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Endocrinology > Hyperprolactinemia and Hyperaldosteronism > Flashcards

Hyperprolactinemia and Hyperaldosteronism Flashcards

1
Q

Hyperprolactinemia

-epidemiology

A

-condition of elevated serum prolactin

  • women are more likely to be diagnosed than men
  • women aged 25-34 years
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2
Q

Hyperprolactinemia

-pathogenesis (6)

A
  • prolactin is produced and secreted by anterior pituitary, inhibited by dopamine
  • prolactin is metabolized by the liver and the kidney
  • if dopamine delivery is impaired –> prolactin secretion increases and hyperprolactinemia develops
  • it may develop as a result of physiological, pharmacological or pathological effect on the hypo-pituitary dopaminergic connections
  • in women –> prolactin inhibits ovulation by blocking GnRH production and secretion –> infertility
  • in men –> elevated prolactin –> GnRH inhibition –> inhibition of spermatogenesis –> infertility
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3
Q
  1. Primary function of prolactin

2. Consequences of prolonged hyperprolactinemia

A
  1. stimulate milk production in response to lactation

2. secondary reduction in bone mineral density

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4
Q

Prolactin synthesis and secretion are affected by:

  1. Prolactin releasing factors
  2. Prolactin inhibiting factor
A
  1. Thyrotropin releasing hormone (TRH), Vasoactive intestinal peptide (VIP), endothelial growth factors, dopamine antagonists, estrogen
  2. Dopamine
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5
Q

Hyperprolactinemia

-etiology (6)

A
  • physiological –> coitus, exercise, lactation, pregnancy, sleep, stress
  • pathological –> pituitary or hypothalamic-pituitary stalk damage
  • systemic disorders –> chronic renal failure, cirrhosis, PCOS, hypothyroidism
  • pharmacological
  • genetic mutations (MEN1)
  • ectopic production
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6
Q

Hyperprolactinemia

  • signs and symptoms:
    1. women (6)
    2. men (6)
A
  1. galactorrhea, oligomenorrhea, amenorrhea, decreased libido, infertility, low bone mass (osteoporosis, osteopenia)
  2. gynecomastia, galactorrhea (rare), decreased libido, infertility, erectile dysfunction, low bone mass (osteoporosis, osteopenia)
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7
Q

Hyperprolactinemia

-diagnostics

A

If serum prolactin is elevated:

  1. exclude physiological and pharmacological causes
  2. neuroradiological imaging of hypothalamic-pituitary region

Lab test

  1. serum prolactin and macroprolactin
  2. breast examination
    * **it is necessary to determine serum prolactin 2 times or more because its secretion is pulsatile
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8
Q
  1. Macroprolactin (4)

2. Normal prolactin ranges

A
  • present in asymptomatic hyperprolactinemia
  • represents large circulating aggregates of prolactin and antibodies –> they are biologically inactive –> can be misdiagnosed as prolactin hypersecretion
  • PEG >65 % - true hyperprolactinemia
  • PEG <30 % macroprolactinemia
  • Women 72-511 (3-25 ng/mL)
  • Men 86-390 (2,2-20 ng/mL)
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9
Q

Hyperprolactinemia

-treatment

A
  • dopamine agonists (DA) –> reduce prolactin hypersecretion and clinical symptoms
  • if asymptomatic –> treatment is not recommended
  • drugs –> most common cause of non-tumor hyperprolactinemia
  • DA - Bromocriptine and Cabergoline
  • Cabergoline is preferred –> higher efficacy, fewer side effects
  • not prescribed during pregnancy
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10
Q

Hyperprolactinemia

  • duration of treatment
  • withdrawal of medication
A
  • after start of treatment –> PRL test i repeated every 1 month and later every 1-2 months
  • normoprolactinemia not achieved –> gradually increase dose
  • normoprolactinemia is achieved –> dose adjustment –> after 2 years, it may be discontinued
  • investigate prolactin level 3 days after stopping it
  • if it rises >50% –> restart treatment
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11
Q

Prolactinoma (4)

A
  • most common cause of PRL excess
  • benign tumor of lactrophs
  • micro <10mm diameter
  • macro >10mm diameter
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12
Q

Prolactinoma

-pathogenesis

A

-tumors inhibit dopamine induced hyperprolactinemia because of pressure on the pituitary stalk or interruption of the vascular connections between the pituitary and hypothalamus

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13
Q

Prolactinoma

-epidemiology (5)

A
  • more common in women
  • microadenomas are more common
  • macroadenomas are more common in men
  • clinical presentation in women are more obvious and present earlier than in men
  • may be associated with MEN1 syndrome
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14
Q

Prolactinoma

  1. Sign and symptoms caused by high prolactin
  2. Sign and symptoms caused by mass effect
  3. Local effects
A
  1. women: oligomenorrhea, amenorrhea, infertility, galactorrhea, low bone mass
    men: decreased libido, impotence, infertility, oligospermia, gynecomastia, erectile dysfunction, low bone mass
  2. headache, visual field defect, external ophthalmoplegic, bitemporal hemianopia
  3. chiasmatic compression, cranial nerve damage, hypothalamic damage, bony invasion: pain, CSF leaks
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15
Q

Prolactinoma

-diagnosis (6)

A
  • when PRL is elevated 10-fold above normal
  • macroprolactinoma 200 and above
  • macroprolactin and serum prolactin
  • MRI of the pituitary with contrast
  • visual field testing
  • no possible markers for predicting the possible malignancy of prolactinoma
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16
Q

The Hook effect (2)

A
  • sometimes, patients can have clear symptoms of hyperprolactemia but lab results are negative because of increased concentration of the hormone.
  • so a dilution method is used to get a clear result.
17
Q

Prolactinoma

-treatment (5)

A
  • medical: dopamine agonist
  • surgical: transsphenoidal surgery
  • radiation treatment
  • surgery and radiation is only done when patient is resistant to medical treatment
  • microprolactinoma - dopamine agonists for 2 years
18
Q

Transsphenoidal surgery

  • indications (4)
  • complications (3)
A
  • the patient is intolerant to high doses of DA
  • resistance to DA
  • macroprolactinoma with threat of optic nerve damage
  • suspected malignancy

-hypopituitarism, diabetes insipidus, cerebrospinal fluid leaks

19
Q

Radiation therapy

  • indications (3)
  • complications (4)
A
  • relapse after surgical treatment, aggressive prolactinoma, malignant prolactinoma
  • hypopituitarism, damage to cranial nerves, increased stroke probability, secondary tumor formation
20
Q

Adrenal gland

-parts

A
  • outer –> adrenal cortex
  • inner –> medulla

the cortex has 3 layers (zones)

  1. Zona glomerulosa (mineralocorticoids)
  2. Zona fasciculata (glucocorticoids)
  3. Zona reticularis (androgens)
21
Q

Primary hyperaldosteronism

  • definition
  • characterized by: (5)
A
  • renin-independent aldosterone hyperproduction syndrome
  • increased aldosterone secretion, decreased plasma renin activity (PRA), increased arterial BP, hypokalemia and metabolic alkalosis
22
Q

Primary hyperaldosteronism

  • most common cause of:
  • Conn’s syndrome
A
  • secondary hypertension
  • patients have a higher incidence of cardiovascular disease

-primary hyperaldosteronism because of aldosterone producing adenoma

23
Q

Primary hyperaldosteronism

-hypersecretion of aldosterone causes: (5)

A
  1. hypertension
  2. affects the cardiovascular system
  3. suppress plasma renin activity (PRA)
  4. decreases sodium excretion in the kidneys
  5. increases potassium excretion –> hypokalemia
24
Q

Renin-angiotensin-aldosterone system

A
  • regulates sodium circulation and BP
  • raises sodium and water reabsorption and increases vasoconstriction
  • main components –> renin, angiotensin II, aldosterone
  1. Renin
  2. Angiotensinogen –> angiotensin I
  3. Angiotensin I + angiotensin converting enzyme (ACE)
  4. Angiotensin II –> stimulates adrenal glands
  5. Aldosterone
25
Q

Factors that stimulate renin secretion (3)

A
  • decreased arterial BP
  • decrease sodium concentration
  • sympathetic nervous system activity (beta 1)
26
Q
  1. Angiotensin II - what does it do (7)

2. Aldosterone - what does it do

A
  1. increases BP, reduced renal blood flow, increases aldosterone secretion, enhances the release of norepinephrine and epinephrine, stimulates center of thirst in hypothalamus, increase osmotic pressure, release ADH
  2. sodium and water reabsorption and potassium secretion –> increase BP, decrease potassium
27
Q

Types of Primary hyperaldosteronism (6)

A
  • aldosterone producing adenoma
  • bilateral idiopathic hyperaldosteronism or idiopathic hyperplasia
  • unilateral hyperplasia or primary adrenal hyperplasia
  • pure aldosterone-producing adrenocortical carcinoma
  • familial hyperaldosteronism
  • ectopic aldosterone secreting tumors
28
Q

Primary hyperaldosteronism

-clinical presentation (4)

A
  • arterial hypertension (severe >150/>100 mmHg)
  • hypokalemia - muscle weakness and cramping
  • mild hypernatremia
  • metabolic alkalosis - due to hypokalemia and aldosterone H+ urinary excretion
29
Q

Primary hyperaldosteronism

-lab tests - diagnosis (4)

A
  • measure plasma renin activity (PRA) or plasma renin concentration (PRC) and plasma aldosterone concentration (PAC)
  • increased PAC/PRA ratio –> suspicious for primary aldosteronism –> screening test
  • oral sodium loading test - high sodium diet for 3 days –> urine test –> measure aldosterone, sodium and creatinine
  • intravenous saline infusion test - after an overnight fast –> values above 10 ng/dL (277 pmol/L) are conclusive
  • Captopril challenge test
30
Q

Primary hyperaldosteronism

-imaging tests - diagnosis (2)

A
  • Adrenal computed tomography (CT) - adrenal carcinoma should be suspected when a unilateral, large (>4cm) adrenal mass is found on CT
  • Adrenal vein sampling (AVS) - before planning surgical management –> invasive, often unsuccessful
31
Q

Primary hyperaldosteronism

-treatment

A
  • surgery –> for patients with unilateral disease
  • medication –> for patient with bilateral adrenal hyperplasia
  • FH type I –> glucocorticoids
32
Q

Primary hyperaldosteronism

-medications

A

Mineralocorticoid receptor antagonist - potassium sparing diuretics:

  • Spironolactone - the most effective, but has antiandrogenic effect (can cause painful male gynecomastia, erectile dysfunction and decrease libido). Contraindicated during pregnancy
  • Eplerenone - has no antiandrogenic effect. Can be used during the pregnancy

Antihypertensive therapy
-ACE inhibitors, ARBs, calcium channel blockers

33
Q

TSH and prolactin (2)

A
  • Primary hypothyroidism causes an elevation of TRH, which can cause an elevation of prolactin along with TSH.
  • Prolactin levels in patients with hypothyroidism tend to be lower than those usually seen with prolactinomas (the latter are usually 150-200 ng/mL or higher).
34
Q

Primary vs Secondary hyperaldosteronism

A
  1. Primary - high aldosterone, low renin

2. Secondary - high aldosterone, high renin

35
Q

Diagnostic steps for the diagnosis of hyperaldosteronism (6)

A
  1. typical symptoms
  2. aldosterone to renin ratio
  3. if abnormal –> confirmatory tests (oral sodium loading test, IV saline infusion, Captopril challenge test)
  4. if confirmatory tests are abnormal –> adrenal CT scanning
  5. if patient is unsuitable for surgery –> medication, if not –> adrenal venous sampling
  6. unilateral –> laparoscopic ADX, bilateral –> MR antagonists
36
Q

Hyperprolactinemia

-treatment - side effects (7)

A
  • nausea
  • vomiting
  • postural hypotension
  • nasal stiffness
  • depression
  • digital vasospasm
  • high doses –> associated with a risk of heart valve regurgitation
37
Q

Who should be tested for primary hyperaldosteronism? (7)

A
  • severe hypertension
  • drug-resistant hypertension
  • hypertension and family history
  • all hypertensive first-degree relatives of patients with PH
  • hypertension and spontaneous or low dose, diuretic induced hypokalemia
  • hypertension with adrenal incidentaloma
  • hypertension with sleep apnea
38
Q

Conditions for examining a patient with hyperaldosteronism (4)

A
  1. potassium levels should be corrected first –> hypokalemia suppresses aldosterone
  2. 2 weeks prior to testing use sufficient amount of salt (>6g/d)
  3. Blood is drawn in the morning after the patient has spent 2hour in the vertical position and sat for 15-60minutes before taking blood
  4. Stop medications which could influence the results
39
Q

When to order macroprolactin values? (2)

A
  • asymptomatic or patients with not so expressed symptoms

- older women with hypophysis tumor and we need to assess for normal deficiency

Endocrinology (11 decks)

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