Endocrine Flashcards
Addison’s disease is
not enough steroids
Addison’s S&S
fatigue, weight loss, hypoglycemia, confusion, hypotension, hyponatremia, fluid volume deficit, hyperkalemic, decreased sex hormones
Adrenal crisis S&S
extreme fatigue, dehydration, fever, hypotension, renal shut down, increase K+, decrease Na
Cushing’s disease is
too much steroids
Cushing’s S&S
thinning hair, facial flush, buffalo hump (fat pads), easy bruising, trunk obesity (redistribution of fat), thin extremities, retaining fluid, htn, weight gain, puffy face (moon face)
hypothalamus releases
thyroid releasing hormone (TRH)
corticotropic releasing hormone (CRH)
pituitary gland releases
thyroid stimulating hormone (TSH)
oxytocin
antidiuretic hormone (ADH, vasopressin)
adrenal glands release
steroids; glucocorticoids and mineralcorticoids
pancreas releases
insulin
glucagon
thyroid gland releases
T3 and T4
Conn’s disease
tumor on adrenal gland causing excess secretion of aldosterone
difference between Cushing’s and Conn’s
Cushing’s is too many steroids (gluco-, mineral-, sex hormones) Conn’s is just too much aldosterone
Pheochromocytoma
tumor on adrenal
gland causing too many catecholamine release (epi and norepi)
in pheochromocytoma we do not palpate the __________ because _____________
abdomen; would cause catecholamines to be released causing an increase in BP and HR
Pheochromocytoma S&S
tachycardia, palpitations, htn, diaphoresis, abdominal pain, chest pain, severe headache
Too much antidiuretic hormone causes
syndrome of inappropriate antidiuretic hormone (SIADH)
not enough antidiuretic hormone causes
diabetes insipidus (DI)
DI S&S
hypotension, tachycardia, headaches, muscle cramps, dilute urine, dry eyes, weight loss
SIADH S&S
euvolemic, decreased urine output, GI upset, low sodium
why does the body stay euvolemic in SIADH
the body is retaining too much water that the kidneys recognize this and begin to help regulate volume this maintains the client has euvolemic instead of becoming hypervolemic… key in diagnosing this condition
not enough thyroid hormones
hypothyroidism
too many thyroid hormones
hyperthyroidism or Grave’s disease
too much TSH -> _______ T3 and T4 -> _______thyroidism
low; hypo
not enough TSH-> _____ T3 and T4 _______ thyroidism
high; hyper
Hypothyroidism S&S
slow HR, weight gain, loss of appetite, hair loss, dry skin, constipation, enlarged thyroid, intolerable to cold, fatigue
Grave’s disease
autoimmune disease with antibodies attacking the thyroid causing hypothyroidism
Grave’s S&S
sweating, exophthalmos, tachycardia, arrhythmia, headache, weight loss, emotional instability, tremor, muscle weakness, n/v, hyperactive GI, goiter
thyroid storm S&S
very high fever, very high hr (200bpm), palpitations, chest pain, SOB
too much parathyroid hormone
hyperparathyroidism
not enough parathyroid hormone
hypoparathyroidism
hypoparathyroidism = low calcium which causes S&S
excitable; tachy, tremors, seizures, etc
hyperparathyroidism = high calcium = S&S
sedative effects
not enough insulin =
diabetes type I or II
too much insulin =
hypoglycemia
insulin enters blood from ______ and glucose enters blood from ______
pancreas; GI tract
no insulin means glucose channel is ______ and this leads to
closed; glucose not being able to enter cells and stays in the blood stream causing an increase in blood glucose
enough insulin means glucose channel is ______ and leads to
open; glucose being able to enter the cell maintaining appropriate blood glucose
Type I S&S
hungry, thirsty, tired because cells do not have enough energy, weight loss because cells do not get enough energy due to glucose channel not being open, blurred vision, increased urine output
DM type I
autoimmune disease, body has destroyed beta cells of pancreas that produce insulin leaving little to no insulin in the body causing very high blood glucose levels in body. no glucose can get into the cells
DKA
blood becomes hypertonic and is an acute exacerbation of type I DM. Polyuria, polydipsia, polyphagia. Because cells don’t have glucose for energy they break down proteins and fats causing ketones to be produced
DKA causes _____ (ABG) causing S&S
metabolic acidosis; kussmaul resporations blowing off CO2, high potassium, thirsty, GI upset, SOB, fatigue
3 Ps of diabetes progressing to DKA
polyuria
polydipsia
polyphagia
DM type II
not enough insulin, insulin resistance or bad insulin. Body is not making enough insulin to keep up with glucose.
DM type II S&S
over weight for longer period of time (pancreas no longer able to keep up), blurred vision, frequent urination, excessive thirst, slow wound healing, fatigue, recurrent infections, numbness and tingling in extremities
Hyperglycemic Hyperosmolar Syndrome (HHS)
Exacerbation of type II DM. high BGL, blood becomes hyperosmolar, kidneys produce more time due to hyperosmolarity of blood, no ketones, symptoms begin over days to weeks (vs hours for DKA)
Hypoglycemia S&S
Tachycardia
Irritability
Restlessness
Excessive hunger
Diaphoresis
Cold and clammy = need a candy
DKA vs HHS
DKA: type one, ketones, acidotic, onset with hours
HHS: type two, no ketones, no acidosis, onset days to weeks
hypoglycemia treatment 15s rule
15 grams of carbs -> check BG in 15 min -> still low? give another 15g carbs and repeat process
after BG rises it is important to give
snack with complex carb and protein to keep the BG up
if hypoglycemic pt unconscious?
IV access push D50W
No iv access? give IM glucagon
