click below
click below
Normal Size Small Size show me how
SIUE Pathophys III
Question | Answer |
---|---|
Anterior pituitatry disease result in what deficiencies? | ATCH deficiency, GH deficiency, and TSH & LH deficiency |
Decreased ATCH results in | decreased cortisol (life threatening because cortisol is required for many aspects of cellular metabolism), N & V, anorexia, fatigue & weakness, and hypoglycemia, loss of body hair, decreased libido |
Decreased GH in children results in | growth failure/dwarfism (although not all children are short in stature), fasting hypoglycemia |
Decreased GH in adults results in | vague symptoms of social withdrawl, fatigue, loss of motivation, diminished feeling of well-being, some osteoporosis |
Increased GH is a result of | Hyperpituitarism (anterior pituitary) |
Decreased GH is a result of | Hypopituitarism (anterior pituitary) |
Increased GH in adults results in ___ & symptoms are? | acromegaly - connective tissue proliferation, increase in size & function of sweat glands, coarse skin & body hair, englargement of facial bones (jaw and forehead), lg joint arthroplasty, barrel chest |
Increased GH in children results in | giantism |
Increased TH levels result in ____ & symptoms are | Hyperthyroidism. Sx: Increased MBR, heat intolerance, exopthalmos, goiter, Increased SNS (tachycardia, sweating), wt loss, hyperreflexia, pretibial edema |
Decreased TH levels results in _____ & symptoms are | Hypothyroidism. Sx: loss of hair, brittle hair, periorbital edema, puffy face, bradycardia (HF), wt gain, cold intolerance, muscle weakness, edema of extremities, myxedema coma |
Hyperfunction of adrenal cortex results in | increased levels of cortisol (cushings disease) from increased ATCH from anterior pituitary. & Hyperaldosteronism |
Hypofunction of adrenal cortex results in | Addison's Disease |
Hyperadlosteronism sx are | result of hyperfunction of adrenal cortex: hypertension & hypokalemia, metabolic acidosis. |
Addison's disease sx: | Hypofunction of adrenal cortex. Sx: fatigue & weakness, N/D, orthostatic hypotension. Mood disturbances. Actually have increased ACTH levels, but decreased cortisol levels. |
Adrenal medulla hypofunction results in | NO KNOWN ALTERATIONS EXIST |
Adrenal medulla hyperfunction typically occurs from ___ and results in _______ | tumors (pheochromocytomas), continual secretion of catecholamines, mostly norepi. Sx: r/t excess catecholamines. Diaphoresis, tachycardia, palpiations, H/A, HTN, hypermetabolism, wt loss, appetite increase, glucose intolerance. |
SIADH caused by | increased secretion of ADH from tumors, CNS injury ,drugs, pulmonary disorders |
SIADH patho | enhanced renal H20 retention from inreased perm to H20 |
SIADH clinical & lab values | serum: low Na+, hypoosmolarity. urine: high Na+, hyperosmolarity. Sx usually occur from serum hyponatremia - neuro changes, heart failure, abd cramping, convulsions & seizures. |
SIADH tx | Give hypertonic saline & fluid restriction |
DI results from | decreased ADH from brain injury or renal disease |
DI patho | decreased renal H20 retention |
DI clinical sx & lab | Polydipsia & Polyuria. Develope large bladder capacities. Serum: high Na+, hyperosmolarity. Urine: dilute, hypoosmolarity, low specific gravity |
DI tx | hydration & DDAVP (or some cases administer ADH) Perform water deprivation test, and will still pee lrg amounts if with-hold H20) |
Diabetes is a dysfunct of the ____ endocrine & characterized by ? | the endcrine system of the pancreas, and a group of disorders characterized by glucose intolerance |
Type I Diabetes is result of ____ & characteristics | an autoimmune-mediated specific loss of beta cells in the pancreatic islets, occurs in childhood. No symptoms of hyperglycemia until 80-90% of beta cells are destroyed, little or no insulin is made, usually normal weight or thin. |
Type I Diabetes are non insulin dependant or insulin dependant | INSULIN Dependent |
Type I diabetes clinically | glucose accumulates in the blood & appears in urine. Osmotic diuresis occurs from intracellular dehydration. Polyuria, polydipsia, polyphagia |
Type II diabetes is a result of | insulin resistance caused by altered metabolism. Obesity and sedentary life style attributes to the cause. |
Type II diabetes sx | recurrent infection & prolonged wound healing, genital puritis, visions changes, diabetic neuropathy, paresthesias, fatigue, obesity. |
Hyperpituitarism is a disease of the | anterior pituitary, usually resulting from pituitary adenomas, which causes usually causes an increase of GH and prolactin. |
Pituitary adenomas usually result in ____ and secrete _____ | hyperpituitarism and result in increased secretion of GH & prolactin. |
Hypersecretion of prolactin is reult of | Hyperpituitarism (anterior pituitarism), usually from prolactinomas. |
Increased prolactin in females causes | amenorrhea, galacctorrhea, hirsutism (excessive hair), osteopenia |
Increased prolactin in males causes | hypogonadism, erectile dysfunction, impaired libido, oliogospermia, diminished ejaculation |
An hypersecretion of GH in children causes _____ and hyposecretion of GH in children causes ______? | 1.) gigantism 2.) dwarfism |
Graves disease is result of | primary hyperthyroidism, most common in women. type II autoimmune. |
Clinical manifestations of Graves Disease | Increased TH, decreased TSH. goiter, pretibial mxyedema, exopthalamos, diplopia, blurred vision, wt loss, increased CO, heat intolerance, hyperreflexia |
Parathyroid hormone deficiency clinical manifestations | inability to maintain calcium levels: hypocalcemia, tetany, dry skin, alopecia, poor dentation, skeletal deformities, muscle spasm |
Chevosks sign is what and indicative of? | If you tap on patients cheek will result in twiching of a lip. Indicative of hypocalcemia (hypoparathyroidism) |
Trousseau sign is what and indicative of? | Sustained inflated BP cuff causes carpal spasm. Indicative hypocalcemia (hypoparathyroidism) |
Hypoparathyroidism lab results | hypocalcemia, hyperphosphatemia, and decreased PTH levels |
Hypothyroidism clinical sx: | goiter (also in hyper), decreased TH, galacterrhea, annovulation, lethargy, confusion, slow movement, decreased reflex, coma, cold intolerance, decreased CO with bradycardia, wt gain, constipation, coarse hair & dry skin |
Thyrotoxicosis is hypo or hyperthyroidism | HYPER (can result in thyrotoxic crisis) |
DKA is more common in | type I diabetes |
DKA is a result & precipitating factors are? | absolute or relative deficiency of insulin. Precipitating factors are intercurrent illness or infection, trauma, surgery, MI stress. |
Clinical manifestations of DKA | polyuria, & dehydration from osmotic diuresis, deficiency in total K+, (not serum K+), decreased Na+, phos, & mag. ketones in urine, BS >250, bicarb < 18, pH < 7.3, presence of anion gap. Kussmal respirations, CNS depression |
HHNK is associated usually with | type II |
Clinical manifestations of HHNK | serum BS > 600, pH > 7.3, bicarb > 15, serum osmol >320, NO ketones, increased BUN & Creatinine, SEVERE VOLUME DEPLETION, more neuro changes from hyperosmolarity, K deficits |
in HHNK the degree of insulin deficienty is ____ than DKA and the degree of volume depletion is _____ | 1.) less 2.) more |
Diabetes Complication | Microvascular & Macrovascular |
Microvascular complication of Diabetes include (3) | Retinopathy, Diabetic Nephropathy, and Diabetic Neuropathy |
Earliest sign of diabetic nephropathy from microvascular complications of diabetes | Microabluminuria (30-300mg/day), followed by proteinuria (> 300mg/day), then a decrease in GFR. Progressive renal failure |
Cushings disease | disease of adrenal cortex, excessive ATCH secretion causes increased in cortisol. |
Cushings clinical manifestations | result of increased cortisol: moon face, truncal obestity, buffalo hump. hypergylcemia, polyuria, protein wasting, muscle thinning in the limbs. bone fx, renal calcium excretion leading to stones |
Delayed puberty is | a delayed development of secondary sex characteristics usually from a physiologic delay, or underlying dieases or chronic diseases like cystic fibrosis, DM, chronic renal defic, malnutrition, excessive exercise |
Delayed puberty is considered no signs of puberty by age __ in males and __ in females | 1.) 14 2.) 13 |
dysmenorrhea is | painful menstruation |
Dysmenorrhea occurs from | 1.) and increased release of excessive amounts of prostaglandins causing excessive uterine contractions. Prostaglandins are myometrial stimulators & vasoconstrictors 2.) Leukotrienes heighten sensitivity of pn fibers. |
Polycystic Ovarian syndrome (PCOS) clinical manifestations | r/t to annovulation & hyperandrogenism: dysfunctional bleeding, ammenorrhea, hirsutism, acne, increased infertility. Increased LH, prolactin, and androgens |
PID pathogenesis | pelvic inflammatory disorder. Acute inflammatory process caused by infection of the uterus, fallopian tubes or ovaries. Microorganisms (usually from STI) migrate and damage the epithelium the lines the upper reproductive tract, traveling to uterus. |
PID results in | tubonecrosis and repeated infections |
cystocele | descent of a portion of the posterior bladder wall & trigone into the vaginal canal. (usually caused by trauma with childbirth) |
Rectocele | buldging of rectum & posterior vaginal wall into the vaginal canal. Symptoms usually ocur after menopause, can result from chronic constipation |
Enterocele | herniation of rectourine pouch into the rectovaginal septum (between rectum & posterior vaginal wall), found in obese people |
Endometriosis occurs from | Unknown sure cause, but theory that 1.) implantation of cells during retrograde menstruation emptying into the pelvic cavity. 2.) impaired cellular & humoral immunity. |
Endometriosis is | disordered immunity in which endometrium cells are permitted to proliferate outside of the uterus, and responds to hormonal fluctuations assoc with menst. cycle. |
Clinical sx of Endometriosis | primarily abd or pelvic pain & infertility. Also includes: dysmenorrhea, dyspareunia, dyschezia, vag bleed, adhesions & scarring. alterations in hormone and prostaglandin secretions |
Phimosis | foreskin is so tight it cannot be retracted back. (cannot be uncovered), usually from scarring and adhesions |
Paraphimosis | foreskin is so tight that it cannot be reduced over the glans. (cannot cover it), usually from scarrin and adhesions |
BRACA1 | clinically significant for ovarian and breast cancer |
Hypertension's effect on cardiovascular system | increased work load of heart, L ventricular hypertrophy, MI, L heart failure. |
Hypertension's effect on coronary arteries | accelerated atherosclerosis, MI, myocardial ischemia |
Hypertension's effect on the aorta | weakened vessel wall resulting in an aneurysm |
Hypertension's effect on the kidneys | Increased RAAS by decreased blood flow. Na+ and H2O retention, increased BV, tissue damage, decreased GFR, kidney ischemia |
Hypertension's effect on brain | decreased blood and O2 supply which could lead to TIA, infarct, hemorrhage, cerebral thrombosis |
Hypertension's effect on eyes | decreased blood flow causing retinal sclerosis, increased arteriolar pressure causing exudate and hemmorrhage. |
Hypertension's effect on arterial vessels of lower extremities | decreased blood flow, increased pressure in arterioles, intermittent claudication, arterial thrombosis, gangrene |
Pulmonary embolism most common cause is from | DVT |
Buergers disease (Thromboangiis Obliterans) | inflammatory disease of the peripheral arteries, the inflam lesions are accompanied by thrombi and by vasospasm of arterial segments which can occlude and obliterate protions of small & med sized arteries causing pain |
Varicose Veins develop because of | 1.) damaged valves resulting in pooling of blood from prolonged standing 2.) decreased activity of the muscle pump which causes increased pooling |
varicose veins can result in | chronic venous insufficiency, leading to a decreased in venous return causing tissue ischemia, edema, venous statis ulcers, hyperpigmentation of skin, feet, & ankles, DVT |
Superior Vena Cava Syndrome | is the progressive occlusion of superior vena cava resulting in venous distention in the upper extremities and head. Leading cause is bronchogenic cancer. |
LDL | Bad cholesterol, responsible for delivery of cholesterol to the tissues. Consists mainly of cholesterol & protein. |
an ____ LDL level is a strong indicator of coronary risk | INCREASED |
Causes of increased LDL | genetic predisp, high dietary intake of cholesterol and fat. |
HDL | the good stuff, consists of mainly phospholipids and proteins, responsible for the reverse cholesterol transport, returning excess cholesterol from tissues to the liver converting it to bile. Participates in endothelial repair. |
an ___ HDL level is a strong indicator of coronary risk | LOW (<40) |
and increased HDL is thought to | protect from athersclerosis |
You can increased your HDL by | exercise, diet, fish oil, niacins and statins |
Myocardial ischemia is | result of local deprivation of coronary artery supply. Insufficient blood flow for and increased demand. |
Myocardial cells become ischemic after | 10 seconds of decreased flow |
Myocardial cells are viable for how long after ischemia occurs | 20 minutes. If perfusion is not restored and MI occurs |
As myocardial ischemia occurs what happens in the heart | decreased contractility, decreased CO, conduction abnormalities, dysrhythmias and the anaerobic process takes over |
Myocardial infarction occurs | after 20 min of ischemia, when blood flow is interrupted for an extended period of time, usually from atherosclerotic CAD, coronary spasm, or embolism. |
Myocardial infarction is considered reversible or irreversible injury | Irreversible. Hypoxic injury causes cellular death (necrosis). When repairing myocardial stunning, hibernating myocardium, myocardium remodeling. |
Angina (4 types) | stable, prinzmetal, silent, angina pectoris |
Stable Angina | recurrent, stable, predictable chest pain, usually occurs with exercise |
Prinzmetal Angina | unpredictable chest pain from vasospasm or coronary vessels without atherosclerosis at rest or sleeping, mostly at rest |
Silent ischemia | undetectable symptoms. Usually in in DB patients or those with dysfunction of nerves. Non-specific symptoms like N/V/D, back pain |
Angina Pectoris | typical, substernal CP, sensation to pressure, radiating into L arm, jaw, neck. Pallor & dyspnea are assocaited (text book CP) |
MI Labs | EKG, Troponins, CKMB, LDH, Glucose |
Troponin | most specific for MI, see in the first 2-4 hours, remaining elevated for 7-10 days. |
CKMB | less specfic than troponin. see in 2-4 hours, peaks in 24 hours. Also can be seen in renal disease. |
LDH in MI | increased after 12 hours or more |
Hyperglycemia in MI | seen 72 hours post MI |
Right heart failure | inability of R ventricle to provide adequate blood flow into the pulmonary circulation. |
Right heart failure usually results from | Left heart failure |
Sx of R heart failure | JVD, peripheral edema, hepatosplenomegaly, increased pressure in systemic circulation, increased workload. |
Left heart failure is | results of pulmonary congestion and inadequate systemic perfusion. |
SX of left heart failure | dyspnea, orthopnea, cough, frothy sputum, fatigue, decreased urine output, decreased CO, pulmonary edema, S3 or S4 gallop |
Aortic Stenosis | most common valvular prob. Oriface of aortic valve narrows causing decreased blood flow from L ventricle ejected out to aorta, leading to increased pressure in L ventricle, increased LVED volume, decreased CO & SV, hypertrophy, and heart failure. |
Mitral stenosis | impairs blood flow from L atrium to L ventricle, inflammation and scarring of valvular leaflets and shortening of tendinea cordis. Sx: dyspnea, orthopnea, cough, angina, syncope, palpitations, pulm crackles, irreg pulse. |
Aortic regurgitation | inability of the aortic valve leaflets to close properly during diastole, leaking blood back into the L ventricle |
Mitral regurgitation | permits the backflow of blood from left ventricle into L atrium during ventricular systole causing a loud pansystolic murmur. |
Tricuspid regurgitation | permits backflow of blood from R ventricle into the R atrium during ventricular systole. Usually occurs with failure of R ventricle secondary to pulmonary hypertension. |
Renal stone composition | 1.) calcium oxalate or phosphate (70-80%) 2.) struvite stones from mag, ammonium, and phos (15%) 3.) uric acid stones (7%) 4.) cystine stones (rare 1%) |
Renal stones are considered | masses of crystal protein, primary salts make up stones. |
Risk factors of developing kidney stones | first stone prior to age 50, men, inadequate fluid intake (dehydration), excessive vitamin D & calcium ingestion, vitamin A deficiency, decreased exercise, geographic location, gout, UTI |
cystitis | inflammation of the bladder most common site of uti. Usually from STI or Ecoli. NO FEVER or chills. |
Sx of cystitis | dysuria, increased frequency & urgency, pain in lower abd, supra pubic, & low back. Heamturia, foul smelling urine. NO FEVER OR CHILLS |
Pyleonephritis | infection occurs proximal to the bladder, in the ureters, renal pelvis, or parenchyma. Usually from e-coli, proteus or psuedomonas. |
Sx of pyleonephritis | systemic sx like FEVER & Chills. increased frequency, low back and suprapubic pain. Onset is usually acute. See WBC casts. |
Creatinine | provides measure of GFR estimating function of renal tissue and glomeruli filtration. Norm (0.7-1.2mg/dl) |
Pre-renal kidney injury | most common cause of AKI. caused by renal hypoperfusion that occurs rapidly over a period of hours with increased plasma BUN and creat. from hypovolemia, hemorrhage, burns, vomiting & diarrhea, shock, renal art stenosis. |
Intra-renal kidney injury | results from injury to glomeruli or tubules and result from acute tubular necrosis, acute glom nephritis, allograft disease. Oliguria is common. |
Post-renal kidney injury | usually occus with UTI that affects the kidney bilaterally. From UTI, prostate disease, urethral obstruction. Obstruction causes decreased in GFR. Hrs of anuria with flank pain followed by polyuria. |
Why are STI's more frequent and severe in women? | Because of Female anatomy. |