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Endocrine Exam 2 > Conditions > Flashcards

Conditions Flashcards

1
Q

Occurs in growing bone

A

rickets

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2
Q

enlargement of cartilage at growth plates of costochondral junctions (rachitic rosary in ribcage) and long of long bones
bowing of long bones of legs

A

rickets

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3
Q

Same thing as rickets except in mature bone

A

osteomalacia

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4
Q

almost all filtered calcium is?

A

reabsorbed

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5
Q

Calcium handling in the kidney: PTH independent

A

*Most (passively in the proximal tubule *
some in the thick ascending limb driven by a voltage gradient created by NA/K/Cl reabsorption

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6
Q

Normal Calcium Handling in the kidney: PTH dependent

A

PTH dependent calcium reabsoption occurs in the *distal convuluted tubule *

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7
Q

what upregulates the mediators of Ca reabsorption in the DCT

A

PTH

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8
Q

low bone mass and/or microarchitectural changes that lead to bone fragility and increased risk of fracture

A

osteoporosis

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9
Q

what is sthe most common cause of osteoporosis?

A

most causes of osteoporosis occur because bone remodeling becomes “uncoupled” with bone resorption outpacing bone formation

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10
Q

What are two mechanisms that can treat osteoporosis?

A

decrease bone resorption- inhibit osteoclasts (these are call antiresoptive agents)

stimulate bone formation- stimulate osteblasts (these are called anabolic agents)

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11
Q

what stimulates the maturation of osteoblasts and prolongs their lifespan?
what inhibits the matruation of osteoclasts and shortens their lifespan?

A

estrogen!

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12
Q

what is the net effect of estrogen

A

supporting bone formation and suppressing bone resorption

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13
Q

what does estrogen inhibit the expression of?

A

RANK-L (decreasing osteclast activity)

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14
Q

parathyroid has this receptor on their surfaces which detects the level of free calcium in the blood

A

calcium sensing

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15
Q

a decline in calcium levels would cause PTH to?

increased levls of calcium would lead PTH to?

A
  • declince in calcium levels lead to release of PTH
  • Elevated levels leads to suppression of PTH
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16
Q

other than parathyroid, where else are CaSR cells present?

A

in the thick ascending loop of henle

when Ca bind to renal CaSR, leads to calcium excretion in the kidney

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17
Q

what is the primary stimulus for PTH secretion

A

hypocalcemia

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18
Q

what is necessary for proper PTH secretion

A

Magnesium

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19
Q

decreases PTH levels?

A

Vitamin D (supresses PTH gene transcription)
Magnesium

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20
Q

increases PTH levels?

A

Calcium
phosphate

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21
Q

what is PTH action at the kidney?

A

PTH increases calcium reabsorption
inhibits renal phosphate reabsorption- promotes phosphaturia
PTH increases the transcription of 1alpha-hydroxylase, the enzyme that activates vitamin D

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22
Q

PTH receptors are found where?

A

osteoblasts (bone building cells)

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23
Q

what do osteoblasts do?

A

signal osteoclast precursors to develop mature, active osteoclasts. RANKL is one of these signals

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24
Q

what can mimic excess PTH? How?

A

PTH- related protein (PTHrp)
it is structurally similar to PTH and shares a receptor

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25
Q

why can’t excess sun not cause vitamin D toxicity?

A

Prolonged UV light exposure also breaks down vitamin D to inactive forms

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26
Q

what is the predominant form of Vitamin D in the body, and considered the storage form?

A

Vitamin is converted in the liver by hydroxylation to 25-hydroxy vitamin D(25-(OH) vitamin D

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27
Q

what serum level is the best marker of vitamin D status in an individual? Why?

A

25-(OH) Vitamin D
it reflects the total amount of Vitamin D entering the system; it is also the predominant storage form

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28
Q

what is the active form of vitamin D? how does it become active? what induces the active form? what suppresses it?

A

25-(OH) vitamin D is hydroxylated in the kidney by 1alpha-hydroxylase to 1,25-dihydroxy vitamin D
enzyme is induced by PTH and hypophosphatemia

suppressed by calcium and by its product 1,25-(OH)2 vitamin D

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29
Q

What does vitamin D do in the GI tract, in the Parathyroid, in the bone?

A

GI: stimulates calcium absorption in the intestine
Parathyroid: decreases the transcription of PTH
Bone: main role is to maintain (via GI absorption) the availability of adequate calcium and phosphate for bone mineralization

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30
Q

what is the most common cause of primary hyperparathyroidism? what is an occasional cause? what do you see left often? very rarely?

A
  • most commonly caused by a parathyroid adenoma in one gland
  • occasionally more than one adenoma can occur simultaneously
  • less often: diffuse hyperplasia of all glands can occur
  • very rare: parathyroid carcinoma
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31
Q

main clinical concerns in primary hyperparathyroidism?

A

detrimental effect on bone density and the risk of kidney stones

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32
Q

treatment of primary hyperparathyroidism?

A

surgical removal of the abnormal glands (usually curative)

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33
Q
  • rare disorder caused by loss of function mutation of the CaSR (i.e, it is less sensitive to calcium)
  • it is transmitted in an autosomal dominant fashion
  • the mutation leads to requirement for higher than usual serum calcium levels before PTH secretion is supressed
A

familial hypcalciuric hyperplasia

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34
Q

clinical manifestation: mild hypercalcemia, high-normal or mildly elevated PTH, and low urinary calcium levels.

A

familial hypocalciuric hypercalcemia

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35
Q

treatment for familial hypocalciuric hypercalcemia?

A

no treatment needed
parathyroidectomy would not solve because the problem lies in all cells

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36
Q

mechanisms of hypercalcemia of malignancy?

A
  • invasion/destruction of bone by tumor- appears that tumor cells secrete signals that stimulate osteoclast activity and cause release of calcium from bone
  • production of PTHrP by tumor- buinds to the same receptor as PTH increasing serum calcium levels
  • production of Vitamin D by tumor- certain hematologic malignancies can produce hypercalcemia related overproduction of 1,25(OH)2 vitamin D
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37
Q

when does vitamin D cause hypercalcemia?

A

Very high doses of oral vitamin D (vitamin D intoxication) - the hypercalcemia is due to vitamin D-mediated increases intestinal calcium absorption and increase resorption of bone

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38
Q

how does sarcoidosis and granulomatous lead to hypercalcemia?

A

granulomatous cells can have unregulated 1alpha-hydroxylase activity, leading to excess active Vitamin D

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39
Q

how does hyperthyroidism (severe) cause hypercalcemia

A

Excess thyroid hormone stimulates bone resoption directly

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40
Q

how does immobilization lead to hypercalcemia?

A

can be seen in the setting of prolonged immobilization related to elevated bone resorption

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41
Q

disorder of inadequate PTH secretion. In the absence of PTH the following are impaired
* activation of Vitamin D/GI absorption of calcium
* mobilization of calcium from bone
* resorption of filtered calcium at the kidney

A

Primary hypoparathyroidism

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42
Q

characterized by low calcium and low PTH

A

hypoparathyroidism

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43
Q

what factors can cause primary hypoparathyroidism?

A

absence or destruction of the parathyroid glands
* congenital
* post surgical
* autoimmue

Impaired PTH secretion from intact glands
* hypomagnesemia

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44
Q

Hypocalcemia can be caused by?

A

vitamin D deficiency

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45
Q

hypocalcemia caused by Vitamin D deficiency would show?

A

mildly low or normal calcium level, low phosphate, low urinary calcium, elevated PTH, low 25-(OH) Vitamin D
normal 1,25-(OH)2 Vitamin D

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46
Q

Other than Vitamin D deficiency, what is another cause of secondary hyperparathyroidism?

A

chronic kidney disease

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47
Q

how are secondary hyperparathyroidism and chronic kidney disease related?

A

renal clearance of phosphate is impaired
renal 1aphla-hydroxylase activity is impaired
* both are triggers for PTH secretion

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48
Q

bone modeling occurs when?
bone remodeling occurs when?

A

bone modeling occurs during growth
bone remodeling occurs throughout life

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49
Q

denser outer portion of bone, most shafts of long bones. 80% of all bone

A

cortical bone

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50
Q

“spongy” inner area of bone spicules. 20% of bone but most surface area so it is an active site of bone remodeling

A

trabecular bone

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51
Q

secrete matrix proteins & faciliate mineraliztion- contian most receptors for hormones affecting bone remodeling- communicates these signals to osteoclasts, which keeps bone buidling and breakdown coupled

A

osteoblasts

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52
Q

osteoblast that has been completely surrounded by bone
involved in sensing mechanical stresses and communicating this information to osteoblasts on the bone surface

A

osteocytes

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53
Q

derived from hematopoietic precursors
create small cavities during bone remodeling which are filled with new bone by osteoblasts

A

osteoclasts

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54
Q

low bone mass and/or microarchitectural changes that lead to bone fragility and increased risk of fracture

A

osteoporosis

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55
Q

osteoporosis can be due to?

A

failure to achieve peak bone mass
* related to genetics, childhood calcium intake, vitamin D status, physical activity
bone loss
* related to accelerated bone resorption or decreased formation

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56
Q

most common type of osteoporosis?

A

postmenopausal osteoporosis

57
Q

when is bone loss the most rapid in postmenopausal women? why?

A

in the first few years after menopause
bone resorption outpaces bone formation

58
Q

risk factors for osteoporosis

A
  • female gender (men get osteoporosis too, only later)
  • increasing age
  • postmenopausal status (or testosterone deficiancy in men)
  • low weight
  • smoking
  • family history of osteoporosis
  • risk factors for falls/fractures: poor muscle strength, impaired balance or vision
59
Q

STRONGEST risk factor for future fragility fracture

A

is previous fragility fracture, these patients are at high risk of more fractures and aggressive risk reduction should be implemented

60
Q

most common osteoporotic fracture

A

vertebral compression fractures

61
Q

have high morbidity and mortality

A

hip fractures

62
Q

fracture that often occurs in younger women?

A

distal radius fracture (colles fracture)

63
Q

osteoporosis due to identifiable risk factors (other than age and menopause)

A

osteporosis

64
Q

what are examples of secondary osteoporosis?

A

glucocorticoid-induced: meds or endogenous cushings syndrome
endocrine issue: low testosterone, hyperparathyroidsm, hyperthyroidism
malignancies: multiple myeloma, other lymphoproliferative malignanicies

65
Q

how are steroids bad for bones? when would you see a increased fracture risk?

A

decrease intestinal calcium absorption
increase expression of RANKL on osteoblasts
suppress maturation and increase apoptosis of osteoblasts
increase renal Ca and Phos losses
* increased fracture risk within a few months of therapy and with low doses*

66
Q

What is whipple’s triad?

A
  • decreased plasma glucose
  • symptoms consistent with hypoglycemia
  • relief of symptoms by correction of hypoglycemia
67
Q

why do we care about the insulin level?

A

the normal response to hypoglycemia is feedback inhibition of insulin secretion
* therefore, an elevated insulin level in the context of hypoglycemia is suggestive of **Endogenous Hyperinsulism **

68
Q

what is C-peptide? what does it measure?

A

C-peptide is a fragment of endogenously produced proinsulin that is split from proinsulin as insulin if formed.
As a result C-peptide level can only increase if endogenous insulin production is increased

69
Q

what are adrenergic mediated symptoms of hypoglycemia?

A

Sweating
pallor
tachycardia
palpatiations
tremor/shaking
nervousness/anxiety
tingling, parasthesias (mouth and fingers)

70
Q

Neuroglycopenic

A

Headache
drowsiness
lightheadedness/syncope
mental dullness/confusion
amnesia
seizures
coma

71
Q

often misdiagnosed as post-partum anxiety and depression
usually self-limited

A

postpartum thyroiditis

72
Q

what is postpartum thyroiditis?

A

a postpartum patient that may experience hyperthyroid phase followed by hypothyroid phase before returning to euthryoid state

73
Q

may be present with thyrotoxicosis, hypothyroidism, euthyroid states.
can be due to benign or malignant disease

A

Goiter

74
Q

when do you treat low TSH with normal free T4 and Free T3?

A

Symptomatic
arrthymia
bone loss
consider if desires pregnancy

75
Q

what are pharmacological causes of hypothyroidism?

A
  • lithium (impaires release of T4 and T3)
  • amiodarone
  • methimazole
  • PTU
  • interferon (cuases hashimoto’s thyroiditis like presentation, resovles after drug stopped)
  • Rifampin (increased levothyroxine metabolism- concern for comprised function of baseline
76
Q

Treament options of hypothyroidism?

A

Levothyroxine(drug of choice)
liothyronine (may use for faster onset)
dessicated thyroid

77
Q

Treament options of hypothyroidism?

A

Levothyroxine(drug of choice)
liothyronine (may use for faster onset)
dessicated thyroid

78
Q

the zona glomerulosa makes

A

aldosterone

79
Q

Zona fasciulata makes

A

cortisol and adrenal androgens

80
Q

Zona reticularis makes?

A

Cortisol and adrenal androgens

81
Q

what is the major regulator of cortisol?

A

ACTH

82
Q

Cortisol exerts what type of feedback on ACTH and CRH secretion

A

negative feedback

83
Q

what regulates ACTH?

A

CRH

84
Q

what are actions of corticosteroids?

A
  • Mobilization of energy stores
  • lipolysis and increased delivery of FFA
  • increased hepatic glucose production by gluconeogenesis
  • inhibits glucose uptake in muscle, fat and lymphoid tissue
  • protein degredation etc.
  • anti-inflammatory effects
  • stimulates bone resorption and inhibits new bone formulation
85
Q

a constellation of symptoms due to excess glucocortioids (exogenous glucorticoids, ectopic ACTH, ETC)

A

Cushing’s syndrome

86
Q

disease due to excess pituitary secretion of ACTH (about 70% of cases are endogenous)

A

Cushing’s disease

87
Q

What are common causes of ACTH dependent cushing’s disease? (80% of cases)

A

Pituitary adenoma (cushing’s adenoma)
Ectopic ACTH syndrome (oat cell ca, carcinoid tumor)
Medullary ca or the thyroid, pheocromocytomas

88
Q

causes of ACTH independent (20% of cases- much higher in kids)

A

iatrogenic- exogenous glucocorticoids (very common)
adrenal adenomas
adrenal cancer
micor and macronondular hyperplasia

89
Q

Common symptoms of cushing’s syndrome

A

moon facies
facial plethora
supraclavicular fat pads
buffalo hump
truncal obesity
weight gain
purple striae

90
Q

common cause of iotrogenic cushing’s disease

A

Glucorticoid therapy

91
Q

when would you use radiation therapy for cushing’s syndrome

A

for larger pituitory tumors and/or persistent hormonal hyperfunction despite surgical intervention

92
Q

what is aldosterone under the control of?

A

renin-angiotensin system
Na/k levels

93
Q

what stimuli causes release of aldosterone?

A

decrease in vascular volume
sympathetic nervous system stimulation of renin
rise in serum potassium concentrations

94
Q

signs and symptoms of primary aldosterone?

A

hypertension
hypokalemia
metabolic alkalosis
muscle weakness/cramps

95
Q

what causes primary aldosternism?

A

aldosterone-producing adrenal adenoma
bilateral hyperplasia of the zona glomerulosa (idiopathic hyperaldosteronism)
primary adrenal hyperplasia
adrenal carcinoma

96
Q

usually small (<2cm)
more commonly occur in L adrenal gland
produce more aldosterone than in any other conditions

A

aldosterone producing adenoma

97
Q

what do levels look like in APA?

A

demonstrate normal or semi-normal response to ACTH- because of that plasma aldosterone is highest in A.M, lowest in late afternoon

98
Q

PTH Low, Calcium Normal

A

PTH independent
malignancy
granulomatous disease
milk-alkali

99
Q

Calcium High, PTH normal/High

A

PTH dependent
primary hyperparathyroidism
Familial hypercalciuric hypercalcemia
lithium

100
Q

Calcium Low, PTH Low/normal

A

primary hypoparathyroidism
autoimmune hypoparathyroidsim
post surgical
congenital/genetic
hypomagnesemia

101
Q

PTH high, calcium low

A

Vitamin D deficiency
chronic kidney disease

102
Q

what are scenarios where the parathyroid is responding normally?

A

PTH independent
secondary hyperparathyroidsim
PTH normal, calcium normal

103
Q

PTH high, calcium normal

A

secondary Hyperparathyroidism

104
Q

High BP
low K
adrenal adenoma on CT

A

primary aldosteronism- Conn’s syndrome

105
Q

what medication inhibits thyroid hormone release?

A

Lithium

106
Q

What is the initial screening test for thyroid?

A

TSH

107
Q

When should you obtain a free T4 and Free T3?

A

If the TSH is abnormal
*reverse T3 only in critical illness
* total T4 monitored in pregnancy

108
Q

if evaluating antibodies for thyroid- which would you evaluate for hypothyroidism? Which for hyperthyroidism

A

TPO and TG antibodies in hypothyroidism
TSI and TRab in hyperthyroidism

109
Q

What level is used as a tumor marker for thyroid cancers?

A

Thryroglobulin

110
Q

Elevated levels of: TSH
Free T4, Free T3:
Anitbodies:
Thyroglobulin:

A

Elevated TSH: Hypothyroidism
Elevated T4, T3: Hyperthyroid
Antibodies: either
Thyroglobulin- thyroid cancer

111
Q

Suppressed levels: TSH
Free T4, T3
Thyroglobulin

A

Suppressed TSH: Hyperthyroidsim
Free T4, Free T3- hypothyroidism
thyroglobulin- thyroid cancer

112
Q

TSH elevated
Free T4 is normal or low
Free T3 often remains low until late in disease course

A

Primary hypothyroidism

113
Q

seen with hypothalmic/pituitary failure, pituitary gland abnormality
* TSH is low-normal or low
* Free T4 is low

A

central hypothyroidsim (secondary disorder)

114
Q

TSH is low
Free T4 is high
Free T3 high

A

Thyrotoxicosis (hyperthyroidism)

115
Q

TSH is normal or high
Free T4 elevated
Free T3 elevated

A

TSH secreting tumor or central thyroid hormone resistance syndrome

116
Q

what should you be aware of with thyroid hormone measurements?

A
  • Estrogen increases total T4 and T3 due to increased TBG
  • Illness decreases total T4 and T3 due to decreased protein levels

Can cause the appearance of abnormality, when fx is normal

117
Q
  • thyroid enlargement
  • may be present with thyrotoxicosis, hypothyroidism or euthyroid states
  • can be due to benign or malignant diseae
  • size does not dictate function
A

Goiter

118
Q

signs as symptoms of hyperthyroidism?

A

increasd metabolic rate: palpitations, tachycardia, arrhythmia
heat intolerance
weight loss
decreased menstrual flow, infertility,
increased spontaneous abortion rate
hyperdefecation

119
Q

can occur due to omission of anti-thyroid therapy, surgery, MI, CVA or infection in patient with underylying thyrotoxicosis

A

thyroid storm

120
Q

what are some causes of hyperthyroidism?

A
  • High iodine uptake: Grave’s disease, toxic multinodular goiter, autoimmune polyglandular syndrome 1&2
  • Low iodine uptake: Thyroiditis (subacute, silent, postpartum)
  • drug induced (iodine, amiodarone, thyroid hormone)
121
Q

Diseases of hyperthyroidism

A

grave’s disease
toxic multinodular goiter
toxic adenoma
TSH secreting pituitary adenoma

122
Q

often presents after URI
thyrotoxic symptoms
anterior neck pain, thyroid tenderness
results from inflammation of gland

A

Subacute thyroiditis

123
Q

treatment for subacute thyroiditis?

A

treat with NSAIDS +/- steroids
use beta blockers for HR (propranolol)
self-limited

124
Q
  • similar to subacute thyroiditis but without pain
  • often a diagnosis of exclusion
  • monitor for improvement
  • treat hormone excess or deficiency as needed
A

silent thyroiditis

125
Q
  • often misdiagnosed as post-partum anxiety and depression
  • usually occurs within 6 months of delivery and is self limited
  • tends to recur with subsequent pregnancies
A

post-partum thyroiditis

126
Q

what is postpartum thyroiditis?

A

patient may experience hyperthyroid phase followed by hypothyroid phase before returning to euthyroid state

127
Q

Complications of total thyroidectomy or lobectomy?

A

recurrent laryngeal nerve injury
hypoparathyroidism
permanent hypothyroidism
may precipitate thyroid storm

128
Q

Isolated increased TSH with normal free T4 and free T3

A

subclinical hypothyroidism

129
Q

when do you treat subclincial hypothyroid

A

symptomatic
arrhythmia
bone loss
consider if desires pregnancy
if TSH > 10 (levothyroxine therapy)
goiter
family history
TPO antibodies
hypercholesterolemia

130
Q

Symptoms of hypothyroidism

A

fatigue
cold intolerance
weight gain
dry skin
brittle nails
hyponatremia
etc.

131
Q

pharmacologic causes of hypothyroidism?

A

Lithium (impairs release of T3 and T4)
amiodarone
methimazole, pTU
interferon (causes hashimoto’s thyroiditis like presentation)
rifampin (increased levothyroxine metabolism)

132
Q
  • severe hypothyroidism with mental status changes
  • usually occurs in longstanding untreated hypothyroidism with an acute precipitating event
  • most common in older women
  • may have history of lithium or amiodarone treatment
A

myxedmea coma

133
Q

Presentation: hypotension, hypothermia, hyponatremia, hypoglycemia, hypoventilation, bradycardia

A

myexedma coma

134
Q

most common thyroid cancer
excellent prognosis
treatement: thyroidectomy(may be curative or radioactive iodine +/- TSH supression
metastasizes via lymphatics

A

papillary thyroid cancer

135
Q

10-15% of thyroid cancers
good prognosis depending on extent of extra-thyroidal extension and vascular invasion
*hurthle cell variant may be aggressive

A

follicular carcinoma

136
Q

uncommon 5-10% of cases
sporadic (75%) or familial (24%)
calcitonin is a serum marker
can diagnose with FNA
tends to metastasize early, even before tumor is palpable

A

medullary carcinoma

137
Q

uncommon 5-10% of cases
sporadic (75%) or familial (24%)
calcitonin is a serum marker
can diagnose with FNA
tends to metastasize early, even before tumor is palpable

A

medullary carcinoma

138
Q

rare <5% of cases
more common in elderly
very poor prognonsis 100% mortality
treatment: palliative
presents as rapidly expanding, fixed, hard thyroid mass
may be seen as late differentiation of papillary TCA

A

anaplastic carcinoma

Endocrine Exam 2 (4 decks)

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