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19 Cards in this Set
- Front
- Back
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Hyperaldosteronism |
primary or secondary - primary form AKA Conn’s disease caused by aldosterone secreting adenoma but could also be related to adrenal hyperplasia or defective enzymes - secondary: caused by arterial hypertension, heart failure, liver failure and ascites Check for aldosteronism in patients with: hypertension, renal mass, hypokalemia, familial history of aldosterone secreting tumors - conn’s disease is more frequent than pheochromocytomas but it’s rare If BP is normal there is no chance to have hyperaldosteronism at least the primary form |
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Symptoms of aldosteronism |
- hypokalemiam, asthenia, cramps, arrhythmia, hyperglycemia, diabetes, high risk of osteoporosis |
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Diagnosis of aldosteronism |
- based on renin and aldosterone serum sampling - aldosterone is high and renin is low because of negative feedback measured in different conditions (orthostatic and clinostatic) - in clinostatin: aldosterone and renin are low Interfering drugs: anti-hypertensive drugs (except from doxasozin), all diuretics acting on serum potassium levels (both sparing and wasting potassium), that can create positive/negative results because changes in potassium levels may increase/decrease aldosterone levels - when having potassium sparing diuretics, you are going to have high aldosterone levels and potassium wasting diuretic, low aldosterone - high intake of sodium= high BP, low renin, lower than aldosterone |
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Dynamic tests for aldosteronism |
- administration of physiological saline solution = increasing blood volume, high sodium administration, aldosterone should decrease in normal conditions - fludrocortisone suppression test= administration of synthetic aldosterone and serum aldosterone levels should be suppressed in physiological conditions - captopril test: ACE inhibitors, aldosterone goes down, the enzyme involved in synthesis of angiotensin II STIMULATES ALDOSTERONE PRODUCTION |
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Adrenal vein sampling |
- imaging: CT and MRI If we can’t detect any lesions/or have bilateral lesions with high levels of aldosterone= we are unsure about diagnosis and perform 24h aldosterone analysis to evaluate daily secretion of aldosterone If we want to detect the adrenal gland responsible for hypersecretion, we perform adrenal vein sampling, we check for aldosterone levels at the vena cava and below the kidney veins (ALDOSTERONE SHOULD BE HIGHER ABOVE) - we check for lateralisation and sample blood coming from right adrenal vein and left renal vein and check for difference between them. We have to be sure we are in the adrenal vein and since it is the only one secreting cortisol, we administer synachten (Synthetic ACTH) and check for cortisol + aldosterone - ACTH has no influence on aldosterone release but it has on cortisol release and if cortisol is high we are in adrenal veins, while if its low/the same as in the periphery we are not sure we are in the adrenal vein |
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Therapy for aldosteronism |
- 1st line: adrenalectomy You perform it after normalization of BP if not, risk of surgical complications is high. After surgery since this is always a benign lesion, recurrence is unlikely= withdraw anti-hypertensive drugs + maintain adequate hydration - 2ndary form of therapy: US, Doppler study for renal arteries |
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Drugs used to control hyperaldosteronism |
- specific diuretics like spironolactone=inhibits aldosterone (mineralocorticoid receptor agonist), its anti-androgen drug SO WE CANNOT USE IT IN MALES We use it in women with PCOS and hirsutism Spironolactone is teratogenic and if you prescribe it it has to be in combined therapy with oral contraceptive pill - |
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Male hypogonadism |
- most cases are surgical (varicocele, cryptorchidism, testicular torsions and viral orchitis) - cryptorchidism testes descend in the scrotal sac during gestation - gonadal function is controlled by pituitary, by secretion of LH AND FSH. LH = leydig cell function and testosterone, FSH = serotoli cells, spermatogenesis Why? The testes need to be at 2 degree Celsius under body temperature that’s why they are positioned outside of the body. Testosterone stimulates this descend. |
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Morris syndrome: androgen insensitivity syndrome |
- receptors insensitivity to testosterone - a form of intersexuality - no menses, cannot get pregnant, testes remained in the abdomen, physiological and psychiatric part is most relevant - complete or partial resistance to androgens. If complete= no chance to develop male sex characteristics but if incomplete= androgen insensitivity = complete hermaphrodite Hermaphrodites develop phallus-like clitoris or penis, closed labia= reconstructive surgery needed if patient wants to identify a specific gender |
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Semen analysis |
- 74-90 days to produce spermatozoa - at the basal level: spermatogonia, meiosis proceeds creating spermatids with no flagella (developed at the end= in epididymis) - important for sperm exams to check how spermatozoa looks like, we evaluate volume of the sperm (3-5ml is normal) The volume tells you about function of prostate and seminal vesicles. - check number of spermatozoa (millions) - check for mobility in a straight direction (normal) - check for morphology: head, neck, body and tail - check for malformations: 2 heads |
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Hypogonadism |
- defined on gonadotropic levels High= primary disease, testes problem inappropriately normal or low= pituitary or hypothalamus damage - 2ndary or hypogonadotropic hypogonadism (patients with pituitary adenoma)= sperm production less compromised than testosterone secretion - negative feedback is due to testosterone and inhibin B All these conditions should be bilateral |
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Klinefelter syndrome (congenital disease) |
- karyotype: 47XXY - spermatogenesis not functioning because mitosis isn’t complete - scleroyalinosis of seminary tubules, small and thicker testes, diagnosed after puberty, testosterone secretion compromised, less hair in beard, less muscle mass, mental retardation, pear shape body type) - fertility problems - mental retardation (most severe) |
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Diagnosis of Klinefelter syndrome |
- low testosterone - high LH and FSH + azospermia - high risk for testes cancer and breast cancer - mandatory follow-ups - have to present gnecomastia which disappears by itself= signs of testes cancer, can be due to an increase in estrogen or ratio between estrogen and testosterone - pseudogynecomastia could reflect increase of adipose tissue at fat level while real gynecomastia = breast cancer but is unlikely and mono lateral - check for prolactin (hyperprolactinemia exclusion) - in case of hyperprolactinemia, LH AND FSH are low and in Klinefelter and in primary hypogonadism they are high (differential diagnosis) |
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Treatment of klinefelter |
- replacement therapy with testosterone= ameliorate all symptoms ,sexual function and body composition but doesn’t help fertility - in klinefelter: no chance to find any sperm working we can only freeze the sperm possibly found in puberty. - most of the stimulation and therapeutic procedures will occur on women |
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Kallman’s syndrome (congenital) |
- genetic cause of hypothalamic hypogonadism - hypogonadotropic hypogonadism manifests with hypo or anosmia - decrease in gonadal function due to failure in the differentiation/ migration of neurons that arise embryonically in all factory mucosa and take up residents in hypothalamus serving as GnRH neurons - a deficit in GnRH hormone = decreased levels of sex steroids= lack of sexual maturity and absence of secondary sexual characteristics |
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Symptoms of Kallman’s syndrome |
- anosmia: complete loss of smell (onion) - blindness - malformations at nose level |
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Diagnosis of Kallman’s syndrome |
- based on signs and symptoms - small testes or micro penis If it occurs after puberty, micropenis is not an issue since the penis was already developed during puberty and we can use the Tanner’s scale + orchidotomer= phase of puberty - testes volume above 10mm= phase 3 puberty occurred - below 10mm and if patient young= something wrong during puberty - in adults with hypogonadism: volume of testes is above 10mm but below 15mm = tests is compromising when volume is below 15mm If a nodule is present on testes, and if smaller than 1cm, the prognosis is not compromised. |
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Testosterone levels |
- below 2ng/mL= diagnostic - between 2-3ng/mL= grey zone= check for free testosterone and albumin - if free testosterone is low= replacement therapy Testosterone is contraindicated in breast cancer and prostate cancer since they are hormonal sensitive and by administering it we increase malignancy of cancer. - if hematocrite is above 52 in patients with elevated erythrocytosis or in case of elevated PCA= CONTRAINDICATION |
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Treatment of Kallman’s syndrome |
- gonadotropins = induction of puberty with an increase in penis size and then stop them and induce testosterone for fertility |
