Endocrine Flashcards

1
Q

goiter

A

an enlargement of thyroid gland w/ or w/o s/s of thyroid dysfx

Excess TSH

low iodine levels (these goiters tend to be larger)

goitrogens–ie lithium

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2
Q

Hashimoto’s

A
thyroid receptor antibodies
antithyroglobulin antibody (anti-Tg)
antithyroperoxidase antibody (anti- TPO)--hallmark of disorder
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3
Q

Risk factors for hypothyroidism

A
female
age > 50
caucasian
pregnancy
hx of other autoimmune disorders
family hx
meds--lithium, amiodarone
treatments for hyperthyroidism
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4
Q

hypothyroidism

early manifestations

A
cold intolerance
weight gain
lethargy
fatigue
memory deficits
poor attn span
increased cholesterol
muscle cramps
raises carotene levels (yellows skin)
constipation
decreased fertility
puffy face
hair loss
brittle nails
anemia
hoarse voice
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5
Q

hypothyroidism

late manifestations

A
below normal temp.
bradycardia
weight gain
decreased LOC
thickened skin
cardiac complications (cardiomegaly)
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6
Q

myxedema

A
life-threatening
severe hypo (coma) → undiagnosed or untreated
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7
Q

hypothyroidism treatment

A

levothyroxine (synthetic T4, converted to T3 in body)
taken for life
take on empty stomach
↑ risk for bleeding with warfarin

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8
Q

hyperthyroidism (Thyrotoxicosis)

A

excessive secretion of T3 and T4

Primary → Grave’s disease
Secondary (pituitary) → over secretes TSH
Tertiary (hypothalamus)

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9
Q

hyperthyroidism risk factors

A
family hx of Graves
age > 40
female
caucasian
meds
excessive iodine intake
pregnancy
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10
Q

Graves’ disease

A

autoimmune
excess levels of T3 and T4
thyroid-stimulating antibodies → thyroid continues to secrete hormones w/o stimulation from pituitary gland

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11
Q

graves’ disease

clinical manifestations

A
nervousness
insomnia
sensitivity to heat
weight loss
gland usually enlarged and palpable
audible bruit may be heard
atrial fib
myxedema--dermatologic manifestations
exophthalmos
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12
Q

Graves’ disease diagnosis

A
Low TSH
↑ T3
↑ T4
antithyroglobulin
antithyrotropin receptor antibody
ultrasound with color doppler eval
radioactive iodine scanning and measurements of iodine uptake-- ↑ iodine uptake and distributed diffusely
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13
Q

treatment of hyperthyroidism

A
  • propylthiouracil (PTU) - blocks thyroid hormone synthesis, suppresses conversion of T4-T3
  • BLACK BOX - hepatotoxic
  • used in 1st trimester with caution
  • radioactive iodine treatment
  • surgery - hormone replacement needed for life
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14
Q

thyrotoxic crisis

A

overwhelming release of thyroid hormones that exerts an intense stimulus on the metabolism

reaction to major stressor

life threatening condition most commonly precipitated by surgery, trauma, or infection

body revved up and can result in death if not treated within 48 hours

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15
Q

hypoparathyroidism

A

s/s r/t insufficient PTH secretion and the resulting ↓ Ca

muscle cramps
irritability
tetany
convulsions
trousseau's and chvostek's sign
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16
Q

hypoparathyroidism treatment

A

replace PTH

normalize serum Ca and vit D levels

if parathyroid removed, replacement treatments are for life

17
Q

hyperparathyroidism

A

s/s r/t excessive secretion of PTH with hypercalcemia and bone breakdown

muscle weakness
poor concentration
neuropathies
kidney stones
metabolic acidosis
osteopenia
pathological fractures
constipation
depression, confusion, subtle cognitive deficits
18
Q

hyperparathyroidism treatment

A
↓ Ca levels
diuretics
calcitonin
bisphosphonates
Vit D
surgical intervention
19
Q

SIADH etiology

A

malignant tumors
CNS disorders (trauma, stroke, brain tumors)
drug therapy
misc. (hypothyroidism, infection)

20
Q

SIADH

A
↓ serum osmolality
dilutional hyponatremia
↑ urine specific gravity & osmolality
weight gain
↓ urine ouput
21
Q

SIADH clinical manifestations

A
hyponatremia:
dyspnea, fatigue
dulled sensorium, confusion, lethargy
muscle twitching, convulsions
impaired taste, anorexia, vomiting, cramps
22
Q

SIADH treatment

A

treat the underlying cause

chronic SIADH - demeclocyline

severe cases may call for hypertonic solution

23
Q

demeclocycline

A

tetracycline
interferes with renal response to ADH
AE: photosensitivity, teeth staining, nephrotoxic

24
Q

Neurogenic DI etiology

A

hypothalamus or pituitary gland damgage

associated disorders: stroke, traumatic brain injury, brain surgery, cerebral infections

sudden onset, usually permanent

treatment: desmopressin (DDAVP) - synthetic ADH replacement therapy, comes in nasal spray; give as small of dose as possible

25
Q

Nephrogenic DI etiology

A

loss of kidney function
often drug related ie lithium
CKD

slow onset and progressive

treatment: thiazide diuretics

26
Q

Cushings clinical manifestations

A

↑ cortisol

glucose intolerance, hyperglycemia
HTN, capillary friability
muscle wasting, weakness; thinning of skin, osteoporosis and bone pain
redistribution of fat to abd, shoulders and face
impaired wound healing & immune response, risk for infection
mood swings, insomnia

27
Q

drug therapy for cushings

A
  • treatment dependent on cause
  • tumor- surgery or radiation
  • exogenous steroids - taper
  • drug therapy is not primary, but adjunct w/radiation or surgery; helps with elevated cortisol levels
28
Q

aminoglutethimide

A

blocks synthesis of all adrenal steroids

used in ppl awaiting surgery, no longer than 3 months

reduces cortisol levels by 50%

AE: drowsiness, nausea, anorexia, rash

29
Q

ketoconazole

A

antifungal that also inhibits glucocorticoid synthesis

adjunct therapy to radiation, surgery

severe liver damage
do not take with ETOH or other hepatotoxic drugs
teratogenic

30
Q

addison disease clinical manifestations

A
slow onset
early s/s
anorexia, weight loss
weakness, malaise, apathy
electrolyte imbalances
skin hyperpigmentation