Endocrine ABIM Flashcards
1
Q
Hypopituitarism causes (3 most common)
A
- Pituitary Tumor
- Pituitary surgery
- Cranial irradiation
2
Q
Hypopituitarism:
Pituitary Apoplexy (bleeding within organ):
cause, symptoms, treatment
A
- Cause: Pituitary hemorrhage or infarction
- Sx: sudden headache, visual change, opthalmoplegia, AMS
- Tx: Acute admin of glucocorticoids until adrenal insuffiency r/o; May also require neurosurgical decompression
3
Q
Hypopituitarism:
Postpartum pituitary necrosis (Sheehan syndrome)
~ cause, symptoms
A
- Cause: silent pituitary infarction usually associated with obstetric hemorrhage and hypotension.
- Sx: Acutely, vascular collapse.
- More commonly, amenorrhea, inability to lactate, fatigue.
4
Q
Hypopituitarism:
Lymphocytic hypophysitis: what is it?
A
- It causes hypopituitarism, and possibly sx of mass lesion.
- Most cases occur during or after pregnancy.
5
Q
Hypopituitarism:
Signs of pituitary mass effect
A
- Headache
- Loss of peripheral vision
6
Q
Hypopituitarism: Symptoms of anterior hypopituitarism
FSH/LH deficiency - symptoms/testing/findings
A
- FSH/LH: amenorrhea, loss of libido, ED
- Test: depressed FSH, LH, estradiol or testosterone
7
Q
Hypopituitarism:
Symptoms of anterior hypopituitarism:
ACTH deficiency -symptoms/tests/findings
A
- Sx: fatigue, N/V, Wt loss, Abd pain
- Tests: Low cortisol/depressed ACTH;
- depressed response of 11-deoxycortisol and cortisol to metyrapone
- positive cortisol response to ACTH
8
Q
Hypopituitarism: Symptoms of anterior hypopituitarism:
- TSH deficiency - symptoms/tests/findings
A
- TSH: cold intolerance, weight gain, constipation
- Tests: depressed free T4 and TSH
9
Q
Hypopituitarism: Symptoms of anterior hypopituitarism
- GH deficiency - symptoms/tests/findings
A
- GH: loss of muscle mass
- Tests: depressed IGF-1 (serum marker of GH)
- diminished response to insulin tolerance test ~ insulin induced hypoglycemia
10
Q
Hypopituitarism: Symptoms of anterior hypopituitarism:
- DI secondary to ADH deficiency
- Symptoms
- Tests
A
- ADH/DI: polyuria, polydypsia, nocturia
- Tests: Urine osmo < 200 does not increase with water deprivation test
- Positive desmopressin challenge (urine concentrates)
- If positive, order MRI of pituitary
11
Q
Hypopituitarism: Symptoms of anterior hypopituitarism
Visual Changes
A
- Bitemporal loss of vision
- (mass effect on optic chiasm)
12
Q
Hypopituitarism: Symptoms of anterior hypopituitarism: prolactin level
A
Level may be elevated from loss of tonic inhibition ~ hyperprolactinemia
13
Q
Hypopituitarism Treatment
A
- Replace hormone deficiency appropriately
- Hydrocortisone for adrenal insufficiency
14
Q
Hypopituitarism Treatment:
- Central Hypothyroid Tx
A
- Thyroxine dosing based on serum T4 rather than TSH level
- T4 replacement only after hypoadrenalism r/o or treated
15
Q
Pituitary Adenoma: micro vs macro
A
benign tumors; microadenoma < 10mm; macroadenoma > 10mm
16
Q
Pituitary Adenoma: 2 ways they become symptomatic
A
- mass effect causing hypopituitarism ~ ant pit hormone deficiencies + headaches/visual field disturbances, CN dysfn.
- endocrine hyperfunction caused by excess secretion by the tumor
17
Q
Pituitary gland is diffusely enlarged in these 2 situations
A
Normal Pregnancy & Untreated Primary Hypothyroidism
18
Q
Pituitary Adenoma: Galactorrhea/Amenorrhea -
- Think this
- Order this…
A
- Think this: Prolactinoma
- Order this: Serum Prolactin Level
19
Q
Pituitary Adenoma:
Enlargement of hands, feet, nose, lips, or tongue; increased spacing between teeth
- Think think
- Order this…
A
- Think this: Acromegaly
- Order this: Serum IGF-1, OGTT (fails to suppress GH)
20
Q
Pituitary Adenoma:
Proximal muscle weakness, facial rounding, centripetal obesity, purple striae, diabetes mellitus, and hypertension
- Think this
- Order this
A
- Think this: Cushing Disease
- Order this:
- 24-hour urine cortisol excretion
- dexamethasone (manmade cortisol) suppression test (suppresses)
- late night salivary cortisol level (elevated)
- serum ACTH level (elevated or inappropriately normal)
21
Q
Pituitary Adenoma: Goiter and Hyperthyroidism
- Think this
- Order this
A
- Think this: TSH-secreting adenoma (rare)
- Order this: TSH normal or elevated; increased T4
22
Q
Pituitary Adenoma: General Testing Rules
- Who to test?
- If pituitary source indicated, what do you order?
- If mass effect, what do you order?
- What syndrome do you always eval for?
A
- Test all patients w/incidentally discovered pituitary adenoma for hormone hypersecretion
- Order MRI if testing indicates hormonal hypersecretion from pituitary source
- If mass effect is presenting sx, obtain MRI first, endocrine testing later (headache/visual)
- Eval pts with at least 1 component of MEN1 and family hx of MEN1 for a pituitary adenoma (usually hyperparathyroidism)
23
Q
Pituitary Adenoma:
Nonprolactinoma causes of hyperprolactinemia
A
- Usually level < 150ng/mL
- Psychotropic agents, TCAs, Antiseizure meds, Metoclopramide, Domperidone, CCBs, Methyldopa, Opiates, Protease Inhibitors
- Check TSH level (hypothyroidism can cause it)
24
Q
Pituitary Adenoma:
Treatment for:
- women with microprolactinoma/normal menses
- patients with nonfunctioning microadenomas (< 10mm)
A
Observation
25
Pituitary Adenoma:
* Treatment for symptomatic prolactinoma
* Dopamine Agonist (cabergoline preferred to bromocriptine)
* consider withdrawal of RX if prolactin level normalized and mass no longer visible on imaging
* Close follow up ~ recurrence rates up to 50%
26
Pituitary Adenoma:
Treatment for adenomas secreting GH, ACTH, TSH; Tx for adenomas w/mass effect, visual field disturbance, Tx for hypopituitarism and Tx for prolactinomas unresponsive to dopamine agonist
Surgery
27
DI: what is it? central vs nephrogenic
Inability to concentrate urine due to insufficient arginine vasopressin (AVP, ADH) release (central) or activity (nephrogenic)
28
DI: patient history includes...(6 likely scenarios)
1. recent head trauma 2. pituitary mass lesion 3. evidence of anterior hypopituitarism 4. h/o infiltrative disorder (such as sarcoidosis) 5. kidney disease (tubulointerstitial disease) 6. meds such as lithium
29
DI: symptoms/signs of central DI
cravings for water or cold liquids, urinary frequency, nocturia, and, depending on mass effect of pituitary tumor, visual field deficits
30
DI: initial testing/confirmation testing
Initial: 1. urine osmo \< 200 mOsm/kg 2. inability to concentrate urine during water deprivation test Confirmation: 1. desmopressin challenge test (+) urine concentrates = central, order MRI of pituitary; (-) urine does not concentrate = nephrogenic, order u/s kidneys
31
DI: Tx DI after neurosurgery or head trauma
If unable to drink, 5% dextrose in 0.45% sodium chloride IV; Add desmopressin if urine output high or hypernatremia develops
32
DI: Tx DI Chronic Central DI
Intranasal or oral desmopressin
33
DI: Lithium Induced nephrogenic DI
Stop lithium or add amiloride (diuretic)
34
DI: Non-drug induced nephrogenic DI
Thiazide diuretic and salt restriction
35
Empty Sella Syndrome: diagnosis
MRI: pituitary gland not visualized or is excessively small
36
Empty Sella Syndrome: causes
increased CSF entering and enlarging sella; tumor; previous pituitary surgery, radiation, infarction
37
Empty Sella Syndrome: testing in asymptomatic, testing in symptomatic
Asymptomatic: obtain cortisol, TSH, and free or total T4 Symptomatic: testing of all pituitary hormones
38
Hyperthyroidism: Thyrotoxicosis
any cause of hormone excess, including primary, secondary, destructive thyroiditis, excessive exogenous ingestion
39
Hyperthyroidism: destructive thyroiditis causes & testing
causes: subacute (de Quervain), silent (painless), postpartum ~ permanent hypothyroidism may follow all; testing: decreased TSH, normal T3 and T4, no symptoms, decreased or no RAIU uptake
40
Hyperthyroidism: Subacute (de Quervain): presentation, testing
nonautoimmune inflammation presents with firm and painful thyroid gland
41
Hyperthyroidism: Postpartum
painless autoimmune occurring within a few months of delivery
42
Hyperthyroidism: defined (\* = most common)
disorders of increased thyroid hormone production and release ~ destructive thyroiditis, \*Graves disease, \*thyroid nodules, toxic multinoduar goiter
43
Hyperthyroidism: signs/symptoms
nervousness, emotional lability, increased sweating, heat intolerance, palpitations, increased defecation, weight loss, menstrual irregularity, tachycardia, lid lag, fine tremor, muscle wasting, proximal muscle weakness, hyperreflexia
44
Hyperthyroidism: Graves specific findings
goiter, opthalmopathy (proptosis, chemosis, extraocular muscle palsy) and pretibial myxedema; TSH receptor abs - do not need checked unless diagnosis unclear
45
Hyperthyroidism: Thyroid Storm - what? why? testing?
what? life threatening hyperthyroidism associated with cardiac decompensation, fever, delirium, and psychosis. why? following surgery, infection, iodine load (contrast), untreated grave's. diagnosis? clinical diagnosis; levels are not indicative
46
Hyperthyroidism: surreptitious use of thyroid hormone
Suppresses thyroglobulin levels (useful measurement to r/o this cause)
47
Hyperthyroidism: testing - what to order?
order TSH, Free T4 levels; it TSH suppressed but T4 is normal, order free T3 to diagnose T3 toxicosis (rare)
48
Hyperthyroidism: testing - 1: tsh low; free T4 high; 2: tsh low; T3 high; normal fT4 3: low TSH, normal T3 and free T4, w/o sx 4: high TSH, high T3, high free T4
1. Primary hyperthyroidism 2. Primary hyperthyroidism w/T3 toxicosis 3. Subclinical hyperthyroidism 4. Secondary hyperthyroidism from pituitary tumor
49
Hyperthyroidism testing - RAUI uptake: 1. diffuse homogenous increased uptake 2.patchy areas of increased uptake 3.focal increased uptake with decreased uptake elsewhere in gland 4.decreased or no uptake
1. Grave's 2.Toxic Multinodular Goiter 3.Solitary adenoma 4. Iodine load (IV contrast or Amiodarone), Thyroiditis (silent, subacute, postpartum, amiodorone induced), Serruptitious ingestion of excessive thyroid hormone
50
Hyperthyroidism: Treatment options (3)
1. Radioactive iodine therapy (may lead to painful radiation thyroidits and sialadenitis, not used during pregnancy or breastfeeding), frequently restores euthyroidism 2. Antithyroid drugs (may lead to drug free remission in 30-50% of Grave's or bridge to more definitive therapy), 3. Thyroidectomy (when definitive therapy required in patient with severe graves opthalmopathy or if RAI or antithyroid drugs can't be given or aren't tolerated or if large goiter causing local sx)
51
Hyperthyroidism: Antithyroid drugs ~ 1. Methimazole - used for/watch for 2. Propylthiouracil - used for/watch for
1. Methimazole: 1st line antithyroid for most pts; watch for agranulocytosis, drug rash, hepatotoxicity 2. PPU: 1st trimester, thyroid storm (inhibits T4 to T3 conversion); watch for: agranulocytosis, drug rash, frequent hepatotoxicity
52
Hyperthyroidism: Treatment 1. Sympathetic nervous system symptoms 2. Prep for thyroidectomy 3. Severe Graves opthalmopathy 4. Pregnancy 1st trimeser; 2nd/3rd trimester
1. SNS: Atenolol or Propanolol 2. Thyroidectomy Prep: Methimazole 3. Severe Graves optho: MMZ or Thyroidectomy \*Avoid RAI (may worsen unless pretreated with glucocorticoids) 4. Pregnancy: 1st trimester PPU; 2nd/3rd trimester: MMZ (RAI contraindicated)
53
Hyperthyroidism: Treatment 5. Subclinical Hyperthyroidism 6. Subacute Thyroiditis 7. Suspicious Nodule (malignancy) 8. Thyroid Storm
5. Methimazole if TSH \< 0.1 6. NSAIDS, glucocorticoids for pain mgmt; atenolol or propanolol for sx; levothyroxine for sx hypothyroidism; repeat thyroid studies 4-6 mos; 50% normalize without treatment
54
Hyperthyroidism: Treatment 7. Suspicious Nodule (malignancy) 8. Thyroid Storm
7. FNAB followed by thyroidectomy if malignant 8. PPU (preferred) or MMZ, idoine-potassium solutions, glucocorticoids and B blockers
55
Hyperthyroidism: PPU or MMZ + fever or sore throat?
Agranulocytosis until proven otherwise
56
Hypothyroidism: Signs/Symptoms
weakness, lethargy, fatigue, depression, poor concentration, myalgia, cold intolerance, constipation, weight gain, menstrual irregularity or menorrhagia, carpal tunnel syndrome
57
Hypothyroidism: Exam findings
Bradycardia, Hypothermia, diastolic hypertension, husky voice, goiter, cool dry skin, brittle hair, edema, delayed relaxation phase of DTRs
58
Hypothyroidism: Causes (6)
1. chronic lymphocytic thyroiditis (Hashimotos) 2.thyroidectomy 3.previous radioactive iodine ablation 4.history of external beam radiation to the neck 5.medication induced (lithium, interferon alfa, ILK2, amiodarone) 6.central (pituitary disease, previous surgery, radiation to sella)
59
Hypothyroidism: Myxedema coma - defined - caused by - precipitated by
defined: severe hypothyroidism leading to decreased mental status, hypothermia, hypotension, bradycardia, hyponatremia, hypoglycemia, hypoxemia, hypoventilation. occurs with: severe, long-standing, untreated hypothyroidism; may pre precipitated by: acute medical or surgical event or administration of opiates
60
Hypothyroidism: Testing
TSH, free T4; T3 usually not necessary; Antithyroid peroxidase associated w/hashimotos
61
Hypothyroidism: Non thyroidal illness
Low/Normal Free T4 Low TSH (initially) then elevated TSH (recovery phase) Normalization of levels 4-8 weeks after recovery No treatment required
62
Hypothyroidism: 1. High TSH; Low free T4 2. High TSH; Normal T4 3. Low TSH, Low free T4
1. Primary hypothyroidism 2. Subclinical hypothyroidism 3. Secondary (central) hypothyroidism; hypopituitarism
63
Hypothyroidism: How do you treat? Who do you treat?
Levothyroxine; treat subclinical w/serum TSH \> 10 or who are pregnant or are trying; Also thyroxine demand increases by 30-50% during pregnancy
64
Hypothyroidism: 4 causes of decreased levothyroxine absorption
1. Celiac disease 2. Calcium 3. Iron 4. PPIs
65
Hypothyroidism: Levothyroxine dosing 1. Age \< 60 2. Age \> 60 3. Heart disease
1. \< 60: Begin full dose 2. \> 60: Begin at 25 - 50; increase by 25 q6 weeks 3. \<3: Begin at 12.5 - 25
66
Hypothyroidism: Levothyroxine dosing 4. Myxedema coma 5. Pregnancy
4. Begin levothyroxine & hydrocortisone ~ give until adrenal insufficiency ruled out 5. increased by 30% initially; check levels frequently
67
Thyroid nodules: 1st step; what does normal mean? what does low mean? 2nd step; 3rd step
1st: TSH level; commonly normal aka not helpful 2nd: Low TSH level suggests benign 3rd: If low, order radioisotope scan to confirm diagnosis and r/o additional non functioning nodules w/i a multinodular goiter
68
Thyroid nodules: Eval MNGoiter for compressive symptoms (name 3) and further testing as needed (name 4)
1. Dysphagia 2. Hoarseness 3. Dyspnea (tracheal compression from substernal goiter) Testing: Barium Swallow; direct visual cord visualization, spirometry w/flow volume loops and/or CT chest
69
Thyroid nodules: FNAB is indicated for...
1. All thyroid nodules \> 1 cm with suspicious features & normal TSH 2. Nodules \< 1 cm with risk factors for thyroid cancer or suspicious u/s characteristics
70
Thyroid nodules: Management/Treatment 1. Observe who? how? 2. RAI or surgery for who? 3. Surgery for who?
1. Observation: periodic u/s for benign nodules 2. RAI or surgery: hyperfunctioning solitary thyroid nodules with RAI ablation or hemithyroidectomy 3. Surgery: continued nodule growth, malignant cytology, large MN goiters w/compressive sx
71
Hypercortisolism Syndrome: what is it? most common causes?
defined: Ongoing exposure to excessive glucocorticoids MCC: iatrogenic, endogenous (ACTH dependent or non)
72
Hypercortisolism: ACTH dependent
-defined
causes
defined by: inappropriately elevated or normal ACTH levels in relation to cortisol level
1. ACTH secreting pituitary adenoma (cushing disease)
2. ACTH secreting carcinomas and carcinoid tumors
73
Hypercortisolism: ACTH independent
defined by: low or normal ACTH levels in relation to cortisol level | 1. adrenal adenoma 2. adrenal carcinoma
74
Hypercortisolism: Clinical Findings highly specific for Cushing Syndrome
centripetal obesity
facial plethora
supraclavicular or dorsocervical (buffalo hump) fat pads
wide \> 1 cm violaceous striae
75
Hypercortisolism: Testing
First Line Diagnostic Studies
* 1mg overnight dexamethasone suppression test (failure to suppress serum cortisol to \< 3)
* if failure to suppress, order ACTH level
* 24 hour urine cortisol level (elevated)
* late night salivery cortisol level (elevated
76
Hypercortisolism:
1mg overnight dexamethason suppression test fails to suppress serum cortisol \> 3, what's next?
* Order ACTH level to differentiate ACTH-dependent from ACTH-independent hypercortisolism
* If Morning ACTH elevated \> 20:
* Order Pituitary MRI or CT
* If Morning ACTH suppressed or normal (\<5):
* Order Adrenal CT
77
Hypercortisolism:
Treatment for Cushing Syndrome
Treatment of low bone density caused by hypercortisolism
* Treatment for Cushing Syndrome: Surgical resection or adrenal gland, pituitary gland, or ectopic tumor
* Treatment for low bone density: Bisphosphanates
78
What do you do if
* 1mg Dexamethasone fails to suppress serum cortisol \< 3
* ACTH is evelated \> 20
* MRI or CT shows no pituitary tumor
1. Order high dose (8mg) dexamethasone suppression test to differentiate between pituitary and ectopic tumor ACTH production
2. If high dose does not suppress cortisol production: ectopic tumor is releasing ACTH ~ SCLC, bronchial carcinoid, pheochromocytoma, medullary thyroid carcinoma.
1. Order Chest CT
3. If high dose does suppress pituitary ACTH production and adrenal cortisol secretion: the source is pituitary
1. Obtain intrapetrosal sinus sampling
79
Adrenal Incidentaloma: Diagnosis
VS
Adrenal malignancy
Mass \> 1 cm discovered incidentally
VS
Adenomas \> 6cm; common in patients with known
nonadrenal malignancy
80
Adrenal Incidentaloma:
* Testing goals
* Asymptomatic patients
* Patients with HTN and hypoK
Goals:
1. Is adenoma functioning? Is it malignant?
* Asymptomatic patients: 1mg dexamethasone suppression test and measurement of 24 hour urine levels of metanephrines and chatecholamines
* Htn & HypoK: above plus plasma aldosterone and plasma renin activity
81
Adrenal Incidentaloma: Treatment
Treatment:
* Adrenal masses \< 4cm: monitored radiographically; repeat imaging in 6-12 months and screen for hormonal hypersecretion
* Adrenal masses \> 4cm or hyperfunctioning tumors: surgery may be recommended
82
Hypoadrenalism: Diagnosis
* Primary
* Secondary
Diagnosis
1. Primary: caused by disease of adrenal glands (Addisons)
* loss of cortisol, aldosterone, adrenal androgens
1. Secondary: caused by disease of pituitary gland
* loss of cortisol and adrenal androgen deficiencies (aldosterone synthesis is not ACTH-dependent)
83
Hypoadrenalism: Causes
1. Most common cause of primary insufficiency
2. Most common cause of secondary insufficiency
1. MCC Primary insuffiiciency: Autoimmune adrenalitis
* also look for type 1 diabetes, hypothyroidism, and vitiligo
2. MCC Secondary insufficiency: Glucocorticoid use
(hypothalamic-pituitary suppression)
* look for patients who recently discontinued glucocorticoid therapy or did not increase glucocorticoid dose in times of stress
84
Hypocortisolism: Testing
* 8AM serum cortisol \< 3ug/dL diagnoses cortisol deficiency
* ACTH level to differentiate primary vs secondary
* Morning ACTH \> 20: Adrenal CT
* Morning ACTH \< 5: Pituitary MRI
* 8AM serum cortiosl \> 18ug/dL excludes diagnosis
* For nondiagnostic values, select stimulating testing with ACTH (cosynotropin).
* A stimulated serum cortisol \> 18 excludes adrenal insufficiency.
85
Hypocortisolism: Treatment
1. Acute Adrenal Insuffiency
2. Standard Treatment
3. Stress/Surgery dosing
4. Primary Adrenal Insufficiency
1. Acute: high dose (4mg) dexamethasone and IV saline before obtaining cortisol, ACTH levels (dexa does not effect serum cortisol assay)
2. Standard: Hydrocortisone 10-30mg/d
3. Increase dose 2-10 times standard replacement
4. Primary: Fludrocortisone; not reqd if hydrocortisone dose is \>40
86
Pheochromocytoma: Diagnosis
1. What is it?
2. What do they secrete?
3. SIgns/Symptoms
1. Rare tumors arising from chromaffin cells of adrenal medulla
2. They secrete biogenic amines: norepinephrine, epinephrine, dopamien and their metabolites
3. Htn, Headache, Hypermetabolism
Hyperhidrosis, Hyperglycemia, Hypocalcemia
Hypotension during anesthesia induction
87
Pheochromocytoma:
Associations
* MEN2
* Von Hippel-Lindau
* Neurofibromatosis 1
88
Pheochromocytoma: Testing
* Low clinical suspicion
* High clinical suspicion
* If biochemical tests are positive
* Low pretest probability: 24 hour measurements of metanephrines and chatecholamines
* Higher clinical suspicion: Plasma measurements of metanephrines
* If positive, MRI or CT of abd/pelvis
* If scans MRI or CT neg 131I or 123 I-MIBG scan may aid in localization
89
Pheochromoctyoma: Treatment
1. Treatment of choice
2. To control BP preoperatively
3. To maintain intravascular volume
4. Treatment for intraoperartive hypertensive crisis
1. Surgery
2. Phenoxybenzamine
3. IV NS
4. Nitroprusside or Phentolamine
90
Primary Hyperaldosteronism:
Characteristic findings/scenarios
1. difficult-to-treat or resistant hypertension
2. unprovoked or difficult to treat hypokalemia
3. family history of hyperaldosteronism
91
Hyperaldosteronism: Testing
1. Simultaneous measurements of plasma aldosterone and renin
* Plasma aldosterone-plasma renin \>20 with plasma aldosterone \> 15 strongly suggests primary hyperaldosteronism
92
Hyperaldosteronism: Confirmation Testing
* Diagnosis confirmed by demonstrating nonsuppressibility of elevated plasma aldosterone in response to high salt load given IV or PO
* In patients w/o adneoma: aldostrone level is supporessed \< 5
* Once autonomous hyperaldosteronism is diagnosed, order CT or MRI of adrenal glands
* Adrenal V sampling is needed before surgery
\* Testing can be done in pts receiving treatment with all antihypertensives except spironolactone and eplerenone (antagonize aldosterone recepter)
93
Hyperaldosteronism: Treatment
* Adrenal Hyperplasia: Spironolactone or Eplerenone
* Aldosterone producing adenoma: Laprascopic adrenalectomy
* Additional HTN control: Add thiazide diuretic
94
Primary Amenorrhea: definition
* 50% due to?
* 15% due to?
* 4 most common causes of primary amenorrhea
definition: failure of menstruation (never occured)
* 50% due to chromosomal disorders
* 15% have anatomic abnormality
1. Turner syndrome,
2. Hypothalamic/pituitary disorders
3. Androgen-resistnace syndromes
4. PCOS
95
Primary Amenorrhea: TESTING
Most important studies:
1. Pregnancy Test
2. Karyotype
3. FSH, LH, TSH, Prolactin Level
4. Pelvic ultrasound
96
Primary Amenorrhea: 4 MCCs
Turner Syndrome
* Karyotype
* Characteristics
* Karyotype: 45 XO
* Lack of secondary sexual characteristics
* Growth Retardation
* Webbed Neck
* Frequent Skeletal abnormalities
97
Primary Amenorrhea: 4 MCCs
Hypothalamic/Pituitary disorders
Functional: stress, excessive exercise, weight loss
Developmental defects of cranial midline structors, tumors, or infiltrative disorders (sarcoidosis)
98
Primary Amenorrhea: 4 MCCs
Androgen-resistance syndromes
* Karyotype
* Characteristics
* XY Karyotype
* Absence of or minimal pubic and axillary hair
* Shallow vagina
* Labial Mass (testes)
99
Primary Amenorrhea: 4 MCCs
PCOS
most commonly causes secondary ammenorrhea but may cause primary amenorrhea
100
Secondary Amenorrhea:
Diagnosis
* Look for abscence of menstruation for three cycles
* or 6 consecutive months in women with previous menstrual flow
101
Secondary Amenorrhea: Testing
* Test all women for
* Look for:
* Assess hormonal status with:
* Test all women with secondary amenorrhea for pregnancy (most commong cause)
* Look for: structural causes (such as Asherman syndrome)
* If no structural cause, asess hormonal status with: estradiol, FSH, LH, TSH and prolactin levels
102
Secondary Amenorrhea:
Hypogonadotrophic Hypogonadism
* Estradiol level
* FSH level
* LH level
* 4 Causes
* Low estradiol
* Low or inappropriately normal FSH and LH
1. Hypothyroidism
2. Hyperprolactinemia
3. Hypothalamic (stress, weight loss, exericse)
4. Pituitary (tumor, sheehan syndrome)
103
Secondary Amenorrhea: Hypogonadotrophic hypogonadism
What test is performed in these patients?
Progesterone Challenge Test
* No bleeding following a progesterone challenge indicates low estrogen because of hypothalamic hypogonadism
* Measure estradiol to confirm
* Bleeding followign progesterone challenge indicates a normal estrogen state and suggests possible hyperandrogenism (e.g. PCOS)
104
1. Low estradiol + Low/Normal FSH and LH =
1. 4 causes
2. Low estradiol and Elevated FSH and LH =
1. 3 causes
1. Hypogonadatrophic Hypogonadism
1. hypothyroidism, hyperprolactinemia, hypothalamic (stress, weight loss, exercise)
2. Hypergonadotrophic Hypogonadism
1. premature ovarian insuffiency (autoimmune), chemotherapy, pelvic radiation
105
Common Causes of Secondary Amenorrhea:
PCOS
* characteristics
* evaluation
* characteristics:
* ovulatory dysfunction
* evidence of hyperandrogenism
* polycystic ovaries on ultrasonagraphy
* evaluation:
* mild elevation in testosterone & DHEAS
* (not needed for diagnosis)
106
Common causes of Secondary Amenhorrhea
Hyperprolactinemia
* Characteristics:
* May be associated with:
* Related to/Causes
* Evaluation
* Rule out
* Order
* Associated with galactorrhea
* Related to medications, tumors that secrete prolactin or compress pituitary stalk, h/o cranial radiotherapy
* First rule out hypthyroidism
* If TSH is normal and serum prolactin level \> 100, obtain MRI to diagnose tumor
107
Common causes of Secondary Amenhorrhea
Hypothalamic Amenorrhea
* Characteristics/causes
* Evaluation
Characteristics:
* Most commonly functional (related to stress, weight loss, excessive exercise)
* Low or normal LH level, and low estradiol level
108
Common Causes of Secondary Amenorrhea
Hypothyroidism
* Cause
* Evaluation
Causes secondary increase in serum prolactin levels
High TSH, high prolactin
109
Secondary Amenorrhea
Adrenal Tumor
* Signs
* Evaluation
* Signs of hyperandrogenism and virilzation, usually acute onset and severe
* Decreased LH and FSH, increased or normal estradiol, and increased testosterone and DHEAS levels
110
Secondary Amenorrhea
Sheehan Syndrome
* History of
* Eval
* History of difficult delivery (blood loss, hypotension) and inability to breastfeed
* Varying levels of panhypopituitarism
111
Secondary Amenorrhea
Asherman Syndrome
(Uterine adhesions)
* History of
* Eval
* previous d&c amenorrhea caused by fibrous uterine scarring
* normal LH and estradiol levels
* no response to estrogen and progesterone challenge
112
Secondary Amenorrhea:
* Treatment
* Prevent osteoporosis
* Hypothalamic amenorrhea
* Treat underlying disorder
* Prevent osteoporosis with estrogen/progesterone replacement until menstruation returns to normal or age 50 years
* For hypothalamic anemorrhea: reduced exercise, improved nutrition, attention to emotional needs
113
PCOS
* Most common cause of ___ with \_\_\_
* Diagnosis requires two of the following:
* most common cause of hirsutism with oligomenorrhea
1. ovulatory dysfunction (amenorrhea, oligomenorrhea, infertility)
2. labratory or clinical evidence of hyperandrogenism (hirsutism, acne)
3. ultrasonagraphic evidence of polycystic ovaries
114
PCOS: Testing
* PCOS IS A CLINICAL DIAGNOSIS
* Insulin resisrance is an important features of this disorder as is being overweight or obese
* Mild elevation in testosterone and DHEAS levels and LH/FSH ratio greater than 2:1 are typical
\* do not routinely order testosterone or DHEAS b/c PCOS is a clinical diagnosis and lab eval is only necessary when androgen producing neoplasm must be ruled out (androgen secreting ovarian or adrenal tumor)
\* this should be suspected in rapidly progressive hirsutism or virilization
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PCOS: Treatment
* Lifestyle modification: reduce weight, control abdominal obesity, restore insulin sensitivity
1. If fertility is not desired: first line treatment of hirsutism and regulation of menses is OCP. Spironolactone can be added if hirsutism remains problem.
2. If fertility is disired, ovluation induction can be brought about with clomiphene citrate or letrozole
116
Infertility: Diagnosis
Defined: inability to conceive after 1 year of intercourse without contraception \< 35 years and after 6 months in women \> or = 35
* Regular menses is correlated with regular ovulation
* If oligomenorrhea is present, eval like secondary amenorrhea
* Consider structural abnormalities and eval with pelvic u/s
* Semen analysis can be perforemd at any time
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Male Hypogonadism: Diagnosis
* Decreased production of
* May be ___ or \_\_\_
* Characteristic findings
* Defined: When sperm or testosterone production is decreased
* May be primary or secondary
* Characteristic findings: fatigue, decreased strength, poor libido, ED, gynecomastia
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Male Hypogonadism: Causes/Testing
Testosterone deficiency diagnosis
* What if it is equivocal?
* What if it is low?
* Diagnosis: two 8am total testosterone levels below reference range
* If it is equivacol, measure free testosterone level by equilbirum dialysis or mass spectrometry
* If it is low, measure LH, FSH, prolatin levels
119
Male Hypogonadism: Causes/Testing
* Primary testicular failure diagnosis
* Some causes include (name 5)
* Elevated LH and FSH level
Causes:
* klinefelter syndrome (check karyotpe, 47XXY)
* atrophy secondary to mumps orchitis
* autoimmune destruction
* previous chemotherapy or pelvic irraditaion
* hemochromatosis
120
Male Hypogonadism: Causes/Testing
* Secondary hypogonadism diagnosis
* Some causes include (name 4)
* Low or normal LH and FSH
* If confirmed: measure prolactin, iron studies, MRI
Causes:
* Sleep apnea
* Hyperprolactinemia
* Hypothalamic or Pituitary disorders (hemochromatosis, pituitary/hypothalamic tumor)
* Use of opiates, anabolic steroids, or glucocorticoids
121
Male Hypogonadism: Treatment
* Testosterone: transdermal (preferred but expensive), buccal, implantable, or IM prep
* Before initiating and during therapy: monitor hematocrit, PSA to screen for development of erythrocytosis and prostate cancer
* Testosterone replacement and anabolic steroid use results in small testicles and male infertility
122
Hypercalcemia/Hyperparathyroidism
* MCC in outpatients
* Commonly presents as:
* Less common presentations are:
* PTH level
* Phos level
* XRAY features (possible)
Most common cause in outpatients: Primary hyperparathyroidism
1. Common: asymptomatic
2. Less common: kidney stones, osteoporosis, pancreatits, fractures
3. PTH elevated (80%) or inappropriately normal (20%)
4. Phosophrous low
5. Xrays may show: chondrocalcinosis or osteitis fibrosa cystica (rare)
123
Hypercalcemia
Most common cause in hospitalized patients
* PTH level
* Phosphorous level
* PTH related protein
Most common cause in hospitalized patients: Malignancy
* PTH level: suppressed
* Phosphorous level: normal or low
* PTH related protein may be elevated but is not needed for diagnosis
124
Hypercalcemia and Hyperparathyroidism:
* Ingestion of these 4 agents causes hypercalcemia
1. Lithium (PTH mediated)
2. Thiazide diuretics (non PTH mediated)
3. Excessive vitamin D ingestion
4. Excessive calcium ingestion
125
Hypercalcemia
* This disease may be associated with
* Hypercalcemia (10%)
* Hypercalciuria (50%)
Sarcoidosis
126
Hypercalcemia causes:
Local Osteolytic Lesions
* PTH level
* Phospohorous level
* How?
* PTH suppressed
* Phosphorous normal or low
* Lytic bone metastasis result in increased mobilization of calcium from bone
127
Hypercalcemia causes:
Multiple Myeloma
* PTH level
* Phospohorous level
* Presentation
* Diagnose with
* PTH suppressed
* Phosophrous elevated
* Look for patients presenting with new kidney injury & anemia
* Diagnose with serum and urine protein immunoelectrophoresis
128
Hypercalcemia causes:
Granulomatous disease (sarcoidosis and TB)
& B Cell Lymphoma
* PTH level
* Phosophorous level
* Calcitriol level
* PTH suppressed
* Phosphorous elevated
* Calcitriol evelated (particularly in sarcoidosis)
129
Hypercalcemia causes:
Milk Alkali Syndrome
* PTH level
* Phosphorous level
* Creatinine level
* Carbon dioxide level
* Consider in healthy persons when ____ has been excluded
* Excessive ingestion of _____ is a cause (rare)
* PTH level suppressed
* Phosphorous, Creatinine, Carbon dioxide levels elevated
* Consider in healthy person when primary hyperparathyroidism excluded
* Excessive ingestion of calcium containing antacids is a cause
130
Hypercalcemia causes:
Hyperthyroidism
* Frequent incidental finding in hyperthyroidism
* Caused by...
* Caused by direct simultation of osteoclasts by thyroid hormone
131
Hypercalcemia: Acute intervention
* When is acute intervention needed?
* Serum calcium level:
* Symptoms may include:
* Most common in setting of:
* with rapid rise in calcium level
* serum calcium \> 14mg/dL
* symptoms may include: mental status change and coma
* most commong in setting of malignancy
132
Hypercalcemia and Hyperparathyroidism: Testing
* Measure ___ to exclude \_\_\_
* If hypercalcemia confirmed, check these 5 levels
* If PTH is elevated or inappropriately normal w/increased calcium, most likely?
* Measure ionized calcium to exclude pseudohypercalcemia
* Pseudohypercalcemia: total calcium increased; ionized normal
* Hypercalcemia confirmed, check:
* calcium, PTH, phosphate
* creatinine and 25 hydroxyvitamin D
* If PTH elevated or inappropriately normal w/increased calcium: most likely cause is primary hyperparathyroidism
133
Hypercalcemia:
Hypercalcemia + Normal PTH levels
* What do you do next?
* What needs to be excluded?
* Measure urinary calcium excretion
* To exclude familial hypocalciuric hypercalcemia
134
Hypercalcemia and Hyperparathyroidism
1. If hyperparathyroidism is confirmed and surgery is indicated, what do you do next?
Sestamibi parathyroid Scan
To look for an Adenoma
135
What is the most common manifestation of MEN I?
Primary Hyperparathyroidism
136
Hypercalemia:
Two treatments plus
Treatment if cause is MM or Sarcoid
1. Volume Resuscitation with normal saline
2. IV bisphosphanates and serum calcitonin
3. oral glucocorticoid therapy (if caused by multiple myeloma or sarcoidosis)
137
Multiple Endocrine Neoplasia
MEN I vs MEN 2
MEN 1 vs MEN 2
* multigland hyperparathyroidism: MC manifestation vs LC manifestation
* pituitary neoplsms vs medullary thyroid cancer
* Pancreatic NETs vs Pheochromocytoma
138
MEN 1
* most common manifestation
* most common neoplasms
* most common NETs
* most common manifestation: multigland hyperparathyroidism
* pituitary neoplasms: prolactinoma, acromegaly, Cushing disease
* pancreatic NETs: gastrinoma, insulinoma, vip-oma, carcinoid syndrome
139
MEN 2
* Least common manifestation
* Most common manifestation
* Most common NET
* least common manifestation: multigland hyperparathyroidism
* most common manifestation: medullary thyroid cancer (may be associated with a palpable neck mass)
* NET: pheochromocytoma (hypertension and palpitations)
140
What level should you check in ALL patients with hyperparathyroidism???
Serum Vitamin D levels
* about 50% have coexisting vitamin D deficiency
* serum and urine calicum levels may be decreased
141
MEN: Treatment
1. Primary hyperparathyroidism and hypercalcemic complications (kidney stones, bone diease, hypercalcemic crisis)?
2. Asymptomatic patients are surgical candidiates if they have any of the following?
Parathyroidectomy for:
1. primary hyperparathyroid + complications
2. asymptomatic + any of the following:
1. serum calcium \> 1 above UNL
2. estimated GFR \< 60
3. reduction in bone mineral density
4. age \< 50 years
142
MEN: Treatment
* Fall in calcium ater parathyroidectomy is due to?
* What do you monitor?
* How do you treat?
* Due to relative hypoparathyroidism "hungry bone syndrome"
* Monitor serum calcium after surgery
* If mild hypocalcemia develops, give oral calcium
143
MEN
How do you treat patients who are not candidates for surgery?
Cinacalcet or Bisphosphonates
144
Hypocalcemia
* most cases caused by?
* what is ical in these cases?
* what is the formula?
* low serum albumin levels
* ionized calcium is normal
* total calcium declines by 0.8 for each 1g/dL decrement in serum albumin
145
Hypocalcemia
* Symptoms/Signs: Name 4
* circumoral and acral parasthesias
* carpal-pedal spasm
* positive trousseau sign (blood pressure cuff carpopedal spasm)
* positive chvostek sign (contraction of ipsilateral facial muscles elicited by tapping facial nerve)
146
Hypocalcemia:
1. Most common cause of acquired hypocalcemia?
2. Name 5 other causes
* Surgical excision of or vascular injury to parathyroid glands
* Other causes include:
* neck irradiation
* congenital hypoparathyroidism (DiGeorge syndrome)
* autoimmune destruction
* infiltrative disease
* complication of plasmapheresis
147
Hypocalcemia:
Name 7 causes aside from hypoparathyroidism
1. hypomagnesemia
2. pancreatitis
3. pseudohypoparathyroidism
4. vitamin d deficiency
5. rhabdomyolysis
6. kidney injury
7. tumor lysis syndrome
148
Hypocalcemia:
Tests to order in evaluation
* Calcium
* Phosphate
* Magnesium
* Creatinine
* PTH
* 25-hydroxyvitamin D
* albumin
* ionized calcium
* EKG to evaluate for QTc prolongation
149
1. Hypocalcemia due to Hypoparathyroidism
2. Hypocalcemia due to psuedohyoparathyroidism (resistance to PTH)
Phosphate Level
* Phosphate Level
* PTH Level
* Vitamin D Level
1. Hypoparathyroidism
* PO4 elevated
* Low PTH
* Variable Vit D
2. Pseudohypoparathyroidism
* PO4 elevated
* PTH elevated
* Normal Vit D
150
Hypocalcemia due to psuedohyoparathyroidism (resistance to PTH)
* Phosphate Level
* PTH Level
* Vitamin D Level
* Elevated PO4
* Elevated PTH
* Normal Vitamin D
151
1. Hypocalcemia due to CKD
* Phosphate Level
* PTH Level
* Vitamin D Level
2. Hypocalcemia due to Vitamin D deficiency
* Phosphate level
* clinical signs
1. CKD
* Elevated PO4
* Elevated PTH
* Low 1, 25 hydroxyvitamin D levels
2. Vitamin D deficiency
* Low PO4
* bone tendernress or fibromyalgias like syndrome, weakness, gait difficulty, osteomalacia
152
Hypocalcemia causes: Key Features
1. Impaired PTH secretion and PTH resistance
2. "Hungry Bone" Syndrome
1. Impaired PTH secretion and PTH resistance:
* Magnesium deficiency
* (small bowel bypass, diarrhea, alcoholism, diuretic therapy)
2. Hungry Bone Syndrome
* Recent parathyroidectomy
153
Hypocalcemia: Treatment
* Acute symptomatic hypocalcemia
* Chronic hypocalcemia
* Acute: IV calcium gluconate and vitamin D
* Chronic: oral calcium supplements and vitamin D
154
Hypocalcemia:
How do you choose the type of Vitamin D for supplementation?
* kidney disease: calcitriol (1,25 dihydroxyvitamin D)
* liver disease: 25-hydroxycholecalciferol
* any other cause of hypocalcemia: cholecalciferol
155
Osteoporosis: Screening
* Who do you screen BDM with DEXA in?
* Women \>/= 65 years old
* Postmenopausal women \< 65 yo who are at increased risk per formal clinical risk assessment tool such as FRAX
* increased risk defined by using the FRAX tool as a predicted 10-year fracture risk \> 8.4%
* Screen men and women with risk factors for secondary osteoporosis (glucocorticoid use, hyperparathyroidism, ADT, malabsorption)
\* most experts recommend 10 to 15 years as screening interval for women with normal or slightly low BMD with no risk factors
156
Osteoporosis: Diagnosis
* what is it?
* what is DEXA?
* what is T score?
* T score: osteopenia
* T score: osteoporosis
* also defined by history of:
* Defined: silent skeletal disorder characterized by compromised bone strength and increased predisposition to fractures
* Dexa is machine used to determine BMD
* T score: comparison of healthy persons BD to yours
* Osteopenia: dexa T score -1 to 2.4
* Osteoporosis: dexa T score \< or = 2.5
* Osteoporosis also diagnosed by history of fragility fracture (fracture from a fall at standing height or lower)
157
Osteoporosis: causes
* Most common cause in women/men
* Secondary causes (name 7)
* MCC in women: estrogen deficiency
* MCC in men: testosterone deficiecy
* Secondary causes:
* hyperthyroidism, hyperparathyroidism, Cushing syndrome
* malabsorption (crohn disease, intestinal resection, celiac)
* rheumatoid arthritis
* medications (excessive glucocorticoids, thyroid hormone, phenytoin)
* multiple myeloma
* CKD, chronic liver disease
* vitamin D deficiency
158
Osteoporosis Treatment
* Lifestyle
* Indications for antiresorptive therapy
Lifestyle:
* stop smoking, reduce alcohol intake, begin resistance exercises
* exposure to sunlight
* supplement calcium and vitamin D intake
Indications for antiresorptive therapy
* osteoporosis
* osteopenia (if additional high risk factors present)
* previous fragility fracture
* vertebral or hip fracture
159
Osteoporosis Treatment:
* Antiresporptive treatment is cost effective when
* risk of major osteoporotic fracture is ? per FRAX
* risk of hip fracture is ? per FRAX
10 year probablity
* \> or = to 20%
* \> or = to 3%
160
Osteoporosis: Treatment
* Antiresorptive drugs:
* First line
* Patients with CKD 4 or intolerant to 1st line
* Approved for: glucocorticoid induced osteoporosis with high risk of fracture, postmenopausal women, men with hypogonadism related osteoporosis at high risk of fracture
* Pain for osteoporosis high risk fracture
* Antiresorptive drugs:
* First Line: aldrenoate or risedronate
* IV zoledronate once yearly
* ALL contranindicated in patients with CKD or esophageal disease
* Denosumab
* Teriparatide
* Calcitonin
161
Osteoporosis:
When is it reasonable to stop therapy?
* No recommended duration of therapy is specified
* Stopping therapy after 5 years is reasonable in women who have
* stable BMI
* no history of fracture
* are at low risk of fracture
162
Osteoporosis: Adverse effects of drugs used
* oral bisphosphonate
* IV bisphosphonate and denosumab
* teriparatide
* oral bisphosphonate: erosive esphagitis and atypical hip fracture
* IV bisphosphonate and denosumab: osteonecrosis of the jaw
* teriparatide: osteosarcoma
* limit to 2 years
163
Osteoporosis
When do you do a follow up DEXA after beginning therapy for osteoporosis?
No concesus exists.
24 months after beginning therapy is reasonable.
164
Osteomalacia:
What is it?
* A metabolic bone disease resulting from failure of organic matrix to mineralize because of lack of available calcium or phosphorous
* Many cases are realted to abnormalities in Vitamin D
* May also result from lack of calcium or phosphate.
165
Osteomalacia: Signs and Symptoms
* Fatigability, malaise, bone pain
* Generalized bone tenderness
* Proximal muscle weakness
* Looser zones (bands perpendicular to the bone surface visible on x rays)
* Hypocalcemia and Hypophosphatemia
* elevated serum alkaline phosphotase level
166
Osteomalacia:
Testing
Diagnosis
Testing:
Evaluate for underlying conditions that may lead to malabsorption of Vitamin D, such as celiac disease, or abnormalities in vitamin D metabolism,
such as liver and kidney disease.
Diagnosis:
Confirmed with bone biopsy
167
Osteomalacia: Treatment
If osteomalacia is secondary to vitamin D deficiency -
* treat with oral ergocalciferol 1000 to 2000 U/d and
* elemental calcium 1g/d
168
Vitamin D Deficiency:
* Screening
* Diagnosis
* Testing
* Population with lower levels
* Treatment of deficient patient
* Screening: Not enough evidence to screen
* Diagnosis: Prolonged, severe defieincy will cause secondary hyperparathyroidism, osteomalacia and symptoms of bone pain, muscle weakness and fracture
* Testing: 25 hydroxyvitamin D best inidicator of status
* Lower levels: obestiy, glucocorticoids, orlistat, malabsoprtion
* Treatment: 50,000 U ergocalciferol of cholecalciferol is recomended, followed by maintenance of 1500-2000 U/d
169
Paget Disease:
What is it?
How is it usually suspected?
Focal disorder of bone remodeling that leads to greatly accelerated rates of bone turnover, disruption of the normal architecture of bone, and sometimes gross defomities of large bone
Most patients are asymptomatic and the disease is suspected with an isolated alkaline phosphotase level in the absence of liver disease
170
Paget Disease:
* Symptoms and Signs
Signs/Symptoms:
* Bone pain, fractures
* Cranial nerve compression syndromes, spinal stenosis, nerve root syndromes
* high-output cardiac failure
* angioid retinal streaks
171
Paget Disease:
Testing
Asymptomatic Patient
* With elevated Alkaline Phosphatase (bone)
* Order bone scan and follow up X rays in areas that localize radionucleotide
Symptomatic Patient
* Obtain X rays of painful area
* Xrays will reveal pathognomonic pagetic lesions: focal osteolysis with coarsening of trabecular pattern, cotton wool skull, and cortical thickening
172
Paget Disease:
Treatment
* Indidications to treat Paget Disease include bone pain, radiculopathy, involvement of weight bearing bone or joint, regardless of symptoms
* Bisphosphonates are first line agents
173
Diabetes Mellitus Type 1 Diagnosis:
* Initial confirmation testing
* 20% develop...
* GAD65 and IA-2 antibodies
* 20% develop organ-specific autoimmune diseases, such as celiac disease, Grave's disease, hypothyroidism, addison disease, pernicious anemia and vitiligo
174
Diabetes Type 1: Treatment
* Basal dose accounts for what % of daily total insulin?
* examples
* The remaining % covers?
* examples
* Basal dose: covers 40-50% total daily dose
* Insuline glargine, detemir, degludec
* 10pm dose covers noctural plasma glucose levels and levels between meals; counters dawn phenomenon
* NPH intermediate: morning and evening to provide basal levels to suppress hepatic gluconeogenesis
* Remaining insulin cover preprandial doses
* insulin aspart, glulisine, lispro. Rapid acting 5-15 mins before meals to modulate postprandial rise in glucose level.
* Regular insulin: 30 mins before meals to prevent postprandial elevations
175
Diabetes: How do you resttore sensitivity to hypoglycemia?
Lowering insulin dose and allowing average plasma glucose level
to increase for several weeks
176
Type 2 Diabetes:
Characteristic findings of long standing disease
* polyria, polyphagia, polydypsia
* retinal microaneurysms, dot and blot hemorrahges, macular edema
* symmetric sensory stocking glove peripheral neuropathy
* cardiovascular and kidney disease
177
Diabetes Type 2: Risk Factors
* positive family history
* history of gestational diabetes or PCOS
* member of certain racial or ethnic groups
* AA, American Indian, Alaskan Native, Asian American, Hispanic, Latino, Native Hawaiian or Pacific Islander
178
Type 2 Diabetes: Screening
USPSTF recommends
* Screen for abnormal blood glucose as part of cardiovascular risk assessment in adults aged \_\_\_who are \_\_\_
* Also consider screening in\_\_\_
ADA recommends
* Screen overweight adults with \_\_\_\_
* Screen all patients \>\_\_yo
USPSTF
* Aged 40-70yo who are overweight or obese
* Earlier if one or more risk factors for diabetes
ADA
* overweight adults with at least one additional risk factor
* and all patients \> 45 yo
179
DM 2
What tests do you use to screen?
* fasting plasma glucose
* 2 hour postprandial glucose during oral glucose tolerance test
* hemoglobin A1c
* if two seperate tests are done simultaneously and both are abnormal, diagnose diabetes
* if one of the two tests is abnormal, repeat the abnormal test
180
DM 2
* Increased risk for diabetes
* Diabetes
* fasting glucose
* random glucose
* 2 hour glucose during OGTT
* hgbA1c
Increased risk:
* FG: 100-125
* RG: 140-199
* 2HR: 140-199
* HgbA1c: 5.7-6.4%
Diabetes
* FG: \>126
* RG: \>200 w symptoms (diagnostic w/o repeat measurement)
* 2HR: \>200
* \> 6.5%
181
