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Endocrinology Flashcards

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USMLE® Step 1 flashcards
1
Q

What is the name of the anterior and posterior lobes of the pituitary gland?

A
  • Anterior: Adenohypophysis.

- Posterior: Neurohypophysis

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2
Q

What are the hormones produced from the pituitary gland ?

A

Anterior:

  • Growth Hormone GH
  • Prolactin
  • Thyroid stimulating hormone TSH
  • Adrenocorticotropic hormone ACTH
  • Luteinizing hormone LH
  • Follicle-stimulating hormone FSH

Posterior:

  • Antidiuretic hormone ADH (Vasopressin).
  • Oxytocin
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3
Q

What is the cause of amenorrhea in Galactorrhea - amenorrhea syndrome ?

A

Amenorrhea is caused by inhibition of the hypothalamic release of Gonadotropin- releasing hormone (GnRH) with a decrease in Luteinizing hormone (LH) and follicle - stimulating hormone (FSH) secretion.

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4
Q

What is the most common presentation of Hyperprolactinemia in men?

A
  • Erectile dysfunction

- Decreased libido.

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5
Q

What is the most common functioning pituitary adenomas ?

A

Prolactinoma.

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6
Q

Name the medications that can cause hyperprolactinemia.

A
  • Drugs that block Dopamine synthesis ( Phenothiazines and Metoclopramide).
  • Dopamine- depleting agents (alpha-methyldopa and reserpine).
  • Tricyclic antidepressants.
  • Narcotics.
  • Cocaine.
  • SSRIs
  • Risperidone.
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7
Q

What os the clinical presentation of hyperprolactinemia ?

A

In females:

  • Galactorrhea.
  • Menstrual abnormalities (Amenorrhea/ oligomenorrhea.
  • Osteopenia.
  • Osteoporosis.
  • Infertility
  • Gynecomastia.

In males:

  • Hypogonadism.
  • Erectile dysfunction.
  • Decreased libido.
  • Infertility
  • Gynecomastia.
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8
Q

How to diagnose hyperprolactinemia ?

A
  • Rule out: Pregnancy , lactation, hypothyroidism and meds.
  • Prolactin level > 100 ng/mL suggest pituitary adenoma.
  • Prolactin level > 100 ng/mL = 1 cm prolactinoma.
  • Prolactin level > 200 ng/mL = 2 cm Prolactinoma.
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9
Q

What is the management of Prolactinoma ?

A
  • Cabergoline or Bromocriptine (Dopamine-agonist).
  • Cabergoline : less S/E and treats galactorrhea.
  • Surgery IF nor responsive to Tx or there is significant compressive neurological effects.
    Radiation if both drug therapy and surgery were ineffective.
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10
Q

What is the indication of Pituitary MRI ?

A

Basal, fasting, morning Prolactin level > 100 -200 mg/L in non pregnant women.

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11
Q

What is the normal level of Prolactin ?

A

< 20 mg/L

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12
Q

What is the name of the syndrome caused by excessive secretion of broth hormone?

A

Acromegaly

Gigantism in children

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13
Q

What is the most common cause of death in acromegaly ?

A

Cardiovascular mortality.

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14
Q

What are the clinical findings of acromegaly ?

A
  • Skeletal and soft tissue changes.
  • Enlargement of hands and feet.
  • Coarsening of facial features.
  • Thickened skin folds.
  • Enlarged nose and mandible.
  • Deeper voice.
  • Increased sweating.
  • OSA.
  • Enlarged internal organs.
  • Interstitial edema
  • Osteoarthritis.
  • Entrapment neuropathy.
  • Menstrual problems.
  • cardiac anomalies.
  • Metabolic changes (DM, Impaired glucose intolerance.
  • HTN
  • H/A and visual fiels loss
  • Proliferated articular cartilage causing sever joint disease.
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15
Q

How to diagnose acromegaly ?

A

Initial: High level of Insulin- like Growth Factor IGF-1.
Confirmatory: Give 100g of glucose orally, then measure growth hormone GH, if > 5ng/mL) then POSITIVE.

“normally glucose suppress level of GH.

Imaging: to localize tumor AFTER GH excess is documented biochemically. MRI better than CT.

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16
Q

What is the primary treatment of acromegaly ?

A

Transsphenoidal surgery.

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17
Q

What is the first and second line medical treatment of acromegaly ?

A

First line:
Somatostatin analogues :
- Octreotide (The best)
- Inareotide

Second line:
Pegvisomant (a growth hormone analogue ).

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18
Q

How does Pegvisomant (the second line treatment of acromegaly) works ?

A

It is a growth hormone analogue which antagonizes endogenic GH by blocking peripheral GH binding to its receptor in the liver.

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19
Q

What is the side effects of Octreotide (the first line treatment of acromegaly)?

A

Cholestasis, leading to cholecystitis.

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20
Q

What are the complications of acromegaly ?

A
  • Tumor pressuring on surrounding structures.
  • Invasion of tumor into brain or sinuses.
  • Cardiac failure.
  • Diabetes mellitus
  • cord compression
  • visual field defect.
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21
Q

What is the most common cause of death in acromegaly ?

A

Cardiac failure.

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22
Q

What are the condition that can lead to hypopituitarism ?

A
  • large pituitary tumors or cysts.
  • Hypothalamic tumors (craniopharyngiomas, meningiomas, gliomas).
  • Pituitary apoplexy syndrome.
  • Inflammatory diseases:
    • Granulomatous diseases (Sarcoidosis, TB, syphilis.
    • Eosinophilic granuloma
    • Autoimmune lymphocytic hypophysitis\
  • Trauma
  • Radiation
  • Surgery
  • Infections.
  • Vascular diseases: e.g (Sheehan postpartum necrosis)
  • Infiltrative disease: e.g ( hemochromatosis and amyloidosis)
  • Stroke
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23
Q

What is hypopituitarism ?

A

It is partial or complete loss of anterior function that results from any lesion which destroys the pituitary or hypothalamus or which interferes with the delivery of releasing and inhibiting factors to the anterior hypothalamus.

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24
Q

What is the most common cause of Panhypopituitarism ?

A

Pituitary adenomas.

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25
Q

What is Pituitary apoplexy syndrome ?

A

It is a syndrome associated with acute hemorrhagic infarction of a pre-existing pituitary adenoma and manifest as severe headache, nausea, vomiting and depression of consciousness.

It is a medical and neurosurgical emergency.

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26
Q

In which order does the pituitary hormones are lost in hypopituitarism ?

A
  1. Gonadotropin deficiency (LH and FSH).
  2. GH deficiency
  3. Thyrotropin deficiency (TSH).
  4. Adrenocorticotropin ACTH.
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27
Q

What is the clinical manifestation in patients with gonadotropin deficiency (LH and FSH) ?

A

Female:

  • Amenorrhea
  • Genital atrophy
  • Infertility.
  • Decreased libido
  • Loss of axillary and pubic hair.

Males:

  • Impotence.
  • Testicular atrophy
  • Infertility
  • Decreased libido
  • Loss of axillary and pubic hair.
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28
Q

What is the clinical manifestation in patients with Growth hormone GH deficiency?

A

In adults: Not clinically detectable:

  • Fine wrinkles
  • Increased sensitivity to insulin (Hypoglycemia).
  • Asymptomatic increase in lipid levels.
  • Decrease in muscle, bone and heart mass.
  • May accelerate atherosclerosis
  • Increase visceral obesity.

In children:

  • Growth failure.
  • Short stature.
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29
Q

What is the clinical manifestation in patients with Thyrotropin TSH deficiency?

A

Hypothyroidism:

  • Fatigue.
  • Weakness.
  • Hyperlipidemia
  • Cold intolerance
  • Puffy skin without goiter.
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30
Q

What is the clinical manifestation in patients with decreased cortisol ?

A
  • Fatigue
  • Decreased appetite
  • Weight loss
  • Decreased skin and nipple pigment
  • Decreased response to stress as well as fever, hypotension and hyponatremia.
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31
Q

Why does electrolyte changes like hyperkalemia and salt loss are minimal in secondary adrenal insufficiency ?

A

Because aldosterone production is mainly dependent on the Renin-Angiotensin system. ACTH (Adrenocorticotropin hormone) deficiency does not result in salt wasting, hyperkalemia and death that are associated with aldosterone deficiency.

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32
Q

What is the most reliable stimulus for GH secretion ?

A

Insulin- induced hypoglycemia. After injecting 0.1 u/kg of regular insulin, blood glucose declines to <40 mg/dL, in normal conditions that will stimulate GH level to > 10 mg/L and exclude GH deficiency .

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33
Q

What is the alternative to Insulin- induced hypoglycemia in order to stimulate GH release ?

A

Arginine infusion.

No risk of developing hypoglycemia.

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34
Q

What is the diagnostic test for adrenocorticotropin hormone ACTH deficiency ?

A

Insulin tolerance test:

  • Giving 0.05-0.1 U/kg of regular insulin.
  • Measure serum cortisol
  • Plasma cortisol should increase > 19 mg/dL.
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35
Q

How does Metyrapone test works for decreased adrenocorticotropin hormone ACTH production ?

A

Metyrapone blocks Cortisol production, which should increase ACTH levels.
A failure of ACTH to rise after giving Metyrapone would indicate pituitary insufficiency.

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36
Q

How to diagnose gonadotropin deficiency ?

A

In female :
- Mesure LH, FSH and Estrogen
In males:
- Mesure LH, FSH and Testosterone.

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37
Q

How to diagnose TSH deficiency ?

A

Measure serum thyroxine T4 and free Triidothyronine T3

Which are low with a normal - low TSH

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38
Q

What is the most important hormone that should be replaced in hypopituitarism ?

A

Cortisol

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39
Q

What is Empty Sella syndrome ?

A

sella turcica is either partially filled with cerebrospinal fluid and a very small associated pituitary gland lying in the floor of the sella. Caused by herniation of the suprasellar subarachnoid space through an incomplete diaphragm sella.

No pituitary gland visible on CT or MRI

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40
Q

Who is at risk of having Empty Sella syndrome and what is the management ?

A
  • Obese
  • Multiparous women with headache

Tx: reassurance

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41
Q

What happen if there was an :
A- Excess
B- Deficiency

in Vasopressin/ anti- diuretic hormone ?

A

A: Syndrome of inappropriate secretion of ADH. (SIADH).

B: Diabetes Insipidus (DI)

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42
Q

What are the types of Diabetes Insipidus (DI) ?

A
  • Central Diabetes Insipidus (CDI):
    It is a disorder of the neurohypophyseal system, caused by partial or total deficiency of ADH.
  • Nephrogenic Diabetes Insipidus (NDI) :
    Renal resistance to the action of vasopressin (ADH)
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43
Q

What are the causes of Nephrogenic Diabetes Insipidus (NDI) ?

A
  1. Idiopathic
  2. Secondary to:
    - Hypercalcemia
    - Hypokalemia
    - Sickle cell disease.
    - Amyloidosis
    - Myeloma
    - Pyelonephritis
    - Sarcoidosis
    - Sjogren Syndrome
    - Meds: Lithium - Demeclocycline - Colchicine.
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44
Q

What is the clinical findings of Diabetes Insipidus ?

A
  • Polyuria
  • Nocturia
  • Excessive thirst (Polydipsia)
  • Hypernatremia
  • High serum osmolarity
  • Low urine osmolarity
  • Urine specific gravity < 1.01
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45
Q

What is the diagnosis of Diabetes Insipidus ?

A

Water deprivation test:

In normal person:

  • Decreased urine volume
  • Increased urine osmolality

In DI patients:
- Urine volume remains increased despite volume depletion.

In CDI: ADH is low
In NDI: ADH High

46
Q

What is the DDx of Diabetes Insipidus ?

A
  • Psychogenic polydipsia.
  • Drug- induced polydipsia (Chlorpromazine , anticholinergic , Thioridazine)
  • Hypothalamic disease.
47
Q

What is the management of Diabetes Insipidus ?

A

CDI:

  • Hormone replacement:
    • Vasopressin SubQ
    • Desmopressin SubQ or PO or Intranaslly.
  • Drugs stimulate the secretions and stimulate release of ADH:
    • Chlorpropamide
    • Clofibrate
    • Carbamazepine

NDI:
- Amiloride or HCTZ to enhance reabsorption of fluid from proximal tubule

  • Chlorthalidone
  • Correction of Ca and K abnormalities.
48
Q

What are the causes of Syndrome of inappropriate secretion of ADH. (SIADH) ?

A
  1. Malignancy:
    - Small cell carcinoma
    - Carcinoma of the pnacreas
    - Ectopic ADH secretions.
  2. Nonmalignant pulmonary disease:
    - TB
    - Pneumonia
    - Lung abscess.
  3. CNS disorders:
    - Head injury
    - Cerebral vascular accident
    - Encephalitis.
  4. Drugs:
    - Chlorpropamide
    - Clofibrate
    - Vincristine
    - Vinblastine
    - Cyclophosphamide
    - Carbamazepine
49
Q

How to diagnose Syndrome of inappropriate secretion of ADH (SIADH) ?

A

labs:
- Plasma osmolality < 270 most/Kg
- Hyponatremia < 130 mEq/L
- Urine Na concentration > 20 mEq/L
- Maintained hypervolemia
- Suppression of Renin-angiotensin system
- Low BUN , Creatinine , Serum uric acid and albumin

50
Q

What is the management of Syndrome of inappropriate secretion of ADH. (SIADH) ?

A
  • Treat the underlying cause
  • Restrict fluid 800 - 1000 mL/day. To increase serum Na.
  • Demeclocycline (inhibits ADH action at collection duct.
  • Conivaptan and Tolvaptan V2 receptors blockers indicated in moderate to severe SIADH.
  • For symptomatic pt:
    IV hypertonic saline (3%) 200-300 mL in 3-4 hrs

Rate correction should be 0.5 - 1 mmol/h serum Na.

51
Q

What is the most sensitive test in thyroid disease ?

A

TSH

52
Q

What is Graves’ disease (toxic diffuse goiter) ?

A

It is an autoimmune disorder of the thyroid gland, it causes the production of antibodies (Thyroid Stimulating Immunoglobulin) TSI, which stimulates the thyroid gland to secrete T4 and T3.

53
Q

What is the causes of Osteoporosis and hypercalcemia in Graves’ disease?

A

It is a result of increase osteoclast activity.

54
Q

What are the clinical findings of Graves’ disease?

A
  1. Nervous symptoms (Young patients).
  2. Cardiovascular and myopathic symptoms (older patients.)
  3. Atrial fibrillation.
  4. Emotional lability, inability to sleep, tremors.
  5. Frequent bowel movement.
  6. Excessive sweating and heat intolerance.
  7. Weight loss (despite increased appetite)+ loss of strength.
  8. Proximal muscle weakness.
  9. Dyspnea, Palpitations, angina, cardiac failure.
  10. Warm and most skin.
  11. Palmar erythema, fine and silky hair.
  12. Ocular signs: Exophthalmos, lid lag, infrequent blinking.
  13. Oligomenorrhea.
  14. Osteoporosis and hypercalcemia.
55
Q

How to diagnose Graves’ disease (lab wise) ?

A
  • Increased TSI.
  • Increased Antithyroglobulin.
  • Increased Antimicrosomal antibodies.
  • Increased free T4 and T3
  • Increased RAIU (Radioactive iodine uptake test).
  • Decreased TSH
56
Q

How to treat the adrenergic hyperfunction caused by Graves’ disease?

A

By Beta-adrenergic blockade (Propranolol).

57
Q

How to treat hyperthyroidism ?

A

Methimazole:

  • Longer half life
  • Reverse hyperthyroidism more quickly.
  • Lesser side effects.
  • Requires 6 weeks to lower T4 levels.
  • Used once daily.
  • Causes agranulocytosis.

Propylthyiouracil :

  • Used only if Methimazole is not appropriate.
  • Causes liver damage.
  • Used 2-3 times daily.
  • Causes agranulocytosis.
58
Q

How to treat hyperthyroidism during pregnancy and nursing ?

A

In pregnancy:
First trimester : Propylthyiouracil.
Second and third trimesters: Methimazole.

During nursing:
Methimazole is better to prevent liver damage.

59
Q

What is agranulocytosis ?

A

Also known as agranulosis or granulopenia.
It is an acute condition involving a severe and dangerous leukopenia, most commonly of neutrophils, and thus causing a neutropenia in the circulating blood

60
Q

What is the permanent therapy for Graves’ disease ?

A

Radioactive iodine.

61
Q

What are the indications of Radioactive iodine therapy in graves’ disease?

A
  • Large thyroid gland.
  • Multiple symptoms of thyrotoxicosis.
  • High levels of thyroxine.
  • High titers of Thyroid Stimulating Imunnoglobulin (TSI).
62
Q

What is the manifestation of thyroid storm ?

A
  • Extreme irritability.
  • Delirium
  • Coma
  • Tachycardia
  • Restlessness.
  • Vomiting.
  • Diarrhea
  • Jaundice
  • HTN
  • Dehydration
  • High fever
63
Q

How to treat thyroid storm?

A
  1. Supportive therapy: Normal saline + glucose hydration.
  2. O2
  3. Cooling blankets.
  4. Propylthiouracil
  5. Iodine to inhibit hormone release.
  6. Adrenergic antagonist (Beta-adrenergic blockers)
  7. Dexamethasone to provide adrenal support.
64
Q

What is the Wolff–Chaikoff effect ?

A

Reduction in thyroid hormone levels caused by ingestion of a large amount of iodine.

65
Q

What are the causes of hypothyroidism ?

A

Primary:

  • Secondary to chronic thyroiditis (Hashimoto disease).
  • Postablative surgery.
  • Post radioactive iodine.
  • Heritable biosynthetic defect.
  • Iodine deficiency
  • Drugs: Lithium , acetylsalicylic acid, Amiodarone, interferon, Sulfonamides.

Secondary (Pituitary causes)
Tertiary (Hypothalamic causes).

66
Q

What is Amiodarone ?

A

It is an anti arrhythmic drug used to treat ventricular and supra ventricular tachyarrhythmia. Structurally similar to T4 and contains 40% of iodine.

67
Q

What are the types of Amiodarone- Induced thyrotoxicosis and how to treat each type?

A

Type 1:

  • Occurs in patients with underlying thyroid pathology (Autonomous nodular goiter or Graves’)
  • Tx: Anti-thyroid therapy.

Type 2:

  • Occurs as a result of Amiodarone.
  • Causing subacute thyroiditis that releases thyroid hormones in circulation.
  • Tx: Glucocorticoids.
68
Q

How to take Levothyroxine (Instructions) ?

A
  • On an empty stomach
  • With no other drugs or vitamins , multivitamins, (Ca, iron) it may decrease its absorption.
  • If patient has a coronary heart disease and needs intervention, do intervention first before starting hormone replacement.
69
Q

If you are suspicious of supra-thyroid hypothyroidism, what should you give to the patient?

A

Levothyroxine + Hydrocortisone.

70
Q

How to deal with hypothyroidism during pregnancy ?

A
  • Treated with Levothyroxine.
  • Serum TSH goal should be kept in lower reference range.
  • TSH should be measured at 4-6 weeks of gestation.
  • Then measure TSH Q4-6 weeks until 20 weeks of gestation.
71
Q

How to treat myxedema coma ?

A

Very high doses of T3 and T4.

72
Q

What is the clinical manifestation of subacute thyroiditis ?

A
  • Follows upper respiratory tract infection.
  • Malaise
  • Fever
  • Pain over the thyroid
  • Pain referred to the lower jaw , ears, neck and arms.
73
Q

What are the lab findings in subacute thyroiditis ?

A
  • High ESR (erythrocyte sedimentation rate.
  • Decreased Radioactive iodine uptake.
  • Initial elevated T3 and T4 as there is hormonal leak from the gland.
  • Followed by hypothyroidism as the hormone is depleted.
74
Q

What is the treatment of subacute thyroiditis ?

A
  • NSAIDs
  • Prednisone
  • Propranolol

until subside and returns to normal.

75
Q

How to treat lymphocytic (silent, painless, or postpartum) thyroiditis ?

A

Symptomatic with Propranolol.

76
Q

What is the management of hyper functioning thyroid adenomas?

A

Ablation and radioactive iodine.

77
Q

What is the most common type of thyroid adenomas ?

A

Follicular adenoma

78
Q

What is the treatment of thyroid Follicular carcinomas. ?

A

Total thyroidectomy with postoperative radioiodine ablation.

79
Q

What is the most common type of thyroid carcinoma?

A

Papillary carcinoma

80
Q

What is the treatment of Papillary carcinoma ?

A

Surgery + radiation + TSH suppression therapy with Levothyroxine.

81
Q

Which type of thyroid cancer is associated with high levels of Calcitonin ?

A

Medullary Carcinoma

82
Q

What is the components of Multiple Endocrine Neoplasia type 1 , type 2 a and type 2b (MEN 1 & 2) ?

A

MEN type 1:

  • Hyperparathyroidism
  • Pituitary tumors
  • Pancreatic tumors.

MEN type 2a (Sipple syndrome):

  • Pheochromocytoma
  • Medullary thyroid carcinoma
  • Parathyroid hyperplasia.

MEN 2b:

  • Pheochromocytoma
  • Medullary carcinoma
  • Neuroma
83
Q

Which type of cancers can increase Calcitonin levels ?

A
  • Medullary thyroid cancer
  • Lung cancer
  • Pancreas cancer
  • Breast cancer
  • Colon cancer.
84
Q

What is the only effective treatment of medullary thyroid cancer?

A

Thyroidectomy.

85
Q

Calcium regulation involves 3 tissues and 3 hormones, what are they?

A
  • Bone
  • Kidney
  • Intestine
  • PTH (Hypercalcemia)
  • Calcitonin (Hypocalcemia)
  • Activated Vit D (Hypercalcemia)
86
Q

What is the most common cause of hypercalcemia ?

A

Primary hyperparathyroidism

87
Q

What is Familial Hypocalciuric Hypercalcemia FHH ?

A

It is a benign form of hypercalcemia. It presents with :

  • Mild hypercalcemia.
  • Family history of hypercalcemia
  • Urine calcium to creatinine ratio <0.01
  • Urine calcium <200 mg/day (hypocalciurea).

most cases associated with CaSR gene mutation.

88
Q

How to treat sever, life-threatening hypercalcemia ?

A
  • Give vigorous fluid replacement, normal or half-normal saline.
  • Then, loop diuretics : Furosemide (to promote calcium loss).
  • Use IV Biphosphonate: Zoledronate or Pamidronate (to inhibit osteoclast and stimulate osteoblast).
  • If nothing works. give Calcitonin (inhibits osteoclast).
89
Q

What are the indications of surgery in primary hyperparathyroidism ?

A
  • Symptomatic hypercalcemia
  • Calcium > 11.5 mg/dL
  • Renal insufficiency
  • Age < 50
  • Nephrolithiasis.
  • Osteoporosis.
90
Q

Define Hungry bone syndrome.

A

It is hypocalcemia that occurs after surgical removal of a hyperactive parathyroid gland, due to increased osteoblast activity. It usually presents with rapidly decreasing calcium, phosphate , and magnesium 1-4 weeks post-parathyroidectomy.

91
Q

How to diagnose DM ?

A
  1. Patient is symptomatic : Polyuria, polydipsia, ketonuria, weight loss + random glucose > 200 mg/dL .

or

  1. Asymptomatic + fasting blood glucose >/= 126 mg/dL + HbA1C > 6.5 %
92
Q

How to start oral hypoglycemic ?

A
  • Metformin is drug of choice.
  • If not controlled, add Sulfonylurea.
  • If still not controlled, switch to Insulin or add Glitazone.
  • If Metformin can’t be used, use Glucagon-Like-peptide-1 (GLP-1) agonist (second line agent, can be used individually if Metformin can’t be used or used with Metformin).
93
Q

Which oral hypoglycemic agent is linked to bladder cancer?

A

Pioglitazone ( from Thiazoildinediones class).

94
Q

What are the classes of oral hypoglycemic drugs and their generic names ?

A
  1. Sulfonylureas:
    - Glyburide
    - Glipizide.
    - Glimeppiride.
  2. Biguanides:
    - Metformin.
  3. Thiazolidinediones:
    - Rosiglitazone
    - Pioglitazone.
  4. Glucosidase inhibitors:
    - Acarbose
    - Miglitol
  5. Meglitinides:
    - Repaglinide.
    - Nateglinide.
  6. Dipeptidyl peptidase IV (DPP-IV):
    - Sitagliptin
    - Saxagliptin
    - Linagliptin
  7. Glucagon-like-peptide-1 (GLP-1) / Injection:
    - Exenatide
    - Liraglutide.
95
Q

Name the insulin types.

A
  1. Ultra - short acting:
    - Insulin lispro
    - Insulin aspart
  2. Rapid:
    - Regular
    - Semilente
  3. Intermediate:
    - NPH
    - Lente
  4. Long- acting:
    - Levemir
    - Glargine .
96
Q

How to diagnose DiabeticKeto acidosis DKA?

A
  • High blood glucose
  • Increased serum level of acetoacetate, acetone, hydroxybutyrate.
  • Metabolic acidosis
  • Increased anion gap
97
Q

What is Hyperosmolar nonketotic coma HONK ?
What is the precipitating factors ?
What is the clinical manifestation?
How to diagnose?

A

It is a syndrome that is characterized by severe hyperglycemia ( > 700 mg/dL) in the absence of significant ketosis.

precipitating factors :

  • noncompliance with treatment + inability to drink enough water to keep up with urinary losses.
  • Infections
  • Strokes
  • Steroids and immunosuppressant agents.
  • Diuretics

clinical manifestation:
weakness, polyuria , polydipsia, lethargy, confusion, convulsion and coma

Diagnosis:

  • Blood glucose > 700 mg/dL
  • extremely high serum osmolality
98
Q

What is the equation of serum osmolality?

A

Serum osmolality in most/L=

2NA) + (glucose /18) + (BUN/ 2.8

99
Q

What is the lipid goals for adults with DM ?

A
  • LDL < 100 mg/dL
  • HDL > 50 mg/dL
  • Fasting triglyceride < 150 mg/dL
100
Q

When does protineuria is detected on a standard urine dipstick ?

A

When the level >300 mg / 24 hrs.

101
Q

How to know if the cause of hypoglycemia is an exogenous insulin administration ?

A

Hypoglycemia triad:

  1. High immunoreactivity.
  2. Insulin
  3. Suppressed plasma C-peptide
102
Q

What are the clinical manifestations of cushing syndrome?

A
  1. Deposition of adipose tissue:
    - upper fat
    - Moon facies.
    - Interscapular buffalo hump
    - Mesenteric bed
    - Truncal obesity
  2. HTN
  3. Muscle weakness
  4. Fatiguability related to mobilization of peripheral supportive tissue.
  5. Osteoporosis due to increased bone catabolism.
  6. Cutaneous striae.
  7. Easy bruisability.
  8. Women:
    - Acne
    - Oligomenorrhea / amenorrhea
  9. Emotional changes: Irritability, severe depression or psychosis.
  10. Glucose intolerance.
  11. Leucocytosis and hypokalemia.
  12. Delayed wound healing
  13. Renal calculi
  14. Glaucoma.
  15. Increased susceptibility to infections.
103
Q

How to treat unresectable adrenal tumors?

A

With Ketoconazole or Metyrapone.

104
Q

What is the normal function of Aldosterone ?

A

Reabsorb sodium and excrete potassium and acid H+.

105
Q

How to diagnose hyperaldosteronism ?

A

Plasma Aldosterone Concentration (PAC) & Plasma Renin Activity (PRA):
- PAC/PRA ratio > 20:1
AND
- PAC > 15.

To confirm:
NaCl challange:
after giving NaCl PAC should be suppressed. IF PAC is still elevated, then this confirms the diagnosis.

106
Q

How to treat bilateral adrenal hyperplasia ?

A

Spironolactone, which blocks Aldosterone.

107
Q

What are the clinical findings of Primary adrenocorticoid insufficiency (Addison disease) ?

A
  1. Weakness
  2. Paresthesias
  3. Cramping
  4. Intolerance to stress.
  5. Personality changes
  6. Small heart
  7. Weight loss
  8. Sparse axillary hair
  9. Hyperpigmintation of skin: diffuse brown, tan, bronze darkening of both exposed and unexposed body parts.
  10. Arterial hypotension
  11. Mild anorexia, wight loss, nausea, vomiting and diarrhea.
108
Q

What is the clinical findings of acute addisionian crisis ? and how to treat it ?

A
  • Fever
  • Hypotension
  • Abdominal pain
  • Vomiting.
  • Altered mental status
  • Vascular collapse.
  • Hyponatremia
  • Hyperkalemia
  • Mild acidosis.

Treatment:

  • Get cortisol level
  • Rapid adminstration of fluids and hydrocortisone.
109
Q

How to diagnose Addison’s disease ?

A

measuring plasma cortisol after giving 250 microgram of Cosyntropin (ACTH) IM or IV.

Normal person should show a brisk rise in cortisol level.

110
Q

What is Pheochromocytoma?

A

It is a benign tumor that arises from the Chromaffin cells of the sympathetic nervous system.

111
Q

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

A

Cardiac arrhythmia and stroke.

112
Q

What is Klinefelter syndrome?

A

It is a primary fevelopemnatal abnormalitiy causing hypogonadism (testicular damage):

  • 47, XXY karyorype
  • Gynecomastia
  • High LH and FSH
  • Sterility and lack of libido
  • Small and thin testes.
  • Intellectual disability
  • Low/normal urinary 17-ketosteroids
  • Low to normal serum testosterone
  • High serum estradiol
  • Tx: Testosterone replacement.

Medical (6 decks)

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