Endocrine Disorders Flashcards
Endocrinology
- define
- evaluation
Study of glands and hormones they produce
-not strictly defined by anatomy
Primarily via hormone concentration
-immunoassay - antibodies to detect certain hormones
—2-step process: 1 Ab links to hormone to fix it to slide, another Ab attached to fluorescent/chemical marker
Gland + hormone
- pineal
- parathyroid
- thyroid
- testis/ovary
- adrenal
- hypothalamus/pituitary
Pineal - malatonin (circadian)
Parathyroid - calcium-phosphate homeostasis
Thyroid - temperature and metabolism control
Testis/ovary - testosterone, estrogen, progesterone
Adrenal - adrenaline, aldosterone, cortisol
Hypothalamus/pituitary - a lot
Endocrine disorders
-3 major divisions + usual causes
Hormone deficiency - glandular destruction (autoimmune, surgery, infection, hemorrhage, etc.), mutations of hormone or receptor/channels
Hormone excess - benign glandular adenoma
Hormone resistance - severe = inherited, functional = impairment (e.g. DM2)
Endocrine disorders
-3 major divisions + common treatments
Hormone deficiency - replacement therapy
Hormone excess - removing tumors (sx), or reducing hormones (medically)
Hormone resistance - medication, etc.
Grave’s Disease
- leading cause of
- who
- type of condn
Thyrotoxicosis (excess thyroid hormone), which leads to hyperthyroidism (excessive thyroid function) and incr metabolism
Women : men = 10:1
Ages 20-50
Chronic, sometimes goes into remission
Usually treatable/manageable, but potentially fatal if not addressed
Grave’s Disease -pathopysiology —type of disorder —normal vs Grave’s thyroid stimulation —factors
Autoimmune
Normal: thyroid hormones released in response to TSH from pituitary
Grave’s: antibodies (thyroid stimulating immunoglobulins (TSI)) bind to surface receptors of thyroid and stimulate hormone release
Combo of environmental and genetic-> TSI
Grave’s Disease
-signs/symptoms (generally)
= increased metabolism
Examples: anxiety, fine tremor, heat intolerance, weight loss, rapid HR, frequent bowel movements
Grave’s Disease -diagnosis —physical exam —blood tests —imaging
Physical: goiter, pulse/BP, tremor, other/ocular findings
Blood:
- TSH lower than normal
- thyroid hormones higher than normal
- TSI levels
- hormone levels are not a very accurate way to measure metabolic disorders due to fluxuations
Imaging: radioactive iodine uptake, ultrasound, CT, MRI
Grave’s Disease
-treatment
—goals
—specific tx (4)
Goals: inhibit production of thyroid hormones and/or decr amount of thyroid tissue
Radioactive iodine therapy (#1 USA) -destroys overactive thyroid cells, usually need HRT later
Anti-thyroid meds -usually supplemental before/after radioiodine
Beta-blockers - suppress SNS
Surgery - partial/complete thyroidectomy, usually need HRT
Grave’s Disease -OD implications —frequency —what —vision-threatening —when —treatments affecting eyes
30%
Lid retraction, EOM enlargement
ON compression (severe EOM enlargement), exposure keratitis/ulceration
Usually w/in a year of dx
Radioiodine may exacerbate ophthalmopathy
Systemic BB lower IOP, pwerfusion of ON
Hashimoto’s Disease
- a leading cause of
- who
- preceded by
Hypothyroidism (impaired function) -> decr metabolism
-not leading, but a leading
Women : men = 4:1 Mean age dx 60 Certain populations (e.g. Japanese)
Subclincial stage -> clinical/overt hypothyroidism
Hashimoto’s Disease -pathophysiology —type of disorder —cause —factors
Autoimmune
Abnormal antibodies cause lymphocytic infiltration of thyroid gland -> atrophy/fibrosis
Combo of environmental and genetic
Hashimoto’s Disease
-signs/symptoms (in general)
= decr metabolism
Examples: tired, poor concentration/memory, weight gain, feeling cold, myxedema (puffy face/hands/feet), alopecia, bradycardia
***may present with goiter or ,later on, atrophy of thyroid tissue
Hashimoto’s Disease -diagnosis —physical exam —blood tests —imaging/procedures
Physical: asymmetric goiter
Blood:
- TSH levels = most sensitive, screening
- unbound T4 levels = confirms clinical hypothyroidism
- antibody testing (TPO, Tg) = confirms etiology
Other: ultrasound, biopsy
Hashimoto’s Disease
-main treatment
HRT with levothyroxine (synthetic hormone)
- clinical effect takes time
- full symptom relief 3-6 mo after normal TSH levels
- subclinical not always treated, recommended to tx women who wish to conceive/are pregnant
Hashimoto’s Disease
-OD implications
—frequency
—medications and eyes
5%
Rarely, levothyroxine replacement -> pseudotumor cerebri in children
Cushing’s Disease
- leading cause of
- who
Leading endogenous cause of Cushing syndrome (hypercorticolism)
Rare
Women>men 4-10x
Byos>girls in pre-pubertal cases
Cushing’s Disease
-complications (6)
Compression fractures of spine Dibetes HTN Infections Kidney stones Mood/psychiatric problems
Cushing’s Disease
-pathophysiology
Pituitary adenoma - benign tumor of gland
Specifically, one producing excess ACTH -> adrenal glands make too much cortisol
Cushing’s Disease
-common signs/symptoms
Moon face Buffalo hump Central obesity Thin skin - purple striae, bruise easily Hyperandrogenism - acne, hirsutism
Cushing’s Disease
-diagnosis
—lab tests
—imaging/procedures
Lab:
- free cortisol in urine - screening
- overnight dexamethasone suppression - principle dx feature***
- elevated midnight serum/salivary samples
- basal plasma/ACTH levels
Other:
- MRI - small tumors
- inferior petrosal venous sampling - localizes pituitary ACTH prod
Cushing’s Disease
-treatment
—primary
—others
Removal of ACTH-producing tumor (sx)
Other:
- trans-sphenoidal resection
- various meds
- pituitary irradiation
- adrenalectomy (last resort)
Cushing’s Disease
-OD implications
—classic problem and manifestation
—systemic pathology affect
Microadenomas - potential for compression of visual pathways/collateral damage during sx
-VF defects
Retinopathy - HTN, DM
Susceptibility to infection
Addison’s Disease
- what
- usual cause
- results
Primary adrenal insufficiency
Autoimmune or genetic
-rarely infection (TB)
Loss of both glucocorticoid and mineralocorticoid secretion
Addison’s Disease
- symptoms
- diagnosis
- treatment
Chronic, non-specific (fatigue, darkening of skin)
Acute = postural hypotension -> hypovolemic shock
Cortisol levels after ACTH stimulation
Acute = immediate rehydration Chronic = HRT
Menopause
- what
- diagnosis
- preceded by
Permanent cessation of menstruation due to loss of ovarian follicular function
-avg age 51
Retrospectively - after 12 mo of amenorrhea
Perimenopause - waning fertility, menstrual irregularity
-precedes by 2-8 years (mean 4)
Menopause
-treatment
—peri
—post
Peri = low dose combined oral contraceptives
- decr symptoms
- contraindicated in smokers, liver disease, thromboembolism
Post = HRT
- benefits = relieves symptoms, slows osteoporosis
- risks = endometrial/breast cancer, venous thromboembolism
Menopause
-OD implications
Dry eye
