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50 Cards in this Set

  • Front
  • Back
Endocrine disorders
- too much or too little hormones secreted by glands
- most common disorder - hypothyroidism
Hormones
Chemical messengers of endocrine system
Endocrine glands
Ductless glands which dump there hormone products directly into the blood stream
Pituitary Gland
Master gland which controls other glands, housed in the hypothalamus
Anterior Pituitary gland
Related to puberty
Cause SIADH
Excess anti-diuretic hormone
- opposite of DI
- Both are fairly rare
- ordinarily a secondary condition
- leads to increased weight and decreased Na+ concentration
Ectopically
abnormally
Most common cause of SIADH
- i.e adenocancer of lung, oat cell cancer due to ectopically produced ADH
Clinical manifestations of SIADH
Increased total body water,weight gain and hypoatremia, increased urine concentration and specific gravity
High specific gravity of urine
Dense, thick, amber colored urine
S/sx of hypoatremia
Confusion and lethargy
1st Treatment of hypoatremia -
Water restriction (less than 1L/day) for chronic conditions
- For acute post-op pts – fluid bolus to kick start urine output
2nd Treatment of hypoatremia -
Isotonic fluids then gradually replace Na+ with hypertonic solutions. If administered quickly, BP increases and cells shrink.
3rd Treatment of hypoatremia -
demeclocycline - blocks ADH effect and increases Na+ levels
Cause of diabetes insipidus
Insufficient action of anti-diuretic hormone
Neurogenic cause of diabetes inspidus
Hypothalamus lesions, brain tumors or lesions
- most common, and can be caused by head trauma – accidental or surgical
Nephrogenic cause of diabetes insipidus
Kidney dysfunction
Tubules don’t reabsorb water
Which cause of diabetes insipidus can be treated with ADH
Neurogenic, because that means that there is deficience of the hormone
Clinical manifestations of Diebetes Insipidus
- Lower TBW
- NA 0 more than 145 meq/L
- hydronephrosis
- high Na value and the constant need to pee
- clear water lost through the bladder
Polydipsia
Excess thirst
-fluid replacement is necessary with diabetes insipidus
- if deprived of water and still peeing like crazy, DI it is
- demopressin is an ADH
ADH replacement
Can be used to prevent Nocturia
Thyroid gland
-plays role in metabolism
- sits in front of the trachea
Hyperthyroidsm
(Grave Disease)
- 10% of thyroid diseases
Increased thyroid hormone
- Autoimmune disease
- antibodies bind to and stimulate TSH receptors
- thyroid cancer could play a role
- exophthalmos – buldging eyes
Complications of exophthalmos
Buldging eyes = dry eyes & eye infections
S/sx of Graves disease
Hyperthermia, tachycardia, delirium, nausea, emlarges thyroid, exophthalmos, increased BP and pulse
Treatment for hyperthyroidism -
Drugs – corticosteroids (which suppress immune system)
- radioactive iodine
- thyroidectomy
Hypothyroidism
- 90% of thyroid disease
- cause – deficiency of thyroxine (of TSH)
- autoimmune
- detected when pt make too much TSH and not enough thyroxine, or too little TSH and too little thyroxine
Clinical Hypothyroidisn
Slow, sluggish, fat and constipated person with headaches, depression and coarse hair

“C” symptoms – coarse hair, constipation, coldness, chubbiness, cranial pain, sluggish
Myxedema coma
Hypothyroidism progresses to coma
- can happen with the withdrawal of thyroid meds
- worst case scenario – pt cant function and fills w/ fluid
Hypothyroism –
Low TSH Something wrong with pituitary
Hypothyroidism – High TSH
Something wrong with thyroid gland
Hypothyroisim treatment
Thyroid replacement - forever
Parathyroid gland
Regulates serum Ca, low calcium leads to more TPH
Ca+ needed for nerve conduction as it regulates the Na+/K pump

Kidney failure = increased parathyroid activity
Location of parathyroid gland
4 glands located around thyroid gland
Causes of Hyperparathyroidism
Renal failure
- the parathyroid glands enlarge and pull Ca. from bones
Clinical manifestations of hyperparathyroidism
Brittle bones
Treatment of Hyperparathyroidism
Removal of parathyroid glands
Consequence of Parathyroid removal
Ca+ supplements forever
Diabetes Mellitus –Type1
-Pancreas makes no insulin
Diabetes Mellitus –Type2
Insufficient insulin made by islet cells of pancreas
Cells that require sugar, don’t allow insulin to do its job
Type 1 causes
Auto immune condition occur due to environmental and heredity factors
Clinical Manifestations Type I
Three Ps
- polydipsia, polyuria, very hungry
Tire easily because cells don’t have the sugar needed to operate
Type 2 causes
Pancreatic cells get overworked with age and obesity
Type 2 Clinical manifestation
Subtle and slow to develop, recurrent infections and visual changes
- more subtle 3 p’s
Complications of Chronic hyperglycemia
Neuropathy (poor nerve transmission)
Nephropathy (kidney dysfunction)
Fat deposits in coronary arteries
Blindness
CAD
Stroke
Effects of diabetes
Stroke, retinopathy, CAD
-Chronic effects due to increased amouts of sugar flowing to certain cells that do not rely on insulin
- Cells take in extra sugar, which draws in extra water which causes cell injury and damage.
Severe complications Type 1
Diabetic ketoacidosis (DKA)
Severe Complications
Type 2
Hyperosmolar hypoglycemic nonketotic syndrome HHNS
DKA -
Insulin deficiency – hyperglycemia – polyuria, cellular starvation – ketones produced in cellular starvation – ketoacidosis
Evaluation of Diabetes
Fasting blood sugars - >126
Glucose tolerance tests >140
HbA1C- three month