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Clin med 1 > Endocrine 4-6 > Flashcards

Endocrine 4-6 Flashcards

1
Q

Which body systems utilize calcium?

A

Nervous, muscular and skeletal system (99% found in bone)

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2
Q

What is calcium regulated by?

A

PTH, calcitonin and active vitamin D

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3
Q

The 1% of calcium circulating in the blood is in what 3 forms?

A
  1. Free ionized form 45%
  2. Bound to proteins 45%
  3. Complex anions 10%
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4
Q

What is the total serum calcium?

A

8.5-10.5mg/dL

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5
Q

What is the net effect of parathyroid hormone?

A

Increase in serum calcium and decrease in serum phosphate

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6
Q

What is calcitriol the active form of?

A

Vitamin D

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7
Q

What is the function of calcitriol?

A

Enhances intestinal cells to absorb calcium and phosphate into the serum

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8
Q

What are the net effects of calcitriol?

A

Increase serum calcium

Increase serum phosphate

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9
Q

Where is calcitriol derived from?

A

Diet or UV light, required enzymatic steps in liver and kidney to become active vitamin D

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10
Q

PTH is synthesized and secreted by what?

A

Chief cells of the parathyroid gland

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11
Q

In response to low serum Ca++ bone does what?

A

Bone: PTH stimulates resorption (osteoclastic) which leads to INCREASE in serum Ca++

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12
Q

In response to low serum Ca+++ kidney does what?

A

PTH promotes Ca++ resorption and stimulates hydroxylation of 25-hydroxyvitamin D (calcidiol) via an enzyme

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13
Q

In response to high serum Ca+++

A

PTH decreases its production

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14
Q

Increased serum calcium leads to what?

A

Decreased PTH

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15
Q

Decreased serum calcium leads to what?

A

Increased PTH

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16
Q

When PTH stimulates the bone what does it do?

A

Increases osteoclastic activity and decreases osteoblastic activity

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17
Q

When PTH stimulates GI tract what does it do?

A

Vitamin D: increased absorption of calcium and phosphate

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18
Q

When PTH stimulates the kidneys what does it do?

A

Activates 1alpha D hydroxylase, increases reabsorption of calcium and increases phosphate excretion

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19
Q

What effect does calcitonin have on the GI tract?

A

None

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20
Q

What effect does calcitonin have on the kidney?

A

Decreases absorption of calcium and phosphate

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21
Q

What effect does calcitonin have on the bone?

A

Increases osteoblastic activity and decreases osteoclastic activity

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22
Q

Hypocalcemia etiologies from the parathyroid

A

Thyroidectomy, iodine therapy, autoimmune, infiltrative disease, PTH resistance

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23
Q

Hypocalcemia etiologies from Vitamin D deficiency

A

CKD: #1 cause, malabsorption syndromes, decrease exposure to sunlight, vitD resistant rickets, hyperphosphatemia, drugs accelerate CP450: Phenytoin

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24
Q

Miscellaneous etiologies for hypocalcemia

A

Hungry bone syndromes, osteoblastic bone metastases, pancreatitis, multiple transfusion, acute respiratory alkalosis, bisphosphonate OD, alcoholics

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25
Q

Hypocalcemia from hypoparathyroidism

A

Requires all 4 parathyroid glands to be affected, therefore uncommon

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26
Q

What are some symptoms of hypocalcemia + hypoparathyroidism?

A

Emotional lability, paresthesia (perioral, hands, feet), SOB (diaphragmatic spasms), voice changes (cataract formation) chronic, personality changes (chronic)

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27
Q

What are some PE findings of hypocalcemia + hypoparathyroidism

A

Tetany, Chvostek’s sign, Trousseau’s sign, muscle stiffness, spasms and cramps, seizures, hypotension, wheezing, voice changes, psychosis, hyperreflexia

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28
Q

What is tetany?

A

Repetitive discharge of peripheral nerves after single stimulus

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29
Q

What can be used to diagnose hypocalcemia + hypoparathyroidism

A

EKG, total calcium (correct calcium for low albumin, ionized calcium), PTH, BUN/creatinine, phosphate, mg, albumin, LFTs, PT/INR

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30
Q

Which VitD labs can be tested for hypocalcemia + hypoparathyroidism

A

Vitamin D levels- 25(OH) cholecalciferol (calcidiol)

1, 25 (OH)2 Cholecalciferol (Calcitriol)- concern for renal dysfunction

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31
Q

How do you treat hypocalcemia + hypoparathyroidism?

A

Oral calcium, IV calcium, Vitamin D, Mg prn, Diet

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32
Q

What are the oral calcium options to treat hypocalcemia + hypoparathyroidism

A

Calcium carbonate 1500mg-2000mg daily

Calcium citrate 1gm/day

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33
Q

What are the IV calcium options to treat hypocalcemia + hypoparathyroidism

A 
Calcium Gluconate (preferred) (1-2gms)
Calcium Chloride
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34
Q

When is IV calcium administered to patients with hypocalcemia + hypoparathyroidism

A 
Sever symptoms (tetany, seizures)
Prolonged QT interval or arrhythmia
Suspected abrupt decrease from normal
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35
Q

What are the indications for using Vitamin D for patients with hypocalcemia + hypoparathyroidism

A

Hypocalcemia secondary to Hypoparathyroidism, hungry bone syndrome, vitamin D deficiency

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36
Q

What forms of vitamin D can be used for hypocalcemia + hypoparathyroidism

A

Calcitriol and Vitamin D2 (Ergocalciferol)

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37
Q

What should be avoided with hypocalcemia + hypoparathyroidism

A

Diuretics

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38
Q

What is the most common electrolyte abnormality in adults with malignancies?

A

Hypercalcemia

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39
Q

What is the most common cause of hypercalcemia?

A

Hyperparathyroidism

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40
Q

Hyperparathyroidism is also seen in what?

A

MEN 1, 2a, and 2b*

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41
Q

SHAMPOO

A 
Sarcoidosis
Hyperparathyroidism
Alkali milk syndrome
Metastastis, multiple myeloma
Paget disease
OSteogenesis imperfecta
Osteoporosis
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42
Q

SHAMPOO is for what?

A

Hypercalcemia etiologies

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43
Q

DIRT

A

D vitamin intoxication
Immobility
RTA (renal tubular acidosis)
Thiazides

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44
Q

DIRT is for what?

A

Hypercalcemia etiologies

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45
Q

The most common cause of primary hyperparathyroidism is what?

A

Single parathyroid adenoma (80%)

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46
Q

Other causes of hyperparathyroidism

A

Hyperplasia, carcinoma, famililar hypocalciuric hypercalcemia

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47
Q

What is secondary hyperparathyroidism?

A

Due to overproduction of PTH due to chronic abnormal stimulus

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48
Q

What can cause secondary hyperparathyroidism

A

Chronic renal failure and VitD deficiency

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49
Q

What is tertiary hyperparathyroidism?

A

Due to a state of excessive secretion of PTH after longstanding secondary

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50
Q

What can cause tertiary hyperparathyroidism?

A

Renal transplant patient

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51
Q

What are the si/sx of hypercalcemia and hyperparathyroidism

A

“bones stones groans and moans”

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52
Q

What happens to the bones with hypercalcemia and hyperparathyroidism

A

Joint pain, bone pain

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53
Q

What is the “stones” when referring to hypercalcemia and hyperparathyroidism

A

Polyuria, kidney stones, hypercalcuria

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54
Q

What is the “groans” when referring to hypercalcemia and hyperparathyroidism

A

Anorexia, N/V/abd pain, constipation, PUD

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55
Q

What are the “moans” when referring to hypercalcemia and hyperparathyroidism

A

Weakness, fatigue, depression, inability to concentrate, anxiety and confusin

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56
Q

PE findings of hypercalcemia and hyperparathyroidism

A

Most of the time PE is non-contributory
Skin: pruritis, skin tenting
Cardiac: HTN, LVH
GI: anorexia, N/V, constipation, pain
Renal: renal colic (kidney stones)
MSK: bone fractures (wrist and vertebrae)
Neuro/Psyc: paresthesias, diminished DTR, muscle weakness, depression

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57
Q

Hypercalcemia diagnostics

A

Calcium level, PTH, 24hour urinary calcium excretion, chloride phosphate, PTHrP, BUN/Creatinine, Calcitriol or Calcidiol, EKG

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58
Q

If the 24hour urinary calcium excretion is high..

A

Primary hyperparathyroidism

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59
Q

If the 24hours urinary calcium excretion is low..

A

Familial hypocalciuric hypercalcemia

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60
Q

PTHrP elevation means what

A

Malignancy

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61
Q

Elevated calcidiol means what

A

Excessive dietary intake of calcium or VitD

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62
Q

Elevated calcitriol with normal calcidiol means what

A

Ectopic production of calcitriol

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63
Q

If PTHrP, calcidiol, and calcitriol are all normal

A

Bone mets, consider rare causes of hypercalcemia and hyperparathyroidism

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64
Q

T or F Imaging studies are not used to make the diagnosis of primary hyperparathyroidism, but may be used to guide the surgeon

A

True!

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65
Q

What diagnostic imaging can be used for hyperparathyroidism?

A

Sestamibi scan, ultrasound of the neck, CT or MRI, bone density measurement by DXA to assess amnt of bone loss, X-ray

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66
Q

DXA

A

Dual XRay absorptiometry: assess the amount of bone loss

Focus on lumbar spine, hip, and distal radius

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67
Q

What can be some XRay findings for hyperparathyroidism?

A

Osteitis fibrosa cystica, “salt and pepper” appearance of skull, brown tumor of long bones

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68
Q

What are the treatment options for hyperparathyroidism?

A

Surveillance, surgical, pharmacological, supportive

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69
Q

Asymptomatic hyperparathyroidism patient treatment

A

STay active, avoid immobilization, drink fluids, modest dietary calcium, VitD recommendation based on age, bisphosphonates, D/C thiazides, VitA, calcium containing antacids

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70
Q

What do asymptomatic hyperparathyroidism patients require annually?

A

Serum calcium and creatinine; bone density scan done 1-2 years

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71
Q

Surgery is recommended for which type of patients with hyperparathyroidism?

A

Symptomatic or pregnant

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72
Q

What is the medical treatment for hyperparathyroidism?

A

Fluids, Furosemide, IV bisphosphonates, calcitonin, cinacalcet, propranolol can help reduce cardiac symptoms

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73
Q

Who is medical treatment for?

A

Indicated for poor surgical candidates, those declining surgery, awaiting surgery with severe symptoms

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74
Q

Hypercalcemia treatment medications

A

Normal saline, loop diuretics, bisphosphonates, calcitonin, Gallium nitrate, dialysis, steorids, magnesium

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75
Q

How does normal saline help hypercalcemia?

A

Decreased calcium levels through dilution, allows for expansino of ECF volume

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76
Q

How do loop diuretics help hypercalcemia?

A

Used with hydration will increase calcium excretion

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77
Q

How do bisphosphonates help hypercalcemia?

A

Inhibit osteoclastic activity

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78
Q

How does calcitonin help hypercalcemia?

A

Inhibits bone removal by osteoclasts, and promotes bone formation by osteoblasts

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79
Q

How does gallium nitrate help with hypercalcemia

A

Inhibits bone resorption directly and may inhibit PTH secretion

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80
Q

When primary hyperparathyroidism is symptomatic, the most common presentation in those over the age of 61 involves what?

A

Nephrolithiasis, fatigue, and bone disease

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81
Q

Surgical treatment for hyperparathyroidism could be considered for who?

A

If patient is symptomatic and/or there are signs of end-organ damage

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82
Q

Medical treatment for hyperparathyroidism with what is an option for nonsurgical candidates?

A

Bisphosphonate and/or cinacalcet

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83
Q

Parathyroid cancer lab results

A

Ca levels >14, PTH levels 5X normal, palpable parathyroid gland

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84
Q

What does treatment of parathyroid cancer consist of?

A

Below the neck exploration with excision of tumor and ipsilateral thyroid lobe

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85
Q

Parathyroid cancer post op care

A

Check Ca levels 2 weeks post op, 6 mos, and annually after

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86
Q

Recurrence of parathyroid cancer has been found in who?

A

15% at 2 years and 67% at 8 years have been reported for MEN1 patients

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87
Q

What is a localized disorder or bone remodeling with excessive bone resorption followed by disorganized bone formation?

A

Paget disease

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88
Q

The bone turnover rate is 20x higher in what?

A

Paget disease

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89
Q

Common bones affected in paget disease

A

Pelvis, lumbar spine, femur, thoracid spine, sacrum, skull, and tinia

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90
Q

What are the 3 phases of paget disease?

A
  1. Lytic: osteoclasts are more numerous and larger, bone turnover rate 20x higher
  2. Mixed phase: Rapid increase in bone formation from numerous osteoblasts
  3. Final phase: bone formed in woven pattern, weak and causes hypervascular bone state
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91
Q

What is the most common symptom for paget disease?

A

Pain, 70-90% are asymptomatic

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92
Q

Si/sx of Pagets disease

A

Osteoarthritis, nerve impingement, hearing loss, bones become soft -> bowed tibias, kyphosis, if skull is involved -> HAs, increased hat size

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93
Q

Diagnosis of Paget disease

A

Alkaline phosphatase will be elevated
Blood levels to asses for bone turnover rate:
Serum N-terminal propeptide of type 1 collagen (NTx)
Serum BetaC-terminal propeptide of type 1 collagen (betaCTx)
Serum calcium, VitD and serum phosphate

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94
Q

Imaging for Paget disease

A

Stage 1: Areas of bone loss
Stage 2: “cotton-wool or picture frame” look for skull and vertebrae
Stage 3: “burn out” phase bone appears enlarged and dense
Bone Scintigraphy: radionuclide bone scans

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95
Q

What are some complications of pagets disease?

A

Pain arthritis, disability, vertebral collapse/fracture, cranial nerve palsies, hearing loss, paralysis

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96
Q

Treament of paget disease involves what?

A

Surveillance for asymptomatic pts, certain criteria for symptomatic pts

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97
Q

Symptomatic paget disease treatment

A

Nitrogen containing bisphosphonates
Extensive disease/elderly: IV Zolendronic Acid (preferred)
Less extensive/young: Risendronate or Alendronate PO
Calcitonin, Calcium, VitD, analgesics, rehab, surgical if needed

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98
Q

What is the treatment of choice of Paget disease?

A

IV infusion of Zolendronate 5mg over 15 minutes

Targeted to achieve a serum alkaline phosphatase in lower half of normal reference range

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99
Q

Paget Disease key points

A

Its a focal disorder of osteoclasts resulting in increased bone turnover and lytic skeletal lesions that primarily affects older individuals

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100
Q

What are some causes of hyperpituitarism?

A

Hyperprolactinemia, acromegaly, gigantism, SIADH

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101
Q

What are some causes of hypopituitarism?

A

Diabetes insipidus, sheehan syndrome, dwarfism

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102
Q

What hormones does the anterior pituitary secrete?

A

GH, PRL, ACTH, TSH, LH, FSH

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103
Q

What hormones are secreted by the posterior pituitary?

A

ADH, Oxytocin

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104
Q

What is another name for ADH?

A

Vasopressin, antidiuretic hormone

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105
Q

Diabetes insipidus is caused by what?

A

A deficiency in vasopressin (ADH) from posterior pituitary

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106
Q

Where is ADH created?

A

Hypothalamus, secreted by posterior pituitary

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107
Q

ADH promotes preservation of water from where?

A

The kidneys

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108
Q

ADH alters water permeability where?

A

In the distal renal tubules

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109
Q

Defined as the passage of large volume (>3L/24hr) of dilute urine (<300 mOsm/kg

A

Diabetes insipidus

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110
Q

Inadequate ADH in diabetes insipidus causes what?

A

Polyuria

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111
Q

What are the two main causes of DI (diabetes insipidus)?

A

Central and nephrogenic

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112
Q

The central cause of DI

A

Due to decreased secretion of ADH

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113
Q

The nephrogenic cause of DI

A

The kidneys are not responding to the normal amount of ADH

114
Q

The central cause of DI can be broken down into what?

A

Primary and Secondary

115
Q

Primary central DI is what?

A

No identifiable lesion on MRI of pituitary or hypothalamus (around 1/3 cases)

116
Q

Secondary central DI is what?

A

Some type of damage to hypothalamus or pituitary stalk by trauma, infection, bleed, tumor, infarction (majority of cases)

117
Q

What is the etiology of central diabetes insipidus?

A 
Cranial surgery (20%) and head trauma (16%)
others: idiopathic, malignant or benign tumors of the pituitary (25%)
118
Q

What is the etiology of nephrogenic diabetes insipidus?

A

Lithium toxicity, hypercalcemia, Demeclocyline, steroids, Ofloxacin, Methicillin, pregnancy (transient), renal disease, congenital

119
Q

What are the si/sx for diabetes insipidus?

A

Polyuria, polydipsia, nocturia, daily urinary output ranges from 3-20L, dehydration, hypotension, hypernatremia

120
Q

What are the clinical manifestations of DI caused by?

A

Absence of ADH

121
Q

Evaluation of DI

A

24 hour urine collection, urinalysis, Serum electrolytes and glucose, plasma and urine osmolality, ADH, water deprivation test, water deprivation + ADH, urine specific gravity, urine osmolarity, MRI

122
Q

What will the serum electrolyte results be for DI?

A

Serum Na will be high, serum glucose normal

123
Q

What will the plasma and urine osmolality be for DI?

A

Plasma osmolality: high

Urine osmolality: low

124
Q

What will the results be for ADH level with DI?

A

Central: Low ADH
Nephrogenic: High ADH

125
Q

What is the treatment for DI?

A

Hypotonic solution D5W targeted at 500-750ml/hr (pts with severe symptoms)

126
Q

What is the goal of treatment for DI?

A

Reduce serum sodium and monitor electrolytes every 4-6 hours

127
Q

How do you treat central DI?

A

Desmopression (DDAVP) intranasal 10-40mc daily or oral 0.1-1.2

128
Q

How do you treat nephrogenic DI?

A

HCTZ 12/5mg-50mg QD- Diuretic that blocks reabsorption of Na into the kidneys

129
Q

What is SIADH?

A

Syndrome of Inappropriate Antidiuretic Hormone

130
Q

What is SIADH characterized by?

A

Excessive release of ADH from the posterior pituitary gland

131
Q

What does the excess ADH do in SIADH?

A

Promotes renal tubule absorption of water and decrease urinary output, causes water retention

132
Q

What does SIADH and excessive ADH result in?

A

Dilutional hyponatremia and low serum osmolality. Hyponatremia can be severe

133
Q

What is the most common cause of hyponatremia in hospitalized patients?

A

SIADH

134
Q

Decreased urinary output will increase what?

A

Urine osmolality

135
Q

What are some etiologies of SIADH?

A

Malignancy (small cell lung cancer, pancreatic cancer), drugs, after pituitary surgery

136
Q

Si/Sx of SIADH?

A

HA/ N/V, seizures, altered mental status, LOC, asymptomatic (if development is gradual)

137
Q

What is the cause of the si/sx for SIADH?

A

Hyponatremia due to water intoxication-severity and onset of hyponatremia determines the extent of symptoms

138
Q

What can be used for diagnosis of SIADH?

A

Urinalysis, urine sodium, urine osmolality, BMP, BUN, serum osmolality, ADH, CT/MRI of head, CXR, CT abd/pelvis

139
Q

What will the result of urinalysis be with SIADH?

A

Specific gravity is high

140
Q

What will the urine sodium be with SIADH?

A

High

141
Q

What will the urine osmolality be with SIADH?

A

High

142
Q

What will the BMP read with SIADH?

A

Serum sodium low

143
Q

What will the BUN read with SIADH?

A

Low

144
Q

What will the serum osmolality be with SIADH?

A

Low

145
Q

SIADH treatment for asymptomatic

A

Restrict fluids <1/5L/day, D/C offending medications, Demeclocycline -> potent inhibitor of ADH

146
Q

SIADH treatment for symptomatic (seizures, altered)

A

3% NaCl (hypertonic solution)
Do not increase Na >0.5-1mEQ/L/hr
Check hourly serum sodium, neuro critical care consult

147
Q

To compare SIADH to DI, SIADH has…

A 
Too much ADH
ECF volume excess
Hyponatremia
Decrease urine output (urine is concentrated and dark)
Hypertensive
148
Q

To compare SIADH to DI, DI has…

A

No ADH
Increase urinary output (>3L/day) urine appears as water
Hypernatremia
Hypotensive

149
Q

What is psychogenic polydipsia characterized by?

A

Polyuria and polydipsia, common occurrence in inpatients with psychiatric disorders

150
Q

What happens in psychogenic polydipsia?

A

Hyponatremia in pts can progress to acute water intoxication, management includes fluid restriction, behavioral and pharmacologic modalities

151
Q

A condition of short stature

A

Dwarfism

152
Q

Most common causes of Dwarfism

A

Familial and delayed growth (non-pathologic)

153
Q

Dwarfism is defined as

A

Height that is 2 standard deviations below mean for children of that sex and age (below the 2.3rd percentile)

154
Q

Achondroplasia is what?

A

Most common bone dysplasia in humans, occurs in all races with equal frequency

155
Q

What are the two main categories of dwarfism?

A

Proportionate Dwarfism and Disproportionate Dwarfism

156
Q

Proportionate Dwarfism

A

Caused by metabolic/hormonal syndromes
Pituitary Dwarfism: GH deficiency syndromes
Laron Syndrome

157
Q

Disproportionate Dwarfism

A

Achondropalsia, sponydyloepiphyseal dysplasia, diastrophic dysplasia

158
Q

What is achondroplasia?

A

Autosomal dominant, spontaneous mutation in FGFR3, normal torso and short limbs

159
Q

What are the si/sx of achondroplasia?

A

Normal torso, short limbs, enlarged skulls, central apnea, obstructive apnea, and hydrocephalus, difficult airway

160
Q

Achondroplasia makes up what % of dwarfism?

A

70%

161
Q

Achondroplasia is associated with what?

A

Advanced paternal age, gene mutation affects bone formation

162
Q

Spondyloepiphyseal dysplasia (SED)

A

Shortened trunk, barrel chest, club feet, cleft palate, severe osteoarthritis

163
Q

SED is associated with what?

A

Variety of medical problems, mainly orthopedic

164
Q

What is the adult height in SED?

A

Varies slightly from under 3 feet to slightly over 4 feet

165
Q

Diastrophic dysplasia

A

Autosomal recessive, rare, shortened forearms and calves, limited ROM, cleft palate, deformed hands/feet

166
Q

Disproportionate dwarfism si of the hands and feet

A

Polydactyly, hitch-hiker thumb, clubfoot

167
Q

Disproportionate dwarfism si of the nails

A

Hypoplastic, short and broad

168
Q

Disproportionate dwarfism si of the thorax and ribs

A

Long, narrow thorax, pear-shaped chest

169
Q

Disproportionate dwarfism si of the heart

A

ASD, single atrium, patent ductus arteriosum, transposition of great vessels

170
Q

Other signs of Disproportionate dwarfism

A

Multiple joint dislocations, long bone fractures

171
Q

How can you diagnose Disproportionate dwarfism?

A

Clinically, based on PE can do genetic testing and skeletal xrays

172
Q

Treatment of Disproportionate dwarfism

A

Symptomatic relief: tracheotomy, cleft palate repair, leg braces, back braces, club foot surgery

173
Q

What is pituitary dwarfism a deficiency in?

A

GH or GHRH (growth hormone releasing hormone)

174
Q

What else can cause pituitary dwarfism?

A

Sellar and parasellar tumors that destroy the pituitary gland itself

175
Q

Auxology

A

Study of human growth

176
Q

Si/Sx of pituitary dwarfism

A

Sever postnatal growth failure, delayed bone age, hypoglycemia, prolonged jaundice, micropenis, high pitched voice, increase body fat, short stature

177
Q

Diagnostic approach to GHD

A

Evaluate for other causes of growth failure, including chronic systemic disease, hypothyroidism, turner syndrome (F), skeletal disorders

178
Q

Diagnostic tests for GHD

A

Insulin-like growth factor 1 (IGF-1)
Insulin0like growth factor binding protein 3 (IGFBP-3)
Bone age

179
Q

If bone age and height velocity are normal, you cane exclude what diagnosis?

A

GHD

180
Q

What provocative tests are used to confirm the diagnosis of GHD?

A

GH provocative testing: Agent that will normally provoke a pituitary to release a burst of GH, blood drawn @ 15 min intervals over one hour

181
Q

What agents are used in the provocative GH testing?

A

Arginine, Levodopa, Clonidine, Glucagon

182
Q

What are the results of provocative GH test?

A

If serum concentrations of GH, IGF-1 and IGFBP-3 remain low, diagnosis can be confirmed
MRI should also be obtained

183
Q

What is Laron Syndrome?

A

Most common known cause of genetically mediated growth hormone insensitivity

184
Q

Laron Syndrome is caused by mutations in what gene?

A

GH receptor gene, unable to bind to receptor

185
Q

What are the mutations associated with Laron Syndrome?

A

Autosomal recessive mutations, causes severe postnatal growth failure, GH levels are normal or high

186
Q

Clinical features of Laron Syndrome

A

Small head circumference, characteristic facies with saddle nose and prominent forehead
Delayed skeletal maturation, small genitalia and testes, short limb length compared with trunk, osteopenia and obesity

187
Q

What are the signs of Turner Syndrome

A

Square “shield” chest, webbed neck, cubitus valgus, genu valgum, shortened 4th metacarpals and Madelung deformity of the forearm

188
Q

What is cubitus valgus?

A

Abnormal angle of forearm when it hangs

189
Q

What is genu valgum?

A

Knees go in and touch

190
Q

What is the treatment of pituitary dwarfism?

A

If its a pituitary/GH problem: GH administer SQ

Laron Syndrome: IGF-1

191
Q

If the childs height is above the 2.3rd percentile?

A

No referral needed

192
Q

If the childs height is below the 2.3rd percentile?

A

Concern, may need referral

193
Q

If childs height if less than the 1st percentile

A

Evaluate the rate of growth, if declines or low, refer to Endocrinologist

194
Q

How is bone age determined?

A

from a radiograph of the left hand and wrist, and requires expert interpretation

195
Q

Delayed bone age with <2SD

A

Refer to endocrinologist

196
Q

Sheehand syndrome is a disease of what?

A

Pituitary

197
Q

Infarction of the pituitary after postpartum hemorrhage, or infarction immediately postpartum

A

Sheehan syndrome

198
Q

Si/sx of Sheehan syndrome

A

History of severe postpartum hemorrhage, severe hypopituitarism: lethargy, anorexia, weight loss, inability to lactate during first days/weeks after delivery

199
Q

SI/sx of Sheehan syndrome with less severe hypopituitarism

A

Failure of postpartum lactation, failure to resume menses in weeks/months after delivery, loss of sexual hair, milder fatigue, weight loss, anorexia

200
Q

Diagnostic studies for Sheehan syndrome

A

MRI, Hormone evaluation

201
Q

Hypopituitarism hormone evaluation

A

Corticotrophin (ACTH), Thyrotropin (TSH), Prolactin, ADH, GH, Gonadotropin

202
Q

Postpartum hypopituitary lab profile

A

Must evaluate for adrenal insufficiency immediately, other hormonal deficiencies can be evaluated 4-6 weeks later

203
Q

MRI results for Sheehan Syndrome

A

Early abnormalities may be seen- enlargement/ischemia

late changes of small pituitary with normal size sella and eventually an empty sella

204
Q

Treatment for Sheehan syndrome

A

Must treat for adrenal insufficiency immediately, other deficiencies can be related 4-6 weeks later
No treatment available for prolactin deficiency

205
Q

ACTH deficiency hypopituitarism treatment

A

Hydrocortisone or glucocorticoid

206
Q

TSH deficiency hypopituitarism treatment

A

Levothyroxine

207
Q

Gonadotropin deficiency hypopituitarism treatment

A

Men: testosterone
Women: Depends on txt goals, estradiol and progestin if pursuing fertility, gonadoptropin or pulsatile GnRH when ovulation induction and fertility

208
Q

GH deficiency hypopituitarism treatment

A

Adults replacement not generally recommended

209
Q

Pituitary in very close to what important structures

A

Optic chiasm, cranial nerves 3, 4, 6, trigeminal ganglion, ophthalmic division of CN V, carotid artery, cerebral circulation

210
Q

What hormones are produced by the anterior pituitary?

A

GH, PRL, ACTH, TSH, LH, FSH

211
Q

What hormones are released by the posterior pituitary?

A

ADH, oxytocin

212
Q

Which pituitary hormones are involved in positive feedback loop?

A

CRH, TRH, GnRH GHRH

213
Q

Which pituitary hormones are involved in negative feedback loop?

A

SST- somatostatin (GHIH growth hormone inhibiting hormone), dopamine

214
Q

What are the two types of pituitary sellar masses?

A

Benign and malignant

215
Q

What type of pituitary sellar mass is benign?

A

Pituitary adenoma, there is a functional and on-functional form

216
Q

The functional pituitary adenoma does what?

A

Produces hormones, about 65-70% of all adenomas

217
Q

What types of pituitary sellar masses are malignant?

A

Germ cell tumor (ectopic pinealoma), sarcoma, chordoma, pituitary carcinoma

218
Q

Pituitary adenoma classifications

A

Micro/macro < or >1cm, by cell type: gonadotroph, thyrotroph, corticotroph, lactotroph, somatotroph, lactrotroph/somatotroph adenomas

219
Q

What type of pituitary adenoma is most common?

A

Lactotroph 40-50% hyperprolactinemia

220
Q

What type of pituitary adenoma is least common?

A

Thyrotoph 1% hyperthyroidism

221
Q

Mutations in what genes can play a role in pituitary adenomas?

A

MEN1, Gs-alpha, PTTG, FGF receptor-4

222
Q

Pituitary adenoma si/sx

A

Neurologic symptoms: visual changes, HA, CSF rhinorrhea (rare), hormonal changes too, can also be asymptomatic

223
Q

Pituitary adenoma visual symptoms

A

Blurry vision, diplopia, bitemporal hemianopia visual field defect, diminished visual acuity
All varies based on tumor size/location

224
Q

Visual changes happen with pituitary adenomas when they are how big?

A

> 2cm

225
Q

Pituitary apoplexy

A

Si of pituitary adenoma, infarct or hemorrhage into the adenoma

226
Q

Si/sx of pituitary apoplexy

A

Severe acute onset HA, vomiting, visual field deficits-diplopia/BTH, other cranial nerve dysfunction (3, 4, 5, 6), fever beck stiffness, impaired consciousness/AMS

227
Q

Diagnostic studies for pituitary adenoma

A

Hormonal evaluation like serum prolactin, insulin-like growth factor 1, 24 hour urinary free cortisol and elevated ACTH, MRI

228
Q

If a thyrotroph adenoma is suspected which lab tests are done

A

Alpha subunit, total or free T4, TSH

229
Q

If a gonadotroph adenoma is suspected, which lab tests are done

A

LH, FSH

230
Q

Diagnosis of pituitary adenoma

A

MRI: consistent with adenoma, hormone hypersecretion (functional vs. non functional), evaluation for visual abnormalities

231
Q

Pituitary adenoma/ incidentaloma evaluation

A

Size >10mm typical hormone evaluation
Size <10mm without clinical findings: measure serum prolactin, could consider MRI at 6 mos and 12 mos, no eval for visual defects

232
Q

Treatment goals of pituitary adenomas

A

Nonfunctioning: relief of visual impairments and other neurologic symptoms, removal of macroadenomas completely to avoid recurrence, management of hormonal deficiencies

233
Q

Pituitary adenoma treatment

A

surgical therapy treatment of choice
Medical therapy: ID hormone deficiency and tx preoperatively
Adjuvant radiation therapy

234
Q

What are some post-op hormone deficiencies from pituitary adenoma?

A

Hypocortisolism, diabetes insipidus and SIADH

235
Q

Outcome of pituitary adenoma surgery

A

Most have reduced size of adenoma, visual function improvement, hormone deficiencies unlikely to improve, mortality rate 1% serious complications 5%

236
Q

Follow-up pituitary adenoma surgery

A

Non-surgical pts: MRI every 6-12 mos, visual field exam every 6-12 mos, monitor and treat hormone deficiencies
Post transsphenoidal resection: 4-6 weeks, residual adenoma monitor with MRI

237
Q

Hyperprolactinemia physiologic causes

A

Sleep, physical exertion, food, stress/trauma, coitus, pregnancy, postpartum state, nursing/nipple stimulation, surgery

238
Q

Pituitary/hypothalamic disorders that cause hyperprolactinemia

A

Prolactinoma, acromegaly, other pituitary tumors, infiltrative disorders (MS), hypothalamic and pituitary stalk disease or damage

239
Q

“Other” causes of hyperprolactinemia

A

Primary hypothyroidism, seizures, PCO, neurogenic causes (chest wall trauma, herpes zoster), renal insufficiency, cirrhosis

240
Q

What can cause hypothalamic-pituitary disease?

A

Lactotroph adenoma (prolactinoma), decreased dopaminergic inhibition of prolactin secretion (drugs or damage), disease in or near hypothalamus/pituitary

241
Q

Drug-induced causes of hyperprolactinemia

A

Ranitidine, Cocaine/amphetamines, metoclopramide, opioids, risperidone, SSRIs, verapamil, hydroxyzine

242
Q

30-40% of all pituitary adenomas are what?

A

Prolactinomas

243
Q

Prolactinomas are frequently diagnosed in who?

A

Women age 20-40. Ones in men are usualyl larger

244
Q

90% of prolactinomas are what?

A

Microadenomas

10% macroadenomas

245
Q

Clinical manifestations of hyperprolactinemia?

A

Galactorrhea, infertility, osteopenia, decrased libido

246
Q

Clinical manifestations of hyperprolactinemia in women?

A

Oligo-amenorrhea, acne/hirsutism, estrogen deficiency sxs/dyspareunia

247
Q

Clinical manifestations of hyperprolactinemia in men?

A

Erectile dysfunction, gynecomastia

248
Q

Hyperprolactinemia labs to evaluate

A

Diluted fasting prolactin, TFTS, LFTs, Ca, Cre/BUN, HCG, IFG-1 (if clinccally indicated)

249
Q

Evaluation of hyperprolactinemia

A

PE, MRI with and without gadolinium
If suprasellar extension: obtain visual fields
If macroadenoma: perform ant pit testing for GH, thyroid and adrenal insufficiency

250
Q

Hyperprolactinemia diagnosis

A

Serum prolactin level will be significantly elevated

MRI with pituitary lesion/adenoma

251
Q

Prolactinoma treatment indications

A

Tumor growth, oligo or amenorrhea/hypogonadism, bothersome galactorrhea, infertility

252
Q

Hyperprolactinemic patients with a microadenoma may be followed without treatment if they are

A

Asymptomatic, eugonadal, have stable MRI scans

253
Q

Prolactinoma therapy

A

Dopamine agonists: first choice in most pts
Cabergoline: first choice
Bromocriptine: first choice for women wanting pregnancy
Can also do surgery and radiation

254
Q

Prolactinoma indications for surgery

A

Visual field defects unresponsive to meds, macroadenomas unresponsive to meds, tumor growth while on meds, intolerance to dopamine agonists, pituitary apoplexy (rare), CS rhinorrhea or >50% shrinkage of tumor with meds

255
Q

Hyperprolactinemia: Goals for dopamine agonist therapy

A

Normalize prolactin levels and achieve remission of associated symptoms, reduce/stabilize tumor size, preserving ant pit function, prevent disease progression

256
Q

What is the presentation of acromegaly?

A

Prognathism, HA, vision defect, skin tags, enlarged tongue/macroglossia, front bossing*, course features, enlarged hands and feet, osteoarthritis, carpal tunnel

257
Q

Which clinical features are most commonly seen in acromegaly?

A

Acral enlargement and or coarse features, sweating, menstrual disorder, HA, arthritis, carpal tunnel syndrome, Diabetes, HTN

258
Q

Why is the diagnosis of acromegaly delayed?

A

Due to gradual development

259
Q

What are some co-morbidities associated with acromegaly?

A

HTN and heart disease, cerebrovascular events and HA, arthritis, insulin-resistant diabetes, sleep apnea

260
Q

Baseline evaluation of acromegaly involves what?

A

IFG-1, pituitary function testing (if macroadenoma), PRL, glucose, LFTs, Cr/BUN, MRI of pituitary, visual fields, CH suppression with oral glucose

261
Q

What is the surgical therapy for acromegaly?

A

Transsphednoial pituitary microsurgery

262
Q

What is the medical therapy for acromegaly?

A

Dopamine agonists, somatostatin analogs, Pegvisomant

263
Q

What is the radiation therapy for acromegaly?

A

Stereotactic radiosurgery

264
Q

What are the goals of therapy for acromegaly?

A

Control tumor size, IGF-1 normal an dOGTT suppression of GH <1mcg/L

265
Q

What somatostatin analogs can be used for acromegaly?

A

Octreotide and Lanreotide

266
Q

Which Dopamine agonists can be used for acromegaly?

A

Bromocriptine and Cabergoline

267
Q

Which GH receptor antagonists can be used for acromegaly?

A

Pegvisomant

268
Q

What are examples of primary neoplastic pituitary tumors?

A

Pituicytoma, Germ cell tumors, sarcomas, chordomas, lymphomas, carcinomas

269
Q

What types of pituitary neoplastic malignant tumors are metastatic?

A

Breast cancer in women, lung cancer in mean

270
Q

Pituicytoma

A

Low-grade indolent glioma. Arises from post pituitary

271
Q

How does Pituicytoma present?

A

Sellar mass; usually mistaken for pituitary adenoma. No known hormonal secretory function

272
Q

Germ cell tumors

A

3rd decade of life, imaging will show mass in 3rd ventricle

273
Q

Si/sx of germ cell tumors

A

HA, N/V, lethargy, diplopia, hypopituitarism, diabetes insipidus, paralysis of upward conjugate gaze (Parinaud’s syndrome)

274
Q

What is Parinaud’s Syndrome

A

Occurs in germ cell tumors. Its the paralysis of upward conjugate gaze

275
Q

Lab studies for germ cell tumors

A

Serum concentrations of B-hCG or AFP may be increased, highly malignant and metastasize readily

276
Q

Chordomas

A

Local aggressive tumors, metastasize

277
Q

Si/sx of chordomas

A

HA, visual impairment, ant pituitary hormonal deficiencies

278
Q

Primary lymphoma

A

HA, visual and oculomotor impairment, ant pituitary hormonal deficiencies, ADH deficiency

279
Q

What will MRI show of a primary lymphoma?

A

Sellar mass with variable extrasellar extension

280
Q

Metastatic Disease

A

Metastases to the pituitary and hypothalamus, accounts for 1-2% of sellar masses

281
Q

Who is metastatic disease commonly seen in?

A

Breast cancer in women and lung cancer in men (and many other cancers)

282
Q

Symptoms of metastatic disease

A

Diabetes insipidus, visual field defects, ant pituitary hormonal deficiencies, retroorbital pain and ophthalmoplegia, poor prognosis

Clin med 1 (9 decks)

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