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SIUE Pathophys III

QuestionAnswer
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.
Created by: asaranita
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