Patho Exam 3 Flashcards
hypothalamus gland
activates, controls, integrates peripheral ANS and somatic functions like body temp, sleep, and appetite
hormones produced by the hypothalamus
CRH GnRH GHIH GHRH MIH PIH TRH
pituitary gland
“master gland” controlled by hypothalamus. anterior and posterior.
hormones produced by the pituitary gland
FSH LH prolactin ACTH TSH GH
hormones produced by the posterior pituitary gland
vasopressin/ADH
oxytocin
destruction of the pituitary gland leads to what s/s?
extreme weight loss, emaciation, endocrine gland/organ atrophy, hair loss, impotence, amenorrhea, hypo metabolism, hypoglycemia
95% of pituitary tumors are…?
benign
what are the s/s of a pituitary tumor?
increased pressure, headache, vision changes, loss of peripheral vision, hormone level changes
diabetes insipidus
low ADH levels because pituitary is not producing enough. characterized by large quantities of dilute urine, electrolyte imbalances (hypernatremia), excessive thirst (dehydration)
SIADH
overproduction of ADH @ pituitary or elsewhere. Characterized by increased blood volume, low quantities of concentrated urine and dilutional hyponatremia (b/c retaining so much water, dilutes salt concentration). S/s include: thirst, mild cramping, nausea, confusion, seizures, coma, irritability, restlessness, dec. appetite, weakness, hallucinations, stupor.
SIADH is commonly the 1st sign of…?
lung cancer
thyroid gland
butterfly shaped gland at the base of the neck. Controls metabolism via control of HR, RR, C/PNS, body weight, muscle strength, menstrual cycles, body temp, and cholesterol levels.
what hormones does the thyroid gland produce?
uses iodine from foods to make T3 (triiodothyronine) and T4 (thyroxine). Levels are maintained by hypothalamus and pituitary via TRH and TSH. Regulate speed at which cells work (i.e. metabolism)
hypothyroidism
decreased levels of thyroid hormones that lead to s/s such as: inc. sensitivity to cold, constipation, weight gain, puffy face, hoarseness, muscle weakness, inc. blood cholesterol levels, muscles aches/stiffness, joint pain/swelling, heavy or irregular periods, thing hair, slow HR, depression, dec. memory
myxedema
life threatening event of severe uncompensated hypothyroidism. s/s include: hypothermia, unconsciousness, low BP, dec. RR, coma. Can be fatal.
what population is most likely to experience myxedema?
older women during cold months
severe hypothyroidism is characterized by what?
inc. cholesterol lebels, atherosclerosis, coronary artery disease, poor left ventricular function, and myxedema coma.
how do you dx hypothyroidism?
TSH level > 10 is considered hypothyroidism free T4 level and anti-thyroid peroxidase (antibody) levels
what is the presence of anti-tthyroid peroxidase indicative of?
Hashimoto’s thyroiditis
what are some causes of hypothyroidism?
Hashimoto's thyroiditis (autoimmune) thyroid atrophy (aging) radioactive iodine/thyroidectomy medications (lithium iodine, antithyroids) infiltrative thyroid disease (cancer)
what are some complications of hypothyroidism?
birth defects goiter heart problems (inc. LDL, pericardial effusions) infertility (dec. ovulation) mental health (depression)
hyperthyroidism
overactive thyroid leads to overproduction of thyroid hormones
causes of hyperthyroidism?
Grave's disease toxic nodular or multi-nodular goiter thyroiditis excessive iodine consumption pregnancy
signs and symptoms of hyperthyroidism?
increased metabolism. fatigue, muscles weakness, hand tremors, mood swings, nervousness, restlessness, anxiety, inc HR, inc. RR, palpitations, dry skin, trouble sleeping, weight loss, inc. freq. of bowel movements, light or skipped periods. Speeds up body processes.
parathyroid gland
four small glands in neck that produce parathyroid hormone (parathormone) and calcitonin.
hyperparathyroidism
overproduction of parathormone leading to bone decalcification and inc. calcium in the blood stream, which may result in calcium-containing kidney stones. signs and symptoms include: apathy, fatigue, muscle weakness, nausea, vomiting, constipation, hypertension, and cardiac dys-arrhythmias
how do you dx hyperparathyroidism?
persistent hypercalcemia and elevated parathormone levels. bone changes on x-ray or bone scan.
hypoparathyroidism
underproduction of parathormone which leads to hypocalcemia. usually occurs after recent neck surgery, with family hx, or with autoimmune diseases like Addison’s.
s/s of hypoparathyroidism?
tetany (muscle spasms/cramps @ fingers and hands), paresthesias (tingling), LOC with grand mal seizures, malformation of teeth, impaired kidney function, heart arrhythmias, fainting, stunted growth, slow mental development, calcium deposits a@ brain, cataracts. cannot reverse complications once happen, but may be able to prevent or keep from progressing.
adrenal gland
two glands @ top of kidneys. 2 main components include the cortex (outer) and medulla (inner) parts.
cortex of the adrenal
outer portion of the gland. produces hormones vital to life such as cortisol (metabolism, stress) and aldosterone (BP control). Produces 2 main groups of corticosteroids: glucocorticoids and mineralocorticoids.
what controls the release of glucocorticoids?
signals from hypothalamus (CRH) and pituitary glands (ACTH)
what controls the release of mineralocorticoids?
signals from the kidney
what hormones are released from the cortex of the adrenal gland?
hydrocortisone
corticosterone
aldosterone
sex hormones
medulla of the adrenal
inner portion of the adrenal gland that produces non-essential hormones after physical or emotional stress.
hormones produced by the medulla of the adrenal gland?
epinephrine (inc. HR, RR, BGC, etc.)
norepinephrine (vasoconstriction, inc. BP
Addison’s disease
adrenal cortex does not produce enough cortisol or aldosterone
adrenal cancer
rare, but aggressive cancer that usually becomes malignant
Cushing’s syndrome
uncommon, characterized by overproductions of cortisol. Also happens with chronic corticosteroid use. “Moon face.”
congenital adrenal hyperplasia
genetic. low cortisol levels and other hormone issues like low aldosterone
pheochromocytoma
rare adrenal tumor that results in over-release of epinephrine and norepinephrine. always in “fight or flight” mode. s/s include: pain (chest), irritability, nervousness, pallor, palpitations, inc. HR, severe headache, sweating, weight loss, hand tremor, sleeping problems, inc. BP. Occurs in “attack” as adrenal medulla releases hormones every 15-20 min.
how to dx pheochromocytoma?
abdominal CT, biopsy, serum catecholamines, glucose, serum metanephrien, MRI, urine tests
primary aldosteronism
adrenal glands produce too much aldosterone, so you lose potassium and retain sodium, which leads to water retention along with inc. blood volume and BP. if untreated, stroke, heart disease. HTN that occurs with this may be curable. resistant hypertension
pancreatic islets
islets of Langerhorn. endocrine cells @ pancreas that control the pancreatic feedback system that regulates blood glucose, insulin, glycogen, glucagon, and somatostatin levels.
diabetes
group of metabolic diseases characterized by hyperglycemia that result from insulin production defects or insulin action defects. Affects nearly 10% of the US population. Results in huge healthcare expenditures.
hospitalization rates for adults and kids with diabetes?
2.4 and 5.3x greater than average population
T1 diabetes
destruction of pancreatic beta cells (genetic, triggered by env. event like infection) results in dec. insulin production and unchecked glucose production at the liver. Glucose requires insulin to enter cells, so cannot enter cells. To meet energy needs, body metabolizes fat to glycerol and free fatty acids. Body uses glycerol as glucose and F.A. are broken down to ketones that are excreted in the urine with large amounts of water. Fasting hyperglycemia.
T2 diabetes
pancreas produces enough insulin, but fat/liver/muscle cells fail to respond to it correctly (insulin resistance). Glucose cannot enter cells resulting in hyperglycemia. 90-95% of patients with diabetes are T2.
diabetic ketoacidosis
common with T1 but not T2 diabetes. Fat is broken down in to free fatty acids, which is metabolized to ketones. Ketones & glucose build up in bloodstream, excreted @ urine with large amounts of water. Dehydration results, worsening ketoacidosis (dec. pH). Causes low BP and shock.
s/s of diabetic ketoacidosis
osmotic diuresis vomiting acidosis cerebellar dysfunction cerebral edema fluid/electrolyte depletion shock
s/s T2 diabetes
NOT diabetic ketoacidosis
fatigue, irritability, polyuria, polydypsia, poor healing wounds, vaginal infections, blurred vision (with hyperglycemia)