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Internal Medicine > Endocrine > Flashcards

Endocrine Flashcards

1
Q

a 25-year-old man concerned about some “bizarre symptoms” that he has been. He tells you that approximately 6 months ago, he began to experience the following symptoms: headaches, visual defects, weight gain, an appearance of his forehead growing, enlarging hands and feet (he could no longer get his gloves and shoes on), and increased sweating. On examination, mental status is normal, and the apical impulse is felt in the fifth intercostal space, midclavicular line. His blood pressure is 170/ 105 mm Hg. He does have a protruding brow, and three discrete visual field defects are noted (two in the left eye and one in the right eye). His tongue appears enlarged, and he is sweating profusely. What is the likely diagnosis

A

Acromegaly

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2
Q

What is the different between acromegaly and gigantism

A

igantism occurs if growth hormone (GH) hypersecretion begins in childhood, before the closure of the epiphyses

Acromegaly involves growth hormone GH hypersecretion beginning in adulthood; a variety of bony and soft tissue abnormalities develop

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3
Q

What is the main cause of both gigantism and acromegaly q

A

a pituitary adenoma that secretes excessive amounts of Growth Hormone; rarely, they are caused by non-pituitary tumors that secrete GHRH

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4
Q

What are the diagnostic tests for gigantism and acromegaly

A

GH test 2 hour after glucose load
Increased IGF-1
MRI/CT shows a pituitary tumor

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5
Q

What is the treatment of gigantism and acromegaly

A

Removal of pituitary tumor

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6
Q

a 25-year-old male presents complaining of fatigue, weight loss, and recurrent nausea and vomiting. On physical exam, he appears weak and has skin that appears abnormally tan. Her blood pressure is 90/70. A basic metabolic panel reveals hyponatremia and hyperkalemia. What is the likely diagnosis

A

Addisons disease

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7
Q

What causes Addisons disease

A

Typically autoimmune. May be due to Tuberculosis in endemic areas

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8
Q

What is Addison’s disease

A

Destruction of the adrenal cortex resulting in loss of cortisol production (↓ cortisol)

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9
Q

What are the typical lab findings with Addisons disease

A

↓ sodium, ↓ 8 AM cortisol, ↑ ACTH (primary), ↑ potassium (primary), low DHEA

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10
Q

What is the role of DHEA and where is it produced

A

It is produced in the adrenal gland and helps with the production of testosterone and estrogen

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11
Q

How do you diagnose Addison’s disease

A

High dose cosyntropin (synthetic ACTH) stimulation test

-Blood or urine cortisol is measured after an IM injection of cosyntropin (synthetic ACTH)

*The normal response is a rise in blood and urine cortisol levels after synthetic ACTH is given
Primary adrenal insufficiency results in little or no increase in cortisol levels (< 20 mcg/dL) after ACTH is given

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12
Q

How do you treat Addison’s disease

A

Hydrocortisone/prednisone PO daily

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13
Q

If someone is experiencing an Addisonian crisis, what will their presenting symptoms be and how would you treat it.

A

Hypotension, altered mental status

treatment: emergent IV saline, glucose, steroids

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14
Q

a 32-year-old woman who comes to the clinic because of new skin markings on her abdomen. Physical exam shows a round face, large purple striae over the abdomen, and several ecchymoses over her trunk, arms, and legs. She describes easy bruising, as well as a significant weakness when she tries to stand up from sitting on the ground. Her 24-hour urine free cortisol is 3 x the upper limit, her late-night serum cortisol is elevated and her plasma ACTH level is < 5 pg/mL. What is the likely diagnosis

A

Cushings disease

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15
Q

What is cushings disease

A

Cushing’s syndrome is a collection of signs and symptoms due to prolonged exposure to excess cortisol

-ACTH secreting pituitary microadenoma usually very small on anterior pituitary

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16
Q

Which gender is more susceptible to cushings disease

A

Females (3x)

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17
Q

What are common symptoms seen with cushings disease

A

buffalo hump, moon facies, supraclavicular pads, HTN, thirst, polyuria, hypokalemia, Proximal muscle weakness, pigmented striae; backache, headache, oligomenorrhea/amenorrhea emotional lability/psychosis

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18
Q

How do you diagnose cushings disease

A

Confirming high cortisol with a 24 hr urine free cortisol, late-night serum cortisol, and/or low-dose dexamethasone suppression test

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19
Q

What is the most reliable index of cortisol secretion

A

24-hour urinary free cortisol

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20
Q

How do you confirm the source of the high cortisol

A

ACTH level

*If it is an ACTH dependent cause, an MRI of the brain should be done to look for a pituitary adenoma (Cushing disease). If it is an ACTH independent cause, a CT of adrenals should be done to look for an adrenal mass such as an adenoma

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21
Q

How does the dexamethasone suppression test work to diagnose cushings syndrome

A

Give a steroid (dexamethasone) ⇒ failure of steroid to decrease cortisol levels is diagnostic ⇒ proceed next to high dose dexamethasone suppression test ⇒ no suppression = Cushing’s syndrome

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22
Q

How do you treat cushings syndrome

A

Transsphenoidal selective resection of pituitary tumor cures 75-90%

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23
Q

a 25-year-old male complaining of an unabated thirst that began three weeks ago. He is constantly drinking and goes to the bathroom around five times a night. He has lost five pounds over the last few weeks. The patient is on lithium for bipolar disorder. His BP is 115/70. The patient’s labs are significant for serum Na of 145 mEq/L (normal: 135-145). Urine osmolality is 185 mOsm/kg, and urine specific gravity is 1.004 (normal: 1.012 to 1.030). What is the likely diagnosis

A

Diabetes insipidus

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24
Q

What is diabetes insipidus

A

Diabetes insipidus (DI) is caused by a deficiency of or resistance to vasopressin (ADH), which decreases the kidneys’ ability to reabsorb water, resulting in massive polyuria

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25
Q

What are the 2 different types of diabetes insipidus

A

Central
Nephrogenic

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26
Q

What is central diabetes insipidus

A

destruction of the posterior pituitary from either an autoimmune issue or some type of brain trauma

Results in no ADH production

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27
Q

What is nephrogenic diabetes insipidus

andwhat can cause it

A

There is a partial or complete insensitivity to ADH

Can be due to: drugs (Lithium, Amp B), hypercalcemia and hypokalemia affecting the kidney’s ability to concentrate urine, acute tubular necrosis

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28
Q

How do you diagnose diabetes insipidus

A

Serum osmolality (concentration) is high (unable to stop the secretion of water into the kidneys so blood becomes more concentrated) and urine osmolality is low because it is so dilute

  • use a water deprivation test or desmopressin stimulation test
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29
Q

What will be seen with the Desmopressin stimulation test for DI

A

Central: reduction in urine output indicating a response to ADH

Nephrogenic: continued production of dilute urine (no response to ADH) because kidneys can’t respond

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30
Q

How do you treat central DI

A

DDAVP

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31
Q

How do you treat Nephrogenic DI

A

Sodium and protein restriction, HCTZ, indomethacin

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32
Q

an 11-y/o girl brought to you by her mother who reports weight loss along with increased thirst and urination. The patient has felt tired and nauseous. On examination her weight is below the 5th percentile, she looks thin, and her skin is pale. her blood pressure is 100/70 and her pulse is 104 bpm. Her respirations are deep at a rate of 28 breaths/minute. Her breath smells fruity. What is the likely diagnosis

A

T1DM

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33
Q

Which type of DM is due to islet cell antibodies

A

T1DM

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34
Q

What is the common presentation of T1DM

A

Children
Polyuria, polydipsia, polyphagia, fatigue, and weight loss

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35
Q

T1DM is often first recognized and DKA… how will the patient present and how will you treat them

A

Fruity breath, nausea, vomiting, dehydration

IV regular insulin

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36
Q

What is Dawn phenomenon

A

Normal glucose until 2-8 am when it rises. Results from decreased insulin sensitivity and a nightly surge of counter-regulatory hormones during nighttime fasting

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37
Q

How do you treat Dawn phenomenon

A

Treat with bedtime injection of NPH to blunt morning hyperglycemia, avoiding carbohydrate snack late at night

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38
Q

What is Somogyi effect

A

Nocturnal hypoglycemia followed by rebound hyperglycemia due to a surge in growth hormone

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39
Q

How do you treat Somogyi effect

A

Treat with decreased nighttime NPH dose or give bedtime snack

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40
Q

How do you treat DKA

A

TREAT WITH FLUIDS! Patients with DKA are always dehydrated and need large-volume IV fluid resuscitation, usually isotonic fluids such as normal saline. If the corrected serum sodium level is high, this can be reduced to half-normal saline. Insulin should always be administered by an IV pump to guard against accidental overdose.

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41
Q

How is DM diagnosed

A

random blood glucose level of > 200 mg/dL + diabetic symptoms

2 separate fasting (8 hours) glucose levels of > 126 mg/dL

2-hour plasma glucose of > 200 on an oral glucose tolerance test (3-hour GTT is the gold standard in GDM)

Hemoglobin A1c of > 6.5%

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42
Q

What are high fasting insulin and C-peptide levels suggestive of

A

T2DM

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43
Q

What is the treatment goal for HbA1C

A

<7

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44
Q

What is the treatment goal for finger stick glucose monitoring

A

< 130 mg/dL fasting
< 180 mg/dL peak postprandial

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45
Q

a 35-year-old Mexican American male complaining of increased thirst, frequent urination, hunger, fatigue, and blurred vision random finger stick blood glucose is 225. What is the likely diagnosis

A

T2DM

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46
Q

How do you diagnose T2DM

A

2 random glucose measurements of >200
OR
2 fasting glucose >126

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47
Q

What is the first line treatment for T2DM
How does it work
What class does it belong to

A

Metformin
decreases hepatic glucose production
Biguanides

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48
Q

At what creatinine level should metformin be stopped at

A

> 1.5

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49
Q

How do Sulfonylureas work
what are examples of sulfonylureas
What are some side effects

A
  • stimulates pancreatic beta-cell insulin release
  • Glipizide, glimipiride, Glyburide
  • Hypoglycemia

*they are cheap and rapidly effective making them desirable

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50
Q

How do Thiazolidinediones work
What are examples
What are some contraindications

A

increases insulin sensitivity in peripheral receptor site adipose and muscle has no effect on pancreatic beta cells

Pioglitazone, Rosiglitazone

CHF, liver disease, fluid retention, weight gain, bladder cancer (pioglitazone), a potential increase in MI (rosiglitazone)

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51
Q

How do Alph-glucosidase inhibitors work
What are some examples
what are some side effects

A

Delays intestinal glucose absorption

Acarbose, miglitol

GI side effects, three times a day dosing

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52
Q

What do Meglitinides do
What are some examples

A

stimulates pancreatic beta-cell insulin release
Nateglinide, Repaglinide

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53
Q

How do GLP1 meds work
what are some examples

A

lowers blood sugar by mimicking incretin - causes insulin secretion and decreased glucagon and delays gastric emptying

Semaglutide, Dulaglutide, Exanatide, Liraglutide

*can cause gastroparesis but can help reduce CV mortality

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54
Q

How do DPP-4 inhibitors work
What are some examples

A

inhibits degradation of GLP-1 so more circulating GLP-1

Sitagliptan, saxagliptan

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55
Q

How do SGLT2 work
What are some examples
What are some side effects

A

inhibition lowers renal glucose threshold which results in increased urinary glucose excretion

Canagliflozin

Vulvovaginal candidiasis, urinary tract infections, bone fractures, lower limb amputations

56
Q

When is insulin utilized in those with T2DM

A

When A1C >9

57
Q

What is the most common complication of using insulin

A

Neuropathy

58
Q

What is normal fasting glucose

A

70-100

59
Q

What is the goal of post prandial glucose

A

<140

60
Q

What is the serum total calcium to qualify for hypercalcemia

A

> 10.5

61
Q

What are the signs of hypercalcemia

A

Bones, stones, groans, psychiatric overtones

*Shortened QT

62
Q

What is hypercalcemia associated with

A

malignancy or hyperparathyroidism

63
Q

How do you treat hypercalcemia

A

IV NS and furosemide

64
Q

What sodium level is considered hypernatremia

A

> 145mmol

65
Q

What are signs of hypernatremia

A

Poor skin turgor, dry mucous membranes, flat neck veins, hypotension, increased BUN/CR ratio > 20:1

66
Q

What causes hypernatremia

A

diarrhea
Diabetes insipidus
diuretics
hyperglycemia
thirst deficit

67
Q

How do you treat hypernatremia

A

D5W

68
Q

What can occur if you correct hypernatremia too quickly

A

cerebral edema
pontine herniation

69
Q

a 33-year-old woman presents to the emergency department due to diffuse pain and fatigue. The woman states that she feels like her bones and muscles diffusely hurt. She also has experienced some abdominal pain as well and states that she has trouble focusing. What is the likely diagnosis

A

Hyperparathyroidism

70
Q

What is hyperparathyroidism

A

a condition in which one or more of the parathyroid glands become overactive and secrete too much parathyroid hormone (PTH). This causes the levels of calcium in the blood to rise

71
Q

What is primary vs secondary hyperparathyroidism

A

Primary: ↑ PTH is usually caused by a PTH-secreting parathyroid ADENOMA

Secondary: ↑ PTH by a physiologic response to hypocalcemia or vitamin D deficiency

72
Q

What is the most common cause of secondary hyperparathyroidism

A

CKD

73
Q

What will be seen in the urine with hyperparathyroidism

A

hyperphosphaturia, hypercalciuria (all Ca and phosphorus go out through kidneys to urine)

74
Q

How do you treat hyperparathyroidism

A

Primary ⇒ surgical correction to remove the overactive parathyroid gland ⇒ If all 4, remove 3.5 glands
Secondary ⇒ replace cause (vitamin D/Ca supplementation)

75
Q

How to treat someone with severe hypercalcemia coupled with hyperparathyroidism

A

IV fluids, Lasix, calcitonin; treat osteoporosis with bisphosphonates

76
Q

a 34-year-old female complaining of irritability and nervousness, heat intolerance with increased sweating, and weight loss despite an increase in appetite. What is the likely diagnosis

A

hyperthyroidism

77
Q

What is the autoimmune disease that leads to hyperthyroidism

A

graves disease

78
Q

How will someone present with hyperthyroidism

A

Heat intolerance, palpitations, sweating, weight loss, tremor, anxiety, tachycardia

79
Q

How will someone with graves disease present in addition to the usual hyperthyroidism sign

A

Diffuse goiter with a bruit, exophthalmos, pretibial myxedema

80
Q

What will be seen with someone experiencing a thyroid storm

A

Fever, tachycardia, delirium

81
Q

What will be seen on labs with hyperthyroidism

A

Low TSH
High T4

82
Q

What antibodies can be tested for in someone with Graves disease

A

Anti-thyrotropin antibodies

83
Q

What is the treatment for hyperthyroidism

A

Methimazole/PTU
radioactive iodine
Thyroidectomy

84
Q

How do you treat someone experiencing a thyroid storm

A

prompt beta-blockers, hydrocortisone, methimazole/propylthiouracil, iodine

85
Q

What is the most common injury associated with a thyroidectomy

A

Injury to the laryngeal nerve leading to hoarseness

86
Q

If someone has hyperthyroidism or graves disease and becomes pregnant, how do you treat them

A

PTU during the first trimester
Methimazole for the remainder of their pregnancy

87
Q

What is Hashimotos thyroiditis

A

Diffusely enlarged, painless, nodular goiter

88
Q

What is subacute thyroiditis and when does it present

A

Painful enlarged thyroid with dysphagia, mild fever

Young women after a viral infection
*treat with ASA

89
Q

What is postpartum thyroiditis

A

1-2 months of hyperthyroidism after delivery

Completely resolves, give propranolol for cardiac symptoms

90
Q

Which disease will lead to Trousseau’s sign and Chvostek’s sign

A

Hypocalcemia

91
Q

How do you treat hypocalcemia

A

IV calcium gluconate

92
Q

If suspicious of phosphorus or calcium imbalance what should you do

A

order a PTH level

**Always remember it is the effect on the EKG that counts the most, not the serum levels

93
Q

What imbalance is occurring if peaked T waves is seen on EKG

A

Hyperkalemia

94
Q

What defines hyponatremia

A

sodium of < 135 mmol/L

95
Q

What are signs of hyponatremia

A

Peripheral and presacral edema, pulmonary edema, JVD, hypertension, decreased hematocrit, decreased serum protein, decreased BUN/CR

*presents with muscle cramps and seizures

96
Q

what causes Hypervolemic hyponatremia

A

CHF, nephrotic syndrome, renal failure, cirrhosis

97
Q

What causes Euvolemic hyponatremia

A

SIADH (Picmonic), steroids, hypothyroid

98
Q

What causes Hypovolemic hyponatremia

A

sodium loss

99
Q

How do you treat severe hyponatremia

A

Hypertonic saline
mannitol

100
Q

Why should sodium concentration be corrected slowly

A

To avoid osmotic demyelination syndrome

101
Q

a 33-year-old woman whose vision has been steadily declining over the past two years. She further complains that her lips and feet feel numb. Her medical history is notable for medullary thyroid cancer status post total thyroidectomy. What is the likely diagnosis

A

Hypoparathyroidism

102
Q

What occurs in the body with hypoparathyroidism

A

Calcium levels in the blood will increase

103
Q

How will someone with hypoparathyroidism present

A

Tingling
tetany
cataracts
Chvosteks & trousseaus sign

104
Q

What is Chvosteks sign

A

tap facial nerve illicit cheek twitch

105
Q

What is trousseaus sign

A

BP cuff inflation illicit carpal spasm

106
Q

How do you treat someone with hypoparathyroidism

What if they are experiencing tetnany

A

Vitamin D and Calcium

secure airway, IV calcium gluconate

107
Q

a 28-year-old woman with increased fatigue and a 10-lb weight gain over the last 2 months. She states that she “feels cold” all the time, has decreased energy, and is experiencing worsening constipation. Patient has a tender thyroid, increased TSH, elevated antimicrosomal antibodies, and increased antithyroglobulin antibodies. What is the likely diagnosis

A

Hypothyroidism

108
Q

How will someone with hypothyroid present

A

Cold intolerance, fatigue, constipation, depression, weight gain, bradycardia

Congenital: round face, large tongue, hernia, delayed milestones, poor feeding

109
Q

What will be seen on labs with hypothyroidism

A

High TSH
Low T4

110
Q

How do you treat hypothyroidism

A

Levothyroxine

111
Q

a 72-year-old man presents to the emergency department after a fall outside of church. He complains only of right hip pain, which has been progressively worsening for the past six months. He denies hitting his head during the fall, but according to his wife, he has been complaining of worsening headaches. His temperature is 98.6°F (37°C), blood pressure is 110/60 mmHg, pulse is 80/min, and respirations are 18/min. Examination of the right lower extremity reveals mild crepitus at the hip, appropriate range of motion, adequate distal sensation, and palpable posterior tibial and dorsalis pedis pulses. A review of his laboratories reveals a serum alkaline phosphatase level that is markedly elevated. An X-ray of the hips is ordered, demonstrating bone sclerosis, coarse cortical trabeculation, and cortical thickening. What is the likely diagnosis

A

Pagets

112
Q

What is Paget’s disease

A

bone remodeling disorder that results in the formation of an unorganized mosaic of woven and lamellar bone that is less compact and weaker than the normal bone

113
Q

Where does pages disease typically occur in the body

A

Pelvis
Spine
Skull

114
Q

What may pagets disease lead to

A

osteosarcoma

115
Q

An x-ray shows is preformed and shows lytic lesions and thickened bone cortices. A bone biopsy is preformed to exclude malignancies. What is the likely diagnosis

A

pagets

116
Q

What will be seen on labs with Pagets disease

A

↑ alkaline phosphatase and bone-specific alkaline phosphatase; increased osteoclast activity and osteoblastic activity

117
Q

How do you treat pagets disease

A

Bisphosphonates

118
Q

a 43-year-old female with high blood pressure unresponsive to therapy. She complains of headaches, palpitations, and sweating. She has a history of neurofibromatosis type 1, though without any neurological deficits. She has multiple café-au-lait spots on her body. The ECG demonstrates sinus tachycardia. She is found to be hypertensive to 154/121 mmHg. Her 24-hour urine metanephrines and VMA come back elevated. Her abdominal CT demonstrates an adrenal mass. What is the likely diagnosis

A

Pheochromocytoma

119
Q

What is a pheochromocytoma

A

a catecholamine-secreting adrenal tumor that secretes norepinephrine and epinephrine autonomously and intermittently

120
Q

What is pheochromocytoma associated with

A

neurofibromatosis type 1, MEN 2A/B

121
Q

What are the 5 P’s to look for with a pheochromocytoma

A

Pallor
Perspiration
Palpitations
pressure
Pain (H/A)

122
Q

How do you diagnose a pheo

A

4-hour catecholamines including metabolites (metanephrine and vanillylmandelic acid)
MRI or CT of the abdomen to visualize the tumor

123
Q

What is the pre-op treatment for someone with a pheochromocytoma

A

phenoxybenzamine or phentolamine 7-14 days followed by beta-blocker to control HTN

*For HTN crisis: Nicardipine or nitroprusside

124
Q

a 31-year-old woman who complains of irregular, infrequent menstrual periods. On further questioning, she complains of headaches, fatigue, and breast discharge. She takes ibuprofen only occasionally. The serum prolactin level is 380 μg per L. (prolactinoma). What is the likely diagnosis

A

Pituitary adenoma

125
Q

What is a pituitary adenoma

A

Noncancerous tumors in the pituitary gland that don’t spread beyond the skull

126
Q

What are the types of pituitary adenomas

A

Most common tumors are microadenomas that are functional (hypersecretion of pituitary hormones), nonfunctional, or compressive

*If larger than 1cm–> Macroadenoma

127
Q

What are the signs and symptoms of a pituitary adenoma

A

diminished temporal vision, or bitemporal hemianopsia = MC visual

128
Q

What are the s/sx of a prolactinoma

A

menorrhea, galactorrhea, and headache

129
Q

How are pituitary adenomas diagnosed

A

MRI to look at the sella turcica
+
Endocrine studies: Prolactin, GH, ACTH, TSH, FSH, LH

130
Q

How do you treat a pituitary adenoma

A

dopamine agonists cabergoline and bromocriptine

*if unsuccessful at managing symptoms, transphenoidal resection will be preformed

131
Q

What is the greatest risk factor for thyroid cancer

A

Radiation exposure
MC F 40-60 y/o

132
Q

What is the most common type of thyroid cancer

A

Papillary carcinoma

133
Q

How do you dx thyroid cancer

A

ultrasound – all lesions >1 cm should be biopsied; smaller lesions can be followed/reevaluated if they grow

134
Q

On US, what characteristics are highly suggestive of a malignant thyroid lesion

A

microcalcifications, hypoechogenicity, a solid cold nodule, irregular nodule margins,

*to eval malignancy, a thyroid uptake scan will be preformed
*If uptake is cold… do an FNA of the nodule

135
Q

What is the treatment for thyroid cancer

A

Always involves complete/partial thyroidectomy with chemo and radiation for anaplastic thyroid CA

Recommended TSH level for pt: 1-2.0

Internal Medicine (8 decks)

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