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Endocrinology Flashcards

1
Q

What are the hormones released by the anterior pituitary?

A
  • ACTH, adrenocotropic hormone
  • PRL Prolaction
  • GH Growth Hormone
  • LH Luteinizing Hormone
  • FSH Follicle-Stimulating Hormone
  • TSH Thyroid Stimulating Hormone
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2
Q

What are the hormones released by the posterior pituitary?

A
  • Anti-diuretic homone (ADH) vasopressin

- Oxytocin

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3
Q

What is the function of Oxytocin?

A

1 uterine contraction during delivery
2 enhances breast milk flow
3 behavior, memory, sperm transport

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4
Q

What is the function of LH (leutinizing hormone)?

A

-regulates gonadal function

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5
Q

What is the function of LH in men?

A

-stimulates testosterone production

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6
Q

What is the function of LH in women?

A
  • stimulates estrogen and progesterone production from the ovary
  • mid-menstrual cycle causes ovulation
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7
Q

When is LH increased in women?

A

-during the follicular phase

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8
Q

What is the function of Follicle-Stimulating hormone (FSH) in men?

A

-stimulates testicular growth

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9
Q

What is the function of FSH in females?

A

-develops ovarian follicle

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10
Q

What does prolactin stimulate?

A

-stimulates lactation in the postpartum period

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11
Q

What does Hyperprolactemia do in men?

A
  • decreased testosterone synthesis
  • decreased libido
  • decreased spermatolgenesis
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12
Q

What does Hyperprolactemia do in women?

A
  • hypogonadism
  • anovulation
  • amenorrhea
  • infertility
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13
Q

What is the function of TSH?

A

-stimulates the thyroid to produce T3/T4

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14
Q

What does a pituitary adenoma do to pituitary function?

A

-most common cause of hypothalamic-pituitary disfunction

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15
Q

What are the types of pituitary adenoma?

A

-Prolactinomas are the most common

  • Microadenoma < 1cm in diameter
  • Macroadenoma > 1cm in dameter
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16
Q

What is the Tx for a pituitary adenoma?

A
  • transsphenoial microsurgery
  • radiation
  • medical Tx: *Bromocriptine for prolactinoma
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17
Q

What is the most common cause of hyperprolactinemia?

A

-Prolactinoma (a pituitary adenoma)

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18
Q

What are the other causes of hyperprolactinemia?

A
  • pregnancy
  • hypothyroidism
  • renal failure
  • cirrhosis
  • chronic nipple stimulation–nipple piercing
  • drugs: OC, tycyclic antidepressants, cimetidine
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19
Q

What are the S/Sx of hyperprolactinemia?

A

Galactorrhea, Infertility (Galactorrhea is excessive or inapropriate production of milk)

—Male Gonadal dysfunction
erectable dysfunction
decreased libido
gynocomastia

–Female Gonadal dysfunction
oligomenorrhea
amenorrhea

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20
Q

What other things need to be ruled out when a lab of hyperprolactinemia is found?

A
  • pregnancy
  • hypothyroidism
  • renal failure
  • cirrhosis
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21
Q

How is a prolactinoma Dx?

A

MRI of pituitary and hypothalamus

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22
Q

What is the Tx for hyperprolactinemia?

A

1 Dopamine Agonists: initial choice
Bromocriptine* fatigue, N, dizziness
orthostatic hypotension
Capergoine : more potent, longer acting,
better tolerated

2 Surgery : transsphenoidal pituitary surgery

3 Radiation

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23
Q

When does Acromegaly occur?

A

occurs after the closure of epiphyses

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24
Q

When does Giantism?

A

occurs before the closure of epiphyses

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25
Q

What is the etiology of Acromegaly & Giantism?

A

-almost always due to a pituitary adenoma

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26
Q

What are the characteristics of Acromegaly & Giantism?

A

-Excessive growth of hands, feet, cranium, jaw internal organs

  • increased glove/ring size, increased shoe width
  • protrusion of the lower jaw
  • increased hat size
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27
Q

What are the S/Sx of Acromegaly and Giantism?

A
  • overgrowth of bone & soft tissue overgrowth
  • doughy hands and moist handshake
  • carpal tunnel syndrome : parathesias
  • deeper voice
  • facial features coarsen
  • tooth space widens
  • macroglossia
  • hypertension
  • cardiomegaly
  • diabetes mellitius: insulin resistance
  • headaches
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28
Q

What are the lab findings for Acromegaly and Giantism?

A

-evelvated GH > 10ng/ml

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29
Q

What are the radiographic/MRI findings with Acromegaly and Giantism?

A

-MRI will show pituitary tumor

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30
Q

What is the Tx for Acromegaly & Giantism?

A
  • -surgery : transphenoidal pituitary microsurgery
  • -medical : Octreotideespecially if acromegaly persists after surgery
  • -Radiation
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31
Q

What are the 2 types of Dwarfism?

A

-Pituitary and Achondroplasia

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32
Q

What is pituitary dwarfism?

A

-short stature with proportional parts due to deficiency of growth hormone

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33
Q

What is Achondroplasia dwarfism?

A
  • 70 % of dwarfism with limbs being disproportionally short compared to the trunk
  • autosomal dominant disorder with a faulty allele
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34
Q

What is the height of a dwarf?

A

-adult height under 4 feet 10 inches

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35
Q

Where does ADH (vasopressin) originate?

A

-ADH/vasopressin is produced by the hypothalamus but is stored and secreted in the posterior pituitary gland

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36
Q

What are the effects of ADH/vasopressin?

A
  • regulates the body’s retention of water by conserving water and concentrating the urine
  • causes moderate vasoconstriction in high doses
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37
Q

What stimulates ADH/vasopressin?

A

-Angiotension II

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38
Q

What is the antagonist of ADH/vasopressin?

A

Ethanol

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39
Q

What is Diabetes Insipidus?

A

-deficiency of vasopressin causing increased thirst and large quantities of urine with low specific gravity

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40
Q

What is the Etiology of Diabetes Insipidus?

A

Vasopressin Deficiency**

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41
Q

What are the causes of vasopressin deficiency?

A
  • tumor
  • trauma
  • infection
  • last trimester of pregnancy
  • renal failure
  • pylonephritis
  • myeloma
  • potassium depletion
  • sickle sell anemia
  • sorgrens’s syndrome
  • chronic hypercalemia

-Drug induced

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42
Q

What drugs cause vasopressin deficiency?

A
  • Lithium**
  • demeclocycline
  • foscarnet
  • methicillin
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43
Q

What are the S/Sx of Diabetes Insipidus?

A
  • Intense thirst, especially for ice water
  • Polyuria : 2-20L per day
  • Dehydration
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44
Q

What are the Lab finding with Diabetes Insipidus?

A
  • Hypernatremia

- Hyperuricemia

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45
Q

How is Diabetes Insipidus Dx?

A
  • MRI

- Vasopressin Challenge Test

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46
Q

What is the differential for polyuria?

A
  • Cushing’s syndrome
  • steroid Tx
  • lithium
  • Parkinson’s Disease
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47
Q

What is the Tx for Diabetes Insipidus?

A

Desmopressin

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48
Q

What is SIADH?

A

Syndrome of Inappropriate Antidiuretic Hormone (caused by excess Vasopression/ADH)

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49
Q

What causes SIADH?

A

excess vasopressin

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50
Q

What is the etiology of SIADH? What causes excessive vasopressin/ADH?

A

Ectopic production of vasopression (cancer)

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51
Q

What are the type of cancer that cause the Ectopic production of vasopression?

A
  • Bronchogenic carcinoma
  • carcinoma of duodenum
  • carcinoma of pancreas
  • uterine carcinoma
  • prostate cancer
  • bladder cancer
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52
Q

Which drugs induce SIADH?

A
  • Desmopression
  • oxytocin
  • carbamazepine
  • ecstasy
  • SSRI
  • TCA’s
  • MAOI
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53
Q

What pulmonary disorders cause SIADH?

A
  • pneumonia

- Tuberculosis

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54
Q

What are the Clinical Criteria for SIADH?

A
  • increased sodium excretion
  • increased osmolality
  • Inappropriate concentrations of the urine
  • Clinical euvolemia
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55
Q

What are the S/Sx of SIADH?

A

**Hyponatremia*

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56
Q

What is the Tx for SIADH?

A
  • Discontinue hypotonic fluids
  • restriction of free water
  • Hypertonic NaCl (3%0
  • IV Conivaptan (Vaprisol) : blocks the effects of vasopressin of the V2 receptor agonists in the kidney
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57
Q

What is the etiology of Grave’s Disease?

A

Grave’s disease is autoimmune (90%) causing the thyroid to produce too much T4

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58
Q

What type of disorder is Graves’ Disease?

A
  • hyperthyroidism

- autoimmune disorder with autoantibodies to TSH receptors

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59
Q

What are the other conditions associated with Graves’ Disease?

A
  • pernicious anemia
  • myasthenia gravis
  • diabetes mellitus
  • Addison’s disease
  • celiac diseas
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60
Q

What are the Lab findings for hyperthyroidism?

A
  • Decreased TSH
  • increased T4
  • increased receptor antibody
  • increased antithyrogrobulin
  • increased ANA
  • increased anti-double stranded DNA
  • Radioactive iodine uptake and scan show high uptake
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61
Q

What are the symptoms of Graves’ Disease?

A
  • heat intolerance
  • sweating
  • weight loss
  • increased appetite
  • nervousness
  • loose stools
  • frequent urination
  • muscle cramps
  • irritability
  • fatigue
  • weakness
  • dyspnea on exertion
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62
Q

What are the signs of Grave’s Disease?

A
  • Eye
  • thyroid
  • cardiac
  • M/S
  • Skin
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63
Q

What are the Eye PE finding with Graves’ Disease?

A
  • exophthalmos
  • chemosis
  • conjunctivis
  • proptosis
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64
Q

What are the thyroid PE findings with Grave’s Disease?

A

-goiter (enlarged thyroid) with bruit

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65
Q

What are the cardiac PE findings with Graves’ Disease?

A
  • palpitations
  • sinus tachy
  • Atrial Fibrillation
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66
Q

What are the M/S physical exam findings with Graves’ disease?

A
  • fine resting tremor

- hyperreflexia

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67
Q

What are the skin PE findings in Graves’ Disease?

A
  • warm moist skin
  • fine hair
  • onycholysis (separation of the nail from the nail bed
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68
Q

What is the Tx for Graves’ disease?

A
  • B-Blockers control symptoms
  • Thiourea drugs (agranulocytosis)
    • Methimazole
    • Propylthiouracil–drug of choice in pregnancy and breast feeding women

-Radioactive iodine is preferred to surgery for permanent control (not in pregnancy)

-Surgery- larger goiters, malignancy
(often caused hypothyroidism)

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69
Q

What is the etiology of Hypothyroidism (Myxedma)?

A
  • Hashimoto’s throiditis
  • Thyroid surgery
  • radiation therapy
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70
Q

What are the S/Sx of Myxedema (Hypothyroidism)?

A
  • Fatigue*
  • lethargy
  • anorexia
  • constipation
  • depression
  • muscle stiffness
  • memory impairment
  • cold intolerance
  • dry skin
  • weakness
  • weight gain
  • **hoarseness**
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71
Q

What are the Lab findings in Myxedema (hypothyroidism)?

A
  • elevated TSH
  • decreased T3/T4
  • anemia
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72
Q

What is the lab finding in Hashimoto’s ?

A

+ antithyroid peroxidase and antithyroglobulin antibidies

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73
Q

What is the Tx for Myxedema/hypothyroidism?

A

-Levothyroxine

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74
Q

Describe how thyroid cancer is characterized?

A

painles mass : “Cold Nodule”* on scan

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75
Q

What are the 4 types of thyroid cancer?

A

1 Papillary
2 Follicular
3 Medullary Carcinoma
4 Anaplastic Carcinoma

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76
Q

How prevalent is Papillary cancer of the thyroid?

A
  • 76% of thyroid cancers
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77
Q

Which is the least aggressive of the thyroid cancer?

A

-Papillary thyroid cancer is least aggressive

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78
Q

What percentage of thyroid cancers is Follicular?

A

-16%

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79
Q

What percentage of thyroid cancers are Medullary Carcinoma?

A

-4% are medullary carcinoma of the thyroid

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80
Q

What factors are unique to Medullary Carcinoma of the thyroid?

A
  • 1/2 is familial
  • associated with MEN type 2 (hereditary condition associated with three primary types of tumors: medullary thyroid cancer, parathyroid tumors, and pheochromocytoma)
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81
Q

Describe Anaplastic Carcinoma?

A
  • 1% of all thyroid carcinomas are Anaplasica
  • Most aggressive of all thyroid carcinomas
  • Worse prognosis
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82
Q

What is Thyrotoxic Crisis also known as?

A

-Thyroid Storm

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83
Q

Is Thyrotoxic Crisis/Thyroid Storm serious?

A

-it is life threatening

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84
Q

What are 3 times that Thyroid Storm/Thyrotoxic Crisis occurs?

A

1 following a stressful event
2 thyroid surgery
3 radioactive iodine

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85
Q

What are the S/Sx of Thyroid Storm/Thyrotoxic Crisis?

A
  • high fever
  • tachycardia
  • vomiting
  • diarrhea
  • dehydration
  • marked weakness
  • muscle wasting
  • extreme restlessness
  • comfusion & emotional lability
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86
Q

What is the Tx for Thyroid Storm/Thyrotoxic Crisis?

A
  • Beta Blockers
  • Hydrocortisone
  • supportive therapy
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87
Q

What secretes Calcitonin?

A

-calcitonin is secreted by the parafollicular C cells in the thyroid

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88
Q

What are the effects of Calcitionin?

A
  • Decreases serum calcium*

- does this by inhibiting osteoclastic bone resorption

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89
Q

What cancer conditions is a Lab draw for Calcitonin important?

A

calcitonin is an important tumor marker in medullary carcinoma of the thyroid?

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90
Q

What are the therapeutic uses of calcitonin as an inhibitor of osteoclastic bone resorption?

A
  • Paget’s disease of the bone
  • Hypercalcemia
  • Osteoporosis
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91
Q

What are the effects of Parathyroid Hormone (PTH)?

A
  • increases serum calcium*

* decreases serum phosphorus*

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92
Q

What 3 organs does PTH effect?

A
  • Bone
  • Intestinal mucosa
  • Kidney
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93
Q

What is the effect of PTH on Bone?

A

-releases calcium and phosporus

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94
Q

What is the effect of PTH on the Intestinal Mucosa?

A

-increases calcium reabsorption

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95
Q

What is the effect of PTH on the Kidney?

A
  • increases production of Vitamin B
  • increases reabsorption of calcium
  • decreases reabsorption of phosphate & bicarbonate
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96
Q

What is Hyperparathyroidism?

A

-the excessive secretion of PTH producing frank hypercalcemia

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97
Q

Is hyperparathyroidism seen more in men or women?

A

2-3 x more common in women

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98
Q

What is the etiology of hyperparathyroidism?

A
  • single parathyroid adenoma (8%)

- hyperplasia (15%)

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99
Q

What are the complaints of patient symptomatic with hyperparathyroidism?

A

bones, stones, abdominal groans, psychic moans, & fatigue overtones

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100
Q

What are the body areas that are characteristically effected most by hyperparathyroidism?

A
  • bone loss
  • kidney disease
  • psychic disturbances
  • abdominal symptoms
  • cardiac
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101
Q

Are people with hyperparathyroidism symptomatic or asymptomatic?

A

-most are symptomatic

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3
4
5
Perfectly
102
Q

What are the bone S/Sx of in hyperparathyroidism?

A
  • bone pain & pathologic Fx’s, increased ALP*

- osteoporosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What are the kidney disease S/Sx of hyperparathyroidism?

A
  • kidney stones* (calcium oxalate)

- possible renal insufficiency

104
Q

What are the CNS S/Sx of hyperparathyroidism?

A
  • Malaise, fatiuge, depression, increased sleeping

- Disorientation, psychosis, stupor

105
Q

What are the Cardiac S/Sx of hyperparathyroidism?

A
  • Bradyarrhythmias, heart bock, asytole*

- HTN, prolonged PR interval, shortened QT interval

106
Q

What are the GI S/Sx of hyperparathyroidism?

A

**abomimal pain, N/V, anorexia, constipation

107
Q

What are the Lab findings with hyperparathyroidism?

A
  • hypercalcemia, low-normal phosphorus*
  • high urine calcium & phosphate excretion
  • increase Alkaline phospatase (only in bone disease)
  • Vitamin D deficiency is common
108
Q

How is Hyperparatyroidism Dx?

A
  • 99m Tc-sestmibescanning
  • CT
  • MRI
  • Ultrasound
109
Q

What is the tx for hyperparathyroidism?

A

-surgery (parathyroidectomy) = definitive Tx
-Medical
-Biphosphonates : inhibit bone resorption (Pamidronate and Zoledronic Acid)
(they help prevent bone loss)
-Estrogen therapy (minimal improvement)

110
Q

What is the etiology for Hypoparathyroidism?

A
  • thyroidectomy
  • heavy metals (iron, from thalassemias)
  • Mg++deficiency (poor aborbtion in the gut)
  • Drugs
    • loop diuretics
    • phenytoin
    • alendronalte (Fosmax)
    • foscarnet (tx CMV in aids patients)
111
Q

What are the S/Sx with hypoparathyroidism?

A
  • tetany, muscle cramps, Carpopedal spasms*
  • parasthesias around mouth, hands, feet*
  • letargy, personality changes, convulsions
  • Chvostik sign : facial muscle contraction on tapping on the facial nerve in front of head
  • Trousseau sign : carpal spasm after BP is increased
  • hyperactive deep tendon reflexes
112
Q

What are the lab findings in hypoparathyroidism?

A
  • low serum calcium, high serum phosphate*
  • low urinary calcium
  • normal ALP, low PTH level
113
Q

What gives the definitive Dx in hypoparathyroidism?

A
  • -respiratory alkalosis
  • -also
    - paresthesias, muscle cramps, or tetany
114
Q

What is the Tx for hypoparathyroidism?

A
  • IV calcium gluconate

- oral calcium

115
Q

What is the recommended daily intake for vitamin D?

A

-400 units of vitamin D

116
Q

How does sunlight produce Vitamin D?

A
  • vitamin D is formed in the epidermis with sunlight (pro hormone)
  • it is metabolized in the liver to (OH) D, kidney to 1.125(OH) 2D
117
Q

What foods are sourced of Vitamin D?

A
  • milk
  • fish oils
  • fish liver
  • eggs
118
Q

How is Vitamin D absorbed from foods?

A

-absorbed in small intestine

119
Q

Where in the body is vitamin D stored after absorbtion?

A

-vit D is stored in adipose tissue

120
Q

What drugs reduce serum 25 (OH) D levels?

A
  • phenytoin

- phenobarbital

121
Q

Who takes phenytoin and who takes phenobarbital?

A

phenytoin : siezures, certain irregular heartbeats

phynobarbital : seizures, tremor, insomnia, narcotic withdrawal

122
Q

When is vitamin D increased in the kidney?

A
  • in response to decreased phosphorus
  • in response to decreased serum calcium
  • in response to increased PTH
123
Q

What are the diseases of Vit D deficiency?

A
  • Rickets

- Osteomalacia (adults)

124
Q

What is Osteomalacia?

A

-inadequate calcium mineralization

125
Q

What is the etiology for Osteomalacia?

A
  • vitamin D decficiency (renal failure, no sun)
  • low calcium intake
  • Rickets
  • malabsorpion
126
Q

What are the S/Sx for Osteomalacia?

A
  • bone pain

- painful proximal muscle weakness

127
Q

What are the Lab findings for Osteomalacia?

A
  • increased ALP*
  • decreased Vit D
  • decreases calcium
  • increased PTH
128
Q

What is Paget’s disease of Bone?

A

-Paget’s is a focal disorder of bone remodeling that leads to greatly accelerated rates of bone turnover

129
Q

What are the S/Sx of Paget’s bone disease?

A
  • 2/3 are asymptomatic

- pain, fractures, deformities (1/3)

130
Q

What are the Lab findings in Paget’s?

A
  • ALP is markedly elevated*

- serum calcium & phosphorus are normal

131
Q

What is the TX for Paget’s disease of bone?

A

-Biphosphonates & calcitionin

132
Q

What are the effects of Glucocorticoids (Cortisol) on Gulcose Metabolism?

A

-increased glucose (increased glucogeneis, decreased glucose uptake)

133
Q

What are the effects of Cortisol on WBC’s?

A
  • increased neutrophils

- decreased lymphocytes

134
Q

What are the effects of Cortisol on Immunology?

A
  • anti-inflammatory

- immunosuppressive

135
Q

What are the cardiac effects of Cortisol?

A
  • increased cardiac output

- increased peripheral vascular tone

136
Q

What are the effects of Cortisol on the Nervous System?

A
  • Eurphoria

- Psychologic abnormalities

137
Q

What are the effects of Cortisol on the Thyroid?

A

-minimal decrease in T3 & T4

138
Q

What is the effect of Cortisol on the Gonadal Function?

A

-decreased testosterone and LH (decreased estrogens & progestins causing amenorrhea?

139
Q

What are the effects of cortisol on the GI system?

A

-promotes peptic ulcer disease

140
Q

What are the Ophthalmologic effects of Cortisol?

A

-increased intraoccular pressure

141
Q

What type of hormone is Aldosterone?

A

-it is a mineralcorticoid

142
Q

Where is Aldosterone produced?

A

-made exclusively in the zone glomerulosa (outer layer) of the adrenal cortex

143
Q

How is Aldosterone released?

A

-it is controlled by the renin-agiotnesion system

144
Q

What are the effects of Aldosterone?

A
  • stimulated by hypovolemia & hyperkalemia
  • causes the renal tubule to resorb sodium and excrete potassium
  • maintain normal exracellular fluid volume
  • inhibited by atrial natriuretic factor & dopamine
145
Q

What is Cushing’s Syndrome?

A
  • Cushing’s Syndrome is glucocorticoid excess

- increased cortisol

146
Q

What is the major etiology of Cushing’s Syndrome?

A

70% Cushing’s Disease, due to excessive pituitary ACTH secretion

147
Q

What are the other etiology of Cushing’s Syndrome?

A

(15%) Nonpituitary neoplasm small cell carcinoma

(15%) Adrenal tumor–adenoma (most) or carcinoma
only cause that has low ACTH due to negative feedback

148
Q

What are the S/Sx of Cushing’s Syndrome?

A
  • Obesity: most common manifestation
  • “Moon facies & Buffalo hump”
  • Hyperlipidemia (70%)
  • **Glucose intolerance (70%)
  • Skin changes (60%)
  • ***Hirsutism (75%) : facial is most common
  • CNS 85%)* emotional lability, anxiety, depress
  • muscle weakness (60%)*
  • ***osteoporosis/osteopenia (80%) Fx, AVN
  • Renal Calculi (15%)*glucocorticoid-induced hypercalcuria
  • thirst and polyuria: due to hyperglycemia
149
Q

What type of obesity is seen in Cushing’s Syndrome?

A

Central obesity, face, neck, trunk, and

150
Q

What are the skin changes seen in Cushing’s Syndrome?

A
  • thinning of the skin: transparency, easy bruising
  • Striae : red to purple, acne, slow wound healing
  • fungal infections
151
Q

What is the Lab findings for Cushing’s Syndrome?

A

elevated cortisol levels (100%)
Hyperglycemia
-elevated ACTH : due to tumor in pituitary or ectopic
Normal/low ACTH if caused by adrenal tumor

152
Q

How is Cushing’s Syndrome Dx?

A

-CT or MRI for adrenal or pituitary tumor
Dexamethasone Suppression Test
-urine-free cortisol: highly accurate and specific
-Diurnal Rhythm
cortisol & ACTH are usually highest in a.m. and lowest in the pm

153
Q

What is the Tx for Cushing’s Syndrome?

A

1 microsurgery, radiation therapy
2 adrenal adenoma : unilateral adrenalectomy
3 adrenal carcinoma: Mitotane (meds), radiation, chemotherapy
4 meds such as ketoconazole block steroid synthesis

154
Q

When Tx Cushing’s syndrome with unilateral adrenalectomy what else does this patient need for tx?

A

require glucocorticoid therapy during and after surgery until the remaining adrenal recovers

155
Q

What is Hirsutism?

A
  • Hyperanrogenism of testosterone*, &

- DHEAS (Dehydroepiandosterone)

156
Q

What is the etiology of Hersutism?

A

POCSpolycysitic ovarian syndrome

  • Ovarian tumors
  • Adrenal carinoma
157
Q

What are the S/Sx of Hirsutism?

A

*Menstrual irregularities : amenorrhea, anovuation

Virilization : Frontal balding, muscularity, clitoromegaly, deapin voice

158
Q

What is the Tx for Hirsutism?

A
  • spironalactone
  • OC, birth control pill
  • metformin
159
Q

What is Addison’s disease? What 2 hormones are released by the adrenal glands?

A

a disorder that occurs when the adrenal glands do not produce enough of their hormones, cortisol: and less often aldosterone

160
Q

What is Addison’s also called?

A

“chronic adrenal insufficiency” or hypocortisolism

161
Q

What are the functions of Cortisol?

A

1) helps the body deal with stress

  • helps regulate body’s use of protein, carbohydrates, & fat
  • helps maintain blood pressure and cardio function
  • controls inflammation
162
Q

What are the functions of aldosterone?

A
  • helps kidneys regulate salt and water

- blood pressure control

163
Q

What are the two forms of Addison’s Disease?

A

1 primary adrenal insufficiency when the problem is the adrenal glands themselves
2 secondary adrenal insufficiency if the adrenal glands are affected by a problem somewhere else such as the pituitary gland

164
Q

With Addison’s Disease where is the problem usually at?

A

-most cases result from a problem with the adrenal glands themselves (primary adrenal insufficiency)

165
Q

What is the usual cause of the adrenal glands to stop producing enough cortisol?

A

1 autoimmune disease accounts for 70% of Addison’s disease

-this occurs when the body’s immune system mistakenly attacks the adrenal glands, and the autoimmune assault destroys the outer layer of the glands

166
Q

Can infections harm the adrenal glands?

A

long-lasting infections such as TB, HIV and fungal infections can cause the hypothalamus or pituitary gland probs, which can turn on or off the production of hormones to the rest of the body

-improper use of prednisone can cause secondary adrenal insufficiency

167
Q

What are the symptoms of Addison’s Disease (adrenocortical insufficiency)?

A
  • Hyperpigmentation of the skin*
  • Weakness and fatigue*
  • Weakness and fatigue*(100%)
  • Weight loss and anorexia* (100%)
  • GI disturbance (50%)–NV
  • Hypotenston (90%)
  • hypogylcemia
  • Amenorrhea
168
Q

What are the Lab findings with Addison’s Disease?

A
  • Hyponatremia, Hyperkalemia*

* low cortisol levels, increased ACTH*

169
Q

What is the Dx test for Addison’s Disease?

A

Cosynropin Stim Test

170
Q

What is the Tx for Addison’s Disease?

A

-Cortisol (hypdrocortisone) : 100mg IV Q 6 hours X 24 hours, then taper (acute adrenal crisis)

  • Cortisol : 10 - 15 mg in am, 5-15 mg in pm
    • increased doses during stress
171
Q

What is Primary Aldosteronism?

A

-abnormally high aldosterone level causing

hypertension, hypokaklemia, weakness

-also causing sodium retension & suppression of plasma renin

172
Q

What is the etiology of primary aldosteronism?

A

-adrenal ademoma (75%)

173
Q

What are the S/Sx of primary aldosteronism?

A
  • Hypokalemia (muscular weakness, fatigue, HA)
  • Hypertension : due to increased Na+ and volume retention
  • Polyuria & Polydipsia
174
Q

How is Aldosteronism Dx?

A

-established by suppressed plasma renin activity and elevated aldosterone production that is not suppressed by high salt intake

175
Q

What are the Lab findings for Aldosteronism?

A
  • Hypokalemia*
  • low plasma renin activity
  • mild metalbolic aklalosis
  • 24 hr urinary aldosterone > 21 ug/24hr
  • plasma aldosterone (8 am or hour after recumbency) > 25 ng/dl
176
Q

What further tests are needed to Dx the Aldosteronism problem?

A

-CT or MRI to identify the tumor

177
Q

What is the Tx for Aldosteronism?

A
  • Spirolactone or eplerenone

- Adrenolectomy

178
Q

What is Pheochromocytoma?

A

-tumor of there adrenal medulla causing abnormal secretion of epinephrine and norepinephrine

179
Q

What is the adrenal medulla?

A
  • the inner part of the adrenal gland, it is located in the center of the gland, being surrounded by the adrenal cortex
  • it helps an individual deal with physical and emotional stress
180
Q

What does the adrenal medulla secrete?

A

-it synthesizes and secretes epinephrine and norepinephrine

181
Q

What are the symptoms of pheochromocytoma?

A 
****Hypertension*****
Headache
Perspiration
Palpitations
*****Tremor****
  • anxiery
  • trachyarrythmias
  • Abd pain
  • N/V
  • weight loss
  • heat intolerance
  • Heart failure
182
Q

How is Pheocromoaytoma Dx?

A

-CT or MRI to identify the tumor of the adrenal medulla

183
Q

What is the Tx for Pheochromocytoma?

A

-Surgery
-Medical : alpha blockers
CCB
Beta Blockers*

184
Q

What is Diabetes Mellitus?

A

-inappropriate hyperglycemia due to either deficiency of insulin and or insulin resistance

185
Q

How many people in the US have Diabetes Mellitius?

A

24 million

186
Q

What are the types of Diabetes Mellitus?

A
  • Type I
  • Type II
  • Metabolic Syndrome / Syndrome X
187
Q

What is Type I Diabetes?

A

-Immune-mediated > Idiopathic

188
Q

What is Type II DM?

A

-Insulin resistance

189
Q

What is Metabolic Syndrome?

A
  • a combination of medical disorders that, when together, increase the risk of developing cardiovascular disease and diabetes. Up to 25% of the general population and prevalence increases with ages.
190
Q

What is the criteria for Dx of Diabetes Mellitus?

A

-2 fasting glucose > or equal to 126 mg/mg/dl
(on 2 different days)

  • Fasting glucose > 200 with symptoms
  • perform glucose tolerance test if needed
191
Q

Describe the glucose tolerance test normal and abnormal values?

A

2 hours after 75g glucose load

  • normal < 140
  • impaired glucose tolerance > 140 - 190
  • Diabetes Mellitus > or equal to 200
192
Q

What is Type 1 Diabetes Mellitius?

A

-decreased or absent insulin production

193
Q

What is the etiology of Type I DM?

A

-immune-mediated (90%)
-starts commonly in children and young adults
-genetic and environmental factors
-most have antibodies against pancreatic islet
cells

194
Q

What are the S/Sx of Type 1 diabetes?

A
  • polyuria, polydipsia, polyphagia*
  • weight loss
  • postural hypotension
  • paresthesias
  • ketoacidosis
  • hypeglycemia
195
Q

What other disorder is associated with Type 1 diabetes?

A

-celiac sprue

196
Q

What are the Lab findings for Type 1 diabetes?

A
  • elevated HBGA1C (Glycosolated Hbg) > 7%

- Urine : + glucose and ketones

197
Q

What is the Tx for DM Type 1?

A
  • Insulin : preprandial + basal or long acting
  • Exercise
  • Healthy diet
  • Blood pressure control
  • Lipid management
198
Q

What is the HbgA1C level goal in Type 1 DM?

A

HgbA1C < 7%

199
Q

What is the preferred BP n Type 1 DM ?

200
Q

What is the preferred LDL in Type 1 DM?

201
Q

What is the preferred level of HDL in Type 1 DM?

202
Q

What is the preferred level of Trigliycerides in Type 1 DM?

203
Q

What is the preferred Preprandial glucose level in Type 1 DM?

A

90-130 mg/dl

204
Q

What is the preferred postprandial glucose level in Type 1 DM?

A

<180 mg/dl

205
Q

Why are ACE-1 used in Type 1 DM?

A

to prevent kidney damage

206
Q

What is the Dawn Phenomenon?

A

elevated blood sugars in the morning due to cortisol

207
Q

How is Dawn Phenomenon Tx?

A
  • increase bedtime insulin

- avoid carbs before bedtime

208
Q

What is the Somongyi Effect?

A

Nocturnal hypoglycemia causes reactive morning hyperglycemia

209
Q

What is the Tx for the Somogyi effect?

A

decrease the amount of dinner or bedtime insulin

210
Q

Is Diabetic Ketoacidosis a serious condition?

A

it is life threatening

211
Q

What patients are more likely to get ketoacidosis?

A

it is the usual presentation for people with Type 1 DM

212
Q

Why does ketoacidosis occur?

A

the body cannot use glucose for fuel because there is no insulin available, so the body begins to breakdown fat for fuel and results in build up of wastes called ketones

213
Q

What are the S/Sx of Diabetic Ketoacidosis?

A
  • N/V
  • 3-Polys (dipsia, phagia, uria)
  • dehydrated
    • / - stupor
214
Q

What are the PE findings for debetic ketoacidosis?

A
  • fruity breath

- hypotension

215
Q

What is found with testing Arterial Blood Gas with diabetic ketoacidosis?

A

-metabolic acidosis

216
Q

What is the Lab findings for Diabetic Ketoacidosis?

A
  • Ketones
  • glucose in urine
  • BS > 250 mg/dl
217
Q

What is the Tx for Diabetic Ketoacidosis?

A

-fluids
-insulin
-potassium monitoring
+/- bicarbonate

218
Q

What are the severe acute possible effects of Type 2 DM?

A
  • DKA (diabetic ketoacidois) is rare

- Hyperosmolar coma may occur

219
Q

What is the Tx for Type 2 DM?

A
  • Diet*
  • Excercise*
  • oral hypoglycemics
  • insulin
220
Q

How prevalant is Metalbolic Syndrome?

A

25% of the general non obese non diabetic population has insulin resistance

221
Q

What are the factors that are considered in the criterial for Dx of Metabolic Syndrome?

A
  • central obesity, waist size
  • triglycerides
  • HDL’s
  • Blood Pressure
  • Fasting blood sugar levels
222
Q

What is the waist size (central obesity) in metabolic syndrome?

A
  • men, 40 inches

- women, 36 inches

223
Q

What is the triglyceride level in metabolic syndrome?

224
Q

What are the HDL levels in metabolic syndrome?

A

< 40 in women

< 50 in men

225
Q

What is the blood pressure in metabolic syndrome?

226
Q

What is the fasting blood sugar in metabolic syndrome?

227
Q

What are the complications of DM?

A

1 macrovascular

2 microvascualr

228
Q

What are the macro vascular complications of DM?

A
  • coronary artery disease
  • periferal artery disease
  • carotid disease
  • stroke
229
Q

What are Ocular microvascular complications of DM?

A

-Ocular–retinopathy, gluacoma, cataracts

230
Q

What are the Renal microvascular complications of DM?

A

diabetic nephropathy

231
Q

What are the microvascual Neuological complications of DM?

A
  • peripheral neuopathy

- foot drop

232
Q

What are the skin microvascular effects os DM?

A
  • ulcers
  • slow healing
  • infections
233
Q

What are the bone microvasclar effects of DM?

A

carpal tunnel syndrome

234
Q

What systems are effected by the vascular complications of DM?

A
  • ocular
  • renal
  • neurological
  • skin
  • bone
235
Q

What two hormones are secreted by the posterior pituitary?

A

-Oxytocin and antidiuretic hormone (ADH, and vasopressin)

236
Q

What is Sheehan’s syndrome?

A

-Ischemia of the pituitary due to volume depletion during or after childbirth.

237
Q

How do glitazones work?

A

-They improve insulin sensitivity.

238
Q

What is the most common pituitary adenoma?

A

-Prolactinoma

239
Q

Large doughy hands should make you think of what diagnosis?

A

-Gigantism

240
Q

Diabetes insipidus is caused by a deficiency of which hormone?

A

-Vasopressin

241
Q

How much more potent is T4 than T3?

A
  • T4, 3-4 times
242
Q

What is the first line treatment for a pheochromocytoma?

A

-Alpha blocker. You should never a pure bata blocker.

243
Q

What is the best imaging for a thyroid nodule?

A

-Ultrasound

244
Q

A patient presents with erectile dysfunction and complains of some numbness in his feet. On second thought he has noticed polyuria and polydipsia. What diagnosis should you be thinking of?

A

-Diabetic neuropathy

245
Q

Pretibial myxedema should make you think of what diagnosis?

A

-Graves’s disease

246
Q

A 35 year old female presents with heat intolerance, weight loss and palpitations. What is the most likely diagnosis?

A

-Hyperthyroidism

247
Q

What are the 3 P’s of Diabetic Ketoacidosis?

A
  • Polydipsia–increased thirst
  • Polyphagia–frequent eating
  • Polyuria–frequent urination
248
Q

What is aldosterone?

A

-a corticosteroid hormone that stimulates absorption of sodium by the kidneys and so regulates water and salt balance

249
Q

How is aldosterone secreted?

A

-production of aldosterone (20-200 micrograms/day in adults) in the zone glomerulosa of the adrenal cortex is regulated by the renin-angiotensin system. Renin is secreted by the kidneys in response to variations in blood pressure and volume and plasma sodium and potassium levels.

250
Q

How does aldosterone affect blood pressure?

A

-it plays a central role in the regulation of blood pressure mainly by acting on organs including the kidney and colon to increase the amount of sodium reabsorbed into the bloodstream and the amount of potassium removed in the urine. Aldosterone also causes water to be reabsorbed along with sodium, this increases the blood volume and therefore blood pressure. Thus, aldosterone indirectly regulates blood levels of electrolytes (sodium, potassium, hydrogen) and helps maintain the blood pH.

251
Q

The drugs stimulate insulin secretion for tx of diabetes Type II.

A

Sulfonylureas

 - glypburide
 - glipizede
 - glimepiride
252
Q

This medication lowers glucose by reducing hepatic glucose production for diabetes Type II tx.

A

-Metfomin (is first line therapy)

253
Q

These medications decrease carbohydrate absorption from the small intestine in Tx of diabetes Type II.

A

-alpha-Glucosiede inhibitors

 - acarbose
 - miglitol
254
Q

In Tx of Type II diabetes these medications increase tissue sensitivity to insulin.

A

-Thiazolidinediones

 - rosiglitazone
 - pioglitazone
255
Q

Name 2 medications that can cause hypothyroidism.

A
  • amiodarone

- lithium

256
Q

Name 2 medications used to tx hyperthyroidism. These help lower the levels of T3 T4.

A
  • Methimazole

- Propylthiouracil (PYU)

257
Q

What is the long term tx for hypothyroidism?

A
  • Levothyroxine (synthetic T4)
  • start on lowest possible dose and is slowly moved up monitoring symptoms and TSH levels, then TSH levels checked yearly (watch for hyperthyroidism)

Endocrinology (6 decks)

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