addition to the β-blocker).
  • Taper β-blocker after 4 to 8 weeks (once methimazole starts to take effect).
  • Continue methimazole for 1 to 2 years.
  • pregnant:
  • propylthiouracil (PTU) is preferred.
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12
Q

For which patients should we consider therapy with radioactive iodine ablation therapy (131i)?

A
  • Elderly patients with Graves’ disease.
  • Patient with solitary toxic nodule.
  • Patients With Graves’ disease in whom therapy with anti-thyroid drugs fails (due to relapse, agranulocytosis)
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13
Q

What are the thionamides and what is the MOA in hyperthyroidism ?

A
  • Methimazole and propylthiouracil (PTU).
  • inhibit thyroid hormone synthesis, and PTU also inhibits conversion of T4 to T3.
  • A major serious side effect is agranulocytosi.
  • skin rash, arthralgias, and hepatotoxicity.
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14
Q

general info about Thyroid storm?

A
  • This is a rare, life-threatening complication of thyrotoxicosis.
  • Characterized by an acute exacerbation of the manifestation of hyperthyroidis.
  • High mortality rate: up to 20% of patients enter a coma or die.
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15
Q

What are the precipitating factors for a thyroid storm?

A

Infection, diabetic ketoacidosis, or stress (e.g., severe trauma, surgery, illness, childbirth).

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16
Q

What are the clinical manifestations of thyroid storm?

A

Marked fever, Tachycardia, agitation, psychosis, confusion, and G.I. symptoms (Nausea, vomiting and diarrhea)

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17
Q

Management of thyroid storm?

A

4 P’s:

  • β-blockers (e.g., Propanolol)
  • Propylthiouracil.
  • Corticosteroids (e.g., Prednisolone).
  • Potassium iodide (Lugol iodine).
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18
Q

What are the causes of primary hypothyroidism?

A
  • Primary hypothyroidism Is the failure of the thyroid to produce sufficient thyroid hormone. This accounts for about 95% of all cases.
  • Hashimoto disease (Chronic thyroiditis): most common.
  • Iatrogenic.
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19
Q

What are the causes of 2ndary and tertiary hypothyroidism?

A
  • Secondary hypothyroidism (due to pituitary disease: i.e deficiency of TSH).
  • Tertiary hypothyroidism ( due to hypothalamic disease, i.e, deficiency of TRH)
  • Both are associated with a low T4 and a low TSH level.
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20
Q

Symptoms of hypothyroidism?

A

a. Fatigue, weakness, lethargy
b. Heavy menstrual periods (menorrhagia), slight weight gain (10 to 30 lb)— patients are not typically obese.
c. Cold intolerance
d. Constipation
e. Slow mentation, inability to concentrate (Mild at first, In the later stages of dementia can occur), dull expression.
f. Muscle weakness, arthralgias
g. Depression
h. Diminished hearing

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21
Q

Signs of hypothyroidism?

A

A. Dry skin, coarse hair: thickened, puffy features.
b. Hoarseness
c. Nonpitting edema (edema due to glycosaminoglycan in interstitial tissues, not
water and salt)
d. Carpal tunnel syndrome
E. Slow relaxation of deep tendon reflexes.
f. Loss of lateral portion of eyebrows.
g. Bradycardia
H. Goiter ( Hashimoto disease: Goiter is rubbery, nontender, and even nodular.
subacute thyroiditis—goiter is very tender and enlarged, although not always symmetrically.)
i. History of upper respiratory infection and fever (sub acute thyroiditis)

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22
Q

Diagnosis of hypothyroidism ?

A
  • High TSH level: most sensitive indicator of hypothyroidism.
  • Low TSH: 2ndary and tertiary hypothyroidism.
  • Low free T4 .
  • Increased antimicrosomal antibodies (Hashimoto thyroiditis).
  • others: Elevated LDL and decreased HDL. And anemia. (mild normocytic)
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23
Q

TTT for hypothyroidism?

A 
* levothyroxine 
(T4): treatment of choice.
- Effect is evident in 2-4 wks.
- Convenient once—daily morning dose.
- Treatment is continued indefinitely.
- Monitor TSH level and clinical state periodically.
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24
Q

Causes of Thyroiditis?

A

A. Subacute (viral) thyroiditis (subacute granulomatous thyroiditis).
B. Subacute lymphocytic thyroiditis (painless thyroiditis, silent thyroiditis).
C. Chronic lymphocytic thyroiditis (Hashimoto thyroiditis, lymphocytic thyroiditis).
D. Fibrous thyroiditis (Riedel thyroiditis).

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25
Q

How to diagnose thyroid nodule ?

A
  1. Fine-needle aspiration (FNA) biopsy. (Test of choice): combined with usg guidance.
  2. Thyroid scan.
  3. thyroid ultrasound.
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26
Q

What kind of thyroid cancers is fine needle aspiration (FNA) is reliable ?

A

All cancers papillary, medullary, And anaplastic.

EXCEPT follicular.

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27
Q

Risk factors of thyroid cancer?

A
  • Head and neck radiation (during childhood).
  • Gardner syndrome and Cowden syndrome for papillary cancer.
  • MEN type II for medullary cancer.
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28
Q

Types of thyroid cancer?

A

A. Papillary carcinoma.

b. Follicular carcinoma.
c. Medullary carcinoma.
d. Anaplastic carcinoma.

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29
Q

Papillary carcinoma ?

A
  • Accounts for 70-80% of all thyroid cancers.
  • Least aggressive thyroid cancer (Excellent prognosis).
  • Most important risk factor is a history of radiation to the head or neck.
  • Positive iodine uptake.
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30
Q

Follicular carcinoma ?

A
  • Accounts for 15% of all thyroid cancers. Avidly absorbs iodine.
  • Prognosis is worse than for papillary cancer.
  • ## May be associated with iodine deficiency.
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31
Q

Hürthle cell carcinoma ?

A
  • Is one variant of Follicular carcinoma.
  • Characteristics cells contain abundant cytoplasm, tightly packed mitochondria, and oval nuclei with prominent
    nucleoli.
  • These tumors are radioiodine resistant.
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32
Q

Medullary carcinoma?

A
  • Accounts for 2-3% of all thyroid cancers.
  • 1/3 sporadic, 1/3 familial, 1/3 associated with MEN II (always screen for pheochromocytoma).
  • Arises from the arafollicular cells (C cells): produces CALCITONON.
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33
Q

Anaplastic carcinoma ?

A
  • Accounts for 5% of all thyroid cancers.
  • Highly malignant.
  • May arise from a long-standing follicular or papillary thyroid carcinoma.
  • Prognosis (grim): Death typically a course within a few months.
  • Mortality is usually due to the invasion of adjacent organs (trachea, neck vessels).
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34
Q

Which type of thyroid cancer should we suspect if we observe high calcitonin levels?

A

Medullary carcinoma.

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35
Q

Treatment of Papillary carcinoma ?

A

A. Lobectomy with isthmusectomy.
B. Total thyroidectomy if tumor is >3 cm, tumor is bilateral, tumor is advanced, or distant metastases are present.
C. Adjuvant treatment: TSH suppression therapy: radioidione theapy for larger tumors.

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36
Q

Treatment of Follicular carcinoma ?

A

total thyroidectomy with postoperative iodine ablation.

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37
Q

Treatment of Medullary carcinoma ?

A

total thyroidectomy.

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38
Q

Treatment of anaplastic carcinoma ?

A

hemotherapy and radiation may provide a modest improvement in survival. Palliative surgery for airway compromise may be needed.

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39
Q

Pituitary Adenomas ?

A
  • Account for about 10% of all intracranial neoplasms.
  • Almost all pituitary tumors are benign.
  • Size: microadenoma (<10 mm) or macroadenoma (>10 mm).
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40
Q

Clinical features of Pituitary Adenomas ?

A
  1. Hormonal effects (occur due to hypersecretion of one or more of the following hormones):
    - Prolactin.
    - GH (result in acromegaly).
    - ACTH (result in cushing disease).
    - TSH.
    - 2. Hypopituitarism.
  2. Mass effects.
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41
Q

Diagnosis of Pituitary Adenomas ?

A
  1. MRI is the imaging study of choice.
  2. Pituitary hormone levels.
  • Although it causes hyperthyroidisim “ still TSH levels will be high”
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42
Q

TTT of Pituitary Adenomas ?

A
  1. Transsphenoidal surgery is indicated in most patients.
    - except patients with Prolactinomas, for which medical management can be tried first.
  2. Radiation therapy and medical therapy are adjacent and most patients.
43
Q

Most common causes of Hyperprolactinemia ?

A
  1. Prolactinoma.
  2. Medications.
  3. Pregnancy.
  4. Renal failure.
  5. Suprasellar mass lesions.
  6. Hypothyroidism.
  7. Idiopathic.
44
Q

Prolactinoma ?

A

a. Most common cause of hyperprolactinemia

b. Most common type of pituitary adenoma (up to 40%)

45
Q

What the outcome of high levels of prolactin ?

A
  • Inhibit secretion of GnRH.
  • This leads to decreased secretion of LH and FSH.
  • Which in turn leads to decreased production of estrogen and testosterone.
46
Q

Clinical features of Hyperprolactinemia?

A
  • Men:
  • Hypogonadism, decreased libido, infertility, impotence.
  • Galactorrhea or gynecomastia (uncommon).
  • parasellar signs and symptoms (visual defects and headaches).
  • Women:
  • Premenopausal: menstrual irregularities, oligomenorrhea or amenorrhea,
    anovulation and infertility, decreased libido, dyspareunia, vaginal dryness, risk
    of osteoporosis, galactorrhea.
  • Postmenopausal: parasellar signs and symptoms (less common than in men)
47
Q

Diagnosis of Hyperprolactinemia?

A
  1. Elevated serum prolactin level.
  2. Order a pregnancy test and TSH level.
  3. CT scan or MRI to identify any mass lesions.
48
Q

Treatment of of Hyperprolactinemia?

A
  1. Treat the underlying cause (e.g., stop medication, treat hypothyroidism).
  2. If prolactinoma is the cause and the patient is symptomatic, treat with bromocriptine (a dopamine agonist that secondarily diminishes the production and release of prolactin).
  3. Consider surgical intervention if symptoms progress despite appropriate medical therapy. However, the recurrence rate after surgery is high.
49
Q

Acromegaly ?

A
  • Acromegaly is broadening of the skeleton, which results from excess secretion of pituitary GH after epiphyseal closure.
  • It is almost always caused by a GH-secreting pituitary adenoma.
50
Q

Clinical features of Acromegaly ?

A
  • Growth promotion.
  • Metabolic disturbances.
  • Parasellar manifestations.
51
Q

Diagnosis of Acromegaly ?

A
  1. IGF-1, also known as somatomedin C, should be significantly elevated in acromegaly.
  2. Oral glucose suppression test—glucose load fails to suppress GH.
  3. MRI of the pituitary.
52
Q

Treatment of 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.
53
Q

Calcification of the supra sellar region seen on brain imaging is nearly diagnostic of?

A

Craniopharyngioma

54
Q

Hypopituitarism ?

A
  • All or some of the hormones released from the anterior pituitary may be absent.
  • Clinical manifestations depend on which hormones are lost.
55
Q

Clinical features of Hypopituitarism ?

A
  1. Reduced GH: growth failure (decreased muscle mass in adults), increased LDL, increased risk of heart disease, increased LDL
  2. Reduced prolactin: failure to lactate
  3. Reduced ACTH: adrenal insufficiency.
  4. Reduced TSH: hypothyroidism
  5. Reduced gonadotropins (LH and FSH): infertility, amenorrhea, loss of secondary
    sex characteristics, diminished libido
  6. Reduced antidiuretic hormone (ADH): diabetes insipidus.
  7. Reduced mealnocyte-stimulating hormone (MSH): decreased skin and hair pigmentation.
56
Q

TTT of diabetes insipidus?

A
  • Central DI:
  • Desmopressin ( nasal spray, orally or by injection).
  • Chlorpropamide.
  • Nephrogenic DI:
  • treat with sodium restriction and thiazide diuretics.
57
Q

What is the main cause of Hypoparathyroidism ?

A
  1. Head and neck surgery accounts for The majority of cases: thyroidectomy, parathyroidectomy, radical surgery for head and neck malignancies.
  2. Nonsurgical hypoparathyroidism is rare.
58
Q

Clinical features of Hypoparathyroidism ?

A
  • Cardiac arrhthmias.
  • Rickets and osteomalacia.
  • Increased neuromascular irritability due to hypocalcemia.
  • Basal ganglia calcifications.
  • Proglonged QT interval on ECG.
  • Cataracts
59
Q

Symptoms of Increased neuromascular irritability due to hypocalcemia ?

A 
A. Numbness/tingling : circumoral, fingers, toes.
B. Tetany:
- Hyperactive deep tendon reflexes.
- Chvostek sign.
- Trousseau sign.
C. Grand mal seizures.
60
Q

Chvostek sign ?

A
  • Tapping the facial nerve elicits contraction of facial muscles.
  • its a sign of hypocalcemia.
  • it could also occur with hypokalemia.
61
Q

Trousseau sign ?

A
  • Inflating the BP cuff to a pressure higher than the patient’s
    systolic BP for 3 minutes elicits carpal spasms
  • its a sign of hypocalcemia.
62
Q

Diagnosis of Hypoparathyroidism ?

A
  1. Low serum calcium
  2. HIGH serum phosphate
  3. Serum PTH inappropriately low
  4. Low urine cAMP
63
Q

TTT of Hypoparathyroidism ?

A
  1. IV calcium gluconate in severe cases, oral calcium in mild to moderate cases.
  2. Vitamin D supplementation (calcitriol).
64
Q

General characteristics of Primary Hyperparathyroidism ?

A
  • One or more glands produce inappropriately high amounts of PTH relative to the serum calcium level.
  • Most common cause of hypercalcemia in the outpatient setting.
65
Q

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

A

Primary Hyperparathyroidism

66
Q

Causes of primary Hyperparathyroidism ?

A
  1. Adenoma (80% of cases): majority involve only one gland.
  2. Hyperplasia (15-20%): all four glands usually affected.
  3. Carcinoma (<1)
67
Q

Clinical features of primary Hyperparathyroidism ?

A
  1. Stones. (a. Nephrolithiasis b. Nephrocalcinosis).
  2. Bones. (boneaches, and Osteitis fibrosa cystica “brown tumors”).
  3. Groans. (Soul pain and weakness, pancreatitis, PUD, Gout, constipation)
  4. Psychiatric overturns. (Depression, fatigue, anorexia, sleep disturbances, anxiety, lethargy).
  5. Others. (Polydipsia, polyuria) (HTN, Shortened QT) (weight loss)
68
Q

Diagnosis of primary Hyperparathyroidism ?

A
  1. Labs:
    - Hypercalcemia.
    - High PTH levels.
    - low serum phosphate.
    - Hypercalciuria.
    - Urine cAMP is elevated.
    - Chloride/phosphorus ratio of > 33 is diagnostic of primary hyperparathyroidism.
  2. Radiographs:
    - Subperiosteal bone resorption.
    - Osteopenia.
69
Q

TTT of primary Hyperparathyroidism ?

A
  1. Surgery is the only definitive treatment, but not all patients require it.
  2. Medical: Encourage fluids. Give diuretics (Furosemide) to enhance calcium excretion if hypercalcemia is severe. (Do not give thiazide diuretics!)
70
Q

What is the most common cause of hypercalcemia in patient in hospital ?

A

Malignancy associated hypercalcemia.

71
Q

Cushing syndrome ?

A
  • Results from excessive levels of glucocorticoids (cortisol is the principal glucocorticoid) due to any cause.
  • Cushing disease results from pituitary Cushing syndrome (pituitary adenoma).
72
Q

Causes of cushing syndrome ?

A
  1. Iatrogenic Cushing syndrome is the most common cause. (androgen excess is absent).
  2. ACTH-secreting adenoma of the pituitary (Cushing disease) is the second most com- mon cause and leads to bilateral adrenal hyperplasia. Androgen excess is common.
  3. Adrenal adenomas and carcinomas (10% to 15%).
  4. Ectopic ACTH production (10% to 15%).
73
Q

Clinical features of Cushing syndrome?

A
  1. Changes in appearance: central obesity, hirsutism, moon facies, “buffalo hump,” purple striae on abdomen, lanugo hair, acne, easy bruising.
  2. HTN.
  3. Decrase glucose tolerance (diabetes).
  4. Hypogonadism (menstrual irregularity and infertility).
  5. Masculinization in females (androgen excess)—only seen in
    ACTH-dependent forms.
  6. Musculoskeletal
  7. Psychiatric disturbances- depression, mania.
  8. Increased likelihood of infections (due to impaired immunity)
74
Q

Diagnosis (Initial screening) of cushing syndrome ?

A
  1. Initial screening:
    a. An overnight (low-dose) dexamethasone suppression test is the initial screening test.
    b. The 24 hour urinary free cortisol level is another excellent screening test.
75
Q

How to differentiate between cushing disease and syndrome ?

A

Patient with Cushing disease may have hyperpigmentation due to Elevated ACTH levels.
Whereas patient with Cushing syndrome due to other causes will not have hyperpigmentation.

76
Q

An overnight (low-dose) dexamethasone suppression test?

A
  • Give the patient 1 mg of dexamethasone at 11 pm. Measure the serum cortisol level at 8 am.
  • If the serum cortisol is < 5 , Cushing syndrome can be excluded (this test is
    very sensitive).
  • If the serum cortisol is > 5 (and often >10), the patient has Cushing syndrome.
  • THEN, Order a high-dose dexamethasone suppression test to determine the
    cause (Cushing disease vs. adrenal tumor vs. ectopic ACTH tumor).
77
Q

Diagnosis ( if Initial screening is positive) of cushing syndrome ?

A
  • ACTH level.
  • High-dose dexamethasone suppression test.
  • CRH stimulation test.
  • Imaging tests.
78
Q

TTT of cushing syndrome?

A
  1. Iatrogenic Cushing syndrome: tapering of glucocorticoid.
  2. Pituitary Cushing syndrome: surgery (transsphenoidal ablation of pituitary adenoma)—usually safe and effective.
  3. Adrenal adenoma or carcinoma: surgery (adrenalectomy).
79
Q

Pheochromocytoma ?

A
  • Are rare tumors that produce, store, and secrete catecholamines.
  • 90% found in adrenal medulla.
  • Curable if diagnosed and treated, but may be fatal if undiagnosed.
80
Q

from where does Pheochromocytoma arises?

A
  • Chromaffin cells of the medulla.

- Sympathtic ganglia ( if extra-adrenal) rare.

81
Q

Rule of 10s for Pheochromocytoma Tumors ?

A
  • 10% are familial.
  • 10% are bilateral (suspect MEN II)
  • 10% are malignant.
  • 10% are multiple.
  • 10% occur in children.
  • 10% are extra-adrenal. (most common site is the organ of Zuckerkandl, which is located at the aortic bifurcation).
82
Q

Clinical features of Pheochromocytoma?

A
  • Acute heart failure.
  • Increase red blood cell count. (secrete erythropoietin)
  • Abdominal pain, constipation and weight loss.
  • HTN.
  • Severe pounding headache.
  • Inappropriate severe sweating.
  • Tachycardia.
  • Palpitation.
  • Anxiety.
  • Feeling of impending doom.
83
Q

Laboratory findings in pheochromocytoma ?

A
  • Hyperglycemia.
  • Hyperlipidemia.
  • Hypokalemia.
84
Q

Diagnosis of pheochromocytoma ?

A
  • Urine screen: test for the presence of the following breakdown products of catecholamines:
    a. Metanephrine
    b. Vanillylmandelic acid, homovanillic acid, normetanephrine.
  • Urine/serum epinephrine and norepinephrine levels.
  • Tumor localization tests—CT, MRI (most valuable).
85
Q

Treatment of pheochromocytoma ?

A
  • Surgical tumor resection with early ligation of venous drainage is the treatment
    of choice.
  • Patients should be treated with α-blockade (typically phenoxybenza- mine) for 10 to 14 days prior to surgery as well as β-blockade (i.e., propranolol) for 2 to 3 days prior to surgery.
86
Q

Primary Hyperaldosteronism?

A
  • Excessive production of aldosterone by the adrenal glands.
87
Q

Causes of Primary Hyperaldosteronism?

A
  1. Adrenal adenoma (in two-thirds of the cases)—aldosterone producing adenoma (Conn syndrome)
  2. Adrenal hyperplasia (in one-third of the cases)—almost always bilateral
  3. Adrenal carcinoma (in <1% of the cases)
88
Q

Clinical features of of Primary Hyperaldosteronism?

A
  1. HTN (most common clinical feature): may otherwise healthy
  2. Headache, fatigue, weakness
  3. Polydipsia, nocturnal polyuria (due to hypokalemia)
  4. Absence of peripheral edema
89
Q

Diagnosis of Primary Hyperaldosteronism?

A
  1. Ratio of the plasma aldosterone level to plasma renin.

2. For definitive diagnosis, one of the two tests is usually performed: (saline infusion test and Oral sodium loading).

90
Q

Adrenal Crisis ?

A
  • And a cute and securely symptomatic stage of adrenal insufficiency that can include severe hypertension and cardiovascular collapse, abdominal pain, acute renal failure, and death.
  • Any stress (eg. trauma infection) surgery can precipitate and adrenal crisis.
  • Can be fetal if untreated.
91
Q

TTT of Adrenal Crisis ?

A
  • IV hydrocortisone.

- IV fluids (saline with 5% dextrose).

92
Q

Causes of primary adrenal insufficiency (Addison diease) ?

A

a. Idiopathic (thought to be autoimmune disease) is the most common type in then industrialized world.
b. Infectious diseases—these include tuberculosis (most common cause worldwide) and fungal infections. Causes also include cytomegalovirus, cryptococcus, toxoplasmosis, and pneumocystis.
c. Iatrogenic—for example, a bilateral adrenalectomy.
d. Metastatic disease—from lung or breast cancer.

93
Q

Causes of 2ndary adrenal insufficiency ?

A

a. Patients on long-term steroid therapy—This is the most common cause of secondary adrenal insufficiency today.

94
Q

Clinical features of Adrenal Insufficiency?

A
  1. Lack of cortisol:
    a. GI symptoms—anorexia, nausea and vomiting, vague abdominal pain, weight loss
    b. Mental symptoms—lethargy, confusion, psychosis.
    c. Hypoglycemia—Cortisol is a gluconeogenic hormone.
    d. Hyperpigmentation
    e. Intolerance to physiologic stress is a feared complication..
  2. Low Aldosterone (only seen in primary adrenal insufficiency)
    a. Sodium loss, causing hyponatremia and hypovolemia, which may lead to:
    - Hypotension, decreased cardiac output, and decreased renal perfusion.
    - Weakness, shock, and syncope.
    b. Hyperkalemia (due to retention of potassium).
95
Q

Why Low Aldosterone only seen in primary adrenal insufficiency ?

A

bcz aldosterone depends on the renin–angiotensin system, not ACTH.
and in primary there is a destruction to adrenal gland it self which leads to decrease both cortisol and aldostrone.

96
Q

TTT of adrenal insufficiency ?

A
  1. Primary: Daily oral glucocoticoid (hydrocortisone or prednisone ) and daily fludrocortisone (mineralocorticoid).
  2. 2ndary: same as primary, EXCEPT that mineralocorticoid replacement is not necessary.
97
Q

prolactin secretion is suppressed by?

A

Dopamine receptor agonists.

98
Q

Standard treatment of multihermanol pituitary insufficiency in young adult is?

A
  • Hydrocortisone, L-thyroxine, gonadal hormones.
99
Q

Patient with central diabetes insipidus?

A

urine osmolality is low and does not change after fluid restriction.

100
Q

Clinical manifestations of MEN 1 ?

A
  • Hyperparathyroidism.
  • Pituitary adenomas.
  • Carcinoid tumors.
  • Adrenal cortex adenoma.
101
Q

Recurrent duodenum, jejunum and gastric ulceration may be a symptom of ?

A

MEN 1

102
Q

What kind of treatment we should propose as the best solution for 34 years old patient with benign autonomic thyroid gland tumor and hyperthyroidism ?

A

the radioiodine After the thyreostatic and fT4 and fT3 normalization with slight suppression of TSH.

103
Q

lab findings of subclinical hyperthyroidism ?

A

TSH: Low - fT4: N - fT3: N

104
Q

Hashimoto thyroiditis antibodies ?

A

Anti-TPO antibodies

1. AA my internal medicine (9 decks)

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