Endocrine Disorders Flashcards

1
Q

Endocrinology

  • define
  • evaluation
A

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

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2
Q

Gland + hormone

  • pineal
  • parathyroid
  • thyroid
  • testis/ovary
  • adrenal
  • hypothalamus/pituitary
A

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

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3
Q

Endocrine disorders

-3 major divisions + usual causes

A

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)

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4
Q

Endocrine disorders

-3 major divisions + common treatments

A

Hormone deficiency - replacement therapy

Hormone excess - removing tumors (sx), or reducing hormones (medically)

Hormone resistance - medication, etc.

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5
Q

Grave’s Disease

  • leading cause of
  • who
  • type of condn
A

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

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6
Q
Grave’s Disease
-pathopysiology
—type of disorder
—normal vs Grave’s thyroid stimulation
—factors
A

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

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7
Q

Grave’s Disease

-signs/symptoms (generally)

A

= increased metabolism

Examples: anxiety, fine tremor, heat intolerance, weight loss, rapid HR, frequent bowel movements

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8
Q
Grave’s Disease
-diagnosis
—physical exam
—blood tests
—imaging
A

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

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9
Q

Grave’s Disease
-treatment
—goals
—specific tx (4)

A

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

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10
Q
Grave’s Disease
-OD implications
—frequency
—what
—vision-threatening
—when
—treatments affecting eyes
A

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

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11
Q

Hashimoto’s Disease

  • a leading cause of
  • who
  • preceded by
A

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

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12
Q
Hashimoto’s Disease
-pathophysiology
—type of disorder
—cause
—factors
A

Autoimmune

Abnormal antibodies cause lymphocytic infiltration of thyroid gland -> atrophy/fibrosis

Combo of environmental and genetic

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13
Q

Hashimoto’s Disease

-signs/symptoms (in general)

A

= 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

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14
Q
Hashimoto’s Disease
-diagnosis
—physical exam
—blood tests
—imaging/procedures
A

Physical: asymmetric goiter

Blood:

  • TSH levels = most sensitive, screening
  • unbound T4 levels = confirms clinical hypothyroidism
  • antibody testing (TPO, Tg) = confirms etiology

Other: ultrasound, biopsy

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15
Q

Hashimoto’s Disease

-main treatment

A

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
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16
Q

Hashimoto’s Disease
-OD implications
—frequency
—medications and eyes

A

5%

Rarely, levothyroxine replacement -> pseudotumor cerebri in children

17
Q

Cushing’s Disease

  • leading cause of
  • who
A

Leading endogenous cause of Cushing syndrome (hypercorticolism)

Rare
Women>men 4-10x
Byos>girls in pre-pubertal cases

18
Q

Cushing’s Disease

-complications (6)

A
Compression fractures of spine
Dibetes
HTN
Infections
Kidney stones
Mood/psychiatric problems
19
Q

Cushing’s Disease

-pathophysiology

A

Pituitary adenoma - benign tumor of gland

Specifically, one producing excess ACTH -> adrenal glands make too much cortisol

20
Q

Cushing’s Disease

-common signs/symptoms

A
Moon face
Buffalo hump
Central obesity
Thin skin - purple striae, bruise easily
Hyperandrogenism - acne, hirsutism
21
Q

Cushing’s Disease
-diagnosis
—lab tests
—imaging/procedures

A

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
22
Q

Cushing’s Disease
-treatment
—primary
—others

A

Removal of ACTH-producing tumor (sx)

Other:

  • trans-sphenoidal resection
  • various meds
  • pituitary irradiation
  • adrenalectomy (last resort)
23
Q

Cushing’s Disease
-OD implications
—classic problem and manifestation
—systemic pathology affect

A

Microadenomas - potential for compression of visual pathways/collateral damage during sx
-VF defects

Retinopathy - HTN, DM
Susceptibility to infection

24
Q

Addison’s Disease

  • what
  • usual cause
  • results
A

Primary adrenal insufficiency

Autoimmune or genetic
-rarely infection (TB)

Loss of both glucocorticoid and mineralocorticoid secretion

25
Q

Addison’s Disease

  • symptoms
  • diagnosis
  • treatment
A

Chronic, non-specific (fatigue, darkening of skin)
Acute = postural hypotension -> hypovolemic shock

Cortisol levels after ACTH stimulation

Acute = immediate rehydration
Chronic = HRT
26
Q

Menopause

  • what
  • diagnosis
  • preceded by
A

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)

27
Q

Menopause
-treatment
—peri
—post

A

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
28
Q

Menopause

-OD implications

A

Dry eye