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Endo/repro Flashcards

0
Q

How are Cortisol and Aldosterone measured?

A

Cortisol: urine free cortisol (reflects unbound, physically active level)
Aldosterone: 24 hr. urine aldosterone

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1
Q

In terms of enzymes, how does the zona glomerulosa of the adrenal gland differ from the zona fasciculata and reticularis?

A
  1. Lacks 17a-Hydroxylase: can’t form cortisol and androgens

2. Has Aldosterone Synthase (CYP11b2): able to form mineralcorticoid - Aldosterone from corticosterone

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2
Q

When are stimulation and suppression tests of the adrenal gland done?

A

Stimulation: when hormone deficiency suspected
Suppression: when hormone excess suspected

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3
Q

When do cortisol levels reach high and low levels

A

Acording to circadian rhythm:
High: 6-7am
Low: 11pm

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4
Q

What are normal daily levels of Cortisol, DHEA, and Aldosterone secretion?

A

Cortisol: 15-30 mg/day
DHEA: 15-30 mg/day
Aldosterone: 0.050-0.250 mg/ day

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5
Q

When measuring urine levels of hormones, what other substance should be considered?

A

Creatinine - ensure kidney secretory function is normal

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6
Q

What is a cosyntropin test and how is it performed? Results?

A

Cosyntropin: ACTH (1-24) given IV w/ cortisol and aldosterone levels checked before and at 30 and 60 minutes post-admin
Normal: cortisol elevation >18mcg/dL (min normal is 9 or more mcg/dL)
Primary adrenal insufficiency: no increase in cortisol or aldo
Long standing secondary: no increase in cortisol but increase in aldo
Recent onset secondary: usually normal result (no time for atrophy)

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7
Q

What binds cortisol in the blood and to what extent?

A

Corticosteroid Binding Globulin (CBG / transcortin): 90%
Albumin: 7%
Free 3%

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8
Q

What binds aldosterone in blood and to what extent?

A

Corticosteroid Binding Globulin (CBG): 17%

Albumin: 47%

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9
Q

How are androgens (DHEA, DHEA-SO4, Testosterone) transported in blood?

A

DHEA, DHEA-SO4: Albumin

Testosterone: 95% bound to SHBG (TeBG)

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10
Q

What is the difference between Cushing’s Syndrome and Cushing’s Disease?

A

Syndrome: excess cortisol action
Disease: ACTH producing pituitary tumor -> excess cortisol production

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11
Q

What is the most common form of Cushing’s syndrome?

A

Exogenous

ex: Iatrogenic (prednisone)
- > negative feedback: decreased ACTH secretion

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12
Q

Major symptoms of Cushing’s

A 
Impaired glucose tolerance
Central obesity
Purpura, ecchymoses, striae
Proximal muscle atrophy
Hirsutism
HTN
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13
Q

How does ectopic ACTH syndrome typically manifest? What tumors is it associated with?

A 
Hypokalemic Alkalosis w/ Diabetes
Associated with:
-Bronchogenic carcinoma (SCLC)
-Carcinoid of Thymus, Pancreas, Ovary
-Medullary carcinoma of thyroid
-Bronchial adenoma
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14
Q

What is ectopic ACTH syndrome?

A

Non pituitary tumor releasing ACTH or CRH -> hyperplasia of adrenal cortex

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15
Q

What is Dexamethasone and how is it used in Cushing’s?

A 
Dexamethasone:  high potency glucocorticoid.  used to test feedback regulation
Give at night - low morning cortisol.  If high - feedback regulation dysfunction
Low dose (2mg/d x 2d) or High dose (8mg/d x 2d):  ability to eventually suppress cortisol highly suggestive of pituitary dysfunction as cause
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16
Q

Diagnostic Strategy for Cushing’s Syndrome

A
  1. Screening and confirm: 1) late cortisol level 2) Dexamethasone suppression test 3) 24 hr urine free cortisol 4) confirm non-suppression w/ low dose Dex test.
  2. Differentials: 1) ACTH level 2) high dose Dex test 3) CRH test 4) Metyrapone test (no longer used)
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17
Q

What is the Metyrapone test?

A

Used in Cushing’s diagnsosis - no longer used clinically
Metyrapone inhibits 11B-hydroxylase (11-DOcortisol -> cortisol)
-> increased ACTH in Cushing’s Disease, no response otherwise
-> increased 11-DOcortisol in Cushing’s Disease (also 17-OHCS in urie)

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18
Q

How does plasma ACTH help differentiate between causes of Cushing’s syndrome?

A

Plasma ACTH levels in:

Cushing’s Disease: normal to high
Ectopic ACTH: very high
Adrenal tumor: low

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19
Q

2 main forms of adrenal insufficiency

A
  1. Primary (Addison’s Disease)

2. Secondary: pituitary failure

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20
Q

What tests are available to verify adrenal insufficiency?

A
  1. Morning cortisol and ACTH (20mcg/dL is N, <5 abnormal, 5-20 req. ACTH stim test)
  2. Cosynotropin (ACTH) test: admin 250 mcg IV/IM, draw for cortisol at 0, 30, 60 mins. Peak of 20+ is N.
  3. Metyrapone overnight test
  4. Insulin tolerance test - Gold Std for HPA axis
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21
Q

How does insulin tolerance testing work?

A

Make patient hypoglycemic via insulin admin
Insulin: 0.1 U/kg IV
Measure Blood glucose at 0 and 30 min (s highly suspected or CAD

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22
Q

What is congenital Adrenal Hyperplasia?

A

AR impairment of Cortisol production due to enzymatic dysfunction
21 hydroxylase: >90%
11 B-hydroxylase: 5%
17 a-hydroxylase: 1%

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23
Q

Symptoms of 21-Hydroxylase defect

A

Depends on severity of enzyme defect
Virilized female infant
w/ Na+ wasting (severe defect) -> hypotension
Precocious male puberty
Adult onset may -> female hirsutism at puberty

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24
Q

What symptoms are seen with 11B hydroxylase deficiency?

A

CYP11B1 (ZF): virilized females w/ hypokalemic HTN

CYP11B2 (ZG): non-virilizing, salt-wasting: hyperkalemic hypotension

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25
Q

What are symptoms of 17a Hydroxylase deficiency?

A

HTN, hypokalemia, hypogonadism
Male: varying degree of ambiguous genitalia at birth
Male and Female: pubertal failure

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26
Q

What is the anatomic location of the pituitary gland?

A

Beneath 3rd ventricle, posterior to optic chiasm, anterior to mamillary bodies, w/ internal carotid aa. on either side

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27
Q

What are Herring Bodies?

A

Seen in Neurohypophysis: Dilated nerve endings containing secretory granules (terminating on blood vessels)

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28
Q

What are ways of classifying pituitary adenoma?

A

Size: Microadenoma (10mm)
Spread: Can also consider confined to sella or invasive
Hormone producing: Functional vs. non
Non-hormone producing: Null-cell

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29
Q

What are different manifestations of GH producing pituitary adenoma (age determined)?

A

Gigantism: if before epiphyses
Acromegaly: if after (overgrowth of soft tissues and organomegaly

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30
Q

What defines pituitary carcinoma?

A

Distant metastases

Very rare

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31
Q

What is an atypical pituitary adenoma?

A

Increased proliferative activity
High rate of recurrence
May express p53 protein

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32
Q

What can cause pituitary inflammatory “Pseudotumors”?

A

autoimmune inflammation: hypophysitis

sarcoidosis

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33
Q

What is Pituitary Apoplexy?

A

“Pituitary stroke”

Infarction of adenoma or hyperplastic gland -> necrosis and/or hemorrhage and acute pituitary insufficiency

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34
Q

What is Primary vs. Secondary Empty Sella Syndrome and who is at risk?

A

Primary: increased CSF compresses pituitary -> insufficiency. sella appears empty in imaging
-Middle aged women w/ hypertension, obesity, and headache

Secondary: Pituitary adenoma infarcts, necrosis -> empty space

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35
Q

What is Craniopharyngioma?

A

Most common sellar tumor in children.
Benign neoplasm derived from Rathke’s Pouch (squamous) epithelium.
Occurs in 2 peaks: 1st 2 decades of life, then again at 45-60.

May form cysts: filled w/ cholesterol rich brownish thick fluid.

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36
Q

What is the description of the microscopic appearance of Craniopharyngioma tissue?

A

Adamantinomatous epithelium

“wet keratin” appearance

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37
Q

What is a Chordoma?

A

Neoplasm derived from vestigial remnants of notochord.
Men > Women, usually >30y.
Parasellar or involving Clivus
Looks like cartilage w/ abundant myxoid stroma

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38
Q

What are primary, secondary and tertiary hypothyroidism?

A

Primary: issue w/ Thyroid itself. High circulating TSH
Secondary: issue w/ Pituitary -> low TSH
Tertiary: issue w/ hypothalamus -> low TRH reaching pituitary and resulting low TSH

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39
Q

2 syndromes of hypothyroidism

A
  1. Cretinism: if hypothyroidism develops in utero or early in childhood
    - mental retardation, short stature, protruding tongue (GAGs), coarse features
  2. Myxedema: development in adulthood
    - slow physical and mental activity, cold intolerance, constipation, coarsening of facial features, enlarged tongue, swelling of arms and legs.
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40
Q

Name 2 long acting insulins and duration of action

A

Glargine (24 hrs) peakless
Detemir (12-20 hrs) relatively peakless
used to maintain basal insulin levels

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41
Q

What infectious agents can produce acute vs. chronic infective thyroiditis?

A

Acute: bacterial
Chronic: mycobacteria or fungi

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42
Q

What is the most common form of adult hypothyroidism?

A

Hashimoto - autoimmune destruction of follicular cells

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43
Q

What is the HLA association with Hashimoto’s Thyroiditis? Other genetic connections?

A

HLA-DR5

Also assoc. w/ Turner and Down’s syndromes

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44
Q

3 mechanisms of cell destruction in Hashimoto’s Thyroiditis?

A

Sensitization of CD4+ helper cells ->

1) CD8+ and cytotoxic Tcell activation and induction of apoptosis (Fas/FasL)
2) cytokine injury (IFN-y -> mac activation)
3) anti-thyroid antibodies (anti-thyroglobulin, anti-thyroid peroxidase)

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45
Q

What are Hurthle cels?

A

Eosinophilic epithelial cels seen in Hashimoto’s at site of thyroid follicle remnants

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46
Q

What diseases are Hashimoto’s patients at risk of developing?

A

Other autoimmune diseases

B-cell Non-Hodgkin’s Lymphoma: MALT

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47
Q

What occurs in deQuervain Thyroiditis?

A

Subacute Granulomatous Thyroiditis
viral infection -> Ag induced cytotoxic cell injury to thyroid follicles -> foreign body reaction to colloid -> granuloma formation

Self-limited, painful w/ initial transient hyperthyroidism

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48
Q

What is Riedel Thyroiditis?

A

Least common thyroiditis - probably autoimmune -> marked fibrosis

thyroid hard and painless

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49
Q

What variant of thyroiditis is found in young women postpartum?

A 
Subacute Lymphocytic (Painless) Thyroiditis
probably autoimmune
produces hypothyroid state
extensive lymphocytic infiltrate, patchy destruction
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50
Q

What is the underlying cause of goiter formation (diffuse or multinodular)?

A

Impaired thyroid hormone synthesis -> increased TSH -> hyperplasia and hypertrophy

Iodine deficiency, enzymatic defect, goitrogen ingestion (brussel’s sprouts, cabbage, cauliflower, cassava)

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51
Q

What is Plummer syndrome?

A

Autonomous nodule in goiter -> hyperthyroidism

Rare. most goiters are euthyroid.

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52
Q

What is the most common thyroid neoplasm?

A

Benign Adenoma
usually non-functional
Requires excision for evaluation

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53
Q

2 types of thyroid carcinoma

A

From follicular epithelial cells: papillary, follicular and anaplastic carcinomas
From C-cells: medullary carcinoma

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54
Q

What is the distinguishing feature of papillary carcinoma of the thyroid?

A

“Little Orphan Annie” eye nuclei - large, clear, ground-glass appearance

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55
Q

Major risk factor for papillary carcinoma of the thyroid

A

Previous exposure to ionizing radiation

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56
Q

How does follicular carcinoma of the thyroid tend to spread?

A

Hematogenously (vs. lymphatics seen in papillary)

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57
Q

Who is at risk of developing follicular thyroid carcinoma?

A

Usually seen in areas w/ endemic iodine deficiency

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58
Q

What is the survival rate for anaplastic thyroid carcinoma and who is at greatest risk?

A

Survival <1 yr.

Older patients, usually w/ concurrent or previous well-differentiated thyroid carcinoma

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59
Q

What is the usual genetic association of Medullary Thyroid Carcinoma?

A

RET proto-oncogene (MEN-2A and 2B)

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60
Q

Wolff-Chaikoff vs. Jod-Basedow

A

Wolff Chaikoff: Increased iodine load -> decreased thyroid hormone excretion
Jod-Basedow: increased iodine load -> hyperthyroidism (usually in iodine deficient person w/ endemic goiter)

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61
Q

Effect of thyroid hormone on: Heart, vascular, skin, GI, skeletal, neuromuscular

A

Heart: increased rate and contractility (increase B1 response)
Vascular: vasodilation -> widened pulse pressure
Skin: warm, smooth, moist
GI: increased motility
Skeletal: increased bone turnover
Neuromuscular: hyperactivity, increased muscle contraction, muscle weakness

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62
Q

What is the T3 Resin Uptake test?

A

Labeled T3 is added to serum, then a T3 binding resin is added.
Assume normal TBG level
Hypothyroid: more labeled T3 binds TBG, low resin uptake
Hyperthyroid: less labeled T3 binds TBG, high resin uptake

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63
Q

What can result from prolonged untreated hypothyroid condition? Characteristics and treatment?

A

Myxedema coma
Decreased mental status, hypothermia, hypotension, bradycardia, high TSH
Treat w/ thyroid hormone

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64
Q

What are reproductive symptoms of hyperthyroidism?

A

Oligo or amenorrhea in women

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65
Q

What can occur in untreated hyperthyroidism? Symptoms? Treatments?

A

Thyroid Storm - life threatening
AMS, Fever, Palpatations, weight loss, diarrhea, heat intolerance, irregular heart beat

Iodine - reduce thyroid hormone
B-blocker - adrenergic effects
Cooling blanket

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66
Q

What is the most common non-thryoidal illness w/ thyroid related manifestation?

A

Decreased activity of Type I deiodinase enzyme (T4 -> T3) -> clinical hypothyroid state
Associated with other severe illness (lung disease in ICU)

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67
Q

2 drugs that inhibit thyroid hormone synthesis / release

A

Iodine

Lithium

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68
Q

How does Amiodarone effect the thryoid?

A

Reduces conversion of T4 -> T3
Blocks T3 binding at nuclear receptor
Direct toxic effect at follicular cells -> destructive thyroiditis

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69
Q

4 synthetic thyroid hormone replacements

A
  1. L-thyronin: T3
  2. Liothyroxine: T3
  3. Liotrix: T3+T4
  4. Levothyroxine: T4: Drug of choice
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70
Q

What is the dose limiting effect of Levothyroxine?

A

CV effects

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71
Q

How should patients receiving Levothyroxine be monitored?

A

Steady state after 6-8 weeks of treatment, then check TSH level.
Once euthyroid monitor every 6-12 mos.

Note: older patients have decreased clearance, so decrease dosage w/ age.

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72
Q

What types of drugs can impact levothyroxine therapy?

A
  1. Resin Binders (cholestyramine, colestipol)
  2. Aluminum containing preps. (hydroxide, sucralfate)
  3. Enzyme inducers (Pheyntoin, Phenobarbitol, Rifampin, Carbamazepine)
  4. Drugs that increase TBG (estrogen, Raloxifene)
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73
Q

What is treatment for Myxedema Coma?

A

1) IV bolus thyroxine: 300-500mcg, then 75-100 daily IV or PO until stable
2) IV hydrocortisone: 100mg q8h (r/o adrenal suppression)
3) supportive therapy: Vent, maintain euglycemia, BP, Temp,

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74
Q

What are the thiourea drugs? Action?

A

Anti-thyroid drugs: Propylthiouracil, Methimazole

  • Inhibit Thyroid Peroxidase
  • Inhibit coupling of Iodotyrosines
  • PTU: inhibits peripheral conversion of T4->T3
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75
Q

In what cases is Propylthiouracil preferred over Methimazole for treatment of hyperthyroid?

A

Thyroid storm

Pregnancy - esp 1st trimester. both cat. D, but PTU has more documented teratogenicity

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76
Q

What medications are given along with I-131 in Radioactive Iodine Treatment?

A

Beta blocker - symptomatic relief - all patients
Thionamide - select patients w/ severe or long standing hyperthyroid, elderly, cardiac disease, withdraw 4-6 days before iodine therapy

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77
Q

What are features and treatment of Thyroid Storm?

A

Thyroid storm: untreated hypertension, fever >103 F (39.4 C), tachycardia, tachypnea, N/V/D, dehydration, delerium, coma
May last 72 hours or up to 8 days w/ inadequate treatment

Treatment: Support vital functions, thionamide/iodide, B-Blocker, correct underlying factors, remove circulating hormones if severe (plasmapheresis / dialysis)

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78
Q

Hyperparathyroidism mnemonic

A

Bones, stones, abdominal groans, psychic moans
mostly due to Ca++
Bones: decreased Ca -> fragility and fractures
Stones: increased circulating Ca -> stones
Abd: hypercalcemia -> constipation
Psy: hypercalcemia -> psych manifestations

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79
Q

Genes assosicated with sporadic and familial hyperparathyroidism

A

Sporadic: PRAD-1 -> increased cyclin D1
inactivation of MEN1
Familial: inactivation of MEN1
RET mutation -> TK activation -> MEN2 syndrome
CASR: Ca++ sensing receptor mutation

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80
Q

What is ostitis fobrosis cystica?

A

End-stage bone disease associated with hyperparathyroidism

Cystic bone spaces filled with brown fibrous tissue (hemorrhage -> hemosiderin filled macrophages)

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81
Q

With what condition is secondary hyperparathyroidism usually associated?

A

Chronic Renal Failure -> low vit D -> persistently low serum Ca++ -> longstanding stimulation of parathyroids

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82
Q

What is the major hormonal contributor to osteoporosis?

A

decreased estrogen (menopause) -> increased osteoblast activity w/ insufficient osteoblast response

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83
Q

3 sites of action of Vitamin D and respective action

A

Bone: Low Ca++: stimulates Ca and PO4 mobilizatoin
Normal Ca and PO4: mineralization of osteoid and epiphyseal
cartilage
Intestine: Increases abs. of Ca++ (upreg. of Ca binding prot. D-28K)
Kidney: Stimulates PTH dependent Ca++ reabs.

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84
Q

Stages of Paget’s disease

A

1) Osteolytic: excessive bone resorption, numerous abnormally large osteoclasts
2) Mixed osteoclast / osteoblast: new bone deposition, marrow replaced by fibrous and granulation tissue
3) Sclerotic stage: Disorganized, excessive bone formation

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85
Q

Complications of Paget’s disease

A

1) pain / fractures / osteoarthritis
2) skeletal deformity
3) high output HF due to increased vascularity of affected bone
4) sarcomas, esp. osteosarcoma

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86
Q

What cellular change is seen in the pituitary with Cushing’s Syndrome?

A

Crooke’s Hyaline change: ACTH producing cells damaged by elevated cortisol levels -> increased cytoplasmic keratin filaments

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87
Q

What is Conn syndrome?

A

Aldosterone producing adrenal cortical adenoma

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88
Q

What happens to renin levels in hyperaldosteronism?

A

Decreased renin due to neg. feedback on RAAS

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89
Q

What is Waterhouse-Friderichsen syndrome?

A

N. meningitidis associated hemorrhage of adrenal glands

Bacteremia -> hypotension and shock -> DIC -> massive hemorrhage of adrenals

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90
Q

What is the most common cause of Addison’s disease?

A

Autoimmune destruction of adrenals

  • Autoimmune polyendocrine syndrome type I (APS1): ARIE gene mutation, chronic mucocutaneous candidiasis, ectodermal dystrophy
  • APS2
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91
Q

What infections are associated w/ Addison’s?

A

TB, Histoplasma capsulatum, CMV, mycobacterium avium intracellulare

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92
Q

Symptoms of Addison’s

A

Weakness, fatigue, hyperpigmentation (MSH), N/V
Hypotension: hyponatremic, hyperkalemic
Hypoglycemia

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93
Q

What is pheochromocytoma?

A

Tumor of adrenal medulla - chromaffin cells

Produces catecholamines

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94
Q

What is found in a 24 hr. urine collection or serum sampling of a patient w/ pheochromocytoma?

A

Increased catecholamines and metabolites such as metanepherine and vanillymandelic acid

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95
Q

What is neuroblastoma?

A

Childhood malignancy of neural crest origin

cells are neuroblasts- intermediate stage of differentiation of sympathetic ganglion cells

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96
Q

What are genetic indicators of prognosis in neuroblastoma?

A 
N-myc amplification:  poor prognosis
1p deletion:  poor prognosis
11q deletion:  poor prognosis
17q gain:  poor prognosis
hyperdiploidy:  favorable!
97
Q

What is a stage IV-S nuroblastoma?

A

Grade II or III tumor w/ metastasis restricted to liver, skin, and bone marrow
Favorable prognosis - often spontaneous regression of tumor

98
Q

What is found in urine of patients w/ neuroblastoma?

A

Increased catecholamines and metabolites: vanillymandelic acid, homovanillic acid

99
Q

what is the effect of lithium on PTH?

A

Lithium antagonizes the CaSR of the parathyroid -> increased hormone productoin.

100
Q

What factors activate and inhibit 1a hydroxylase?

A

Activators: low serum phosphate, PTH
Inhibitors: Ca++ and FGF23

101
Q

What percent of Ca++ is free in the blood vs. bound? What is the effect of pH on this?

A

Usually 50% bound w/ 80% of that to albumin and 20% to globulin
Lowered pH -> decreases binding

102
Q

What is corrected Ca++?

A

corrected Ca++ = serum [Ca] + ((4.0- [albumin]) *0.8)

103
Q

Normal level of vitamin D 25OHD

A

30-70 ng/mL

104
Q

What is the most common presentation of hypercalcemia? Other symptoms?

A

Asymptomatic

Other symptoms: weakness, fatigue, aches and pains, depression, thirst + polyuria, constipation

105
Q

How could one have hypercalcemia with Low PTH?

A
  1. Excessive release of Ca++ from bone due to
    - PTHrP (lung / kidney ca)
    - Metastatic destruction (breast ca., leukemia, lymphoma, mm)
    - high bone turnover: hyperthyroid, immobilization, vit A tox
  2. Excessive absorption of Ca++ from gut
    - Vit D intox, sarcoidosis / granulomatous (1a-hydroxylase)
    - Excessive Ca++ intake (milk alkalai syndrome)
106
Q

Treatments for primary hyperparathyroidism

A
  1. surgical removal of adenoma
  2. hydration
  3. bisphosphonates: reduce osteoclast activity
  4. cinacalcet: calcimimetic: activates CaSR -> decreased PTH
107
Q

What is the effect of hypocalcemia on the nervous system?

A

Excites

108
Q

What are Chvostek and Trousseau’s signs associated w/?

A

Indicators of Hypocalcemia
Chvostek: tap cheek - flinch toward same side (non-specific)
Troussear: inflate cuff above SBP -> PAINFUL spasm of hand

109
Q

Most common cause of hypoparathyroidism

A

Autoimmune destruction

110
Q

What are some genetic causes of hypoparathyroidism?

A

activating mutation of CaSR

DiGeorge (failure of descent of 3rd and 4th pharyngeal pouch)

111
Q

What occurs in pseudohypoparathyroidism?

A

Autosomal Dominant Gs-alpha mutation
1) from mother: PTH resistance + AHO phenotype
2) from father: AHO phenotype only
Tissue resistance to PTH -> elevated PTH w/ symptoms of hypo-PTH
Low Ca++, high PO4

112
Q

What is Albrights Hereditary Osteodystrophy?

A

Associated with pseudohypoparathyroidism

Results in short stature, mild mtard, short 4th and 5th metacarpals,

113
Q

What is the effect of a PHEX gene mutation?

A

PHEX codes for FGF23 degradation enzyme -> excess FGF 23

FGF23: inhibits 1a-hydroxylase -> low levels of active vitamin D -> decreased phosphate absorption and osteomalacia

114
Q

What do Z and T scores of a DEXA scan refer to?

A

DEXA: bone density scan
Z-score: compares patient result to mean and STD of same sex and age control group
T-score: compared patient result to mean and STD of young adult control group of same sex

115
Q

How is T-score on DEXA used?

A

DEXA: bone density scan

T-score: -1.0: normal

116
Q

3 types of primary osteoporosis

A

1) idiopathic in children and young adults
2) post menopausal: low E -> increased osteoclast act. + decreased osteoblast act.
3) senile: decreased ability of osteoblast to divide and produce osteoid

117
Q

Drugs useful in treating osteoporosis

A

1) bisphosphonate : inhibit reabsorption
2) teriparatide / fluoride: stimulates bone deposition
3) strontium ranelate: inhibit reab / stim dep.

118
Q

2 genetic conditions of Rickets

A

1) X-linked hypophosphatemic rickets: PHEX inactivating mutation -> increased FGF 23
2) AD hypophosphatemic rickets: FGF23 mutation -> resistant to inactivation

119
Q

Osteogenesis Imperfecta treatment

A

bisphosphonate

120
Q

What are the most common forms of endocrine HTN?

A

1) renal artery stenosis
2) Primary aldosteronism
3) pheochromocytoma

121
Q

2 primary causes of Renal Vascular HTN

A

1) atherosclerosis (2/3)
2) fibromuscular dysplasia (1/3: young females)
* *hormonal influence implicated: affects women of childbearing age**

122
Q

When are screening tests for Renal Artery Hypertension appropriate?

A

When corrective procedures are an option for treatment

123
Q

What is the preferred treatment for Renal Vascular HTN due to atherosclerotic disease?

A

Medical management: ACEi / ARB, + thiazide if needed

124
Q

Is percutaneous angioplasty more effective in treating Renal Vascular HTN due to atherosclerosis or FMD?

A

FMD.

Atherosclerosis is more progressive and diffuse - low cure rate w/ stenting.

125
Q

Indication for surgical treatment of Renal Vascular HTN?

A
  1. Recent onset of HTN
  2. Young pt.
  3. HTN <5yrs
  4. Inability to tolerate / non-compliant w/ meds
  5. Recurrent flash pulmonary edema or refractory HF
126
Q

What is the recommended screening test for primary aldosteronism?

A

Plasma Aldosterone / Plasma Renin Activity (100% sensitive, 60% spec)
>20 is positive test

Follow w/ suppression test (high Na+ test)

127
Q

How is an aldosterone suppression test performed?

A

Salt tabs or high salt diet for 3 days followed by 24 hr. urine catch.
Adequate salt loading: >200mEq / L
Urine aldosterone >12 mcg / 24 hrs is positive.

Follow w/ imaging and renal vein sampling if needed to determine laterality of lesion

128
Q

What are common locations for extra-adrenal pheochromocytomas to arise?

A

Tissues derived from neural crest: carotid body, aortic chemoreceptors, sympathetic ganglia

129
Q

HTN + sweating, headache, palpitations suggests what?

A

Pheochromocytoma

sensitivity 90% +

130
Q

How and under what circumstances are plasma catecholamines drawn?

A

Patient supine w/ indwelling catheter for 30 mins in a quiet environment to prevent catecholamine spike.

131
Q

What is the incidence of germ line mutations in pheochromocytoma? What gene is usually involved?

A

20% of cases, AD inheritence
Mitochondria Succinate Dehydrogenase
High recurrence rate (15%) - long term follow up

132
Q

What substances inhibit insulin secretion?

A

Serotonin, PGE, a-agonists, thiazides, phenytoin, diazoxide

133
Q

How is an oral glucose tolerance test performed?

A

Oral solution of 75g glucose
Serum glucose measured every 30 mins for 2 hrs.
No value should exceed 200 mg/dL
Value should be <140 at 2 hrs.

134
Q

What are diagnostic criteria for diabetes?

A 
Ant of these:
Random glucose >200 mg/dL + signs / symptoms
Fasting glucose >126 on 2 occasions
HbA1c >6.5%
OGTC results >200 at 2 hrs.
135
Q

What are criteria for Impaired Glucose Tolerance?

A

HbA1c: 5.7-6.4%
Fasting glucose: 100-125
OGTT @2hrs of 140-200

136
Q

Criteria for Gestational Diabetes Diagnosis

A 
Made by OGTT after overnight fast of at least 8hrs.
Any of the following:
Fasting:  >92
1hr:  >180
2hr:  >153
137
Q

What % of Bcells must be destroyed in T1DM for symptoms to manifest?

A

90%

138
Q

3 antibodies found in T1DM

A

Anti-islet cell
Anti-insulin
Anti-glutamic acid decarboxylase

139
Q

Genetic links in Maturity Onset Diabetes of the Young?

A

AD with mutations in glucokinase and mitochondrial genes

140
Q

What is the correlation between adiponectin and insulin sensitivity?

A

Only adipocytokine w/ positive correlation

141
Q

Cholymicron apoproteins

A

Apo-E

Apo-48

142
Q

What apoproteins are on VLDL

A

Apo-B100

Apo E

143
Q

What is the underlying defect found in Familial hypercholesterolemia? What are the levels in Hetero and Homozygous forms?

A

LDL Receptor defect
Autosomal Dominant condition - complete penetrance
Hetero: TC and LDL: 250-600 mg/dL
Homo: TC and LDL: 500-1000 mg/dL w/ early CAD / death

144
Q

What is the underlying defect in Type III hyperlipoproteinemia?

A

apo-E mutation (AR)-> VLDL, IDL, LDL remnants accumulate - can’t bind to LDL receptor effectively
TG and TC elevation: 300-400 mg/dL

145
Q

What is are the symptoms of LDL deficiency?

A 
cholymicron accumulations and very high TG (AR)
early onset (homozygous)
Turbid serum
Eruptive xanthomas
Recurrent pancreatitis
Lipidemia retinalis
Hepatomegaly, splenomegaly
146
Q

When does the process of breast tissue involution begin?

A

Before menopause, age 35-40
Progressive TDLU atrophy and replacement w/ fatty stroma
Failure to involute -> increased risk of br. carcinoma

147
Q

What is the most common breast disorder?

A

Fibrocystic change

>50% of all surgical procedures

148
Q

Presentation of Intraductal Papilloma

A

serous or bloody nipple discharge
sub-areolar tumor
Typically pts. are >60 yrs

149
Q

Does In Situ Carcinoma of the breast usually present as a palpable mass?

A

In 50-75% of cases NO.

Detected as microcalcifications on mammogram

150
Q

What is Paget’s disease of the nipple? Incidence of underlying cancers?

A

Erosion / inflammation of the nipple/areola due to extension of neoplastic cells to the epidermis.
50% have underlying intraductal tumor (CIS)
50% have underlying invasive carcinoma

151
Q

What is the most common breast cancer?

A

Invasive Ductal Carcinoma

cells arranged in nests, cords, tubules, w/ fibrous stroma

152
Q

What is the appearance of invasive lobular carcinoma?

A

Cells invade stroma individually - seen aligned in single file chains
No desmoplastic stroma
more common spread to CSF and elsewhere

153
Q

What is phyllodes tumor?

A 
Low-grade Malignancy that develops w/in a fibroadenoma
Arises from breast stroma
Pts. usually >60
leaf-like projections into cystic space
highly cellular stroma
154
Q

What is the incidence of cancer development in women w/ BRCA-1 mutation?

A

85% chance in carriers
pre-menopausal breast / ovarian cancer
Triple negative cancers: Estrogen, Progesterone, HER-2 receptor negative

155
Q

In what case is breast cancer chemoprevention appropriate? Agents?

A 
Gail index >1.66% risk for 5 yrs
Tamoxifen  (ER antagonist)
Raloxifene  (SERM) if postmenopausal
- (+) estrogen in bone
- (-) estrogen in breast / uterus
156
Q

What is close surveillance for patients at high risk for breast cancer?

A

Mammograms begin 10yrs before onset of youngest affected family member
MRI if 20-25% lifetime risk
Monthly self-exams in late teens
Clinical breast exams q6 mos starting @20 yoa

157
Q

What does HER-2/neu code for? Specific drug?

A

EGFR-2, which dimerizes -> TK activity

158
Q

5 subtypes of epithelial breast cancer and relative survial

A 
Luminal A and B:  ER (+)
Basal:  ER (-)
ERBB2:  HER2/neu, EGFR2 (+)
Normal Tissue:  expresses adipose and non-epithelial genes
Survival:  A>B >> Basal and ERBB2
159
Q

What are the BIRADS categories of breast imaging results?

A

5: Highly suspicious (95% likely malignancy)
4: Suspicious (3-94% likely malignancy)
3: Probably benign (2% likelihood of malignancy)
2: Benign
1: Negative
0: Needs more workup
6: Known malignancy

160
Q

In what cases is “neo-endocrine” adjuvant therapy appropriate?

A 
ER (+) cancer in postmenopausal patients
Agent:  Anastrozole (Amiridex)
Aromatase inhibitor
Plateau in 6-9mos
Continue up to 5 yrs. post-op
161
Q

What are indications for Partial vs. Complete Mastectomy?

A

Partial: Tumor excision w/ clean margins and 30%, active conn. tiss. disease (SLE, systemic sclerosis) (may/ may not req. rad)

162
Q

Is there an increased risk of cancer associated with Lichen Sclerosis?

A

Yes. 1-4% increase in lifetime risk for Sq. Cell Carcinoma

Lesion itself is not pre-cancerous

163
Q

Characteristics of Lichen Sclerosis

A

Flattening of Rete Pegs
Acanthosis
Hydropic degeneration of basal layer
Dermal fibrosis and perivascular lymphocytic infiltrate

164
Q

How is vulvar intraepithelial neoplasia (VIN/CIN) graded?

A

VIN I: Mild dysplasia, involves lower 1/3 of epidermis (LSIL)
VIN II: Moderate dysplasia: involves lower 2/3 of epidermis (HSIL)
VIN III: Severe: full thickness (HSIL)

165
Q

What % of vulvar squamous cell carcinomas are associated with lichen sclerosis?

A

15%

p53 mutation in these

166
Q

What is the gross and microscopic appearance of Paget’s disease of Vulvar (extramammary) Paget’s Disease?

A

Gross: Erythmatous, crusted, limited to epidermis and adnexa

Microscopic: Paget’s cells (large mucinous cells w/ prominent nuclei + nucleoli, clear cytoplasm). Blue staining w/ PAS, Alcian blue, Mucicarmine

Note: no underlying tumor

167
Q

How is Melanoma In Situ differentiated from Extramammary Paget’s?

A

MIS: S-100 (+), Mucin stain (-)

168
Q

What is condyloma acuminatum associated with (infection)?

A

HPV 1 and 6 (low-risk viruses)

Benign lesions

169
Q

Histologic tropisms for HPV viruses

A

HPV-6: always squamous lesion
HPV-16: squamous or glandular
HPV-18: most common in glandular lesions

170
Q

Causes of chronic endometritis

A

Gonorrhea
Miliary TB
IUD
Spontaneous

171
Q

What is the most common cause of dysfunctional uterine bleeding?

A

Anovulatory cycle

Ovulatory failure and no progestational effect -> unopposed estrogen effect

172
Q

What drug has been connected to incidence of endometrial polyps?

A

Tamoxifen - has weak estrogenic effects on endometrium

173
Q

Most common invasive tumor of female genital tract

A

Endometrial carcinoma

174
Q

Type I vs II Endometrial carcinoma

A

Type I: younger women, estrogen related, peri-menopausal, low grade, good prog, PTEN and micro-satellite instability

Type II: older women, no estrogen link, post-menopausal, high grade, poor prog, aggressive, p53 mutation

175
Q

What are the grades of Type I endometrial cancer?

A

FIGO grades

I: well differentiated, glandular architecture, 50% solid w/ increased atypia

176
Q

What is carcinosarcoma of the endometrium?

A

Composed of a mix of malignant glands and malignant stroma
Sarcoma component may mimic other tissues: cartilage, bone, etc.
Not two tumors, but one tumor showing two differentiations

177
Q

Most common uterine tumor?

A

Leiomyoma

benign smooth muscle tumor

178
Q

3 examples of abnormal placentation

A
  1. Placenta accreta: attacment to and invasion of myometrium
    3 types: accreta, increta, percreta
  2. Placenta Previa: abnormal location of attachment - near cervix
  3. Abruptio Placentae: premature separation of placenta from uterus
    -> bleeding and possible fetal death.
179
Q

Causes of complete and partial hyatidiform mole

A

Complete: fertilization of egg that lost chromosomes -> angrogenesis (doubling of paternal chromosomes) -> normal karyogype, usually 46XX. No fetal tissues found.

Partial: fertilization of egg w/ 2 sperm -> triploid / tetraploid karyotype. Fetal tissue present.

180
Q

Risks w/ estrogen meds

A 
Endometrial cancer
Breast cancer:  uncertain - long term use
Cardiovascular outcomes (DVT (50%), stroke / TIA, primary CHD event)
181
Q

What is the oral effectiveness of natural estrogens?

A

Poor - rapid, extensive 1st pass metabolism

Estrogen derivatives: C17 modification: improved bioavailability

182
Q

3 Progestin medications

A

Progesterone
Norethindrone
Medroxyprogesterone

183
Q

What are the effects of Progesterone?

A

Development of secretory endometrium
Maintenance of pregnancy
Suppress menstruation and uterine contractions

184
Q

When can hormone replacement be used to treat osteoporosis?

A

When also treating menopausal symptoms

185
Q

What is POCD treatment?

A

Treat symptoms, modify according to patient goals

  • Lifestyle modification: aerobic exercise, controlled eating, orlistat, tobacco avoidance
  • Eflornithine cream: inhibit ornithing decarboxylase -> reduce hair growth
  • Oral Contraceptives (reduce LH)
  • Spironolactone (anti-androgen)
186
Q

What drugs can be used to induce ovulation in patients with PCOS?

A

Metformin: +/- clompiphene. Incosistent result
Thiazolidinediones (reduce insulin levels)
Clomiphene: Increase FSH / LH (80% ovulate, 50% conceive)
Gonadotropin therapy

187
Q

When is Clomiphene administered for fertility treatment?

A

5 day course on days 3-7 or 5-9 of follicular phase

early admin increases likelihood of multiple follicle recruitment for maturation

188
Q

When does ovulation occur following gonadotropin administration? what is it?

A

24-36 hours
Gonadotropin is injectable FSH or FSH + LH
admin daily throughout follicular phase, then hCG -> ovulation 34-36 hours later

189
Q

What is balanoposthitis?

A

Penile inflammatory condition
Infection of glans and prepuce due to poor hygiene + smegma
Candida, anaerobes, gardnerella, pyogenic bacteria

190
Q

Chancroid agent

A

Hemophilus ducreyi

Painful chancre - rare in US

191
Q

Granuloma inguinale agent

A

Klebsiella granulomatis

192
Q

Virus most assoc. w/ penile carcinoma in situ

A

HPV 16

193
Q

What are Bowen disease and Bowenoid papulosis?

A

Both penile carcinoma in situ usually associated w/ HPV 16
Microscopically indistinguishable, but morphologically distinct.
Bowen: over 35yoa, gray-white opaque plaque. 10% progress to infiltrating squamous carcinoma
Bowenoid: <35 yoa. papules. Never progresses to cancer

194
Q

What are the major causes if epididymitis and orchitis by age?

A

Peds: gram (-) rods, assoc w/ genitourinary malformation
<35: chlamydia, neisseria
Older: E.coli, Pseudomonas

195
Q

What can result from ascendin gonorrheal infection of the male GU tract?

A

Abscesses of epididymis and extensive damage / destruction

196
Q

Where are Leydig cells found?

A

Testicular interstitium - between seminiferous tubules

197
Q

Cells of seminiferous tubule and roles

A

Spermatogenic cells - mature to spermatocytes

Sertoli cells- maintain maturing spermatozoa, secrete Mullerian Inhibiting Factor (MIF)

198
Q

What are risk factors for male germ cell tumors? Common genetic marker?

A 
Cryptorchidism - 10% of cases.  Higher risk w/ higher level of undescended testicle
Genetic - family hx
Testicular dysgenesis (Kleinfelter's)

i(12p) found in 90% of cases

199
Q

Most common male germ cell tumor and marker

A

Seminoma

Shows elevated placental alkaline phosphatase

200
Q

What is spermatocytic seminoma?

A

Develops in older patients (>65 yoa)
Slow growing, does not metastasize, excellent prognosis
No lymphocytic infiltrate
3 cells: medium (most numerous), small, scattered giant cells

201
Q

What is Embryonal carcinoma?

A 
Form of testicular cancer
Rare
20-30 yr age range
epithelial cells, primitive papillary architecture, bizarre cytology w/ syncytial cels
Markers:  hCG, AFP
202
Q

What are the most common testicular tumors by age group?

A

Pre-pubescent: yolk sac tumor
20-30: Embryonal seminoma
30s: Seminoma
>65: Spermatocytic seminoma

203
Q

What is the microscopic feature most frequently associated with yolk sac tumors of the testes?

A

Schiller-Duval bodies : primitive glomerular cell formations

204
Q

Identifying features of testicular choriocarcinoma

A 
Resembles chorionic vili and contains 2 cell types:
-syncytiotrophoblast
-cytotrophoblast
Prominent hemorrhage and necrosis
expression of hCG -> gynecomastia
205
Q

Are teratomas in men benign?

A

In children: yes

Adult: always treated as malignant

206
Q

What is the presentation of Leydig Cell tumors?

A

Usually sexual precocity due to androgen production
May present w/ gynecomastia
Testicular swelling

207
Q

What is seen pathologically in Leydig cell tumors

A

Cicrumscribed nodule, golden color on cut surface

Well differentiated cytology, Rienke crystals

208
Q

How do Sertoli tumors present?

A

Usually hormonally silent (may produce androgen, but low level)
Cells (tall, columnar) arragnged in cordlike structures and tubules

209
Q

What is the most common testicular cancer in older men?

A

Testicular lymphoma

Poor prognosis

210
Q

What is the most common cause of granulomatous prostatitis?

A

BCG (TB vaccine) treatment of bladder cancer

211
Q

Pharm treatments for BHP

A

a-blocker, DHT inhibitor

212
Q

Precursor to prostate cancer

A

High grade intraepithelial neoplasia

213
Q

What is the best tool for determining prognosis of prostate cancer?

A

Gleason grading + stage
Gleason: 1-5 based on differentiation / pattern
1: well differentiated, glandular pattern
5: No differentiation

214
Q

Targets of Testosterone vs. Dihidrotestosterone

A

T: hair, muscle, libido, brain, Wolffian duct
DHT: external genitalia, male pattern body hair, prostate

215
Q

In males what are the respective target cells of FSH and LH?

A

FSH: Sertoli -> spermatogenesis (Inhibin decreases FSH)
LH: Leydig -> testosterone (neg feedback to decrease LH)

216
Q

What can Inhibin B levels be used to estimate?

A

Number of active Sertoli cells

217
Q

In a young male w/ hypgonadism when should testosterone levels be checked?

A

Evening - low levels.

Diurnal variation of Testosterone: high in morning, low in evening

218
Q

What is Klinefelter’s Syndrome?

A

Male w/ XXY genotype -> hypogonadism
Damage to seminiferous tubules and Leydig cells
High gonadotropins, low T

219
Q

What occurs in gonadal dysgenesis?

A

Mutation in sex determining region of Y chromosome -> streak gonads and female external genitalia
High risk of malignancy of gonads
Low GnRH -> low sex hormones

220
Q

What is Kallman’s syndrome?

A

X-linked (usually) hypogonadism
KALIG-1 defect -> failed migration of GnRH cells from olfactory placode -> hypothalmus
anosmia, mid-line defects, R-G colorblindness, neurosensory hearing loss

221
Q

What lab finding constitute male infertility (semen analysis)?

A

3 abnormal samples over a 3 month period

222
Q

What is 17a-alkylated Testosterone?

A

Daily dosing testosterone replacement
May be used for post-putertal hypogonadism
HEPATOTOXIC: not routinely used or recommended

223
Q

What effect can testosterone supplementation have on male fertility?

A

T -> fedback inhibition on LH and FSH -> decreased sperm production and reduced fertility

224
Q

3 GnRH Agonists

A

Leuprolide
Goserelin
Triptorelin

Agonism -> downreg of GnRH receptor -> decreased Testosterone

225
Q

4 GnRH Antagonists

A 
-elix drugs
Cetrorelix:  IVF
Ganirelix:  IVF
Degarelix:  prostate ca
Abarelix:  not in US - paliative prostate ca. care
226
Q

3 non-steroidal AR antagonists used in Prostate Ca

A

Flutamide
Bicalutamide
Nilutamide

Often used w/ GnRH antagonist

227
Q

5a-reductase inhibitors

A

Finasteride
Dutasteride
Bicalutamide

228
Q

How does genetic imprinting occur?

A

Methylation of cytosines on CpG islands in regulatory sequences of DNA

229
Q

What is MEN1?

A

Autosomal Dominant INACTIVATION of tumor suppressor MENIN
Results in multiple endocrine neoplasias of 3Ps:
Parathyroid, Pancreas, Pituitary and others
hypoparathyroidism in >90% of cases
55% of deaths due to reasons other than MEN1

230
Q

What is MEN2?

A

AD ACTIVATING mutation of c-RET proto-oncogene
MEN2A: Pheochromocytoma, hyperparathyroidism, medullary thyroid carcinoma, hirschprung, cutaneous lichen amyloidosis
MEN2B: Marfanoid body, neuromas on tongue and GIT, thick lips and eyelids, NO HYPERPARATHYROIDISM

231
Q

How does psuedohypoparathyroidism type 1a differ from 1b?

A

1a: presents with albright hereditary osteodystrophy due to tissue resistance to hormones other than PTH (inc. LH, FSH, GRF, CRF)
1b: PTH resistance only, no AHO

232
Q

What are the hypothalamic nuclei involved w/ hunger /satiety?

A

Lateral: hunger: lesion -> anorexia
Ventromedial: satiety: lesion -> overeating

233
Q

What is the neurocircuit model of hunger / satiety?

A

Arcuate nucleus is center of hunger / satiety
Neuronal expression of:
NPY / AgRP: increase hunger
aMSH / CART: decrease hunger

234
Q

What is AgRP’s role in obesity?

A

AgRP is specific inhibitor of aMSH at MC4 in hypothalamus -> obesity
Human mutations of AgRP -> increased BMR and obesity resistance

235
Q

What are MC3 and MC4?

A

Melanocortin receptors in hypothalamus that decrease appetite and increase BMR.
Agonized by MSH
Antagonized by AgRP
Agonist drugs: experimental anti-obesity drugs

236
Q

What is the role of Leptin in obesity?

A

produced by adipocytes (increased mass -> increased leptin)
Increases activity of aMSH neurons -> decreased hunger / increased MR
Many obese: resistant to leptin

237
Q

What is orlistat and MOA?

A

drug for treatment of obesity

Inhibits gastric and pancreatic lipase w/in intestine -> reduced TG absorption

238
Q

What is Lorcaserin and MOA?

A

Lorcaserin: obesity drug

5HT2C agonist -> increased POMC production -> increased MSH -> increased activity of MC3 and MC4 -> decrease in hunger

239
Q

Most common type of primary ovarian neoplasm?

A

Surface epithelial tumor

240
Q

What organisms are associated with Pelvic Inflammatory Disease?

A

N. gonorrheae, Chlamydia, anaerobes (bacteroides, peptostrepto), aerobes (E.coli), mycoplasma

M2 (19 decks)

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