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ENDO 2 Exam II (2017) > Kinder CIS > Flashcards

Kinder CIS Flashcards

1
Q

Secondary Hypertension causes

A 
Renal parenchymal disease
Renal artery stenosis
Obstructive sleep apnea
Endocrine:
- Hyperaldosteronism
- Thyroid disease
- Cushing disease
Pheochromocytoma
Coarctation of the aorta
CNS (Brain Tumor)
Medications (NSAID)
Polycythemia
Pre-eclampsia
Hypercalcemia (renal dysfunction and vasoconstriction)
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2
Q

what is essential hypertension?

A

idiopathic

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3
Q

Primary Aldosteronism – Who to screen

A

Blood pressure ≥ 150/100 mm Hg on 3 separate occasions
Drug Resistant Hypertension
BP > 140/90 mm Hg that is resistant to 3 medications including a diuretic
Controlled blood pressure on 4 medications
Hypertension and hypokalemia
Hypertension with an adrenal incidentaloma
Hypertension and sleep apnea
Hypertension with a family history of early onset hypertension or stroke age under 40
Hypertension and first-degree relative with primary aldosteronism

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4
Q

testing aldosteronism- Test Preparation

A

Correct hypovolemia and hypokalemia
Stop spironolactone, eplerenone, amiloride, potassium wasting diuretics, licorice, and chewing tobacco at least one month before testing
Patient should be ambulatory and sitting upright with a morning sample
Substitute antihypertensives:
Verapamil, hydralazine, and doxazosin

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5
Q

Etiologies of Primary Hyperaldosteronism

A

Unilateral aldosterone-producing adenoma ≅ 50%
Bilateral Adrenal Hyperplasia ≅ 50%

Rarer:
Inherited glucocorticoid-remedial aldosteronism
- ACTH instead of angiotensin II regulated
- Suppressed by low dose glucocorticoids
Unilateral adrenal hyperplasia
Bilateral aldosterone producing adenomas
Adrenocortical carcinoma

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6
Q

tests to confirm primary hyperaldosteronism

A

Oral Salt Loading Test – most common test
Saline Suppression Test
Fludrocortisone Suppression Test

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7
Q

Oral Salt Loading Test

A

6 gm salt per day for 3 days
Maintain normokalemia
24-hour urinary aldosterone > 12 mcg/day suggestive of primary aldosteronism

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8
Q

Saline Suppression Test

A

2 liters normal saline infusion over 4 hours

Plasma aldosterone ≥ 10 ng/dL confirms primary aldosteronism

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9
Q

Fludrocortisone Suppression Test

A

Fludrocortisone 0.1 mg po q 6 hours for 4 days
NaCl 1800 mg po tid, High Salt Diet, Supplemental Potassium
Plasma aldosterone > 6 ng/dL day 4 consistent with primary aldosteronism

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10
Q

Adrenal Venous Sampling

A

Best test to determine if small adenoma on CT is secreting aldosterone
Differentiate between bilateral or unilateral hyperplasia

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11
Q

treating adrenal hyperplasia

A

Treat hypertension and hypokalemia with spironolactone and oral potassium supplementation

Unilateral laparoscopic adrenalectomy for unilateral adrenal hyperplasia or unilateral aldosterone producing adenoma

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12
Q

11-β-hydroxysteroid dehydrogenase 2

A

Enzyme expressed in aldosterone-selective epithelial tissues such as kidney, colon, salivary, and sweat glands.
Oxidizes cortisol to the inactive metabolite cortisone preventing illicit activation of the mineralcorticoid receptor.
Glycyrrhizinic acid in black licorice inactivates 11-β-HSD 2 causing pseuodohyperaldosteronism
Syndrome of apparerent mineralocorticoid excess is caused by a genetically inherited deficiency of 11-β-HSD 2

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13
Q

Liddle Syndrome

A

Autosomal Dominant
Dysregulation of epithelial sodium channel (ENaC) due to a genetic mutation that causes the channels to no longer be degraded appropriately
High number of channels present in the collecting ducts lead to pseudohyperaldosteronism (↓PRA, ↓PAC)

Treatment is with potassium sparing diuretics

  • Amiloride
  • Triamterene
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14
Q

17 alpha hydroxylase deficiency

A

mineralocorticoids up
cortisol and sex hormones down

hypertension
hypokalemia
decreased DHT

male: ambiguous genitalia, pseudo-hermaphroditism
female: lack of 2ndary sexual characteristics

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15
Q

21-hydroxylase deficiency

A

decreased mineralocorticoids, decreased cortisol
increased sex hormones

hypotension
hyperkalemia
increased renin activity
increased 17-hydroxyprogesterone

presents in infancy

  • salt wasting
  • precocious puberty
  • female: virilization
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16
Q

11 beta hydroxylase enzyme deficiency

A

decreased aldosterone
increased 11-deoxycorticosterone

decreased cortisol
increased sex hormones

hypertension with low renin

female virilization

17
Q

Hirsutism

A

Due to decreased sex hormone binding globulin leading to increased free testosterone

Decreased estrogen (e.g. prolactinoma)
Insulin
Growth Hormone (acromegaly)
Obesity (especially PCOS)
Hypothyroidism
Glucocorticoids (Cushings)
Androgens
Nephrotic Syndrome
18
Q

causes of hirsutism

A

PCOS (70-80% of cases)
- Irregular menses, central obesity, infertility, acanthosis nigricans, and insulin resistance

Idiopathic hyperandrogenemia (6-15% of cases)
- Clinical and biochemical signs of hyperandrogenemia with regular ovulatory cycles
Idiopathic hirsutism (50% of mild cases)
- Normal androgens, normal ovulation, normal appearing ovaries

Congenital Adrenal Hyperplasia (< 5% of cases)
- Menstrual dysfunction and anovulation

19
Q

Rare etiologies of hirsutism

A 
Acromegaly
Cushing syndrome
Hyperprolactinemia
Hyperthecosis
Thyroid dysfunction
Glucocorticoid resistance
Drugs
- Anabolic Steroids
- Androgenic steroids
- Valproic acid
Androgen secreting adrenal or ovarian tumor
20
Q

Labs for patients with hirsutism

A 
Fasting Glucose/Insulin
TSH
Prolactin 
IGF-1
24 hour urine Cortisol

Testosterone
DHEAS
17OHP

of those last three tests:
Idiopathic or hereditary - all normal
PCOS (LH/FSH > 2) - testosterone mildly increased
CAH - all increased (17 OHP > 500* ng/dL = CAH)

21
Q

Virilization:

A

Increased muscularity, temporal alopecia, deepening voice, acne, clitoromegaly - Adrenal, Ovaries, CAH

Labs usually show increase of:
testosterone (ovarian neoplasm)
DHEAS (adrenal neoplasm)
androstenedione (adrenal or ovarian)

22
Q

Labs for patients with virilization

A
  1. Ovarian tumor
    total testosterone greatly increased with normal
    DHEAS and 17 OHP. (Total Testosterone > 200 ng/dL points to ovary or adrenal)
  2. Adrenal tumor
    greatly increased DHEAS (> 700ng/dL)
  3. CAH
    Total Testosterone, DHEAS, and 17 OHP = all increased.
    (17 OHP > 500 ng/dL = diagnostic)
23
Q

Labs for patients with hirsutism or virilization

A

** Total testosterone > 200 ng/dL = ovarian neoplasm

Serum androstenedione > 1000 ng/dL = adrenal or ovarian neoplasm

** DHEAS > 700mcg/dL = adrenal neoplasm or CAH

17-hydroxyprogesterone = CAH **(> 500 ng/dL is diagnostic); CAH usually has base line > 300ng/dL with ACTH stimulated to > 1000 ng/dL)

ACTH and 24 hour urine cortisol

LH:FSH > 2 (PCOS)

TSH, prolactin,

24
Q

Treatment of Hirsutism

A

Combination Oral Contraceptives

Antiandrogens
- Spironolactone
- Finasteride (5-alpha reductase inhibitor)
- Metformin (reduces hepatic gluconeogenesis)
—- Lowers peripheral insulin sensitivity
—- Lowers insulin levels
—- Not great for hirsutism
GnRH agonists (decrease gonadotropins by constant stimulation)

25
Q

Pheochromocytoma symptoms

A

Classic Triad of Symptoms:
Paroxysmal headache, palpitations, and sweating

Other paroxysmal symptoms:
Anxiety, pallor/flushing, syncope, tremor, blurred vision, heat intolerance, nausea, vomiting, abdominal pain, diarrhea, constipation, polyuria, polydipsia, weight loss, fatigue, chest pain, low grade fever

26
Q

labs to confirm pheochromocytoma

A

24 hour Urinary Fractionated Metanephrines or Plasma Free Metanephrines

  • Metaneprhine (epinephrine metabolite)
  • Normetanephrine (norepinephrine metabolite)

Other testing

  • 24 hour urine catecholamines
  • – Norepinephrine, epinephrine, and dopamine
  • 24 hour urine vanilylmandelic acid (norepineprhine metabolite) , homovanillic acid (dopamine metabolite)
27
Q

pheochromocytoma treatment goals

A

get blood pressure and heart rate down

less than 1 PVC every 5 minutes on EKG
No S-T segment changes or T-wave inversions on EKG

28
Q

meds for pheochromocytoma

A

Alpha-adrenergic blocker - 1st
Phenoxybenzamine

Beta-adrenergic blocker – 2nd
Atenolol

Increase intake of salt and fluid for volume expansion if needed

29
Q

Precipitators of adrenergic crisis

A 
Postural changes or increase in intra-abdominal pressure
Exertion, Trauma
Foods/Beverages
--- Banana, cheese, caffeine
Emotional Stress
Urination(bladder pheochromocytoma)
Drugs
--- Corticosteroids, metoclopramide, phenothiazines, tricyclic antidepressants, sympathomimetics, morphine, nasal decongestants, glucagon, chemotherapeutic agents
Induction of anesthesia
Manipulation of the tumor
30
Q

where pheochromocytomas arise

A

80-85% of pheochromocytomas arise in the adrenal
10-20% :
symphathetic ganglia in pelvis, mediastinum, or neck
Along cranial nerves
Vagus (parasympathetic)
Most common site in the abdomen is at the origin of the inferior mesenteric artery

31
Q

Pheochromocytoma Rules of 10

A 
10% Extra-adrenal
10% Bilateral
10% Malignant
10% Children
10% Familial
10% not associated with hypertension
10% contain calcification
32
Q

Genetic Disorders associated with Pheochromocytomas

A

MEN 2A
MEN 2B
Von Hippel Lindau Syndrome
Hereditary Paraganglioma-Pheochromocytoma Syndromes

33
Q

Multliple Endocrine Neoplasia 2A (Autosomal Dominant)

A

Mutation of germline RET (neural crest cells)
Pheochromocytoma
Parathyroid Tumors
Medullary Thyroid Cancers

34
Q

Multiple Endocrine Neoplasia 2B (Autosomal Dominant)

A

Mutation of germline RET
Medullary Thyroid Cancers
Pheochromocytoma
Mucosal Neuroma
Intestinal ganglioneuromas
Muscle, joint, and spinal problems – Marfinoid body habitus
Facial Features including swollen lips, and thick eyelids

35
Q

Von Hippel-Lindau Syndrome – Autosomal Dominant

A 
Retinal angiomatosis
Cerebral hemangioblastoma
Pheochromocytoma
Renal cyst/Carcinoma
Pancreatic cysts
Endolymphatic sac tumor
Bilateral papillary cystadenomas of the epididymis in men and broad limagment of the uterus in women
Genetic: VHL
36
Q

Hereditary Paraganglioma-Pheochromocytoma Syndromes

A

Autosomal Dominant
Paragangliomas in the skull base, upper mediastinum, and neck are usually parasympathetic and generally do not secrete.
Paragangliomas in the lower mediastinum, abdomen, and pelvis are typically associated with the sympathetic nervous system and hypersecrete catecholamines

37
Q

Gynecomastia etiologies

A 
Physiologic - 25% 
- Neonatal, pubertal, or aging
- 90 % newborns, 50% of boys during puberty, 65% of hospitalized men age 50-80
Idiopathic – 25%
Medication- 10-25%
Cirrhosis 8 %
Hypogonadism
Tumors
Hyperthyroidism
Chronic Renal Insufficiency
Obesity
Drugs:
Cimetidine
Finasteride
Cannabinoids
Omeprazole
Ranitidine
Spironolactone
Diazepam
Phenytoin
Phenothiazines
Opioids
38
Q

Testing for gynecomastia

A

Pubertal Gynecomastia
Does not need further testing in most cases

Testing when etiology unclear:
Liver and kidney function
Thyroid function
Testosterone, LH, FSH, and Prolactin
Serum estradiol
Beta-HCG, AFP  - rule out germ cell tumors
DHEA-Sulfate – adrenal androgens

Testicular Ultrasound

  • Testicular mass
  • Gynecomastia > 5 cm
  • Elevated hCG
  • Elevated estradiol
  • Unclear etiology for gynecomastia

Breast Cancer suspicion

  • Breast ultrasound and mammogram
  • Biopsy

Abdominal CT if adrenal tumor suspected

39
Q

treatment of gynecomastia

A

Pubertal boys reassurance and watchful waiting
Asymptomatic men with long standing gynecomastia no treatment necessary
Stop offending medications
Medications
- Antiestrogens – tamoxifen or raloxifene
- Androgens – danazol
Surgery

ENDO 2 Exam II (2017) (19 decks)

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