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Patho Pharm Charm
Exam 1
| Question | Answer |
|---|---|
| increased blood presure increased blood glucose derease in urination missing or infrequent bowel sounds pale. clammy or sweaty skin | acute stress response |
| Dilated pupils increased heart rate increased respiratory rate and bronchdilation | acute stress response |
| blood glucose wBC Count | Lab test that needs to be monitored during acute stress response |
| insmonia emotional disturbance gastric and duodenal ulcers mild headaches upset tummy rhematic disorders CV and Kidney disease | Physiologic effefct of chronic stress |
| General: effect is a general systemic reaction Adaption: response is in reaction to a stressor Syndrome: Physical manifestations are coordinated and dependent on each other | GAS or General Adaptation Syndrome |
| stimulation of the nervous system and HPA Axis which leads to the release of catecholamines and cortisol | GAS; Alarm Stage |
| the elevated cortisol levels are not needed in this stage as the body chooses the most effective channel of defense | GAS, Resistance Stage |
| sets in if the stressor persists or if the body is overwhelmed by it | GAS, Exhaustion Stage |
| systemic damage and various ailments can appear in this stage, as the body resources are exhausted | GAS, Exhaustion Stage |
| these ailments can occur: insomnia emotional disturbance gastric and duodenal ulcers mild headaches CV, kidney disease | GAS, Exhaustion Stage |
| Evidence also suggects that the ______________, the adrenomedullary hormonal system and sympathetic nervous system are activated differently depending on the type of intensityofstressor. | HPA Axis |
| ________________can stimulate emotional and intellectual growth if it is controllable and brief in nature | mild stress |
| response to ___________can vary depending on conditioning factors such as environment lifestyle factors and life experiences | stress |
| _________occurs better when the change occurs gradually as opposed to suddenly | Adaption |
| Immaturity in age can also slow the ability to adapt (Elderly and infants) | Genetic Endowment and Age |
| Geneticsalso factor in to the patient's ability to adapt, such as someone who may be predisposed to develop a depressive disorder | Genetic Endowment and Age |
| Recent research shows that females and males respond to stress differently and post-menopausaland pre-menopausal women also have varied responses to stress. | Gender |
| Physical and mental health status play a major role un adaption to stress. This us because it determ the amount of physiological and psychological reserves available | Health Status |
| Deficiencies or excess of various minerals, lipids, certain fatty acids, vitamins, specific amino acides can alter the pt health status and impair the ability to adapt | Nutrition |
| Disturbances in the sleep-wake cycle or circadian rhythms can impair the ability to a patient to adapt to stressors due to a disturbance in the immune response , hormone secretion, physical and psychlog functioning | Sleep-wake cycle |
| cyclea person's sense of being in control over the environment a sense of purpose in life and an ability to conceptualize stressors as a challenge rather than a threat can improve a patient's ability to cope | Hardiness |
| the social environment can modualte the relationship between stress and health, Those with a stronger social network may have a better ability to cpoe with stress | Psychosocial Factors |
| help maintain homeostasis? Monitors levels of whatever hormone or enzyme is being maintained? Cyclical? Decr in the level of glucose in the blood triggers this? incr glycogenolysis incr in the secretion of insulin | Negative Feedback |
| ______ especially _______ can interact with other CNS depressantsand alcohol and patients should be warned about that. They also have a tendency to cause withdrawal symptoms so a patient needs to be assessed for symptoms of withdrawal. | Antidepressants especially Benzodiazepines |
| sweating shaking confusion palpitations nausea nervousness | Symptoms of antidepressant withdrawal |
| tolerance dependence the pt should always be asked when they took their last dose | Antidepressants |
| stimulation of peripheral nerve fibers that are stimulated by pain that approaches or exceeds stimulus intensity, the pain can be superficial somatic, visceral and deep somatic. | Nociceptive Pain |
| widespread pain that is not explainable. Its evidenced by sensory deficit, burning pain, pain that occurs with light stroking of the skin and attacks that occur without provocation. Caused by damaged neurons that send pain stimuli to the brain. | Neuropathic Pain |
| pain that has a stimulus and is in response to that stimulus where as neuropathic pain has an unknown stimulus and causes a different pain sensation and is caused by damaged neurons as opposed to a thermal, mechanical or chemical stimuli. | Nociceptive Pain |
| sensory deficit and burning pain. | Neuropathic pain |
| inhibit the cyclooxygenase enzymes interfering with the synthesis of prostaglandins. Prostaglandins have many functions but those formed by cyclooxygenase-2 enhance pain and cause inflammation. NSAIDs are well absorbed and | Ibruprofen (P) Motrin, Advil |
| CNS: dizziness, confusion, tinnitus, drowsiness, headache Blood: abnormal bruising or bleeding Respiratory: wheezing, bronchoconstriction CV: edema, HT, Premature closure of fetal ductus arteriosus | Side/Adverse effects of Ibruprofen (NSAIDS) |
| GI: N&V are most common abdominal pain bleeding Salicylic acid is irritating to the gastric mucosa its antiprostaglandin effect reduces the cytoprotective mechanisms of the stomach | SE/AR of NSAIDS (Ibruprofen, Motrin, Advil, IBU) |
| Skin: Urticaria Reproduction: Prolonged labor | SE/AR of NSAIDS |
| cross-allergic w/aspirin and should never be given to any1 who has had a severe allergic rxn to aspirin.Some may be less irritating to the GI tract than aspirin.All cause GI upset. | NSAIDs |
| can increase the risk of gastric ulcers by inhibiting the prostaglandin responsible for formation of the cytoprotective mucin in the stomach. NSAIDs are often given with food to decrease gastric irritation. | NSAIDs |
| appear to interfere with the diuretic effect of loop diuretics and the antihypertensive effect of thiazides, loop diuretics, beta-blockers, and ACE inhibitors. | NSAIDs |
| NSAIDs have caused renal failure when given to subjects with renal insufficiency. ACETAMINOPHEN [Tylenol] | NSAIDS |
| NSAIDs have caused renal failure when given to subjects with renal insufficiency. ACETAMINOPHEN [Tylenol] | NSAID MOA |
| Acetaminophen is completely absorbed from the GI tract, metabolized in the liver (one metabolite is hepatotoxic), and excreted in the urine.No remarkable SE. | NSAIDs |
| Toxicity: Liver damage, especially in alcoholics.The antidote, if given early enough, is N-acetylcysteine (Mucomyst) along with gastric lavage, cathartics,and activated charcoal. | NSAID toxicity |
| Opioids act on receptors(most imp mu & kappa receptors,on neurons in the spinal cord and brain to raise pain threshold and reduce pain perception and the emotional rxn to pain. Some agents may act on sigma receptors and cause hallucinations and dysphoria. | Morphine (P) |
| Well absorbed from sites of administration although some agents have a large first pass effect when given orally Most are metabolized in the liver and the metabolites excreted via the kidney | Opioids |
| activ mu recep & mimic axns of endogenous opioid peptides(enkephalins & endorphins) Medullary axn: Cause resp depression via direct axn on mu receptors in resp control cntr.Suppress medullas resp to CO2 levels.Stim the CTZ...N&V,suppress cough reflex. | Action in the CNS (Opioids) P: Morphine |
| The person becomes drowsy, lethargic, and apathetic. Some subjects become excited (especially with meperidine). They also alter mood, causing euphoria although some patients become dysphoric parasympathetic action, causes miosis | CNS Actions (Opioids/P: Morphine) |
| GI tract: Opioids reduce propulsive mvemnts & peristalsis resul in constip.Cause spasm of biliary duct. Tolerance doesnt devel GU system:spasmogenic on bladder & ureters & increase tone of detrusor musc and sphincter. diminish sensation of full bladder | Actions in the Periphery (Opioids) |
| Decr ability to void CV effects: The opioids have few CV effects at usual doses. (4) Release of histamine may cause urticaria, sweating, vasodilation & bronchoconstriction. | Actions on periphery (opioids) |
| CNS: sedation, drowsiness, ataxia, euphoria, N&V Resp: decr rate and/or depth; bronchoconstric. CV: HT; brady GI: constip; abd obstruction; paralytic ileus. Urinary retention; decr contractibility of the uterus & prol labor; biliary spasm; miosis. | Opioid SE/AR |
| cross the placenta and breast barrier. accum in the fetus,ion trappin incr serotonin lvl; meperidine has caused fatal rxns & dextromethorphan serious rxns when pt on MAOIs.Parnate Deaths:dose dumping,ext-rel cap of morph/hydromorphone when coadmin w/a | OPIOIDS |
| Cause of death is respiratory depression. b. Triad symptoms include pin point pupils, respiratory depression, and loss of consciousness with decreased blood pressure. Tolerance/physical dependence | Opioid Toxicity |
| • Important points to remember for administering morphine for pain -check pain level, last time of admin -check RR, decreased BP -check for pin-point pupils, loss of consciousness, decreased BP, respiratory depression, these are signs of toxicity | Admin Opioids! |
| No autonomic resp,factors that contrib to chronic pain inclu peripheral mech, periph-central mech & central mech.Leads to persis stim of nociceptors,periph sensitiz. Dur 6 mo+, abs of autonomic resp, incr irritability | Chronic Pain |
| assoc depression, somatic preoccu,w/d from outside interest, decr strength of relat,decr sleep,decr libido, appetite changes trmt inclu:dep on cause of pain,trtd by therapy& multi-modal pain meds | Chronic Pain |
| ) is used to provide oxygen at a low flow rate(2-6 liters)and a concentration of 24 to 40%. It has a thin tube with two nozzles that are placed into the patient’s nostrils | nasal cannula NC |
| often used at between 6 and 12 LPM, with a concentration of oxygen to the patient of between 28% and 50%. | Simple face mask |
| which can accurately deliver a predetermined oxygen concentration to the trachea up to 40%. | Venturi masks |
| is based on a simple mask, but features a reservoir bag, which increases the provided oxygen rate to 40–70% oxygen at 5 to 15 LPM. | Partial rebreathing |
| draw oxygen from an attached reservoir bags, w/one-way valves that direct exhaled air out of the mask. When properly fitted&used @ flow rates of 10-15 LPM or higher,they deliv close to 100% oxygen. This type of mask is indic for acute medical emergencies. | Non-rebreather masks |
| Make sure pt has effec airway clearance by chkng to see if cough is prod.Encour deep breathng &coughing to help loosen secretions. Make sure the pt is getting enough oxy,check for signs of hypoxemia, monitor ABG levels, | Priority interventions for taking care of a patient with pneumonia |
| assess respiratory status, monitor fluid I/O, evaluate effectiveness of treatments | Priority interventions for taking care of a patient with pneumonia |
| wheezing, chest tightness, may be worse at night (nocturnal asthma) | Asthma attack |
| chest tightness, increase in respiratory rate and prolonged expiration, cough may accompany wheezing | Mild attack |
| loud wheezing, chest tightness, distant breathing, increase in respiratory rate and prolonged expiration, use of accessory muscles, fatigue, moist skin, signs of anxiety | More severe asthma attack |
| : inability to say more than two words between breaths, breath sounds become inaudible, wheezing diminishes and cough becomes unproductive | onset of respiratory failure |
| Ppl w/infectious pneumonia often have a prod cough, fever,shaking chills, SOB, sharp or stabbing chest pain during deep breaths,confusion, increased RR. More severe symptoms may include:central cyanosis, decreased thirst, convulsions, persistent vomitin | Pneumonia |
| Cough with sputum prod on most days for 3 months of a year, for 2 consec yrs. It's indic by an incr # (hyperplasia)&incr size (hypertrophy) of the goblet cells & mucous glands of the airway. Mucus buildup leads to a narrowing of airways and a prod cough. | Chronic Bronchitis |
| congested lung fields, decr PaO2-less than 65 mmHg, polycythemia and increased PCO2 Patients with chronic bronchitis are referred to as Blue Bloaters due to hypoxia and fluid retention. Their skin and lips are often a bluish color due to the hypoxia | Chronic bronchitis symptoms |
| Restlessness, Anxiety, Disorientation, confusion, lassitude and listlessness, headaches. | Symptoms of mild hypoxemia |
| Cyanosis (skin appearing bluish due to insufficient oxygen) Cheyne-Stokes respiration (irreg pattern of breathing), incr BP, apnea (temporary cessation of breathing), tachy, hypotension (abnormally low BP) below 100 diastolic & 40 systolic. | Symptoms of acute hypoxemia |
| initial incr in cardiac output & rapid decrlater. Ventric fib,Asystole(severe form of CA, heart stops), Polycythemia (abnorm incr in RBCs.Bone marrow may be stim to prod excess RBCs in case of pt suffering from chronic hypoxemia),Coma | Symptoms of acute hypoxemia |
| 7.35-7.45 (acid-base)- indicates if a patient is acidemic (pH < 7.35; H+ >45) or alkalemic (pH > 7.45; H+ < 35) | pH (acid-base) |
| 35-45 mmHg-indic of CO2 prod & elim:for a cnstnt metabolic rate,the PaCO2 is determ by elim thru ventilatn. A high PaCO2(resp acidosis,hypercapnia)indic underventilatn (a hypermetabolic disorder),a low PaCO2 (resp alkalosis,hypocapnia)hyper/overventilatn. | pCO2 (Ventilation) |
| ion indic whether a metabolic prob is present (ketoacidosis).A low ___indic metabolic acidosis, high ___ indic metabolic alkalosis. when given w/ blood gas results is calc by the analyzer, correlation should be chkd w/total CO2 levels as direc measured | HCO3: 22-26 (buffer) |
| A low ___indic that the pt is not oxygenating properly, and is hypoxemic. At a PaO2 of less than 60 mm Hg, supplemental oxygen should be admin. At a PaO2 of less than 26 mmHg, the pt is at risk of death and must be oxygenated immediately. | pO2: 80-100 mmHg (oxygenation) |
| abn incr in RBCs which stems from bone marrow being stim to prod more RBcs bc chronic hypoxemia.COPD,chronic hypoxemia leads to it bc the body wants more oxy&amt of blood cells dont prov enuf oxy bc poor oxy.Chronic bronch(1of2 cond under COPD, emphysema) | Polycythemia |
| Short acting B-2 adrenoceptor agonists, albuterol.1st line trtmt for asthma symp. Anticholinergic meds, ipratroprium bromide, prov benefit when used in combo w/albuterol in moderat/severe symp. Anticholin bronchodil r used i ppl cant tolerate albuterol | What would be the medications used in acute asthma attack? |
| usually treated with dialysis. When the GFR decreases to 50%, plasma levels of urea and creatinine show significant increases. Due to the kidney’s adaptive ability, it can adjust for destruction of less than 50% of the total GFR. | • What is the pathophysiology of CKD? How does bone disease and anemia develop in CKD and how are they treated? |
| When GFR is decreased to 50% creatinine levels will double. This results in hypertrophy and hyperfiltration of the remaining nephrons and can lead to renal dysfunction. This leads to glomerulosclerosis. | • What is the pathophysiology of CKD? How does bone disease and anemia develop in CKD and how are they treated? |
| •Systemic HT •Acute insults from nephrotoxins/decr perfusion •Proteinuria •Incr renal ammoniagenesis w/ interstitial injury •Hyperlipidemia •Hyperphosphatemia w/Ca phosphate deposition •Decr levels of nitrous oxide •Smoking •Uncontrolled diabetes | Factors other than the underlying disease process and glomerular hypertension that may cause progressive renal injury include the following: |
| metabolic acidosis and salt and water imbal also occur. Anemia devel from a decrin erythropoietin synthesis, which makes RBCs.starts early in disease stage and becomes worse as it progr. This can cause bleeding from uremia induced platelet dysfunction. | Hyperkalemia |
| Other causes of anemia in chronic kidney disease include the following: chronic blood loss, secondary hyperparathyroidism, inflammation, nutritional deficiency, accumulation of inhibitors of erythropoiesis. | Hyperkalemia |
| High-turnover bone disease due to high parathyroid hormone (PTH) levels, Low-turnover bone disease (adynamic bone disease), defective mineralization (osteomalacia), mixed disease, beta-2-microglobulin associated bone disease. | Different types of bone disease occur with chronic kidney disease |
| mineral and bone disorder (CKD-MBD) involves biochemical abnormalities, (ie: serum phosphorus, PTH, vitamin D levels, and alkaline phosphatase) related to bone metabolism. | Chronic kidney disease |
| •Hyperphosphatemia •Hypocalcemia •Decr renal synthesis of 1,25-dihydroxycholecalciferol (1,25-dihydroxyvitamin D, or calcitriol) •Intrinsic altratn in the parathyroid gland,cause incr PTH secretion & incr parathyroid growth •Skeletal resistance to PT | Secondary hyperparathyroidism develops in chronic kidney disease because of the following factors: |
| develops primarily from decreased intestinal calcium absorption because of low plasma calcitriol levels and possibly from calcium binding to elevated serum levels of phosphate. | Hypocalcemia |
| indep trigger PTH synth & secretn.stimuli persist in chronic kidney disease,more adv stages,PTH secretn bc maladapt¶thyroid glands,initially hypertrophy,becum hyperplastic. persis elev PTH levels exacerb hyperphosphatemia 4rm bone resorp of phosphate | Low serum calcitriol levels, hypocalcemia, and hyperphosphatemia |
| If serum levels of PTH remain elevated, a high bone turnover lesion, known | osteitis fibrosa |
| one of several bone lesions, which as a group are commonly known as? These lesions develop in patients with severe chronic kidney disease and are common in those with ESRD. | Renal osteodystrophy |
| prevalence in US has incr&it has been descr b4 dialysis.pathogenesis is not well def but a#of factors contrib,high Ca load,use of vit D sterols,incr age, prev corticosteroid therapy,peritoneal dialysis &incr lvl of N-terminally truncated PTH frag. | adynamic bone disease |
| in the setting of chronic kidney disease is associated with aluminum accumulation. It is markedly less common than high-turnover bone disease. | Low-turnover osteomalacia |
| from beta-2-microglobulin accumulation in patients who have required chronic dialysis for at least 8-10 years is another form of bone disease. It manifests with cysts at the ends of long bones. | Dialysis-related amyloidosis |
| ...is treated with dietary phosphate binders and dietary phosphate restriction. | Hypocalcemia |
| hormonal imbalance of DHT in conjuction with testosterone can lead to BPH, there is evidence that estrogen can also lead to BPH. Age is also a factor. Symptoms of BPH include: Urgency, Hesistancy, frequency and urinary retension | • What is the etiology and clinical manifestations of BPH? |
| Acute glomerulonephritis occurs after streptococc infec,strep throat.if its the cause,cond:acute poststreptococc glomerulonephritis(APSGN)/postinfec glomerulonephritis can occur bc toxins,paint/glue inhaled,then excr thru urine | • What is the etiology of APSGN and how will you differentiate between (assuming she meant Nephrotic and nephritic) nephrotic syndrome and nephritic syndrome? |
| pores are large enuf to allow protein thru to cause proteinuria, but not large enuf to let RBCs thru to cause hematuria. Its imp to know the diff is that nephritic syndrome will have proteinuria and hematuria and nephrotic syndrome only has proteinuria. | Nephrotic syndrome |
| hypovolemia, decreased cardiac output, cardiac failure, decreased peripheral vascular resistance, decreased reno-vascular blood flow, hemorrhagic blood loss | • Identify the Pre-renal, renal and post-renal causes of Acute renal failure? Pre-renal |
| . While chronic glomerulonephritis occurs as a symptom of certain diseases, its cause is not known. | • What is the etiology of APSGN and how will you differentiate between (assuming she meant Nephrotic and nephritic) nephrotic syndrome and nephritic syndrome? |
| prolonged ischemia, nephrotoxic injury, acute glomerulonephritis, toxemia of pregnancy | renal causes of Acute renal failure? Intra-renal |
| prostate hyperplasia, bladder cancer, calculi formation, prostate cancer, spinal cord disease | renal causes of Acute renal failure? Post-renal |
| is an inflammation of the urinary bladder whereas pyelonephritis is an inflammation of the kidney. They can both be a type of urinary tract infection, but when the UTI is in the bladder it is cystitis and if it manifests in the kidney it is pyelonephritis | • Differentiate between cystitis and pyelonephritis and how they differ in clinical manifestations |
| General symptoms of cystitis include urgency, frequency, dysuria, and, occasionally, hematuria, dyspareunia, abdominal cramps, and/or bladder pain and spasms. | • Differentiate between cystitis and pyelonephritis and how they differ in clinical manifestations |
| high fever, pain on passing urine, and abdominal pain that radiates along the flank towards the back. There is often associated vomiting. There can also be signs of infection (fever, malaise, weight loss) and hematuria. | Symptoms of pyelonephritis |
| Output greater than intake, dry skin/mucous membranes. Minor: Increased serum sodium. Increased pulse from baseline. Decreased or excessive urine output. Concentrated urine. Urinary frequency. Decreased fluid intake.Poor skin turgor.Thirst/nausea/anorexia | • Clinical manifestations of fluid volume deficit and what are the lab values pertaining to fluid status? |
| Calcium 8.8 - 10.3 mg/dL Calcium, ionized 2.24 - 2.46 meq/L Chloride 95 - 107 mEq/L Magnesium 1.6 - 2.4 mEq/L Phosphate 2.5 - 4.5 mg/dL Potassium 3.5 - 5.2 mEq/L Sodium 135 - 147 mEq/L | Electrolyte values are used to determine fluid status |
| Normally the body maintains a balance of fluid in tissues by ensuring that the same of amount of water entering the body also leaves it. The circulatory system transports fluid within the body via its network of blood vessels. | • Explain the mechanics of fluid shift and development of edema |
| The fluid, which contains oxygen and nutrients needed by the cells, moves from the walls of the blood vessels into the body's tissues. After its nutrients are used up, fluid moves back into the blood vessels and returns to the heart. | Explain the mechanics of fluid shift and development of edema |
| lymph sys(ntwk of chan in body that carry lymph,colorless fluid w/WBCs to fight infec)also absorbs & trans this fluid.edema:too much fluid moves bl vess in tissues/not enuf fluid moves 4rm tissues bk in blood vess.Fluid imbal cause mild 2 severe swelling | Explain the mechanics of fluid shift and development of edema |
| Third spacing is fluid trapped in one of several possible transcellular spaces. Examples: pleural effusion, pericardial effusion, ascites. | • What is third spacing? Provide some examples. |
| Muscle cramping and weakness, abdominal cramping, nausea, vomiting, headache, confusion, lethargy, seizures, coma, death | • Signs and symptoms of hypernatremia? |
| Calcium less than 8.0 mg/dl symptoms include: Neuromuscular irritability, Paresthesias, Muscle cramping, Hyperactive reflexes, Tetany, hypotension, Cardiac dysrhythmias | • Clinical findings in hypocalcemia |
| Decreased renal function, Potassium IV fluid: too much or too fast, Crushing injury, Potassium sparing diuretics, Excessive oral ingestion | • Etiology of hypokalemia |
| Dialysis may be required to help remove excess potassium from poorly functioning kidneys. | • How is hyperkalemia related to renal function? |
| Serum osmolality • Determined mainly by serum Na+ concentration; one of the most reliable measures of hydration. 275 to 295 mOsm/kg •Increases in dehydration •Decreases with water excess | • What are the components of renal function tests and know the normal values |
| BUN (blood urea nitrogen)10 to 20 mg/dL •Refl diff btwn rates of urea synth in liver & its excre by kidneys.Urea is main end prod of protein catabolism | • What are the components of renal function tests and know the normal values |
| Serum glucose 70-110 mg/dL Markedly elevated glucose in blood stream caues osmotic diuresis and fluid volume deficit. | What are the components of renal function tests and know the normal values |
| Urine osmolality 50 to 1200 mOsm/L (depends upon the circulating titer of ADH and the rate of urinary solute excretion • Measures number of solute particles per unit of water in urine; determines diluting and concentrating ability of kidneys | What are the components of renal function tests and know the normal values |
| Reflects changes in urine contents more accurately than specific gravity, but depends on the prior state of hydration. It should be 12 times that of serum osmolality. Conc. urine has osmolality > 1000. | What are the components of renal function tests and know the normal values |
| Incr w/decr renal blood flow/decr urine prod (red urea clearance),dehydration, neoplasms & certain antibio(less spec for renal failure than creatinine) Decr in preg,overhydration,severe liver disease & low protein intake Incr in fluid vol deficit | What are the components of renal function tests and know the normal values |
| Decr w/low RBCs or w/norm hemoglob in pres of fluid vol excess | What are the components of renal function tests and know the normal values |
| 1.010 to 1.030 • Measures degree of concentration of urine; determined by number and weight of solute particles in urine. | Urine Specific Gravity (S.G.) |
| Increases with any condition causing hypoperfusion of kidneys leading to oliguria, i.e., dehydration, shock. | Urine Specific Gravity (S.G.) |
| Decreases when renal tubules lose their ability to reabsorb water and concentrate urine as in early pyelonephritis. | Urine Specific Gravity (S.G.) |
| : urine volume less than 400 ml per 24 hours; increased serum creatinine, urea, uric acid, organic acids, potassium, and magnesium; lasts 3 to 5 days in infants and children, 10 to 14 days in adolescents and adults. | • • Clinical and lab findings in Different phases of acute renal failure?Oliguric-anuric phase: |
| begins when urine output exceeds 500 ml per 24 hours, end when BUN and creatinine levels stop rising; length is availabe. | • • Clinical and lab findings in Different phases of acute renal failure?Diuretic phase: |
| asymptomatic; last several months to 1 year; some scar tissue may remain. | • • Clinical and lab findings in Different phases of acute renal failure?Recovery phase: |
| decreased tissue turgor, dryness of mucous membranes, weight loss, flat neck veins, hypotension, tachycardia. | • • Clinical and lab findings in Different phases of acute renal failure?In prerenal disease |
| difficulty in voiding, changes in urine flow. | • • Clinical and lab findings in Different phases of acute renal failure?In postrenal disease: |
| presentation varies; usually have edema, may have fever, skin rash. | • • Clinical and lab findings in Different phases of acute renal failure?In Intrarenal disease |
| • Nausea, vomiting, diarrhea, and lethargy may also occur. | • Clinical and lab findings in Different phases of acute renal failure? |
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