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Patho Test # 3
SIUE NIcole's Patho Test #3
| Question | Answer |
|---|---|
| SIADH is characterized by high levels of what? | ADH in the absence of normal physiologic stimuli for its release. |
| Most common cause of SIADH is what? | Ectopically produced ADH by tumor cells. Can also be caused by pituitary surgery because stored ADH is released. |
| Cardinal features of SIADH are the result of enhanced water retention, why does this happen and what else does it result in? | ADH increases the kidney's permeability to water thus increasing water resorption. This increases extracellular fluid volume leading to dilutional hyponatremia, hypoosmolarity, and urine that is inappropriately concentrated compared to serum osmolarity. |
| What are some of the symptoms in SIADH and what are they usually the result of? | SIADH symptoms are usually the result of hypotonic dilutional hyponatremia. Thirst, impaired taste, annorxia, dyspnea on exertion, fatigue, dulled sensorium, more severe are GI symptoms, most severe are confusion, lethargy, muscle twitching & convulsions. |
| Serum Na+ levels below 110-115 mEq/L can lead to what type of problem? | Severe irreversible neurological damage. |
| What findings are indicative for a Dx of SIADH? | 1)serum hpoosmololity (<280 mOsm/kg)and hyponatremia (serum Na+ <135 mEq/l) 2)urine hyperosmolarity 3)urine Na excretion 4)normal renal, adrenal and thyroid function 5)absence of conditions that can alter volume status. |
| What is the cause of D.I.? | Insufficiency of ADH |
| What does a deficiency of ADH in D.I. lead to? | Polyuria, and ploydipsia. |
| What are the two types of D.I. and what happens in each type? | Neurogenic-any organic lesion of the hypothalamus, pituitary stalk, or posterior pituitary interferes w/ ADH synthesis, transport, or release. Nephrogenic-insensitivity of the renal collecting tubules to ADH. |
| Neurogenic D.I. ADH levels are insufficient, Nephrogenic D.I. ADH levels are what? | They are normal, but the collecting ducts do not respond to ADH stimulation. |
| What does D.I. cause? | Causes the inability of the kidney to increase permeability to water, causing excretion of large volumes of dilute urine, polydipsia, increase in serum Na. |
| What are the S&S of D.I.? | polyuria, nocturia, continuous thirst, polydispia. |
| Posttraumatic or postneurosurgical D.I. develop a three-phase syndrome, what happens? | 1)initially sig. diuresis occurs, as a result of acute damage to the hypothalamic centers involving ADH secretion.2)Antidiuresis may represent necrosis of denervated tissue of posterior pituitary release of ADH 3)Polyuria & polydispia-perm. loss of ADH. |
| What is the basic criteria to diagnose D.I.? | Polyuria, polydispia, low urine specific gravity <1.010, low urine osmololity <200 mOsml/kg, hypernatremia, high serum osmolality 300mOsm, and continued diuresis despite serum Na 145 mEq/L or greater. |
| What are the major differences between D.I. and SIADH? | D.I.-decrease in ADH stimulation or production SIADH-increase in ADH. D.I.-Large amount of dilute urine, increase serum Na, polydispia,polyuria,increased thirst SIADH-increase ECF volume, dilutional serum Na, concentrated urine. |
| Type 1 D.M. is caused from? | Autoimmune destruction of pancreatic beta cells (HLA-DQ, HLA-DR), nonimmune destruction of beta cells from other diseases, leading to an absolute insulin deficiency . |
| Type 2 D.M. is caused from? | Genetic abnormalities combined with environmental influences, such as obesity result in insulin resistance, and decreased insulin secretion by beta cells. Resistance can be from abnormal insulin molecule or insulin receptor. |
| Type 1 occurs primarily in children, what are the clinical manifestations? | Polydispia-high BS water is taken out of cells resulting in intracellular dehydration, polyuria, polyphagia, weight loss, and fatigue, acidosis produces kussmaul respiration's and acetone breath. |
| Insulin normally stimulates lipogenesis and inhibits lipolysis, thus preventing fat catabolism, what happens with insulin deficiency? | lypolysis is enhanced and there is an increase in the amount of nonesterified fatty acids delivered to the liver, increase in glyconeogenesis contributing to high glucose and production of ketone bodies. |
| In type 1 diabetes what the accumulation of ketone bodies cause? | decrease in pH, triggering of the buffer systems. |
| How does the lack of insulin contribute to weight loss? | Lack of insulin causes the breakdown the protein and fat, thus contributing to the wt loss. |
| What are the Manifestations of type 2 D.M.? | Same symptoms of type 1 polyuria, and polydipsia, but will more often have nonspecific symptoms such as fatigue, pruritus, recurrent infections, visual changes, or symptoms of neuropathy. |
| What is the most common cause of hyperpituitarism? | Pituitary adenomas that are usually benign slow growing tumors that arise from cells of the anterior pituitary, most commonly those that secrete GH and prolactin. |
| Expansion of the pituitary adenoma can cause what type of deficits? | Neurologic and secretory defects. |
| Pituitary adenomas that arise from hormone producing cells of the pituitary are most often associated with hyper or hypo secretion of GH and prolactin? | Hypersectretion |
| What results in hyposecretion of anterior pituitary cells. | The pressure produced by the primary adenoma. Can cause reduced amounts of TSH, ACTH. |
| What is the autoimmune disease that results in stimulation of the thyroid gland and resultant hyperthyroidism? | Graves disease-multi system syndrome consisting of one or more of the following 1)hyperthyroidism, 2)diffuse thyroid enlargement Goiter 3)opthalmopathy 4)dermopathy |
| What happens in Graves to cause an increased amount of TH? | T-lymphocytes are sensitized to thyroid antigens and stimulate B cells to produce IgG (TSI) antibodies in whoch bind to TSH receptors on the thyroid gland and stimulate TH excretion. |
| Are TSH and TRH high in Graves disease? | No they are low because of the normal negative feedback system in which stops the production of TRH and TSH in the presence of high TH levels. |
| What are some of the symptoms with hyperthyroid? | Pretibial edema, warm skin sweaty palms, wt. loss, tachycardia, goiter, exophthalmos, visual disturbances. |
| What can happen when the thyroid gland enlarges as a normal response to puberty, pregnancy, or iodine deficiency? | The increase in follicles can result in irreversible changes in some of the follicles resulting in them functioning autonomously and producing excessive TH. |
| Once thyrotoxicosis results what is the condition called? | Toxic multinodular goiter or if only one nodule is hyperfunctioning toxic adenoma. |
| What is the difference in hyperthyroid manifestations between toxic multinodular or toxic adenoma with Graves? | Infiltrative ophthalmopathy and myxedema do not occur. |
| Hypothyroidism is characterized with what deficiency | TH |
| Hypothyroidism may be primary or secondary, what are these? | Primary-defective hormone synthesis resulting from autoimmune thyroiditis, endemic iodine deficiency, or iatrogenic loss of thyroid tissue after surgery. 2) Congenital defects Secondary-conditions that cause either pituitary or hypothalmic failure. |
| With primary thyroid malfunction in hypothyroidism what will you see as far as the levels of TH, TSH, and TRH? | Low levels of TH, and high levels of TSH and TRH. Lack of TH negative feedback on pituitary TSH secretion and hypothalmic TRH secretion. |
| In secondary hypothyroidism what will you see if there is pituitary malfunction? | Low levels of TSH and TH and high levels of TRH. Lack of the negative feedback to hypothalmic release of TRH by TSH and thyroid TH. |
| In secondary hypthyroidism if there is hypothalmic malfunction what will you see? | Low levels of TRH, TSH and TH because there is decreased TH. |
| Manifestations of hypothyroidism? | decreased energy metabolism, heat production, cold intolerance, lethargy, slightly lowered body temp, myxedema is characteristic of long time standing hypothyroidism. |
| Hypoparathyroidism is characterized by what hormone deficiency? | Abnormally low PTH most commonly caused by damage to parathyroid glands during thyroid surgery. |
| In hypoparathyroidism a lack of circulating PTH causes what to Ca and Phos? | Depressed serum Ca and increased serum phosphate. |
| If there is an absence of PTH what happens as far as Ca? | Impaired Ca resorbtion from bone and regulation of Ca reabsorbtion form the renal tubules. Hypocalcemia causes a lowering threshold for nerve and muscle excitation so that nerve impulses are initiated by a slight stimulus. |
| What are the manifestations of parathyroid deficiency? | Muscle spasms, hyperreflexia, tonic-clonic convulsions, laryngeal spasms, and severe cases death from asphyxiation, dry skin, loss of body hair, hypoplasia of developing teeth, horizontal ridges on nails, basal ganglia calcifications. |
| What electrolyte deficiency can cause a decrease in PTH? | Magnesium- once mag levels return to normal PTH levels should start to return to normal. |
| G.H. deficiency or excess is the result of a diseased ___? | Anterior Pituitary in which G.H. is released from. |
| In children what does a lack of G.H. and insulin like growth factor result in? | Delayed growth, dwarfism-with G.H. insensitivity in which the G.H. receptor is altered. Adults are more vague and include social withdrawl, fatigue, loss of motivation and diminished feeling of well being, osteoporosis and reduced lean body mass. |
| In Adults what does lack of G.H. cause? | Social withdrawl, fatigue, loss of motivation, and feeling of well-being. |
| In adults what does an increase in G.H. cause? | Acromegaly-enlarged tongues, interstitial edema, increase function and size of sebacous glands, course hair, enlargement of facial bones hands & feet, protrusion of lower jaw bone & forehead, elongation of rib bones, arthritis, HA, HTN, L heart failure. |
| In children whose epipyseal plates that have not closed the effect of increase G.H.? | Increase long bone-giantism |
| When does DKA develope? | When there is an absolute or relative deficiency of insulin. Most commonly occurs with Type 1 D.M. |
| What are the signs and symptoms of DKA? | Polyuria, dehydration, glucose and ketones in urine, Na, Phos, and Mag and K deficits. Metabolic acidosis, kussmaul respirations, acetone breath, CNS depression, anorexia, nausea, abd. pain, thirst. |
| What labs would you commonly see in a person with DKA? | Serum glucose of > 250mg/dl, serum bicarb <18mg/dl, serum pH <7.30, presence of an anion gap, presence of urine and serum ketones. Decreased serum Na, K, Phos, mag. Increased plasma levels of B-hydroxybutyrate, acetoacetate, and acetone. |
| HHNKS is most often followed by what and is it a medical emergency? | HHNKS is most often brought on by infections, medications, nonadherence to diabetes treatment, or coexisting disease and is a life threatening emergency. Most commonly seen with type 2 D.M. |
| How does HHNK differ from DKA? | Less profound insulin deficiency, and more fluid deficient, levels of free fatty acids are lower, lack of ketosis, bc insulin levels are sufficient to prevent excessive lipolysis, but not to use glucose properly. |
| What labs would you see in a person with HHNKS? | Serum glucose >600mg/dl, pH >7.30, serum bicarb >15mg/dl, high serum osmolarity, little or absent ketone in serum and urine,loss of electrolytes including K. |
| What are some signs that kidney failure is resulting from D.M.? | Microalbuminuria is the first manifestation of renal dysfunction, proteinuria, hypoproteinemia, Decreased G.F.R. <10/ml/min. |
| This syndrome is caused by excess levels of ACTH secreted by the anterior pituitary. | Cushing syndrome and occurs whenever there is an excess level or cortisol regardless of the cause. |
| What are the clinical manifestations of cushing syndrome? | Weight gain is the most common feature, resulting in the accumulation of adipose tissue in the trunk face, and cervical areas. Glucose intolerance, protein wasting leading to muscle weakness and thinning of the limbs, pathologic fx. |
| What leads to the pathologic fx, osteoporosis, vertebral compression, bone and back pain, and kyphosis in cushing syndrome? | Hypercortilism leads to increase bone resorption, inhibits bone formation, decreases intestinal ca absorbtion, and increases renal calcium excretion. |
| The loss of collagen in cushings causes what? | Thin weakened integumentary in which capillaries are more visible,vessel susceptible to rupture causing easily bruising. Easily damaged skin leading to skin breaks and ulcers. |
| What is cushings syndrome mostly likely caused from? | A ACTH secreting pituitary tumor, and ACTh secreting carcinoid tumors or small cell carcinoma of the lung, or adrenal tumor or dysfunction of the adrenal cortex. |
| Hyperfunction of the adrenal cortex can lead to? | Increased levels of circulating cortisol leading to cushing's and hypersection of adrenal androgens and estrogens leasing to virilization or feminization, and hyperaldosteronism. |
| Hypofunction of the adrenal cortex can lead to what? | Addison's disease. |
| In addison's disease what are your levels of ACTH and what do you see with this level? | ACTH are increased, but cannot stimulate the adrenal cortex because of adrenal atrophy or hypofunction because of autoimmune disease. Weakness, fatigue, anorexia, diarrhea, hypotension, hyperpigmentation. |
| What do women see when there is a decrease in adrenal androgens? | Loss of their secondary sex characteristics such as pubic hair and axillary hair. |
| Hyperfunction of the adrenal medulla is most likely caused by what, and what happens? | Most likely caused by a pheochromocytoma (tumor) on the adrenal medulla, that produces norepi, and larger tumors produce both norepi and epi. Persistant HTN,tachy, palpitations, severe HA, hypermetabolism, warth, heat intolerance, wt. loss. |
| What is delayed puberty? | Delayed puberty is the absence of thelarche (breast development) in girls by the age of 13, absence of menarche by age 15. Absence of testicular enlargement and thinning of the scrotal sac in boys by age 14. |
| What are the majority the causes of delayed puberty? | 95% of cases are a physiologic delay in which hormone levels are normal the the hypothatlmic-pituitary gonadal axis is intact, but maturation is happening slowly. Also any chronic condition that delays bone aging, lung disease, renal failure, cystic fib. |
| The other 5% of causes of delayed puberty are caused from what? | Disruption of the hypothalmic-pituitary gonadal axis with controls the release of LH and FSH, possibly caused by CNS tumors, hypopituitarism, pituitary adenomas. |
| What causes dysmenorrhea? | Usually the result of excessive prostaglandin production, enhanced by progesterone. Women w/ painful periods produce 10x as much prostaglandin, secretory endomorphism produces 3x prostaglandins, and discharged endometrium produces even more. |
| What else is associated with causing dysmenorrhea? | Leukotrienes highten sensitivity to pain in the uterus, and vasopressin contributes to endometrial hypersensitivity, constriction of endometrial blood vessels,--> ischemia, endometrial bleeding, and pain caused by protaglandins. |
| Secondary dysmenorrhea ia caused from what? | Disorders such as endometriosis, pelvic adhesion's, inflammation, cervical stenosis, uterine fibroids, polyps, tumors, cysts, IUD's |
| Women who are on the pill, do they suffer from dysmenorrhea? | Nope |
| Dysmenorrhea may be more sever in who? | Obese, smokers, nulliparous, delayed childbearing, and sexually inactive. |
| What is the chief symptom associated with dysmenorrhea? | pelvic pain associated with the onset of menses, pain often radiates into the groin and may be accompanies by backache, anorexia, vomiting, diarrhea, syncope, and HA. |
| In PCOS at lease two of these have to be present? | oligo-ovulation or anovulation, elevated levels of andorgens, or clinical signs of herandrogenism and polycystic ovaries. |
| In PCOS what things are increased and what is decreased? | Increase in GnRH causes increased LH which then increases androgens from the adrenal glands and testosterone. Androgens--> estrogen--> + feedback for LH and - feedback for FSH. FSH is decreased but still allows for continual follicular growth. |
| What are the clinical manifestations associated with PCOS? | Usually appear within first 2 yrs of puberty but can occur after normal menses or pregnancy. dysfunctional bleeding or amenorrhea, hirsutism, acne, and infertility. Insulin intolerance and hyperinsulinemia. |
| What is PID? | An acute inflammatory process caused by infection. |
| What can cause the infection in PID? What microorganisms? | Polymicrobial infection, can be initiated by chlamydia, gonorrhea, mixed nongonococcal/nonchlamydial bacteria, anaerobes, facultative organisms and genital tract mycoplasmas. |
| How do gonorrhea and chlamydia contribute to PID? | They may induce changes in the columnar, epithelium that lines the upper reporductive tract, causing damage and facilitating invasion by other microorganisms. Resultant inflammatory response leads to tubonecrosis and predispose to PID. |
| What are some of the symptoms associated with PID? | Symptoms most likely to develop during or immediately after menstration. Low bilateral abd. pain with fever, may be severe and sudden or no symptoms. May worsen with walking, jumping, or intercourse. Dysuria and irregular bleeding. |
| What is a cystocele? | Descent of a portion of the posterior bladder wall and trigone into the vaginal canal and is usually caused by childbirth. |
| What is a rectocele? | Bulging of the rectum and posterior vaginal wall into the vaginal canal. May sustain during childbirth, but symptoms usually do not develop until after menopause. |
| What results when there is functioning endometrial tissue or implants outside the uterus and responds to the hormonal fluctuations of the menstrual cycle? | Endometriosis |
| What are some of the proposed causes of endometriosis? | Retrograde menstruation, impaired cellular & humoral immunity cytotoxin t cell and NK cell activity is depressed, machrophages contribute to the endometrial cell proliferation outside the uterus. |
| What will you see with endometriosis? | Infertility and pain, dysmenorrhea, dyschezia (hallmark symptom), dyspareunia, abnormal bleeding asymptomatic pelvic mass if located in pelvis. |
| What is phimosis? | Condition in which the foreskin cannot be retracted back over the glans, most commonly caused by poor hygiene and chronic infections. Can occur in circumcised males with extra foreskin. |
| What is paraphimosis? | The foreskin is retracted and cannot be moved forward to cover the glans. If foreskin cannot be manually moved forward and edema occurs surgery has to be done to prevent necrosis by the constricted blood vessels. |
| What is the significance of BRCA-1 gene? | It is a breast CA susceptibility gene that is passed by an autosomal dominant mechanism. Women who inherited Breast CA or ovarian CA have tumors associated with alterations in particular genes mainly BRCA-1 and BRCA-2. |
| What is hypertension? | Consistent elevation of systemic arterial blood pressure 140/90. Caused by increased CO or increased peripheral resistance or both. |
| How does HTN contribute to organ dysfunction and damage? | Walls of systemic blood vessels are damaged w/ sustained HTN. Within the walls of the arteries and arterioles smooth muscles cells undergo hypertrophy, and hyperplasia causing fibrosis decreasing blood flow. |
| What other factors contribute to fibrosis of the tunica intima and media? | endothelial dysfunction, angiotensin II, catecholamines, insulin resistance, and inflammation. |
| What are the target organs for failure or dysfunction in HTN? | kidney, heart, brain, extremities, and eyes. |
| What effect does HTN have on the heart? | LV hypertrophy,angina pectoris, CHF, CAD, MI, and sudden death. HTN causes an increased workload on the heart causes a large hypertrophied heart, diminished BF through coronary arteries from fibrosis and constriction. |
| What effect does HTN have on the kidneys? | Renin and aldosterone secretion stimulated by reduced BF-retention of Na and H2O, causing increased BV perpetuating HTN further. |
| What effect does HTN have on the brain? | Reduced BF and O2 supply weakened vessel walls, accelerated atherosclerosis. |
| What effect does HTN have on the LE? | reduced blood flow and high pressures in arterioles accelerated atherosclerosis. |
| Where is the usual source of PE? | Embolus that gets lodges in a pulmonary vessel, usually originate in the venous circulation mostly from deep veins in the thigh and pelvis or LE, venous thromboembolism. Embolis can be a thrombus (blood clot), tissue fragment, lipids, or air bubble. |
| Risk factors associated with PE can be associated with the Virchow triad which states what? | 1)Venous stasis 2)hypercoagubility 3)injuries to the endothelial cells that line the vessels. |
| What is Buerger disease? | An inflammatory disease of the peripheral arteries, associated mostly with smoking, but also can be caused by frostbite, trauma, or the use of sympathomimetic drugs. |
| What happens in Buerger disease? | The inflammatory lesions are accompanied by thrombi, and sometimes vasospasm of arterial segments in which can eventually occlude and obliterate portions of small and medium sized arteries. |
| Arteries supply what in Buerger's are mostly affected? | Digital, tibial, and plantar arteries of the feet and digital, palmar, and ulnar arteries of the hands. |
| What symptoms to do see with Buerger's disease? | Pain and tenderness at affected site, sluggish blood flow, and rubor caused by dilated capillaries, cyanosis from blood remaining in capillaries after O2 has diffused, ischemia causes thin and shiny skin, nails thick & malformed, and possible gangrene. |
| What is a varicose vein? | It is a vein in which blood has pooled. Typically involves the saphenous veins of the legs. |
| What are varicose veins caused by? | Trauma to the saphenous veins that damages one of more valves, or gradual venous distention caused by the action of gravity on blood in the legs. |
| What can varicose veins eventually lead too? | Distention of varicose veins progresses until the pressure in the vein damages venous valves, which cannot maintain normal venous pressure. Chronic venous insufficiency. |
| Chronic venous insufficiency then leads to other problems such as? | Venous HTN, circulatory stasis, and tissue hypoxia lead to an inflammatory rxn in vessels and tissue leading to fibrosclerotic remodeling of the skin and then to ulceration. Hyperpigmentation of skin and edema may extend to the knees. |
| A decrease in circulation as a result of CVI can cause? | Decrease in circulation to the extremities can become so sluggish that the metabolic demands of the cells for O2, nutrients, & waste removal are barely met. Any trauma or pressure can lower O2 and cause cell death and necrosis, infection. |
| What is Superior vena cava syndrome? | Progressive occulusion of the superior vena cava that leads to venous distention in upper extremities and head. |
| What causes SVCS? | The SVC is a low pressure vessel and can be easily compressed. Leading cause is bronchogenic CA, followed by lymphomas and mets of other CA. Benign- thrombosis, histoplasmosis, TB, mediastinal fibrosis, cystic fibrosis, retrosternal goiter. |
| What are clinical manifestations of SVCS? | Edema & venous distention of the upper extremities, face & occular beds. Feeling of fullness in the head, tighter shirt collars, necklaces & rings, Cerebral & CNS edema-HA,visual disturbances, impaired LOC,skin of face & arms is purple and taunt, Res.Dis. |
| What is LDL? | Low density lipoprotein composed mainly of cholesterol and protein. Increased levels is a strong indication of coronary risk. |
| What is LDL's function? | Delivery of cholesterol to the tissues and also plays a role in endothelial injury, inflammation, and immune responses that contribute to atherosclerosis. |
| What is HDL? | High density lipoprotein composes mostly of phospholips and protein. Low levels are indicative of coronary risk. |
| What is HDL's function? | Responsible for reverse cholesterol transport which returns excess cholesterol from the tissues to the liver to be processed & eliminated as bile or converted to cholesterol containing steroids, participates in endothelial repair & decreases thrombosis. |
| Myocardial ischemia develops when? | If the supply of coronary blood cannot meet the demand of the myocardium for O2 and nutrients. |
| Ischemia can be caused by what factors? | Thrombus formation from a plaque rupture or ulceration, coronary spasm, hypotension dysrhythmias, decrease in the O2 carrying capacity of the blood (anemia, hypoxemia). |
| 10 seconds of myocardial occlusion myocardial cells become what? | Ischemic |
| What happens after several minutes of coronary occlusion? | The heart cells loose the ability to contract, and CO decreases, conduction abnormalities, anaerobic processes take over and lactic acid accumulates. |
| At 20 min of coronary occlusion what happens to the myocardial cells? | If perfusion is restored within 20 min the cardiac cells remain viable, if not infarction occurs. |
| During an MI if thrombus breaks up before complete distal tissue necrosis occurs, what does the infarction involve and what is shown on the EKG? | The infarction will only involve the myocardium directly under the endocardium. ST depression, T wave inversion- NON STEMI |
| If thrombus lodges permanently during an MI what does it involve and what is shown on the EKG? | The infarction will extend through the myocardium all the way to the epicardium. ST elevations STEMI Severe cardiac dysfunction. |
| What would your labs reveal after an MI? | Increase in Cardiac troponins, increase in CPK-MB and LDH. |
| What occurs with stable angina? | Chest pain that is caused by a gradual luminal narrowing and hardening of arterial walls, so the vessels cannot dialate in response to increase myocardial demand with physical exertion or emotional stress. Usually lasts 3-5 min. Relief w rest & nitrates. |
| In stable angina what may a person do in response to chest pain and where can it radiate? | Clenching fist over left sternal border, pain can radiate to the neck, lower jaw, L arm, L shoulder, or back and down R arm. |
| What occurs with unstable angina? | Fissuring or superficial erosion of the plaque leads to transient episodes of thrombotic vessel occlusion and vasoconstriction at the sire of plaque damage. Reversible ischemia. |
| In unstable angina, the liable thrombus occludes vessel no more than how long? | 10-20 minutes |
| Unstable angina presents as a new onset angina that occurs when? | occurs at rest and increasing in severity or frequency. |
| Silent angina is characterized by what? | Myocardial ischemia that does not present with angina, but with non-specific symptoms such as fatigue, dyspnea, or feeling of unease. |
| What causes silent angina? | Presence of a globular or regional abnormality in L ventricular sympathetic afferant innervation, might occur in DM, or following denervation in coronary artery bypass. |
| What is aortic stenosis? | The orifice of the aortic semilunar valve narrows, causing diminished BF from L ventricle to aorta. Outflow obstruction increases pressure in L ventricle-->hypertrophy increase demand for O2--> Ischemia |
| Mitral stenosis | Impairment of the inflow of blood from L atrium to L ventricle. Inflammation and scaring leads to fibrous leaflets. Incomplete emptying of L atrium and elevated L atrium pressures causing dilation and hypertrophy. Increase pulm HTN, & R heart failure. |
| Aortic regurgitation | The inability of the leaflets valve in aorta to close properly during diastole resulting in backflow of ejected blood in ventricle. Increase volume bc receiving blood from atrium and backflow. |
| Mitral regurgitation | Permits blood to backflow from L ventricle to L atrium. Increase in atrial pressure, increase pulm pressure, and R ventricle failure. |
| Tricuspid regurgitation | lease to volume overload in R ventricle, increase systemic venous pressure, R heart failure. |
| What make up the composition of renal stones? | Calcium oxalate or phosphate, Struvite-mag., ammonium, & phosphate Uric acid, cystine stones are rare. |
| What are some risk factors for developing a renal stone? | Age, gender, race, geographic location, seasonal factors, fluid intake, diet, occupation, UTI, HTN, obesity, avg. temp, humidity and rainfall. |
| Where does the infection reside in pyelonephritis? | Infection of one or both upper uninary tracts ureter, renal pelvis and interstitium. Unrinary obstruction and reflux of urine are common risk factors. |
| In pyelonephritis what does the infection cause? | Medullary infiltration of WBC with renal inflammation, renal edema and purulent urine. Fever, chills, flank or groin pain, frequency dysuria. |
| Where does cystitis occur? | Inflammation of the bladder and is the most common site of UTI. |
| What does cystitis cause? | Mild inflammation-mucosa is red, more advanced diffuse hemorrhage, pus formation or exudates on epithelial surface, dysuria, frequency, urgency, pain in lower abd, hematuria and foul smelling urine. |
| Some differences in pyelonephritis and cystitis? | Pyelo is infection of the upper urinary tract while cystitis is of the lower or bladder. Pyelo has pus in the urine and cystitis has blood. Pyelo pain is in flank or groin while cystitis is in lower abd. |
| What is creatinine and what does it indicate? | Creatinine is constantly released from muscle & excreted primarily by glomerual filtration & measures the index of changing glomerular function. As GFR declines plasma creatinine increases by a reciprocal amount to maintain a constant rate of secretion. |
| Acute renal injury commonly occurs from what? | Extracellular vol depletion, decrease renal blood flow, or toxic/inflammatory injury to kidney cells. |
| Prerenal acute kidney injury | Impaired renal blood flow (hypoperfusion) that occurs rapidly. Early phases GFR is maintained but then falls w a decrease in filtration pressure. BUN and creatinine are increased. |
| Intrarenal acute kidney injury | Injury to the glomeruli or tubules. Ischemic acute tubular necrosis, nephrotoxic ATN (radioconstrast dye), acute glomerulonephritis, vascular disease, malignant HTN, DIC, allograft rejection, interstitial diseases (drug allergy). Oliguria |
| Postrenal acute kidney injury | Bilateral urinary tract obstruction that affects the kidneys bilaterally. Obstruction causes increase in intraluminal pressure upstream with decrease in GFR. Several hours of anuria with flank pain followed by polyuria. |
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ngawlik
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