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Endocrinology Flashcards

1
Q

diagnosis for diabetes made by ONE of the following (4 different ways)

A
  1. 2 FASTING glucose greater than or equal to 126
  2. ONE RANDOM glucose greater than or equal to 200 WITH symptoms (polyuria, polydipsia, polyphagia)
  3. ABNORMAL GTT (2-hour GTT with 75G glucose load)
  4. HbA1c greater than 6.5%
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2
Q

STRONGEST indication for screening for diabetes

A

HTN

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3
Q

mechanism for type 2 diabetes

A

excess fat = insulin deficiency

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4
Q

best INITIAL treatment for type 2 diabetes

A
  • DIET
  • EXERCISE
  • WEIGHT LOSS
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5
Q

best INITIAL MEDICAL treatment for type 2 diabetes

A

metformin (biguanide)

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6
Q

metformin MOA

A

blocks gluconeogenesis

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7
Q

main advantages of metformin (2)

A
  • no risk of hypOglycemia

- does NOT increase obesity

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8
Q

metformin CONTRAindications (2 main ones)

A
  • renal insufficiency

- use of contrast

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9
Q

name the sulfonylureas (3)

A
  • glyburide
  • glimepiride
  • glipizide
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10
Q

sulfonylurea MOA

A

increase insulin RELEASE from pancreas

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11
Q

sulfonylurea ADVERSE EFFECTS (2 main ones)

A
  • hypOglycemia

- SIADH

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12
Q

name the dipeptidyl peptidase 4 (DPP-4) inhibitors

A
  • sitaGLIPTIN
  • linaGLIPTIN
  • aloGLIPTIN
  • saxaGLIPTIN
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13
Q

dipeptidyl peptidase 4 (DPP-4) inhibitor MOA

A

block metabolism of INCRETINS

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14
Q

mechanism of incretins (GLP and GIP)

```
GLP = glucagon-like peptide
(GIP = glucose insulinotropic peptide)
~~~

A

increase insulin and decrease glucagon secretion from pancreas

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15
Q

name the thiazolidinediones

A
  • rosiGLITAZONE

- pioGLITAZONE

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16
Q

thiazolidinedione MOA

A

increase PERIPHERAL insulin sensitivity

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17
Q

thiazolidinediones CONTRAindication

A

CHF

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18
Q

name the a-glucosidase inhibitors

A
  • acarbose

- miglitol

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19
Q

a-glucosidase inhibitor MOA

A

block glucose ABSORPTION in intestinal lining

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20
Q

name the insulin secretagogues

A
  • nateGLINIDE

- repaGLINIDE

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21
Q

secretagogue MOA

A

increase insulin RELEASE from pancreas

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22
Q

name the SGLT inhibitors (sodium-glucose transport)

A
  • canaGLIFLOZIN
  • dapaGLIFLOZIN
  • empaGLIFLOZIN
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23
Q

SGLT inhibitor MOA

A

inhibits glucose reabsorption in kidneys

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24
Q

name the GLP (glucagon insulinotropic peptide) analogs

A
  • exenaTIDE

- liragluTIDE

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25
Q

GLP analog MOA

A

slow gastric emptying and promote weight loss

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26
Q

name long-acting insulin

A
  • glargine (daily)
  • detemir (daily, or Q12H)
  • NPH (Q12H)
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27
Q

name short-acting insulin

A
  • aspart
  • lispro
  • glulisine
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28
Q

mechanism for type 1 diabetes

A

underproduction of insulin d/t destruction of pancreas

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29
Q

DKA presentation

A
  • hyperventilation d/t metabolic acidosis
  • “fruity” breath from acetone
  • confusion from hyperosmolar state
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30
Q

best INITIAL tests for DKA

A
  • chemistry
  • arterial blood gas
  • acetone level
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31
Q

marker of ketone production

A

B-hydroxybutyrate

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32
Q

DKA lab findings

A
  • hyperglycemia (> 250)
  • hyperkalemia
  • low bicarb
  • low pH
  • elevated AG
  • elevated acetone, acetoacetate, and B-hydroxybutyrate
  • +/- pseudohyponatremia
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33
Q

INITIAL treatment for DKA

A

NS bolus

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34
Q

once DKA is confirmed, next step in management

A

IV insulin

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35
Q

complications of diabetes:

BP goal

A

less than 140/90

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36
Q

complications of diabetes:

LDL goal

A

diabetes = CAD
less than 100

if BOTH DM AND CAD, less than 70

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37
Q

complications of diabetes:

retinopathy

A

ANNUAL dilated eye exam to detect PROLIFERATIVE RETINOPATHY

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38
Q

treatment for proliferative retinopathy in DM

A

laser photocoagulation

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39
Q

complications of diabetes:

nephropathy

A

microalbumin

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40
Q

if ANY protein is found in urine of DM patient, should be treated with

A

ACEI/ARB

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41
Q

complications of diabetes:

neuropathy

A

ANNUAL foot exam

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42
Q

treatment for diabetic neuropathy

A

gabapentin, or pregabalin

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43
Q

complications of diabetes:

erectile dysfunction

A

no routine screening test: just ask

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44
Q

treatment for erectile dysfunction

A

PDE inhibitor (e.g. sildenafil)

n.b. CI with nitrates

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45
Q

complications of diabetes:

“bloating,” constipation, abdominal fullness, and diarrhea

A

gastroparesis

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46
Q

treatment for gastroparesis

A

metoclopramide, or erythromycin

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47
Q

hypOthyroidism:

  • weight =
  • intolerance =
  • hair =
  • skin =
  • mental =
  • heart =
  • muscle =
  • reflexes =
  • fatigue? =
  • menstrual changes =
A
  • gain
  • cold
  • coarse
  • dry
  • depressed
  • bradycardia
  • WEAK
  • diminished
  • yes
  • yes
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48
Q

hypERthyroidism:

  • weight =
  • intolerance =
  • hair =
  • skin =
  • mental =
  • heart =
  • muscle =
  • reflexes =
  • fatigue? =
  • menstrual changes =
A
  • loss
  • heat
  • fine
  • anxious
  • tachycardia, tachyarrhythmias (e.g. atrial fibrillation)
  • WEAK
  • N/A
  • yes
  • yes
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49
Q

mechanism of weight gain in hypOthyroidism

A

low thyroid = decreased metabolic rate (decreased use of glucose and FFA) = weight gain

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50
Q

best INITIAL tests for hypothyroidism

A
  • free T4 (decreased)

- TSH (increased)

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51
Q

treatment for hypothyroidism

A

levothyroxine (T4 replacement, which gets converted in tissues to T3)

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52
Q

4 forms of hyperthyroid

A
  1. Graves (diffuse toxic goiter)
  2. silent thyroiditis
  3. subacute
  4. pituitary adenoma
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53
Q

Graves disease (diffuse toxic goiter):

  • physical findings
  • RAIU (radioactive iodine uptake)
  • treatment
A
  • eye, skin, and nail findings
  • elevated
  • radioactive iodine ablation (RAI)
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54
Q

silent thyroiditis

  • physical findings
  • RAIU (radioactive iodine uptake)
  • treatment
A
  • none
  • low
  • none
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55
Q

subacute thyroiditis

  • physical findings
  • RAIU (radioactive iodine uptake)
  • treatment
A
  • tender thyroid gland
  • low
  • aspirin
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56
Q

pituitary adenoma

  • physical findings
  • RAIU (radioactive iodine uptake)
  • treatment
A
  • none
  • elevated
  • surgery
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57
Q

ophthalmopathy seen in Graves disease

A
  • exophthalmos (eyes are bulging)

- proptosis (eyelids are retracted)

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58
Q

dermopathy seen in Graves disease

A

pretibial myxedema

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59
Q

nail finding seen in Graves disease

A

onycholysis (separation of nail from nailbed)

60
Q

ACUTE treatment for Graves disease

A

PTU (propylthiouracil), or methimazole

61
Q

definitive treatment for Graves disease

A

radioactive iodine ablation (RAI)

62
Q

treatment for symptoms in Graves disease (tremor, and palpitations)

A

propranolol

63
Q

PTU (propylthiouracil) MOA

A

inhibits thyroid peroxidase:

  • iodination of tyrosine residues of thyroglobulin
  • coupling of DIT and MIT
  • decreases PERIPHERAL conversion of T4 to T3
64
Q

methimazole MOA

A

inhibits thyroid peroxidase:

  • iodination of tyrosine residues of thyroglobulin
  • coupling of DIT and MIT
65
Q

silent thyroiditis may have which antibodies?

A
  • thyroid peroxidase Ab

- antithyroglobulin Ab

66
Q

ONLY cause of hyperthyroidism with ELEVATED TSH

A

pituitary adenoma

67
Q

treatment for pituitary adenoma

A
  • MRI of brain

- surgery

68
Q
  • elevated T4
  • low TSH
  • nonpalpable thyroid d/t atrophy of gland
A

exogenous thyroid hormone abuse

69
Q
  • acute
  • SEVERE
  • life-threatening hypERthyroidism
A

thyroid storm

70
Q

treatment for thyroid storm

A
  • iodine (blocks iodine uptake and hormone release)
  • PTU, or methimazole (blocks thyroxine production)
  • dexamethasone (blocks PERIPHERAL conversion of t$ to T3)
  • propranolol (blocks PERIPHERAL EFFECTS)
71
Q

can you determine etiology thyroid function from presence of goiter?

A

NO, can hypOthyroidism, hypERthyroidism, or normal thyroid

72
Q

next best in management if there is a solitary thyroid nodule

A

fine needle biopsy (FNA)

73
Q

if solitary thyroid nodule shows cancer, next step in management

A

surgery

74
Q

MCC of hypercalcemia

A

PRIMARY hyperparathyroidism

75
Q

other causes of hypercalcemia

A
  • malignancy
  • granulomatous disease
  • vitamin D toxicity
  • thiazide diuretics
  • TB
  • histoplasmosis
  • berylliosis
76
Q

mechanism of PTH (parathyroid hormone) (4 effects)

A
  • reabsorbs Ca++ at DISTAL tubule
  • excretes phosphate at PROXIMAL tubule
  • activates vitamin D
  • reabsorbs Ca++ and phosphate from bone
77
Q

target organ damage from hyperparathyroidism

A
  • kidney stones
  • osteoporosis/osteomalacia/fractures
  • confusion
  • constipation (initially, diarrhea)
78
Q

diagnostic tests for hyperparathyroidism

A
  • PTH (elevated)

- Ca++ (elevated)

79
Q

treatment for hyperparathyroidism

A

surgery

80
Q

when is surgical removal the answer for hyperparathyroidism?

A
  • symptoms
  • renal insufficiency
  • markedly elevated 24H URINE Ca++
  • serum Ca++ more than 12.5
81
Q

acute, severe hypercalcemia presentation

A
  • confusion
  • constipation
  • polyuria/polydipsia (from nephrogenic DI)
  • short QT syndrome
  • renal insufficiency (ATN/kidney stone)
82
Q

treatment for acute, severe hypercalcemia

A
  1. hydration (high volume: 3-4 liters of NS)
  2. bisphosphonate (very potent, but slow)
  3. furosemide (ONLY AFTER hydration)
  4. calcitonin (IF hydration and furosemide do NOT work quickly enough)
  5. steroid (IF etiology is granulomatous disease)
83
Q

mechanism of volume depletion in hypercalcemia

A
  • inhibits ADH effect in collecting duct = nephrogenic DI

- high Ca++ filtration promotes osmotic diuresis

84
Q

causes of hypocalcemia

A
  • surgical removal of parathyroid glands
  • hypomagnesemia (PTH needs magnesium to work)
  • vitamin D deficiency
  • acute hyperphosphatemia (binds Ca++)
  • fat malabsorption (binds Ca++ in gut)
  • PTH resistance (pseudohypoparathyroidism)
85
Q

presentation of severe hypocalcemia

A
  • seizures
  • neural twitching (Chvostek’s and Trousseau’s signs)
  • arrhythmia/prolonged QT
86
Q

treatment for hypocalcemia

A
  • replace Ca++

- vitamin D if deficient, or hypoparathyroidism

87
Q

clinical presentation, regardless of cause, of hyperadrenalism AKA hypercortisolism (Cushing syndrome)

A
  • fat REdistribution
  • easy bruising and striae
  • HTN
  • muscle wasting
  • hirsutism
88
Q

name the 3 sources of Cushing disease

A
  1. pituitary tumor
  2. ectopic ACTH production
  3. adrenal adenoma
89
Q

Cushing disease: pituitary tumor

  • ACTH level
  • effect of high-dose dexamethasone
  • specific test for diagnosis
  • treatment
A
  • high
  • suppression
  • MRI, or petrosal vein sampling
  • removal
90
Q

Cushing disease: ectopic ACTH production

  • ACTH level
  • effect of high-dose dexamethasone
  • specific test for diagnosis
  • treatment
A
  • high
  • NO suppression
  • scan chest and abdomen
  • removal
91
Q

Cushing disease: adrenal adenoma

  • ACTH level
  • effect of high-dose dexamethasone
  • specific test for diagnosis
  • treatment
A
  • LOW
  • NO suppression
  • scan adrenals
  • removal
92
Q

lab findings in hypercortisolism

A
  • hyperglycemia
  • hyperlipidemia
  • osteoporosis
  • leukocytosis
  • metabolic alkalosis (d/t increased urinary loss of H+)
93
Q

mechanism of metabolic alkalosis in hypercortisolism

A

cortisol = mineralocorticoid/aldosterone effects

increased H+ excretion at a-intercalated cell of late distal/early collecting duct

94
Q

best INITIAL diagnostic tests

A
  • 1 mg overnight dexamethasone suppression testing

- 24-hour urine cortisol

95
Q

LOW ACTH level

A

adrenal gland ORIGIN

96
Q

HIGH ACTH level

A

either pituitary gland or from ECTOPIC production

97
Q
  • fatigue
  • anorexia
  • weight loss
  • weakness with hypOtension
  • thin patient with hyperpigmented skin
  • hypERkalemia, with mild metabolic acidosis
  • hyponatremia
  • may have hypoglycemia and neutropenia
A

adrenal insufficiency (Addison disease)

98
Q

MOST ACCURATE test for adrenal insufficiency

A
  • cosyntropin (synthetic ACTH) stimulation test

- CT scan of adrenal glands

99
Q

treatment for ACUTE addisonian (hypoadrenal) CRISIS

A
  • check cortisol level

- IVF and hydrocortisone

100
Q

treatment for STABLE (nonhypotensive) adrenal insufficiency

A

prednisone

101
Q

treatment for adrenal insufficiency, if patient is STILL hypotensive AFTER prednisone

A

fludrocortisone

102
Q
  • HTN
  • hypOkalemia
  • metabolic alkalosis
A

hyperaldosteronism (Conn syndrome)

103
Q

diagnostic tests for hyperaldosteronism

A
  • LOW renin
  • HIGH aldosterone
  • HTN
104
Q

how do you confirm diagnosis for hyperaldosteronism

A

CT scan of adrenal glands

105
Q

treatment for hyperaldosteronism: solitary adenoma

A

surgical resection

106
Q

treatment for hyperaldosteronism: hyperplasia

A

spironolactone

107
Q
  • HA, palpitations, tremors, anxiety, flushing (all nonspecific)
  • EPISODIC HYPERTENSION
A

pheochromocytoma

108
Q

best INITIAL tests for pheochromocytoma

A
  • serum and urinary catecholamine levels (HIGH)

- serum free metanephrine and VMA levels

109
Q

MOST ACCURATE test for pheochromocytoma

A

CT or MRI of adrenal glands

110
Q

what test is used to detect metastatic disease in pheochromocytoma?

A

MIGB scan

111
Q

FIRST treatment used for pheochromocytoma

A

phenoxybenzamine (alpha blockade)

112
Q

treatment for pheochromocytoma AFTER a-blocker

A

propranolol

113
Q

definitive treatment for pheochromocytoma

A

surgery

114
Q

ALL forms of congenital adrenal hyperplasia (CAH)

A
  • elevated ACTH
  • low aldosterone
  • low cortisol
  • treatable with prednisone
115
Q

name the 3 kinds of CAH

A
  • 21-hydroxylase deficiency
  • 11-hydroxylase deficiency
  • 17-hydroxylase deficiency
116
Q

MOST COMMON TYPE of CAH

A

21-hydroxylase deficiency

117
Q
  • hirsutism (virilization)

- HYPOTENSION

A

21-hydroxylase deficiency

118
Q

diagnostic test for 21-hydroxylase deficiency

A

increased 17-hydroxyprogesterone level

119
Q
  • hirsutism (virilization)

- HYPERTENSION

A

11-hydroxylase deficiency

120
Q
  • HYPERTENSION ONLY

- NO hirsutism (virilization)

A

17-hydroxylase deficiency

121
Q

MC pituitary tumor

A

prolactinoma

122
Q

presentation for prolactinoma: men

A
  • impotence
  • decreased libido
  • gynecomastia
  • presents LATE
  • MORE LIKELY to have signs of mass effect (HA, and visual disturbance)
123
Q

presentation for prolactinoma: women

A
  • amenorrhea
  • galactorrhea in ABSENCE of pregnancy
  • presents EARLY
124
Q

MOST ACCURATE test for prolactinoma

A

MRI of brain

125
Q

best INITIAL treatment for prolactinoma

A
  • dopamine agonist (bromocriptine, or cabergoline)

- surgery, if medicine doesn’t work

126
Q
  • growth hormone-secreting adenoma in pituitary

- excess production of growth hormone (GH)

A

acromegaly

127
Q

acromegaly presentation

A
  • enlarged head, fingers, feet, nose, and jaw

- intense sweating (enlarged sweat glands)

128
Q

acromegaly also causes

A
  • joint abnormalities
  • amenorrhea
  • cardiomegaly
  • HTN
  • colonic polyps
  • DM
129
Q

best INITIAL test for acromegaly

A

insulinlike growth factor (IGF)

130
Q

which test is NOT done first for acromegaly, and why?

A
  • growth factor

- bc max secretion is in middle of night and has short half-life

131
Q

MOST ACCURATE test for acromegaly

A

GH suppression with glucose EXCLUDES acromegaly

132
Q

treatment for acromegaly

A

transsphenoidal resection

133
Q

somatostatin analog that has some effect on inhibiting GH release

A

octreotide

134
Q

dopamine agonists that inhibit GH

A

bromocriptine, and cabergoline

135
Q

GH receptor antagonist

A

pegvisomant

136
Q

primary amenorrhea causes

A
  1. Turner syndrome

2. testicular feminization

137
Q

secondary amenorrhea causes

A
  1. pregnancy (MCC)
  2. exercise
  3. extreme weight loss
  4. hyperprolactinemia
  5. polycystic ovary syndrome (PCOS)
138
Q
  • short stature
  • webbed neck
  • wide-spaced nipples
  • scant pubic and axillary hair
  • XO karyotype
A

TURNER SYNDROME

139
Q
  • genetically male, but looks/acts/feels female

- does not menstruate (no cervix, fallopian tubes, ovaries, or top 1/3 of vagina)

A

testicular feminization

140
Q
  • obesity
  • amenorrhea
  • hirsutism
  • increased adrenal androgens
A

PCOS

141
Q

treatment for glucose intolerance and DM in PCOS

A

metformin

142
Q

treatment for virilization in PCOS

A

spironolactone

143
Q
  • tall male
  • insensitivity of FSH and LH receptors in testicles
  • XXY karyotype
  • VERY HIGH FSH and LH levels, BUT NO testosterone is produced from testicles
A

Klinefelter’s syndrome

144
Q

treatment for Klinefelter’s syndrome

A

testosterone

145
Q
  • ANOSMIA (key to diagnosis)
  • hypogonadism
  • LOW GnRH, FSH, and LH
A

Kallman’s syndrome

Step 3 (1 decks)

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