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)
what are some risk factors for T2 diabetes?
family history, obesity, race/ethnicity (not Caucasian), age >45, impaired fasting glucose, hypertension, low HDLs, high triglycerides, history of gestational diabetes or delivery of >lb baby.
metabolic syndrome
constellation of symptoms associated with beta cell failure and rising glucose levels. these include: hypertension, high cholesterol, abdominal obesity, and hyperglycemia.
gestational diabetes
any degree of glucose intolerance with onset anytime during pregnancy. Placental hormones can lead to insulin resistance. Clinical manifestations = 3P’s (polyuria, polydipsia, polyphagia.
Normal vs. diabetic levels for A1c, fasting plasma glucose, and oral glucose tolerance test
Normal: A1c ~5%, FPG <99, OGTT <139
Diabetes: A1c 6.5+, FPG 126+, OGTT 200+
what organs are damaged by hyperglycemia?
eyes, kidneys, nervous system, GUT organs, sexual organs, bladder, GI, cardiac system
micro and macro-vascular complications of diabetes
diabetes causes chronic inflammation, which damages micro and macrovascular tissue. These changes lead to inc. risk for coronary artery disease, cerebrovascular disease, diabetic retinopathy, nephropathy, and neuropathy.
hematemesis
blood in vomit
hematochezia
bright red stools (visible blood)
melena
black, tarry stools (blood acted on by GI tract)
occult bleeding
stools look normal but products are present in stool in small amounts (Guiac test)
hyperkalemia and GI
results in hyper excitability of GI smooth muscle and inc. GI motility (diarrhea)
hypokalemia and GI
dec. excitability of GI smooth muscle and motility, so constipation
hypercalcemia and GI
causes dec. excitability of GI smooth muscle, dec. motility, and inc. strength of contractions. Constipation.
hypocalcemia and GI
inc. excitability of GI smooth muscle and inc. motility. dec. strength of contractions. Diarrhea.
osmotic diarrhea
unabsorbable osmotic particles in GI tract cause osmotic movement of water from GI cells to the lumen.
secretory diarrhea
inflammation or infectious process that involves cells of GI tract and causes those cells to secrete excessive fluid into lumen
diarrhea and electrolyte imbalance
potassium and bicarbonate usually reabsorbed in GI tract, but with diarrhea more is lost leading to metabolic acidosis and hypokalemia
dysphagia
difficulty swallowing
esophagitis
infection/inflammation of the esophagus, often related to GERD reflux into lower esophagus
achalasia
dysphagia associated with inability of lower esophageal sphincter to release
GERD
gastro-esophageal reflux disease. backward movement of gastric contents into esophagus, leads to complications like Barrett’s esophagus
Barrett’s esophagus
change in tissue types @ esophagus, increases risk for cancer
hiatal hernia
protrusion of part of the stomach upward into the thorax
esophageal cancer
uncommon. associated with Barrett’s esophagus and long term GERD. Presents with dysphagia.
gastritis
inflammation of stomach
stress ulcers
stress activates SNS, which shunts blood away from GI tract. Stomach acid then irritates ischemia gastric mucosa and causes ulcers. can lead to massive bleeding.
peptic ulcer disease
ulcerative disorder @ duodenum associated with h. pylori infections.
stomach cancer
bulky, irregular shaped ulcers with jagged edges. risk factors include dietary habits and chronic gastritis.
IBS
chronic and recurrent intestinal symptoms not explained by structural or biochemical abnormalities
inflammatory bowel disease
two types: ulcerative colitis and Crohn’s disease
ulcerative colitis
non-specific inflammatory condition at the colon. confined to the colon or rectum. Confluent lesions, pinpoint mucosal hemorrhages, and crypt abscesses
Crohn’s disease
recurrent, granulatomous inflammatory response. Affects various sites along the GI tract (NOT JUST RECTUM/COLON). Skip lesions, cobblestone appearance, and complications such as fistula development.
diverticular disease
pouch-like herniations of the superficial layers of the colon through muscles of bowel wall. Risks include low fiber diet, high intake of processed foods…does not exist in undeveloped nations.
appendicitis
inflammation of the appendix wall. Pain localized at the right lower quadrant with elevated WBC and rebound tenderness.
peritonitis
inflammation of the membrane lining of the abdominal cavity and covering visceral organs.
gallbladder
pear-shaped organ. hollow. R side of abdomen. primary function is to store and secrete bile. (bile salts are recycled)
cholecystitis
inflammation of the gallbladder. s/s include severe pain in RUQ that radiates to shoulder/back. Tenderness w/ palpation. Nausea, vomiting, fever, usually occurs after a large fatty or fatty meal. Caused by gallstones, tumors, or obstruction of bile duct.
cholelithiasis
gallstones. usually asymptomiatic. Most common symptom is biliary colic. Does not cause dyspepsia or fatty food intolerance. Risk factors: 4Fs = fat, female, forty or older, family hx
pancreas
two main functions include 95% exocrine (digestion) and 5% endocrine (blood sugar regulation).
pancreatitis
inflammation of the pancreas. Acute pancreatitis is a medical emergency and char. by severe LUQ pain radiated to pack. Cullen and Grey Turner signs indicate intra-abdomial bleeding. Chronic is usually undetected. Classic s/s include: persistent pain, excess fat in feces, jaundice, LUQ mass as scar tissue replaces pancreatic tissue
causes of pancreatitis
mostly alcohol abuse and gallstones
liver
largest gland of body. ~3lb solid organ. reddish-brown color, rubbery.
Kupffer cells
@ liver. breakdown old RBCs, producing bilirubin.
functions of liver
digestion, metabolism, detoxification, storage, production, immunity.
liver and digestion
produces bile to aid digestion
liver and metabolism
metabolizes carbs, lipids, proteins into bio-useful materials. Absorbs/releases glucose
liver and detoxification
hepatocytes monitor blood and remove toxic substances before they reach rest of body
liver and storage
stores many nutrients, vitamins, minerals, glucose, fatty acids.
liver and production
produces clotting factors like prothrombin, fibrinogen, and albumins
liver and immunity
Kupffer cells are immune cells that capture and digest bacteria, parasites, fungi, old RBCs, and cell debris. Fixed macrophages.
hepatic dysfunction caused by…?
damage to the liver cells, primary liver disease, bile obstruction, problematic hepatic circulation
jaundice
skin, sclera discolored yellow because of too much bilirubin (>3mg/dL causes yellowing)
portal hypertension
increase in blood pressure at portal venous system, leads to ascites and varices
ascites
fluid accumulation in abdominal cavity due to increased BP and decreased albumin levels (pressure gradient). Failure of liver to metabolize aldosterone leads to inc. water and sodium retention @ kidneys.
esophageal varices
abnormal, enlarged veins at esophagus. Rupture, bleeding = major complication of portal hypertension. High mortality rate. 30% of all upper GI bleeds.
osteogenic cells
stem cells @ inner layer of periosteum. Gives rise to osteoblasts.
osteoblasts
build bone
osteoclasts
crush/break down bone matrix (remodeling &calcium release)
osteocytes
mature bone cells
remodeling requires what types of bone cells?
osteoclasts and osteoblasts
compact bone (cortical)
organized, solid, strong.
haversian system.
covers spongy bone, forms cylinder around central marrow cavity, 85% skeleton
spongy bone (cancellous)
no haversian system. contain trabecular, located at ends of bone and center of flat bones, can withstand forces from many directions. “inner” porous bone.
bones in the skeleton? axial? appendicular?
206 80 axial (skull, spine, ribs), 126 appendicular (extremities, shoulder, pelvis)
bone integrity/maintenance includes…
remodeling and repair
4 stages of bone repair?
hematoma formation
fibrocartilage callus formation
bony callus formation
bone remodeling
synarthrosis joints
no movement. Fibrous or fixed joints.
amphiarthrosis
slightly movable joints i.e. intervertebral or pubic symphysis
diathrosis
very moveable. synovial joints, ball& socket, freely movable.
fibrous joints
bone to bone juncture
cartilaginous joints
symphysis and synchondrosis
synovial joints
uni-bi-or multi-axial
joint capsule
fibrous connective tissue that covers ends of bone where they meet in a joint
synovial membrane
smooth inner lining of joint capsule (non-articular portion of synovial joint and any ligaments/tendons in cavity)
synovial cavity
enclosed, fluid-filled space b/t articulating surfaces of 2 bones
synovial fluid
lubricating fluid in joints. superfiltrated plasma from blood vessels. nourishes articulate cartilage pads
articular cartilage
layer of hyaline cartilage that covers the end of each bone to reduce friction and distribute weight-bearing forces.
contraction/relaxation of muscles requires…?
large amounts of ATP and calcium (catalyst for myosin/actin).
