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Diagnosis and Management > Endocrine Part 2 Hyper/HypoCa, Osteo, Pituitary > Flashcards

Endocrine Part 2 Hyper/HypoCa, Osteo, Pituitary Flashcards

1
Q

Calcium Metabolism and Bones Diseases

(3)

A

Hypercalcemia

Hypocalcemia

Osteoporosis

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2
Q

Hypercalcemia

Common medical condition

  • Symptomatic?
  • Severe hypercalcemia is potentially _____
  • (2) causes, effective Rx is often possible–accurate diagnosis is key to definitive treatment
A
  • Often asymptomatic (most often found on a Chem panel)
  • Severe hypercalcemia is potentially fatal
  • Hyperparathyroidism vs. Cancer Effective Rx is often possible–accurate diagnosis is key to definitive treatment

Hypercalcemia more important is the work up than the treatment

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3
Q

Hypocalcemia

Relatively rare

  • Symptomatic?
  • Seen in both _____ and ____ practice
  • Causes (2) - Accurate diagnosis is key to definitive treatment
A
  • May be severely symptomatic
  • Seen in both pediatric and adult practice
  • Hypoparathyroidism vs. Non-PTH deficient Hypocalcemia - Accurate diagnosis is key to definitive treatment

Hypocalcemia treat first then work up

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4
Q

Calcium Labs

(1) 50%

(1) 40%

(1) 10%

A

Ionized Ca++

Albumin (bound calcium)

Organic complexes (citrate, phosphate)

Corrected serum Ca++= total serum Ca++ (mg/dL) + 0.8X (4.0- serum albumin{g/dL})

If albumin is low, can underestimate total serum Ca

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5
Q

pH Effects on Calcium

Acidosis =

Alkalsosis =

A

Acidosis increases Ca

Alkalosis decreases ionized calcium (hyperventilation → alkalosis, symptoms of tetany)

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6
Q

Parathyroid Hormone Regulates Calcium

PTH effect on the

  1. Gut =
  2. Kidneys =
  3. Bones =
A
  1. Forms “active” Vitamin D to increase gut Ca2+ absorption
  2. Stimulates calcium reabsorption and phosphate excretion in the kidney
  3. Osteoblast stimulation which increases bone resorption of calcium
  • Parathyroid glands cannot be palpated bc sit behind thyroid*
  • 3 things that happen we have a low serum calcium*
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7
Q

Vitamin D regulates Ca Absorption

Sources of vitamin D: fortified ____, ___ oils, Rx (2)

Vitamin D absorbed from the skin and gut are stored in the ____

PTH effect on Vitamin D?

What Vitamin D do we measure in primary care?

A

Fortified milk, Fish oils, D2 ergocalciferol, D3 cholecalciferol

Vitamin D stored in the liver

PTH activates the inactivated form of Vit D to its active form - 25 OH Vit D → 125 OH Vit D

We measure the storage form of Vitamin D in primary care

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8
Q

Manifestations of Hypercalcemia

Hypercalcemia favors membrane hyperpolarization → _____ excitability

(2)*

Neurologic: fatigue, ___ness, con____, coma

Gastrointestinal: C_______, abdominal pain, peptic ulcers

Renal: ____uria, de_____, nephro______

Cardiac: palpitations, arrhythmia, _____cardia, _____ QT, AV block

A

Hypercalcemia favors membrane hyperpolarization → reduced excitability

Lethargy, Coma*

Neurologic: fatigue, weakness, confusion, coma

Gastrointestinal: Constipation, abdominal pain, peptic ulcers

Renal: Polyuria, dehydration, nephrolithiasis

Cardiac: palpitations, arrhythmia, bradycardia, short QT, AV block

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9
Q

Clinical Manifestations of Hypercalcemia

Vicious cycle of severe hypercalcemia =

Anything above ___ mg/dL is an emergency! and requires (1)

Anything under ___mg/dL is not concerning, will start to see symptoms when it rises above this level

First treatment will be (1)

A

Hypercalcemia causes osmotic diuresis → reduced GFR → polyuria/n/v → dehydration → hypercalcemia

>13mg/dL is an emergency! requires inpatient eval

<12 not concerning, >12 will start to see sx

HYDRATION

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10
Q

Differential Diagnosis for Hypercalcemia

The most important test is repeat Ca and draw serum PTH

PTH Mediated (1)* - and what will the labs show?

Non-PTH Mediated (1)* - and what will the labs show?

A

Primary Hyperparathyroidism - High Ca and High PTH

Malignancy (non-PTH mediated - humoral, lytic, vitD and/or cytokine production) - High Ca but Low PTH → refer

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11
Q

Primary Hyperparathyroidism

  • PHPT is the ____ common cause of hypercalcemia, affecting 1/1000 persons (more with increased age)
  • Most patients with hyperparathyroidism are ______ at diagnosis
  • (2) lab values is generally diagnostic of PHPT
A
  • PHPT is the most common cause of hypercalcemia, affecting 1/1000 persons (more with increased age)
  • Most patients with hyperparathyroidism are asymptomatic at diagnosis
  • Elevated or unexpectedly “normal” PTH + Elevated albumin adjusted Ca level lab values is generally diagnostic of PHPT

PHPT also concerning bc of kidney stones

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12
Q

Primary Hyperparathyroidism Lab and Imaging Eval

  • Serum C_____
  • P______ hormone
  • 25 OH _______
  • G______ filtration rate
  • Bone d_______
  • (1) imaging to detect stones
A
  • Serum Calcium
  • Parathyroid hormone
  • 25 OH Vitamin D
  • Glomerular filtration rate (check kidneys!)
  • Bone density
  • Ultrasound to detect stones
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13
Q

Primary Hyperparathyroidism Treatment

(1) recommended for pts <50yo with clinically significant hypercalcemia, osteoporosis or fragility fracture, renal calculi, hypercalciuria, impaired renal function

Medical Management

  • correction of dietary (1) and (1) deficiency
  • Rx (1) lowers serum calcium levels
  • Rx (1) improves bone density, but reducing fracture risk unknown
A

Surgery <50 + significant hypercal

  • Correction of dietary calcium and vitamin D deficiency
  • Calcinet
  • Bisphosphonates

If pts <50 yo we generally treat definitively by surgical resection

  • If >50 and asymptomatic – wait and watch*
  • -Tell them to don’t avoid Ca completely – to prevent driving up Ca-**Get bone density and urine tests every few years*
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14
Q

When to Asymptomatic Primary Hyperparathyroidism

Once you find someone with high PTH after presenting with hypercalcemia – get these tests

(2)-(2),(3)

A

Skeletal

  • DEXA for bone mineral density
  • Xray/CT/MRI/VFA for vertebral fracture

Renal

  • CrCl <60ml
  • 24h urine for calcium >400 and increased stone risk
  • Xray/US/CT for nephrolithiasis
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15
Q

PHPT Treatment

  1. Surgical (1)
  2. Medical
    1. Ob_____: maintain hy____, avoid diu______, get (1) to monitor for osteoporosis and treat it
    2. What to do about dietary calcium?
    3. (1)Rx activates CaSR and inhibits PTH secretion
A
  1. Surgical removal of overactive parathyroid gland (localization using neck US, sestamibi scan)
  2. Medical
    1. Observation, maintain hydration, avoid diuretics, get DEXA scan to monitor for osteoporosis
    2. NO NEED TO LIMIT DIETARY CALCIUM
    3. Cinacalcet activates CaSR and inhibits PTH secretion
  • Tx for osteoporosis – give bisphosphonates*
  • Cinacalcet (lowers PTH) and bisphosphonate given if cannot have surgery*
  • Critically important is to maintain hydration to avoid vicious cycle of kidney injury*
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16
Q

Non-PTH mediated Hypercalcemia Causes

M______ - often advanced, poor prognosis

(1) mediated - increased gut absorption

A

Malignancy

Vitamin D mediated

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17
Q

Malignancy Non-PTH mediated Hypercalcemia

  1. ______ hypercalcemia of malignancy - PTHrP
    1. 80% of cases, mostly _____ cancers (cervix, lung, head, and neck)
  2. Local osteo_____ lesions - bone ____
    1. 20% of cases - br_____ ca, pr______ ca, multiple _____
  3. 1,25OH2-vit D mediated
    1. <1% - ly_______
A
  1. Humoral hypercalcemia of malignancy - PTHrP
    1. 80% of cases, mostly squamous cancers (cervix, lung, head, and neck)
  2. Local osteolytic lesions - bone mets
    1. 20% of cases - breast ca, prostate ca, multiple myeloma
  3. 1,25OH2-vit D mediated
    1. <1% - lymphoma
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18
Q

Vitamin D mediated - Non PTH Hypercalcemia

  1. (1) intoxication – excess 25-OH-vitamin D levels
  2. (1) mediated – excess 1,25-OH-vitamin D
    1. Granulomatous Disease – Sarcoid, Crohn’s disease, Tb
    2. Lymphoma
A
  1. Vitamin D intoxication – excess 25-OH-vitamin D levels
  2. Calcitriol mediated – excess 1,25-OH-vitamin D
    1. Granulomatous Disease – Sarcoid, Crohn’s disease, Tb
    2. Lymphoma
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19
Q

Treatment of Hypercalcemia

  1. Treat the underlying p______
  2. Enhance _____ calcium excretion
  3. Block ______ activity
  4. Block ______ calcium absorption

How?

A
  1. Treat the underlying pathophysiology
    1. ie surgery for PHPT
  2. Enhance renal calcium excretion
    1. Volume expansion promotes calciuresis: saline, then loop diuretics (no thiazides)
    2. Dialysis against low calcium bath (if CA <18mg/dL)
  3. Block osteoclastic activity
    1. Pamidronate/Zoledronate (IV bisphosphonates
  4. Block intestinal calcium absorption
    1. Low calcium diet, avoid calcium supplements, glucocorticoids if Vit D mediated
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20
Q

Response to Hypocalcemia

A
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21
Q

Clinical Manifestations of Hypocalcemia

Hypocalcemia favors membrane depolarization (Na+ channel effects) → ______ excitability

(2) signs, Se_______

  • Neurologic: t______, B_____ reflexes, Ch______ isgn, se______
  • MSK: muscle ______, T______ sign, carpopedal sp______, t_____*
  • Cardiac: _____ QT, arrhythmia

Any of these S/S/ Ca

A

Increased excitability

Chvostek’s and Trousseau’s sign, Seizures

  • Neurologic: tingling, brisk reflexes, Chvostek’s sign, seizures
  • Musculoskeletal: muscle cramps, Trousseau’s, carpopedal spasm, tetany
  • Cardiac: long QT, arrythmia

S/S, Ca <8.5 → ER

  • Chvostek’s = tapping on facial nerve → cheek will twitch*
  • Trouseau’s (Pic)*
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22
Q

Differential Diagnosis of Hypocalcemia

(2) (2), (2)

A

Hypoparathyroid (PTH low, Phos high)

  1. Genetic
  2. Acquired

Non-PTH deficient (PTH elevated, Phos variable)

  1. Chronic Kidney Disease
  2. Vitamin D deficiency or resistance
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23
Q

Genetic vs. Acquired Hypoparathyroidism

What is the most common cause of hypoparathyroidism?

  1. Genetic
    1. ____immune (polyglandular syndrome type 1)
    2. Parathyroid dev_______ (22g deletion = DiGeorge syndrome, TBX1, GCM2)
  2. Acquired
    1. Post (1) ~75%
    2. M_____ deficiency (alc, mag wasting meds, diarrhea etc)
    3. H_____ bone syndrome (post parathyroidectomy for PHPT)
    4. (1) inhibitors
A

Post neck surgery ~75%

  1. Genetic
    1. Autoimmune (polyglandular syndrome type 1)
    2. Parathyroid development (22g deletion = DiGeorge syndrome, TBX1, GCM2)
  2. Acquired
    1. Post neck surgery ~75%
    2. Magnesium deficiency (alc, mag wasting meds, diarrhea etc)
    3. Hungry bone syndrome (post parathyroidectomy for PHPT)
    4. Immune checkpoint inhibitors

Magnesium deficiency – decreases function of PTH

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24
Q

Differential Diagnosis of Hypocalcemia Chart

Takeaway - Check (4)

A

PTH, PO4, Mg, Cr or EGFR

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25
Q

Treatment of Hypocalcemia

For Acute, Symptomatic Hypocalcemia

(1) followed by (1)

Once normalized?

For Hypoparathyroidism

(2) supplements for a goal calcium LLN + Monitor (1) urine calcium and sx

A

For Acute, Symptomatic Hypocalcemia

Rapid IV Ca++ followed by Oral supplements

Once normalized, it is then important to differentiate between PTH-deficient and non-PTH-deficient causes to determine treatment strategy

For Hypoparathyroidism

Calcitrol (1,25 OH Vitamin D) supplements for a goal calcium LLN + Monitor 24 urine calcium and sx

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26
Q

Calcium Metabolism - Bone - A Dynamic Organ

(1) buildup bone
(1) breakdown bone

These processes should happen ______, over time less ____ and more breakdown

Any breakdown in any of these steps → _______ will develop (low bone ____ + low bone _____)

A

Osteoblasts buildup bone

Osteoclasts breakdown bone (bone resorption)

These processes should happen together, over time less pairing and more breakdown

Any breakdown in any of these steps → osteoporosis will develop (low bone mass + low bone quality)

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27
Q

Calcium Metabolism-Bone

Which type of bone is very sensitive to PTH excess?

Which type of bone is very sensitive to glucocorticoids?

A

Cortical Bone (wrist > hip > vertebrae)

Cancellous Trabecular Bone (vertebrae > hip > wrist)

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28
Q

Osteoporosis Definitions

Clinical Definition

DEXA Definition

A

Poor bone strength (density + quality)

T score > -2.5 SD below the mean for young adults

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29
Q

Osteoporosis Patho

  • Systemic skeletal disease characterized by low bone _____ and m____architectural deterioration of bone tissue (q_____)
  • Bone Quality – m___architecture, m____architecture, microdamage accumulation, degree of m_____ization, rate of bone t______
  • Consequently – there is an increase in bone fr_____ and risk of fr_____
A
  • Systemic skeletal disease characterized by low bone mass and microarchitectural deterioration of bone tissue (quality)
  • Bone Quality – macroarchitecture, microarchitecture, microdamage accumulation, degree of mineralization, rate of bone turnover
  • Consequently – there is an increase in bone fragility and risk of fracture
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30
Q

Peak Bone Mass and Rate of Bone Loss

  • Intrinsic Factors
    • G_____, wnt pathway
  • Extrinsic Factors
    • Es_____ Status
    • XRC/Nu_____
    • Tob_____
    • Ca____/Vitamin __ status
    • Ch____ Diseases
    • Med______
A
  • Intrinsic Factors
    • Genes, wnt pathway
  • Extrinsic Factors
    • Estrogen Status
    • XRC/Nutrition
    • Tobacco
    • Calcium/Vitamin D status
    • Chronic Diseases
    • Medications
31
Q

Secondary Osteoporosis

Due to Systemic Diseases

  1. Endocrine (3)
  2. Oncologic (1)
  3. Nutritional Disorders (1)
  4. Inflammatory Arthritis (1)
  5. Medications associated with OP (2)
A
  1. Hypogonadism (Hyperprolactinemia), Cushing’s, Primary Hyperparathyroidism
  2. Multiple Myeloma
  3. Celiac sprue
  4. Rheumatoid Arthritis
  5. Glucocorticoids, PPI’s
32
Q

Prevalence of Osteoporosis and Incidence of Fracture

  • Half of ___yo have osteoporosis*
  • Most common fracture is radiographic asymptomatic _______ fracture*
  • We worry most about ___ fracture → decreased QOL, increased mortality*
A
  • Half of 80yo have osteoporosis*
  • Most common fracture is radiographic asymptomatic vertebral fracture*
  • We worry most about hip fracture → decreased QOL, increased mortality*
33
Q

Risk Factors for Fracture

Major Risk Factors

  • Personal _____ of fracture as an adult
  • History of fragility fracture in a first (1)
  • ____ body weight
  • Current sm______
  • Use of oral (1) therapy (daily dose equivalent, > 5mg of prednisone) for more than 3m

Additional Risk Factors

  • Impaired v_____
  • Es_______ deficiency at an early age (before 45y)
  • Poor health or fr_____
  • Recent f_____
  • Low C_____ intake (lifelong)
  • Low physical ac_____
  • Al_____ in amounts greater than 2 drinks per day
A

Major Risk Factors

  • Personal history of fracture as an adult
  • History of fragility fracture in a first degree relative
  • Low body weight
  • Current smoking
  • Use of oral corticosteroids therapy (daily dose equivalent, > 5mg of prednisone) for more than 3m

Additional Risk Factors

  • Impaired vision
  • Estrogen deficiency at an early age (before 45y)
  • Poor health or frailty
  • Recent falls
  • Low Calcium intake (lifelong)
  • Low physical activity
  • Alcohol in amounts greater than 2 drinks per day
34
Q

Osteoporosis Treatment

Most common med (1)

Only one that promotes bone formation (1)

Lifestyle measures = adequate weight _____ exercises, _____ cessation, avoid excess _____ intake, (2) supplements

A

Bisphosphonates (Risedronate)

PTH hormone*

Adequate weight bearing exercises, smoking cessation, avoid excess alcohol, Calcium supplementation, Vitamin D

35
Q

Bisphosphonates

  • Bind “av_____” to hydroxyapatite crystal
  • Impair osteo_____-mediated bone resorption–“anti-_____”
  • Enhance osteoclast ap_____
  • Orals: poorly absorbed, risk of esoph______
  • IV: can cause “___ like reaction”
  • Contraindicated if ____ < 30-35%
A
  • Bind “avidly” to hydroxyapatite crystal
  • Impair osteoclast-mediated bone resorption–“anti-resorptive”
  • Enhance osteoclast apoptosis
  • Orals: poorly absorbed, risk of esophagitis
  • IV: can cause “flu like reaction”
  • Contraindicated if GFR < 30-35%

Must drink with full glass of water and nothing else

36
Q

How well do Bisphosphonates reduce fracture risk?

A

70% risk reduction

37
Q

MOAB that blocks osteoclast activation

Reduces fracture risk by?

Route =

Concern =

A

Denosumab*

68% risk reduction

Subq injection

If patient stops abruptly, will experience acute loss of bone in SPINE

38
Q

Rare complication that happens with recurrent IV treatment of Bisphosphonates

A

Osteonecrosis of the Jaw

39
Q

Rare complication that occurs with long term use of bisphosphonates

A

Atypical Femur Fracture

Happens distal to lesser trochanter to just proximal to supracondylar flare

No or minimal trauma, complete or incomplete

Minor features: prodromal pain, cortical thickness, periosteal reaction

40
Q

Bisphosphonate rare SE vs. osteoporosis fracture

How often do these atypical fractures occur? Is it worth it to take a bisphosphonate?

A

Bottom line – your more likely to suffer a osteoporosis fracture than a SE risk fracture – these meds are very very safe

41
Q

Metabolic Bone Disease - Estrogen/HRT

Effects on Hip fractures/osteoporosis?

A

Estrogen/HRT reduces risk of Hip fractures

42
Q

Calcium Metabolism - The role of Vitamin D

How does Vitamin D deficiency effect calcium?

Preferred range for Serum 25OHD stores?

(1) enhances intestinal calcium transport 45-65%

Intestinal ______ transport increases to 80%

A

Vitamin D deficiency → poor absorption of calcium (10-15) and phosphorus

30-60ng/mL

1,25 OHD enhances intestinal calcium transport (45-65%)

Intestinal phosphorus transport increases to 80%

Bones cannot calcify, will become weak

43
Q

What imaging modality is used to visualize the pituitary?

pic = saggital view

A

Sella Protocol MRI - Fine pituitary cuts

(group of MRI sequences put together to improve sensitivity and specificity for the assessment of lesions of the pituitary gland)

pic = coronal view

44
Q

What hormone is in excess in these pictures of twins?

A

Excess growth hormone = gigantism

45
Q

Growth Hormone Excess S/S

GF/IGF-1 effects - dependent on hormone levels

  1. Ac___ changes and soft tissue ____growth
  2. Musculoskeletal involvement
    1. Prognathism =
    2. Jaw Mal______
    3. Frontal B_____
    4. Proximal myopathy
  3. Visceromegaly
    1. T______, prostate, thyroid, salivary glands, liver, spleen, kidney
  4. Skin - H____hydrosis
  5. Cardiovascular
    1. Arrythmia, H____tension and valvular heart disease (~60%)
    2. Concentric myocardial hypertrophy can lead to diastolic _____ heart _____
  6. Entrapment Neuropathy
    1. Median nerve - (1) syndrome (can be bilateral)
A
  1. Acral changes and soft tissue overgrowth
  2. Musculoskeletal involvement
    1. Prognathism = protruding of lower jaw
    2. Jaw Malocclusion
    3. Frontal Bossing
    4. Proximal myopathy
  3. Visceromegaly
    1. Tongue, prostate, thyroid, salivary glands, liver, spleen, kidney
  4. Skin - Hyperhydrosis
  5. Cardiovascular
    1. Arrythmia, Hypertension and valvular heart disease (~60%)
    2. Concentric myocardial hypertrophy can lead to diastolic congestive heart failure
  6. Entrapment Neuropathy
    1. Median nerve - carpal tunnel syndrome (can be bilateral)
46
Q

Growth Hormone Excess S/S

GH/IGF-1 Effects -dependent on hormone levels

(1) effect on joints

(2) effects on pulmonary

(1) effect on endocrine

(2) local tumor mass effects

Mortality due to C______, R_____ disease and C____ Cancer

A

Arthritis

Obstructive or Central Sleep Apnea

Diabetes mellitus*

Headaches, Visual field deficits

Cardiovascular, Respiratory disease, Colon Cancer

47
Q

70% of acromegaly is secondary to a (1)

A

Benign Pituitary Macroadenoma

48
Q

Acromegaly Diagnostic Labs

(2) Tests*

A

IGF-1 Level**

GH Glucose Suppression Testing - Glucose fails to suppress growth hormone in acromegaly

49
Q

Growth Hormone Excess - Confirming the Diagnosis

A
50
Q

Growth Hormone Excess Treatment Goals

Remove the ______

_______ GH secretion

Preserve the ______ function

A

Remove the adenoma

Normalize GH secretion

Preserve the pituitary function

51
Q

GH Excess Treatment

S______, R_____ therapy

S______ analogues

(1) antagonist, (1) agonist

A

Surgery , Radiation therapy

Somatostatin analogues

GH Rec antagonist, Dopamine agonists

  • If pituitary tumor confirmed -> then surgery*
  • If surgery not fully effective can add on medical tx like meds/RT*
52
Q

Prolactin Regulation

_____ inhibits prolactin

Hyperprolactinemia presents in women with O____menorrhea A____horrea, or G______hea syndrome

A

Dopamine inhibits prolactin

(dopamine goes down after pregnancy so mother can secrete breast milk)

Hyperprolactinemia presents in women with Oligomenorrhea Amenhorrea, or Galactorrhea syndrome

53
Q

Causes of Hyperprolactinemia

(1) most common cause

(1) Rx

A

Microadenomas and Macroadenomas (tumor secreting its own prolactin is most common cause)

Anti-Dopaminergics

54
Q

Patho of Hyperprolactinemia

Prolactinomas present with ______

Increase in prolactin _____ (1) which then _____ (2)

(3)* effects

A

Prolactinomas present with Hypogonadism

Increase in prolactin suppresses GnRH which then suppresses LH, FSH

Amenhorrhea

Infertility

Impotence

55
Q

Male Clinical Manifestations of Hyperprolactinemia

Hyperprolactinemia is a cause of Hypogonadotropic Hypogonadism – (central or secondary hypogonadism)

  • Low T_______ with normal or low LH/FSH
  • Decreased l_____ – impotence
    • Delayed diagnosis – macroadenoma more common
  • Inf_____ (less common)
  • ___ Bone Mass/(1)*
A
  • Low Testosterone with normal or low LH/FSH
  • Decreased libido – impotence
    • Delayed diagnosis – macroadenoma more common
  • Infertility (less common)
  • Low Bone Mass/Osteoporosis*
56
Q

Female Clinical Manifestations of Hyperprolactinemia

  • (2)orrhea with normal or low LH/FSH
  • G_____orrhea
  • Decreased l_____ - sexual dysfunction
  • Inf_____
  • Low ____ Mass/(1)*
A
  • Oligo- or amenorrhea with normal or low LH/FSH
  • Galactorrhea
  • Decreased libido - sexual dysfunction
  • Infertility
  • Low Bone Mass/Osteoporosis*

Osteoporosis overtime happens dt decrease in estrogen

57
Q

Treatment of Hyperprolactinemia

(1) Rx - (2)

High levels of prolactin → (1) to endocrine and (1) will be performed

A

Dopamine Agonists

Bromocriptine, Cabergoline

High levels of prolactin -> referral to endocrine and an MRI will be performed

58
Q

Eval of Pituitary Mass - Pituitary Microadenoma

  • Differential Diagnosis of a Pituitary “mass” starts with _____ adenomas and extends to non-pituitary adenomas and also includes inf_____ diseases (not often reported as mass)
  • Always start with the ____ of the adenoma when evaluating pituitary masses. For m____adenomas – evaluate for hyperfunctioning adenoma
A
  • Differential Diagnosis of a Pituitary “mass” starts with pituitary adenomas and extends to non-pituitary adenomas and also includes infiltrative diseases (not often reported as mass)
  • Always start with the size of the adenoma when evaluating pituitary masses. For microadenomas – evaluate for hyperfunctioning adenoma
59
Q

Pituitary Microadenomas

Functional and common (3)

Functional (2)

A

Prolactinoma, Acromegaly, ACTH secreting pituitary adenoma (Cushing’s)

LH/FSH or TSH secreting adenomas

60
Q

Pituitary Macroadenoma

Q1 - is this f_____?

Q2 - is this causing a ____ effect? (main difference)

Q3 - is this causing h____pituitarism

A

Is this functional?

Is this causing a mass effect*?

Is this causing hypopituitarism

  • Additional concerns with macroadenoma*
  • Is this tumor pressing on other things, is it causing destruction of normal pituitary to cause inadequate thyroid function?*
  • Main difference is worrying about mass effect – checking thyroid and cortisol levels asap!**
  • Send to neurosurgeon!*
61
Q

Pituitary Mass Effects

(1)*

Need to see a (1)

Red flag (1)

A

Bitemporal Visual Field Defects*

Neuro-ophthalmologist

CSF rhinorrhea (we worry about bacteria going up into CSF and causing meningitis)

62
Q

Hypopituitarism

Causes target _____ failure

  1. No (1) → Diabetes Insipidus
  2. No (1) → amenorrhea/decreased libido
  3. No (1) → failure to lactate
  4. No (1) → short stature, hypoglycemia, mild anemia
  5. No (1) → cold intolerance, poor memory, decreased energy
  6. No (1) → Lack of well being, poor appetite, hypotension, low sodium
A

Target organ failure

  1. No ADH → Diabetes Insipidus
  2. No LH/FSH → amenorrhea/decreased libido
  3. No PR → failure to lactate
  4. No GH → short stature, hypoglycemia, mild anemia
  5. No TSH → cold intolerance, poor memory, decreased energy
  6. No ACTH → Lack of well being, poor appetite, hypotension, low sodium
  • If you have one of these will be called hypopituitarism*
  • If you have all of these pan-hypopituitarism*
63
Q

Causes of Hypopituitarism

  • Congenital: G____ and dev_______ defects
  • Tumors: Pituitary M____adenoma, Craniopharyngioma, other sella or parasella tumors M______ deposition – breast, lung, others
  • Inflammation/Infiltrative: Sar____, T_, Hypophysitis, Histiocytosis X
  • Vascular/Infarction: Sh_____s*, Pituitary A______**, Parasellar Aneurysms, Trauma
A
  • Congenital: Genetic and developmental defects
  • Tumors: Pituitary Macroadenoma, Craniopharyngioma, other sella or parasella tumors Metastatic deposition – breast, lung, others
  • Inflammation/Infiltrative: Sarcoid, TB, Hypophysitis, Histiocytosis X
  • Vascular/Infarction: Sheehan’s*, Pituitary Apoplexy**, Parasellar Aneurysms, Trauma
64
Q

ICI Hypophysitis

Takeaway?

A

Immune checkpoint inhibitors used in RCC and melanoma are now causing a lot of hypophysitis

AE of drug that activates autoimmunity in endocrine glands

65
Q

Causes of Hypopituitarism - Apoplexy

Acute onset of symptoms referred to the pituitary gland secondary to a h_______ event (less likely can be secondary to a non-hemorrhagic event)

  • Head____ with nausea, emesis, s____ neck, fever
  • +/- ______ Field Deficit – can see BTH or a CN palsy
  • +/- Acute onset of H_____pituitarism
    • Acute secondary ad______ insufficiency is most concerning hormone deficit and results in nausea, emesis, poor appetite, lightheadedness hyponatremia and hypotension
A

Acute onset of symptoms referred to the pituitary gland secondary to a hemorrhagic event (less likely can be secondary to a non-hemorrhagic event)

  • Headache with nausea, emesis, stiff neck, fever
  • +/- Visual Field Deficit – can see BTH or a CN palsy
  • +/- Acute onset of Hypopituitarism
    • Acute secondary adrenal insufficiency is most concerning hormone deficit and results in nausea, emesis, poor appetite, lightheadedness hyponatremia and hypotension

We worry about blood pooling and compressing structures -> n/v, bilateral heminopsia, headache

66
Q

Posterior Pituitary AVP Secretion

  • Posterior Pituitary: N______ bodies are located in the Hypothalamus (2)
  • Ax______ endings release hormones
A
  • Posterior Pituitary: Neuronal bodies are located in the Hypothalamus (Supraoptic, Paraventricular)
  • Axonal endings release hormones
67
Q

ADH and Urine

In the absence of Vasopressin (ADH), what happens to urine?

A

A large volume of dilute (hypotonic) urine is excreted (200-100cc/hr)

68
Q

Diabetes Insipidus

  • Presentation of ____uria
    • Evaluate for _____ diuresis (glucose, etc)
  • When the urine is found to be dilute (hypotonic) - the focus turns to (1) hormone

Types of Polydipsia

  1. (1) = Ingestion of excess volume of fluid
  2. (1) = Reduced production/secretion of AVP
  3. (1) = Enhanced metabolism of AVP
  4. (1) = Reduced responsiveness to AVP
A
  • Presentation of polyuria
    • Evaluate for osmotic diuresis (glucose, etc)
  • When the urine is found to be dilute (hypotonic) - the focus turns to hormone

Types of Polydipsia

  1. Primary Polydipsia = Ingestion of excess volume of fluid
  2. Central DI = Reduced production/secretion of AVP
  3. Central DI = Enhanced metabolism of AVP
  4. Nephrogenic DI = Reduced responsiveness to AVP
69
Q

Diabetes Insipidus Etiology

Post___ectomy

Tumors (Cranio_____)

Secondary (met______)

Granulomas like Sar______

L______ hypophysitis (autoimmune)

  • (1) = Destruction of ADH center alone
  • Destruction of ADH center + Destruction of hypothalamic Thirst center = can be _____
A

Posthypophysectomy

Tumors (Craniopharyngioma)

Secondary (metastasis)

Granulomas like Sarcoidosis

Lymphocytic hypophysitis (autoimmune)

  • Central DI = Destruction of ADH center alone
  • Destruction of ADH center + Destruction of hypothalamic Thirst center = can be Sarcoidosis
70
Q

Water Deprivation Test to Evaluate for DI

=

A

Withhold water then give dose of vasopressin → if urine osmolality goes up → Central DI

If they do not respond, refer to neuro for workup of nephrogenic DI

71
Q

Treatment of Central DI

Drug of Choice (1)*

  • V2 receptor selective, no V1 activity, so no vaso_____/B__ concerns
  • Admin: (4) routes, poor absorption with (1) form so need to correct dosing, (2) routes for inpatient
  • Monitor for ____uria/th____ and serum N__ or os______
A

Desmopressin (ddAVP)

  • V2 receptor selective, no V1 activity, so no vasoconstriction/BP concerns
  • Admin: (Nasal spray, PO, IV, SQ) routes, poor absorption with (PO) form so need to correct dosing, (IV, SQ) routes for inpatient
  • Monitor for polyuria/thirst and serum Na or osmolarity
72
Q

Diabetes and COVID takeaway?

A

People with diabetes 50% more likely to die from COVID-19 compared with no diabetes

And COVID worsens Diabetes outcomes → triggers new onset Diabetes and more frequent and severe DKA

73
Q

Diabetes + Covid Mortality

Increased mortality risk for diabetes patients with COVID-19 with

  • ______ age
  • ______ BMI
  • _____ sex
A
  • Older age
  • Increased BMI
  • Male sex
  • 1 out of 3 people with diabetes and COVID-19 died at Montefiore March-May 2020*
  • Insulin treatment as a proxy for diabetes duration and obesity was predictive of mortality rather than HbA1c levels*
  • Further investigation of underlying mechanisms of mortality and inpatient glycemic control is needed*
  • COVID virus just caused such an intense form of hyperglycemia*

Diagnosis and Management (36 decks)

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