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OMS III > IM Endo > Flashcards

IM Endo Flashcards

1
Q

panhypopituitarism

etiology

A

caused by any condition that compresses or damages the pituitary gland. tumors of many types can copmress the gland such as mets, adenomas, rathke cleft cysts, meningiomas, craniopharyngiomas, or lymphoma. trauma and radiation are damaging to the pituitary. conditions such as hemochromatosis, sarcoidosis, and histiocytosis x or infection with fungi, tb, and parasites infiltrate the pituitary destroying its function. finally, ai and lymphocytic infilatration can damage the gland

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2
Q

panhypopituitarism

presentation

A

the sx are based on the deficiencies of the specific hormone

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3
Q

ultimately, anything that damages the brain, from tumor to stroke to infection can cause

A

panhypopituitarism

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4
Q

panhypopituitarism

prolactin deficiency

A

there are never any symptoms of prolactin deficiency in men

in women prolactin deficiency inhibits lactation after childbirth

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5
Q

panhypopituitarism

lh and fsh

A

women will not be able to ovulate or menstruate normally and will become amenorrheic

men will not make testosterone or sperm, ed and decreased muscle mass

both will have decreased libido and decreased axillary pubic and body hair

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6
Q

kallman syndrome

A

decreased fsh and lh from decreased gnrh

anosmia

renal agenesis in 50%

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7
Q

panhypopituitarism

gh deficiency

A

children present with short stature and dwarfism

adults have fewer sx of GH deficiency bc several other hormones such as catecholamines, glucagon, and cortisol act as stress hormones:
central obesity
increased ldl and cholesterol levels
reduced lean muscle mass

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8
Q

hyponatremia is common secondary to hypothyroidism and isolated glucocorticoid underproduction

A

k levels remain normal bc aldosterone is not affected and aldosterone excretes k

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9
Q

mri detects compressing mass lesions on the

A

pituitary

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10
Q

low tsh and thyroxine

confirmatory test

A

decreased tsh response to trh

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11
Q

decreased acth and decreased cortisol

confirmatory test

A

normal response to cosyntropin stimulation of the adrenal. cortisol will rise (adrenal is normal) in recent disease, but abnormal in chornic disease bc of adrenal atrophy

no response in acth level with crh

an elevated baseline cortisol level excludes pituiatry insufficiency

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12
Q

decreased lh and fsh levels

decreased testosterone levels

confirmatory test

A

no confirmatory test

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13
Q

G levels low, but this finding is not helpful since GH is pulsatile and maximum at night

confirmatory test

A

no response to arginine infusion

no response to GH releasing hormone

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14
Q

prolactin level low, but not helpful

confirmatory test

A

no response to TRH

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15
Q

metyrapone

A

inhibits 11 beta hydroxylase. this decreases the ouput of the adrenal gland, so it should cause ACTH levels to rise bc cortisol goes down and it negatively inhibits ACTH

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16
Q

insulin stimulation

A

when insulin decreases glucose levles, GH should usually rise. Failure of GH to rise in response to insulin indicates pituitary insufficiency

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17
Q

treatment for panhypopituarism

A

replace deficient hormones with:

cortisone
thyroxine
testosterone and estrogen
recombinant human growth hormone

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18
Q

replace cortisol before starting

A

thyroxine

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19
Q

posterior pituitary

A

the 2 products of the posterior pituitary are ADH and oxytocin, there is no deficiency disease described for oxytoxin. oxytocin helps uterine contraction during delivery but delivery still occurs even if it is absent. adh deficiency is also known as central diabetes insipidus

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20
Q

diabetes insipidus

definition

A

a decrease in either the amount of ADG from the pituitary (central) or its effect on the kidney (nephrogenic)

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21
Q

diabetes insipidus

etiology

A

Central: any destruction of the brain from stroke tumore trauma hypoxia or infilatration of the gland from sarcoidosis or infection can cause CDI

Nephrogenic: a few kidney disease such as chronic pyelonephritis amyloidosis myeloma or sickle cell disease will damage the kidney enough to inhbit the effect of ADH. Hypercalcemia and hypokalemia alo inhibit adh’s effect on the kidney

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22
Q

diabetes insipidus

presentation

A

di presents with extrmeely high-volume urin and excesssive thirst resulting in volume depletion or hypernatremia, when hypernatremia is severe there will be neurological sx such as confusion disorientation lethargy and evventually seizures and coma. neurological sx occure only when volume losses are not matched with drinking enough fluid

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23
Q

lithium is a classic cause of

A

NDI

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24
Q

when to do a vasopressin test

A

excessive thirst > increase in urine volume, and decrease in urine osmolarity and sodium > decrease in serum volume and a increase in serum osmolality and sodium > do desmopressin stimulation test

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25
Q

diabetes insipidus

diagnostic tests

A

serum sodium is elevated when oral replacement is insufficient. Urine osmolality and urine sodium are decreased. serum osmolailty which is largely a function of serum sodium is eleveated. urin volume is enormous

the difference between central and nephrogenic di is determined by the response to vasopressin. in central di urine volume will decrease and urine osmolality will increase. with nephrogenic di there is no effect of vasopressing on urine volume or osmolality

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26
Q

diabetes insipidus

treatment

A

central di is treated with long term vasopressin (desmopressin) use.

nephrogenic di is managed by trying to correct the underlying cause, it also responds to hctz, amiloride and prostaglanding inhibitors such as nsaids (eg indomethacin)

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27
Q

Vasopressin (desmopressin) stimulation test

A

Urine volume decrease and osmolality increase > dx is central diabetes insipidus > treat with vasopressin

No effect on urine > dx is nephrogenic diabetes insipidus > treatment is to treat underlying cause, hctz, amiloride and nsaids

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28
Q

acromegaly

definition

A

the overproduction of gh leading to soft tissue overgrowth throughout the body

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29
Q

acromegaly

etiology

A

alnost always caused by a pituitary adenoma, can be associated with multiple endocrine neoplasias when it is combined with parathyroid and pacreatic disorder like gastrinoma or insulinoma. rarely it is caused by ectopic gh or ghrh production from a lymphoma or bronchial carcinoid

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30
Q

acromegaly

presentation/what is the most likely dx

A

causes enlargement in soft tissue like cartilage and bone:

increased ring hat and shoe size

carpal tunnel sydrome and obstuctive sleep apnea from soft tissues enlarging

body odor from sweat glandy hyptertrophy

coarsening facial features and teeth widening from jaw growth

deep voice and macroglossia (big tongue)

colonic polyps and skin tags

arthalgias from joints growing out of alignment

htn for unclear resons in 50%

cardiomegaly and CHF

ed from incrased prolactin taht is cosecreted with the pituitary adenoma

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31
Q

GH abuse can give the same presentation of

A

acromegaly

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32
Q

acromegaly

diagnostic tests

A

lab tests will show glucose intolerance and hyperlipidemia, which contribute to cardiac dysfunction.

the best inital test is a level of insulinlike growth factor (IGF-1).

the most accurate test is the glucose suppression test. normally glucose should suppress growth hormone levels

mri should be done only after the laboratory identification of acromegaly

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33
Q

acromegaly

treatment

A

surgery: it resonds to transpenoidal transection of the pituitary in 70% of cases. larger adenomas are harder to cure

medications
cabergoline: dopamine will inhibit GH release
octreotide or lanreotide: somatostatin inhibits GH release
pegvisomat: a gh receptor antagonist it inihbits IGF release from the liver

radiotherapy: radiation is used only in those who do not respond to surgery or medications

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34
Q

prolactin levels are tested bc of cosecretion with

A

growth hormone

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35
Q

hyperprolactinemia

etiology

A

high prolactin levels can seem confusing bc so many causes have nothing to with a pituitary adenoma. prolactin can be cosecreted with GH, and increase simplybecause of acromegaly. hypothyroidism lease to hyperprolactinemia bc extremely high trh levels will stimulate prolactin secretion

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36
Q

physiologic causes of hyperprolactinemia

A

pregnancy
intense exercise
renal insufficiency
increased chest wall stimulation

cutting the pituitary stalk eliminated dopamine delivery to the anterior pituitary. dopamine inhibits prolactin release

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37
Q

drugs taht cause hyperprolactinemia

A

antipsychotic medications, methyldopa, metoclopromide, opiods, tca’s, and verapamil all raise prolactin levels

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38
Q

verapamil is the only ccb to raise

A

prolactin level

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39
Q

hyperprolactinemia

presentation

A

women present with glactorrhea, amenorrhea, and infertility.

men have ed and decreased libido, gynecomastia, galactorrhea is rare

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40
Q

do not do an mri of the head first in

A

any endocrine disorder

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41
Q

Hyperprolactinemia

diagnostic tests

A

after the prolactin level is found to be high, perform:

thyroid function tests
pregnancy test
BUN/creatinine (kidney disease elevates prolactin)
liver function tests (cirrhosis elevates prolactin)

MRI is done after:
high prolatin level is confrimed
secondary causs liek medication are excluded and
the pt is not pregnant

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42
Q

hyperprolactinemia treatment

A

Dopamine agonists: cabergoline is better tolerated than bromocriptine

transphenoidal surgery is appropriate for those not repsonidng to medications

radiation is rarley needed

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43
Q

always exclude pregnancy first in any woman with a high

A

prolactin level

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44
Q

hypothyroidism

etiology

A

hypothyroidism is almost always from a single cause: failure of the thyroid gland from burnt-out hashimoto thyroiditis. the acute phase is rarely perceived. occasionally pts have hypthyroidism from:

dietary deficiency of iodine
amiodarone

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45
Q

hypothyroidism

what is the most likely dx

A

hypothyroidism is characterized by almost all bodily processes being slowed down-except mentrual flow, which is increased

when TSH is bery high (more than double th eupper limit of normal) with normal T4, replace hormone.

when TSG is ess than double the normal, get antithyroid peroxidase/antithyroglobulin antibodies. if antibodies are positivt, replace thyroid hormone.

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46
Q

High TSH (double normal) + normal T4 =

A

treatment

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47
Q

what to look for in hypothyroidism

A 
bradycardia
constipation
weight gain
fatigue, lethargy, coma
decreased reflexes
cold intolerance
hypothermia (hair loss, edema)
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48
Q

what to look for in hyperthyroidism

A 
tachycardia, palpitations, arrhythmia (atrial fibrillation)
diarrhea (hyperdefecation)
weight loss
anxiety, nervousness, restlessness
hyperreflexia
heat intolerance
fever
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49
Q

antithyroid peroxidase antibodies tell who needs thyroid replacement when

A

T4 is normal and TSH is high

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50
Q

hypothyroidism

diagnostic tests

A

all thyroid disorders are best tested first with a TSH. if the TSH level is supressed, measure T4 levels. TSG levels are markedly elevated if the gland has failed

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51
Q

hypothyroidism

treatment

A

replacing thyroid hormone with thyroxine (synthroid) is sufficient

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52
Q

Hyperthyroidism types

A

graves

subacute thyroiditis

painless “silent” thyroiditis

exogenous thyroid hormone use

pituitary adenoma

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53
Q

only graves disease has

A

eye and skin abnormalities

TSH receptor antibodies

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54
Q

what is the most likely dx

graves disease

A

eye (proptosis) (20-40%) and skin (5%) findings

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55
Q

what is the most likely dx

subacute thyroiditis

A

tender thyroid

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56
Q

what is the most likely dx

painless “silent” thryoiditis

A

nontender, normal exam results

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57
Q

what is the most likely dx

exogenous thyroid hormone use

A

involuted gland is not palpable

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58
Q

what is the most likely dx

pituitary adenoma, thyroid

A

high TSH level

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59
Q

hyperthyroidism

diagnostic tests

A

all forms of hyperhytoidism have an elevated T4 (thyroxine) level.

only pituitary adenomas will ahve a high TSH level. in all others the pituitary release of TSH is inhibited

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60
Q

Lab findings in hyperthyroidism

graves disease

A

TSH: low

RAIU: elevated

Confirmatory: positive antibody testing

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61
Q

Lab findings in hyperthyroidism

subacute thyroiditis

A

TSH: low

RAIU: decreased

Confirmatory: tenderness

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62
Q

Lab findings in hyperthyroidism

painless “silent” thyroiditis

A

TSH: low

RAIU: decreased

Confirmatory: none

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63
Q

Lab findings in hyperthyroidism

exogenous thyroid hormone use

A

TSH: low

RAIU: decreased

Confirmatory: history and involuted nonpalpable gland

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64
Q

Lab findings in hyperthyroidism

pituitary adenoma

A

TSH: high

RAIU: not done

Confirmatory: mri of head

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65
Q

Treatment

graves disease

A

radioactive iodine

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66
Q

Treatment

subacute thyroiditis

A

aspirin

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67
Q

Treatment

painless silent thyroidis

A

none

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68
Q

Treatment

exogenous thyroid hormone use

A

stop use

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69
Q

Treatment

pituitary adenoma

A

surgery

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70
Q

Treatment of acute hyperthyroidism and “thyroid storm”

A

Propranolol: blocks target organ effect, inhibits peripheral conversion of T4>T3

Thiourea drugs (methimazole and ptu): blocks hormone production

iodinated contrast material (iopanoic acid and ipodate): blocks the peripheral conversion of T4 to the more active T3, also blocks the release of existing hormoen

steroids (hydrocortisone)

radioactive iodine: ablates the gland for a permanent cure

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71
Q

graves ophthalmopathy

A

steroids are the best initial therapy. radiation is used in those not responding to steroids. severe cases may need decompressive surgery

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72
Q

Thyroid nodules

A

these are incredible common, and are palpable in as much as 5% of women and 1% of men. 95% are benign (adenoma, colloid nodule, cyst). thyroid nodules are rarely associated with clinically apparent hyperfunctioning or hypofunctioning

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73
Q

methimazole is preferred of

A

ptu

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74
Q

if the pt has a hyperfunctioning thyroid do they need a needle biopsy

A

no bc malignancies of the thyroid or not hyperactive

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75
Q

Thyroid US

A

only gives you size still have to do thyroid function testing or biopsy

76
Q

thryoid nodule

diagnostic tests

A

thyroid nodules grater than 1 cm must be biopsied with a fine needle aspirate if there is normal thyroid funtion (t4/TSH)

nodules in those who are euthyroid should be biopsied

there is no need to ultrasound or do radionuclide scanning bc these tests cannot exclude cancer

77
Q

needle biopsy is the mainstay of

A

thyroid nodule management

78
Q

when a pt has a thyroid nodule

A

perform thyroid function tests (TSH and T4)

if tests are normal, biopsy the gland

79
Q

thyroid follicular adenoma

A

cannot exclude cancer so you must remove the entire nodule, this is an indeterminate finding on fine needle apsiration. a sonogram cannot exclude cancer

80
Q

hypercalcemia

etiology

A

the omst common cause of hypercalcemia is primary hyperparathyroidism (PTH). most of the pts are asymptomatic. For those with severe, acute symptomatic hypercalcemia, there is a high prevalence of cancer and the hypercalcemia of malignancy which is from a pth like particle. other causes are:

vit d intoxication
sarcoidosis and other granulomatous diseases
thiazide diuretics
hypthyroidism
mtastases to bone and multiple myeloma
81
Q

hypercalcemia

presentation

A

acute, symptomatic hypercalcemia presents with confusion, stupor, lethargy, and constipation

short QT and htn

osteoporosis

nephrolithiasis
diabetes inspidus
renal insufficiency

82
Q

hypercalcemia

treatment

A

acute hypercalcemia is treated with:

saline hydration at high volume
bisphosphonates: pamidronate, zoledronic acid

83
Q

the mechanism of htn in what is not clear

A

hypercalcemia

84
Q

primary hyperparathyroidism and cancer account for 90% of

A

hypercalcemia pts

85
Q

prednisone controls hypercalcemia when it is from

A

sarcoidosis or any granulomatous disease

86
Q

give calcitonin when

A

when hypercalcemia is not controlled with saline and bisphosphonates, if it is from malignancy (give cinacalcet if not), use dialysis if renal failure

87
Q

hpyerparathyroidsim

etiology

A

Primary is from:

solitary adenoma (80-85%)
hyperplasia of all 4 glands (15-20%)
parathyroid malignancy (1%)
88
Q

hyperparathyroidism presentation

A

primary hyperparathyroidism often presents as an asymptomatic elevation in clacium elvels found on routine blood testing. when there are symptoms, it can occationally present with the signs of acute, severe hypercalcemia previously described. more often there are slower manifestations such as:

osteoporosis
nephrolithiasis and renal insufficiency
muscle weakness, anorexia, nausea, vomiting, and abdominal pain
peptic ulcer disease (calcium stimulated gastrin)

89
Q

hyperparathyroidism diagnostic tests

A

besides high calcium and PTH levels, you will also find a low phosphate level, low chloride level, EKG with a short QT, and sometimes an elevated BUN and creatinine. alkaline phosphatase may be elevated from the effect of PTH on bone

90
Q

bone x ray is not a good test for what

A

effects of high PTH, dexa densitometry is better

91
Q

when hyperparathyroid what will help before surgery

A

preop imaging of the neck with us or nuclear scanning to help determine the approach.

92
Q

hyperparathyroidism treatment

A

surgical removal of the involved parathyroid gland is the standard of care

when surgery is not possible give cinacalcet

93
Q

hypocalcemia

etiology

A

primary hyperparathyroidism is most often a complication of prior neck surgy, such as thyroidectomy, in which the parathyroids have been removed

other causes are:

hypomagnesemia: magneisum is necessary for PTH to be released from the lgand. low magnesium levels also lead to increased urinary loss of calcium

Renal Failure: other causes include vitamin D deficiency, genetic disorders, fat malabsorption, and low albumin states.

94
Q

for every pon decrease in albumin the calcium level decreases by

A

0.8

95
Q

low albumin causes a decrease in total calcium but the free calcium level

A

is normal hence no symptoms

96
Q

hypocalcemia

presentation

A

signs of neural hyperexcitability in hypocalcemia:

chvostek sign (facial nerve hyperexcitability)
carpopedal spasm
perioral numbness
mental irritability
seizures
tetany (trousseau sign)
97
Q

hypocalcemia

diagnostic tests

A

ekg shows a prolonged QT

slit lamp exam shows early cataracts

98
Q

hypocalcemia

treatment

A

replace calcium and vitamin D this is done orally if sx are mild or absent and iv if sx are severe

99
Q

low calcium =

A

twitchy and hyperexcitable

100
Q

high calcium =

A

lethargic and slow

101
Q

hypercortisolism

definition

A

cushing syndrome can be sued interchangeably iwth the term hypercotisolism, cushing disease is a term used for the pituitary overproduction of ACTH from carcinoid or cancer or from overproduction autonomously in the adrenal gland. prednisone and other glucocorticoid use can cause the same manifestation.

102
Q

hypercortisolism

etiology

A

pituitary ACTH (cushing disease) 70%
adrenals 15%
unknown source of ACTH 5%
ectopic ACTH (cancer, carcinoid)

103
Q

hypercortisolism

presentation

A

fat redistribution: Moon face, truncal obesity, buffalo hump, thin extremitites, increased abdominal fat

Skin: striae, easy bruising, decreased wound healing, adn thinning of skin

osteoporosis

htn: from increased sodium reabsorption in th ekideny and increased vascular reactivity

menstural disorders in women

ed in men

cognitive disturbance: from decreased concentration to psychosis

polyuria: from hyperglycemia and increased freee water clearance

104
Q

hypercortisolism

diagnostic tests

A
  1. Establish the presence of hypercortisolism

2. establish the cause of hypercortisolism

105
Q

Establish the presence of hypercortisolism

A

the best initial test for the presence of hypercortisolism is the 24 hour urin cortisol. if this is not in the choices then andwer is the 1 mg overnight dexamethasone suppression test. the 1 mg overnight dexamethason suppression test should normally suppress the omrning cotisol level. if this suppression occurs, hypercortisolism can be excluded

there are false positives on the 1 mg overnight dexamethasone suppression test

the 24 hour urin cortisol is a more specific test of hypercortisolism if the 24 urin cortisol is elevated the presence of hypercortisolism is confirmed

106
Q

causes of false positive 1 mg overnight suppression testing

A

depression

alcoholism

obesity

107
Q

establish the cause of hypercortisolism

A

ACTH testing is the best inital test to determine the cause or location of hypercortisolism

Low ACTH means an adrenal source

if the ACTH level is elevated teh source coudl be from:
Pituitary (suppresses with high dose dexamethasone)
ectopic production: lung cancer, carcinoid (dexamethasone does not suppress)

once the ACTH level is elevated and does not suppress with high dose dexamethasone, scan the brain with an MRI. if the mri does not show a clear pituitary lesion, sample the inferior petrosal sinus for ACTH, possibly after stimulating the pt with corticotropin-releasing hormone (CRH). An elevated ACTH from the venous drainage of the pituitary confirs the pituitary as the source. the petrosal venous sinus must be sampled bc some pituitary lesions are too small to be detected on MRI.

108
Q

Decreased ACTH =

A

adrenal source

109
Q

if the ACTH is elevated and you cannot find a defect in the pituitary either by MRI or samplingthe petrosal sinus

A

scan the chest looking for an extopic source of ACTH production. you can always confirm teh source of hypecortisolism with biochemical tests before you perform imagins studies

110
Q

CC: I feel weak and tired, and I notice hair growth on my face and strance marks on my stomach

low-dose (1 mg) dexamethasone suppression test

A

decreased=disease excluded

111
Q

CC: I feel weak and tired, and I notice hair growth on my face and strance marks on my stomach

cortisol testing:
24 urine
late-night salivary

A

increased

do ACTH testing if high:
ACTH dependant cushing syndrom

if low:
ACTH independant cushing syndrome

112
Q

at least 10% of the population has an abnormality of what on MRI

A

the pituitary so if you start with a scan you may removed the pituitary when the source is in the adrenals

113
Q

ACTH high?>high dose dexamethasone

A

suppresses: pituitary

Dose not suppress: ectopic + cancer

114
Q

Other lab testing for hypercortisolism

A

cortisol is a stress hormone that is an antiinsulin. in addition, there is some aldosteronelike effect of cortisol that has an effect on the kidneys distal tubule of excreting potassium and hydrogen ions

115
Q

effects of hypercortisolism include

A 
hyperglycemia
hyperlipidemia
hypokalemia
metabolic acidosis
leukocytosis from demargination of white blood cells, at least half of white cells in the blood are on the vessel wall waiting for an acute stress to come into circulation. they are like parked police cars wiating to be called
116
Q

hypercortisolism

treatment

A

surgically remove the source of hypercortisolism. transphenoidal surgery is done for pituitary sources whereas laparoscopic removal is done for adrenal sources

117
Q

evaluation of adrenal incidentaloma

A

how far should you go in the evaluation of an unexpected, asyptomatic adrenal lesion found on CT

metanephrines of blood or urine to exclude pheochromocytoma

renin and aldosterone levels to exclude hyperaldosteronism

1 mg overnight dexamethasone suppresion test

118
Q

4% of the population has adrenal incidenaloma

A

do not start with a scan or you will remove the wrong organ

119
Q

laboratory finding in adrenal disorders

ACTH level

A

Adrenal: low

Pituitary: high

Ectopic: high

120
Q

laboratory finding in adrenal disorders

Petrosal Sinus

A

Adrenal: not done

Pituitary: high ACTH

Ectopic: low ACTH

121
Q

laboratory finding in adrenal disorders

Gigh dose dexamethasone

A

Adrenal: no suppression

Pituitary: suppresses

Ectopic: no suppression

122
Q

ACTH independent cushign syndrome

A

Adrenal mass?

CT adrenal

123
Q

ACTH-dependent Cushing Syndrome

pituitary vs ectopic ACTH production?

high dose dexamethasone suppression test

suppression of cortisol?

A

pituitary adenoma? (cushing disease)

pituitary mass?

pituitary MRI

no mass seen?

pterosal sinus sampling for ACTH

124
Q

ACTH-dependent Cushing Syndrome

pituitary vs ectopic ACTH production?

high dose dexamethasone suppression test

increase ACTH and cortisol?

A

ectopic ACTH secreting tumor

chest CT

125
Q

Hypoadrenalism

definition

A

chronic hypadrenalsim is also called ADDison disease. acute adrenal insufficiency is an adrenal crisis. these conditions are different severities of the same disorder

126
Q

Hypoadrenalism

etiology

A

Addison disease is caused by autoimmune destruction of the gland in more than 80% of cases.

less common causes are:
infection (tb)
adrenoleukodystophy
metastatic cancer to the adrenal gland

127
Q

acute adrenal crisis is cause by

A

hemorrhage

surgery

hypotension

trauma that rapidly destroys the gland

the sudden removal of chronic high dose prednisone (steroid) use can precipitate acute adrenal crisis

it is less comman to have an acute adrenal crisis from the loss of the pituitary bc aldosterone is not under the control o fACTH

128
Q

Hypoadrenalism

presentation

A

weakness

fatigue

altered mental status

nausea

vomiting

anorexia

hypotension

hyponatremia

hyperkalemia

hyperpigmentation is just chronic

129
Q

if hypoadrenalism is from pituitary failure

A

ACTH level is low

130
Q

high acth level means the etiology of adrenal insufficinecy is

A

a primary adrenal failure

131
Q

eosinophilia is common in

A

hypoadrenalism

132
Q

hypoadrenalism diagnostic tests

A

pats have the hooposit of hypercortisolism so they have

hypoglyxemia

hyperkalemia

metabolic acidosis

hyponatremia

high bun

133
Q

what is more important than testing in acute adrenal crisis

A

treatment

134
Q

hypoadrenalism treatment

A
  1. replace steroids with hydrocortisone
  2. fludrocortisone is a steroid hormone that is particularly high in mineralocorticoid or aldosterone-like effect. fludricortisone is most useful if the pt still have evidence of postural instability. mineralocorticoid cupplements hsould be used in primary adrenal insuffciiency when the pat is on oral steroids such as cortisone
135
Q

Signs and sx of hypoadrenalism

weakness hypotension weight loss hyperpigmentation

then to the cosyntropin stimulation test (plasma cortisol before and after cosyntropin IM or IV)

cortisol fails to rise

high ACTH

A

aldosterone also low

primary adrenal insufficiency

136
Q

Signs and sx of hypoadrenalism

weakness hypotension weight loss hyperpigmentation

then to the cosyntropin stimulation test (plasma cortisol before and after cosyntropin IM or IV)

cortisol fails to rise

low ACTH

A

aldosterone an increase

secondary adrenal insufficiency or adrenal atrophy from pituitary insufficiency

137
Q

Primary hyperaldosteronism

etiology

A

Primary hyperaldosteronism is the autonomous overproduction of aldosterone despire a high pressure with a low renin activity. eighty percent are from solitary adenoma. most of the rest is from bilateral hyperplasia. it is rarely malignant

138
Q

Primary hyperaldosteron

what is the most likely dx

A

all forms of secondary htn are more likely in those whose onset:

is under age 30 or above 60
is not controlled by 2 antihypertensive meds
has a characteristic finding on the hx physical or labs

139
Q

Primary hyperaldosteronism

presentation

A

there is high bp in association with a low potassium level.the low potassium level is either found on routine lab testing or bc of sx of muscular weakness or diabetes insipidus from the hypokalemia

140
Q

Primary hyperaldosteronism

diagnostic tests

A

the best initial test is to measure the ration of plasma aldosterone to plasma renin. an elevated plasma renin excludes primary hyperaldosteonism.

the most accurate test to confirm the presence of a unilateral adenoma is a sample of the venous blood draining the adrenal. it will show a high aldosterone level.

141
Q

Primary hyperaldosteronism

CT

A

Ct scan of the adrenals should only be done after biochemical testin confirms:

low potassium

high aldosterone despite a high salt diet

low plasma renin level

142
Q

high bp + hypokalemia =

A

primary hyperaldosteronism

143
Q

never start with what in endocrinology?

A

a scan there are too many incidental lesions of the adrenal

144
Q

Primary hyperaldosteronism

treatment

A

unilateral adenoma is resected by laparoscopy

bilateral hyperplasia is treated with eplerenon or spironolactone

145
Q

spironolactone causes

A

gynecomastia and decreased libido bc it is antiadrenergic

146
Q

pheochromocytoma

definition and etiology

A

pheochromocytoma is a nonmalignant lesion of the adrenal medulla autonomously overproducing catecholamines despite a high bp

147
Q

pheochromocytoma

what is the most liekly diagnosis

A

htn that is episodic in nature

ha

sweating

palpitations and tremor

148
Q

pheochromocytoma

diagnostic tests

A

the best inital test is the level of free metanephrines in plasma. this is confirmed with a 24 hour urine collection for metanephrines. this is more sensitive than the urine vanillylmandelic acid level. direct measurement of epinephrine and norepineprhine are useful as well

imaging of the adrenal glands with CT or MRIis done only after biochemical testing

mibg scanning: this is a nuclear isotype scan that detects the locationo fo pheochromocytoma that originates outside the adrenal gland

149
Q

pheochromocytoma

treatment

A

phenoxybenzamine is an alpha blocker htat is the best initial therapy. of pheochromocytoma. calcium channel blocekr and beta blockers are used afterward

pheos are removed surgically or by laparoscopy

150
Q

Diabetes Mellitus

definition etiology

A

dm is defined as persistently high fasting glucose levels greater than 126 on at least 2 separate occasions

151
Q

Type 1 DM

A

onset in childhood
insulin dependent from an early age
not related to obesity
defined as insulin deficiency

152
Q

Type 2 DM

A

onset in adulthood
directly related to obesity
defined as insulin resistance

153
Q

Diabetes Mellitus

presentation

A

polyuria, polyphagia, and polydipsia are the most common presentation. Type 1 diabetics are generally thinner than Type 2 diabetics. Type 2 DM is more resistant to diabetic ketoacidosis (DKA). both types present with decreased wound healing. Type 2 diabetics are much less likely to present iwth polyphagia.

154
Q

Diabetes Mellitus

diagnostic tests

A

diabetes is defined/diagnosed as:

two fasting blood glucose measurements greater than 125mg/dl

single glucose level above 200mg/dl with above symptoms

increased glucose elvel on oral glucose tolerance testing

hemoglobin a1c greater than 6.5% is a diagnostic criterion and is the best test to follow response to therapy over the last several months.

155
Q

Diabetes Mellitus

treatment

A

Diet exercise and weight loss - weight loss can control asm uch as 25% of cases of Type 2 DM without the need for medications, since decreasing the amoun of adipose tissue helps to decrease insulin resistance. Exercising muscle dose not need insulin.

Oral hypoglycemic medication - the best initial drug therapy is with oral metformin. Sulfonylureasare not used as first line therapy bc they increase insulin release from the pancreas, thereby driving the glucose intracellularly and increasing obesity. The goal of therapy is Hga1c less than 7%

156
Q

Metformin

A

works by blocking gluconeogenesis. it does not increase weight gain. in the absence of renal failure, metformin is clearly the best inital therapy for diabetes

157
Q

metformin is contraindicated in who

A

people with renal dysfunction bc it can accumulate and cause metabolic acidosis

158
Q

DPP-IV inhibitors

sitaglipitin, linagliptin, alogliptin

A

block the metabolism of the incretins, also called insulinotropic peptide (GIP) and glucagon-like peptide (GLP). the term glucagon like peptide is confusing, bc GLP actually inhibits or suppresses glucagon.

159
Q

Incretin Mimetics

exenatide, liraglutide, albiglutide

A

are a direct replacement of incretins. They are generally not gien before the DPP-IV inhibitors, bc they must be administerd by injection. incretin agonists also markedly slow gastric motility and decrease weight. the management of incretins is confusing bc they have seversal names

160
Q

The incretins (GIP and GLP) increase

A

insulin release and decrease glucagon release from the pancreas. They are secreted into the bloodstream when food (especially carbohydrates) enters the duodenum and is metabolized by dipeptidyl peptidase IV (DPPIV). the incretins normally have a half life of only 1-2 minutes. Giving DPP-IV inhibitors- such as sitagliptin, saxaglipitin, and linagliptin-markedly lengthens the half life of incretins.

161
Q

Incretins =

A

glucose insulinotropic peptide (GIP) and glucagon-like peptide (GLP)

DPP-IV inhibitors block their metabolism

all slow gi motility

162
Q

Thiazoladinediones (glitazones)

A

provide no clear benefit over the hypoglycemic medications. they are relatively contraindicated in CHF bc they increase fluid overload.

163
Q

Nateglinide and repaglinide

A

they are stimulators of insulin release in a manner similar to sulfonylureas, but do not contain sulfa. they do not add any therapeutic benefit to sulfonylureas

164
Q

alpha glucosidase inhibitors (acarbose and miglitol)

A

they are agents that block glucose absorption in the bowel. they add about half a point decrease in HgA1C . they cause flatus, diarrhea, and abdominal pain. they can be used with renal insufficiency.

165
Q

pramlintide

A

it is an analog of a protein called amulin that is secreted normally with insulin. amylin decreases gastric emptying, decreases glucagon levels, and decreases appetite

166
Q

insulin

A

insulin is added if the pt is not controlled with oral hypoglycemic agents. insulin glargine gives a steady state of insulinfor the entire day. dosing is not tested. glargine provides much more steady blood levels than NPH insulin, which is dosed twice a day. long acting insulin is combined with a short acting insulin such as lispro, aspart, or glulisine. regular insulin is sometimes used as the short acting insulin, goal of therapy is A1C less than 7%

167
Q

lispro, aspart, glulisine

A

Onset: 5-15 minutes

Peak action: 1 hour

Duration: 3-4 hours

168
Q

Regular insulin

A

Onset: 30-60 minutes

Peak action: 2 hours

Duration: 6-8 hours

169
Q

NPH

A

Onset: 2-4 hours

Peak action: 6-7 hours

Duration: 10-20 hours

170
Q

Glargine

A

Onset: 1-2 hours

Peak action: 1-2 hours

Duration: 24 hours

171
Q

Diabetic Ketoacidosis

A

more common in those with Type 1 diabetes, diabetic ketoacidosis (DKA) can definitely present in those with Type 2 diabetes

Hyperventilation
possibly altered mental status
metabolic acidosis with an increased anion gap
hyperkalemia in blood, but decreased total body potassium bc of urinary spillage
increased anion gap on blood testing
serum is positive for ketones
nonspecific abdominal poin
acetone odor on breath
polydipsia and polyuria
172
Q

Diabetic Ketoacidosis

treatment

A

treat with large-volume saline and insulin replacement. replace potassium when the potassium level comes down to a level approaching normal. correct the underlying cause: noncompliance with medications, infection, pregnancy, or any serious illness.

173
Q

Decrease insulin

A

Increase synthesis of glucose

increase breakdown of glycogen

decrease uptake of glucose by tissues

increase breakdown of fats

174
Q

Increase synthesis of glucose

increase breakdown of glycogen

A

increase liver output of glucose> hyperlgycemia

175
Q

decrease uptake of glucose by tissues

A

hyperglycemia

176
Q

increase breakdown of fats

A

increase free fatty acids in plasma > increase liver output of ketone bodies >ketoacidosis

177
Q

Increase breakdown of proteins

A

increase synthesis of glucose> increase liver output of glucose> hyperglycemia

178
Q

what is the most accurate measure of the severity of dka

A

hyperglycemia is not the best measure of the severity of DKA. the glucose level can be markedly elevated without the presence of ketoacidosis. urine ketones mean very little. although blood ketones are important, they are not all detected. if the serum bicarbonate is very low, the pt is at risk of death. if the serum bicarbonate is high, it does not matter how high the glucose level is, in terms of severity. serum bicarbonate level is a way of saying anion gap. if the bicarbonate level is low, the anion gap is increased.

179
Q

Health Maintenance

all pts with DM should receive:

A

pneumococcal vaccine

yearly eye exam to check for proliferative retinopathy, which needs laser therapy

stain medication if the ldl is above 100mg/dl

ace inhibitors and arbs if the blood pressure is greater than 140/90 mmhg

acei or arb if urine tests positive for microalbuminuria

aspirin, used regularly in all diabetic pts abov the age of 30

foot exam for neuropathy and ulcers

180
Q

Complications of Diabetes

A

Cardiovascular complications

diabetic nephropathy

gastroparesis

retinopathy

neuropathy

181
Q

Complications of Diabetes

Cardiovascular complications

A

diabetic pts are at significantly increased risk of mi, stroke, and CHF from premature atherosclerotic disease. this is why the goal of blood pressure in these pts (below 140/90 mmhg) is lower than in the general population. in addition, diabetes is considered an equivalent of coronary disease for treatment of ldl, and the goal is less than 100mg/dl when initiating treatment with statins

182
Q

Complications of Diabetes

diabetic nephropathy

A

diabetes leads to microalbuminuria early in the disease. the dipstick for urine becomes trace positive at 300 mg per 24 hours. pts with dm should be screened annually for microalbuminuria and started on an ace inhibitor or arb when it i spresent. these agents are proven to decrease the rate of progression of nephropathy by decreasing intraglomerular hypertension and decreasing damage to the kidney.

183
Q

Complications of Diabetes

gastroparesis

A

after several years, DM decreases the ability of the gut to sense the stretch of the walls of the bowel. stretch is the main stimulant to gastric motility. gastroparesis is an immobility of the bowls that leads to bloating, constipation,, early satiety, vomiting, and abdominal discomfort. treatment is with metoclopromide and erythromycin, which increase gastric motility.

184
Q

Complications of Diabetes

retinopathy

A

DM’s effect on microvasculature is especially apparent in the eye. in the united states, nearly 25,000 people go blind from DM each year. the only management for nonproliferative retinopathy is tighter control of glucose. aspirin does not help retinopathy. when neovascularization and vitreous hemorrhages are present, it is called proliferative retinopathy. this is treated with laser photocoagulation, which markedly retards the progression to blindness.

185
Q

Complications of Diabetes

neuropathy

A

damage to microvasculature damages the vasonervorum that surrounds large peripheral nerves. this leads to decreased sensation in the feet-the main cause of skin ulcers of the feet which lead to osteomyelitis. when the neuropathy leads to pain, treatment is with pregabalin, gabapentin, or tricyclic antidepressants.

OMS III (21 decks)

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