Week 6 - Endocrine System Flashcards
Hypothyroidism
Deficient production of TH by the thyroid gland.
Most common thyroid disorder. More prevalent in women and the elderly.
Treatment for hypothyroidism
Levothyroxine
Secondary hypothyroidism
Caused by pituitary or hypothalamic failure to stimulate thyroid to produce TH
What causes hypothyroidism?
1.Usually caused by autoimmune thyroiditis (Hashimoto’s disease)
2. Loss of thyroid tissue after surgery
3. chemo/radiation
5. Medications
6. Iodine deficiency
Symptoms of hypothyroidism
Affects all body systems and occurs insidiously over months/years
Symptoms dependent on degree of deficiency
1. Low energy levels
2. Low basal metabolic rate
3. Cold intolerance
4. Lethargy
5. Tiredness
6. Lowered body temp
7. Diastolic hypertension
8. Goiter
9. weight gain
Myxedema
Myxedema coma – low level of consciousness
Evaluation for hypothyroidism
- clinical symptoms
- increase in TSH levels and decrease in TH levels
Thyroid stimulating hormone
Synthesized and stored in the anterior pituitary gland, circulates to bind with the TSH receptor. Effects include:
i. Immediate increase in release of stored thyroid hormones
ii. Increase in iodine uptake and oxidation
iii. Increases TH synthesis
iv. Increase in synthesis and secretion of prostaglandins by the thyroid
Function of the thyroid
Controls the body’s metabolic processes
Secondary hypothyroidism
Caused by the pituitary’s failure to synthesize adequate amounts of TSH or a lack of TRH.
Pituitary tumors that compress surrounding pituitary cells or the consequences of their treatment are the most common causes
- TBI
- subarachnoid hemorrhage
- pituitary infection
Feedback loop for primary thyroid malfunction
- thyroid doesn’t produce enough TH
- no negative feedback to pituitary and hypothalamus
- .Low TH and high TSH, TRH levels
Feedback loop for pituitary malfunction
- lack of negative feedback to hypothalamic release of TRH by TSH and TH
- low levels of TSH and TH and high levels of TRH
Feedback loop for hypothalamic function
- Decreased TRH due to defect in hypothalamic function
- Low levels of TRH, TSH, and TH
Hyperthyroidism
Excess amounts of TH from the thyroid gland
Causes of hyperthyroidism
- Graves’ disease (an immune system disorder that results in the overproduction of thyroid hormones)
- Toxic multinodular goiter
- Solitary toxic adenoma
- Follicular thyroid carcinoma
Central (secondary) hyperthyroidism
caused by TSH secreting pituitary adenomas
Clinical manifestations of hyperthyroidism
Attributable to the metabolic effects of increased circulating levels of TH
a. Increased metabolic rate
b. Heat intolerance
c. Sensitivity to stimulation by the sympathetic division of the ANS
Diagnostic criteria for primary hyperthyroidism
Diagnosed with elevated T3 and T4 levels and decreased serum TSH
Diagnostic criteria for secondary hyperthyroidism
Normal TSH levels despite increase TH concentrations
(TSH secreting pituitary tumor)
Treatment for hyperthyroidism
Aimed at controlling TH production, secretion or action
Includes radioactive iodine therapy (drug is absorbed by the thyroid tissue causing cell death - goal to kill overactive thyroid tissue), antithyroid drug therapy (methimazole or propylthiouracil) and surgery
What are the two most distinguishing factors of hyperthyroidism?
Pretibial myxedema (a waxy, discolored induration of the skin—classically described as having an orange peel appearance—on the anterior aspect of the lower legs, spreading to the dorsum of the feet, or as a non-localised, non-pitting edema of the skin in the same areas)
Exophthalmos (he protrusion of one or both eyes anteriorly out of the orbit)
Functional abnormalities of hyperthyroidism
Result from hyperactivity of the sympathetic division of the ANS
1. lag of the globe on upward gaze 2. lag of the upper lid on downward gaze
Grave’s Disease
An immune system disorder that results in the overproduction of thyroid hormones
Infiltrative abnormalities of hyperthyroidism
Involving the orbital contents with enlargement of the ocular muscles. Affect more than ½ of individuals with the disease.
- Increased secretion of hyaluronic acid, adipogenesis, inflammation, and edema of the orbital contents result in
- exophthalmos (protrusion of the eyeball)
- periorbital edema
- extraocular muscle weakness leading to strabismus (crossed eyes) and diplopia (double vision)
Environmental Risk Factors for Type 1 Diabetes
- Viral infections (enterovirus), coxsackievirus, other infectious microorganisms
- H pylori
- Exposure to cow’s milk proteins
- Lack of Vitamin D
How is diabetes diagnosed?
An A1c greater than 6.5%
What are the actions of insulin?
Promotes glucose uptake in the liver, muscle, and adipose tissue
What are the autonomic neuropathic complications of diabetes?
Slows everything down
- decreased esophageal motility
- gastroparesis
- delayed gastric emptying
Hypoglycemia
Blood sugar less than 60
Symptoms of hypoglycemia
- Tachycardia
- Palpitations
- Diaphoresis
- Tremors
- Pallor
Cause of primary hyperparathyroidism
Caused by parathyroid gland tumor (something wrong with the gland itself)
Primary hyperparathyroidism
Characterized by inappropriate and excess secretion of parathyroid hormone (PTH) and no feedback loop to control secretion. Usually caused by a parathyroid tumor –> something with the gland itself
Primary hyperparathyroidism results in…
- Increased level of calcium in the blood
- Higher threshold for calcium level feedback is set
- Results in hypercalcemia and hypophosphatemia
Secondary hyperparathyroidism
A compensatory response of the parathyroid glands to chronic hypocalcemia, which is a common complication of chronic kidney disease or vitamin D deficiency.
Symptoms of hypercalcemia
May be asymptomatic or may have
- paresthesias (numbness and tingling)
- muscle cramps
Patients with hypercalcemia may have low bone density (osteoporosis) where is this mostly noted?
The distal third of the radius.
Complications of hypercalcemia
- Kidney stones
- fractures
- Ventricular hypertrophy
- Depression
- Gastric issues
Causes of hypoparathyroidism
- damage to Parathyroid gland during surgery
- genetic syndromes
- idiopathic
- autoimmune causes
- DiGeorge syndrome
Hypoparathyroidism
A lack of circulating PTH causes depressed serum calcium levels and increased serum phosphate levels. In the absence of PTH, resorption of calcium from bone and regulation of calcium reabsorption from the renal tubules are impaired. Therefore phosphate reabsorption by the renal tubules is increased, causing decreased renal phosphate excretion and hyperphosphatemia.
Symptoms of hypocalcemia
- Dry skin
- Loss of body and scalp hair
- Hypoplasia of developing teeth
- Horizontal ridges in nails
- Cataracts
- Basal ganglia calcification
- Bone deformities
- Bowing of long bones
Causes of hypomagnesemia
- Chronic alcoholism
- Malnutrition
- Malabsorption
- Increased renal clearance of MG caused by the use of aminoglycoside antibiotics or certain chemotherapeutic agents, or prolonged Mg deficiency parenteral nutritional therapy
What does hypomagenesemia do?
Inhibits PTH secretion
- if Mg is low, then Ca is high, so don’t want the PTH to increase Ca levels any more
Hypercortisolism
AKA Cushing’s Syndrome
Glucose intolerance because of cortisol-induced insulin resistance and increased gluconeogenesis and glycogen storage by the liver.
Overproduction of ACTH by pituitary adenoma or ectopic secreting nonpituitary tumor.
Happens when there’s extra cortisol in your body. Cortisol, the “stress hormone,” is vital to regulating your blood sugar and turning food into energy. Unfortunately, too much of it caused by a medication or a tumor can cause weight gain, muscle weakness and more.
Characterized by patterns of fat deposition “truncal obesity”, “moon face” and “buffalo hump”
What is the cause of Cushing’s syndrome?
From overproduction of cortisol by the adrenal glands or steroid use.
Adrenocorticotropic Hormone (ACTH)
Hormone produced by the pituitary gland that controls the production of cortisol by the adrenal gland.
Function of cortisol
- Respond to stress
- Fight infection
- Regulate blood sugar
- Maintain blood pressure
- Regulate metabolism, the process of how your body uses food and energy
Adrenal crisis
Onset signified by severe hypotension which can progress to complete vascular collapse and shock .
“adrenal crisis” or “Addisonian crisis” and develops when:
- Undiagnosed disease
- Withdrawal of glucocorticoid therapy
- Infection
- Multiple stressor
This is why we wean steroids.
What hormones do the adrenal glands produce?
Aldosterone and cortisol
Primary Adrenal insufficiency
AKA Addison’s disease
Adrenal gland is unable to produce enough cortisol and aldosterone.
Lab work shows:
- Serum and urine cortisol levels depressed
- ACTH levels are increased
Symptoms may not present until 90% of adrenal cortex is destroyed
When prescribing cortisol remember:
o More cortisol is needed with acute stressors (infection, surgery, trauma) to approximate the amount that would be secreted if normal adrenal function were present
Most common cause of Addison’s disease
Autoimmune destruction of adrenal cortex.
