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ADVANCED PATHOPHYSIOLOGY EXAM 4 QUESTIONS AND ANSWERS ( LATEST UPDATE ), Exams of Nursing

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ADVANCED PATHOPHYSIOLOGY EXAM 4
QUESTIONS AND ANSWERS
1. Kidneys require at least of cardiac output.
ANS 20-25%
2. Reduced perfusion of a kidney activates the system, which causes
constriction of peripheral arterioles.
ANS renin-angiotensin-aldosterone
3. most common type of kidney stone
ANS calcium oxalate
4. Passage of kidney stones can be extremely painful and may produce
to the umbilicus area.
ANS referred pain
5. Referred pain from kidney stones is seen in the area.
ANS umbilicus
6. Sensory innervation of the upper part of a ureter arises from the
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ADVANCED PATHOPHYSIOLOGY EXAM 4

QUESTIONS AND ANSWERS

  1. Kidneys require at least of cardiac output. ANS 20 - 25%
  2. Reduced perfusion of a kidney activates the system, which causes constriction of peripheral arterioles. ANS renin-angiotensin-aldosterone
  3. most common type of kidney stone ANS calcium oxalate
  4. Passage of kidney stones can be extremely painful and may produce to the umbilicus area. ANS referred pain
  5. Referred pain from kidney stones is seen in the area. ANS umbilicus
  6. Sensory innervation of the upper part of a ureter arises from the

thoracic nerve root. ANS 10th

  1. Common clinical manifestations of a in older adults include con- fusion and poorly localized abdominal discomfort. ANS urinary tract infection
  2. infection of one or both upper urinary tracts, including ureter, renal pelvis, and kidney interstitium ANS pyelonephritis
  3. and (vesicoureteral reflux) are the most common underlying risk factors for development of pyelonephritis. ANS urinary obstruction, reflux of urine from the bladder
  4. What are the three most common microorganisms associated with acute pyelonephritis? ANS E. coli, Proteus, Pseudomonas
  5. Urine that is acidic/alkaline on the pH scale increases the risk of stone formation. ANS alkaline

ANS

and , as well as the clinical signs and symtpoms. ANS urine culture, urinalysis

  1. casts indicate a diagnosis of pyelonephritis, rather than cystitis. However, these are not always present. ANS white blood cell
  1. Reduced glomerular filtration rate during glomerular disease is evidenced by elevated plasma , concentration, or reduced clear- ance. ANS urea, creatinine, renal creatinine
  2. includes renal diseases in which glomerular inflammation is caused by immune mechanisms that damage the glomerular capillary filtration membrane including the endothelium, basement membrane, and epithelium (podocytes). ANS acute glomerulonephritis
  3. The classic symptoms of include sudden onset of hematuria in- cluding red blood cell casts and proteinuria (milder than nephrotic syndrome), and in more severe cases, these symptoms are also accompanied by edema, hypertension, and impaired renal function. ANS acute glomerulonephritis
  4. Nephrotic syndrome is the excretion of g or more of protein in the urine per day. ANS 3.
  5. is the excretion of less than 3.0g/dl of albumin per day.

ANS elevated

  1. Changes in serum creatinine level only occur if more than % of glomerular filtration is lost and are often delayed more than hours. ANS 50, 24
  2. What prevents the implementation of early therapy during acute kidney injury? ANS diagnostic delays
  3. Patients with acute kidney injury are prone to develop and meta- bolic. ANS hyperkalemia, acidosis
  1. Acute kidney injury can lead to decreased renal phosphate excretion (AKA ). ANS hyperphosphatemia
  2. Fluid retention causes in cases of acute kidney injury. ANS edema
  3. Symptoms of develop in persons with cardiac disease when acute kidney injury occurs. ANS congestive heart failure
  4. Acute kidney injury commonly results from intracellular/extracellular vol- ume depletion, increased/decreased renal blood flow, or toxic and inflamma- tory injury to kidney cells that result in alterations in renal function that may be minimal or severe. ANS extracellular, decreased
  5. Renal hypoperfusion is referred to as acute kidney injury. ANS prerenal
  6. disorders involving renal parenchymal or interstitial tissue ANS intrarenal
  7. disorders associated with acute urinary tract obstruction ANS postrenal
  8. is the presence of waste products in the blood. ANS uremia
  9. Causes of AKI include hypovolemia, hemorrhagic blood loss, loss of plasma volume due to burns and peritonitis, water and electrolyte losses,
  1. activity is elevated with progressive nephron injury, which promotes glomerular hypertension and hyperfiltration caused by efferent arteriolar vasoconstriction and also promotes systemic hypertension. ANS angiotensin II
  2. Angiotensin II can promote the activity of cells and growth factors that participate in tubulointerstitial fibrosis and scarring. ANS inflammatory
  1. GERD is the reflux of and from the stomach to the esophagus that causes esophagitis. ANS acid, pepsin
  2. (type I) is the most common type of hiatal hernia, and it occurs when the proximal portion of the stomach moves into the thoracic cavity through the esophageal hiatus. ANS sliding
  3. The is an opening in the diaphragm for the esophagus and vagus nerves. ANS esophageal hiatus
  4. A person that has a sliding hiatal hernia will experience symptoms when in the position, because the lower esophagus and stomach are pulled into the thorax. ANS supine
  5. Drugs that can relax the lower esophageal sphincter ANS a , n , c , and n. ANS anticholinergics, nitrates, calcium channel blockers, nicotine
  6. Clinical manifestations of include heartburn, chronic cough, asthma attacks, and laryngitis. ANS reflux esophagitis
  7. may be a trigger for asthma or chronic cough. ANS GERD

ANS intussusception

  1. Causes of intestinal obstructions ANS h , constriction from a , v , and i. ANS hernia, adhesions, volvulus, intussusception
  2. A is a break, or ulceration, in the protective mucosal lining of the lower esophagus, stomach, or duodenum. ANS peptic ulcer
  1. Risk factors for peptic ulcer disease include predisposition, infection of the gastric mucosa, and habitual use of. ANS genetic, H. pylori, NSAIDs
  2. Chronic use of NSAIDs suppresses mucosal synthesis, resulting in decreased bicarbonate secretion and mucin (gut barrier component) pro- duction and increased secretion of hydrochloric acid. ANS prostaglandin
  3. syndrome often follows a partial gastrectomy or pyloroplasty and occurs 20 minutes after eating. It involves rapid gastric emptying and creation of a high osmotic gradient. ANS dumping
  4. Clinical manifestations of include increased pulse, hypotension, weakness, pallor, sweating, and dizziness following a partial gastrectomy or pyloroplasty. ANS dumping syndrome
  5. The pathophysiology of includes rapid gastric emptying and cre- ation of a high osmotic gradient within the small intestine, causing a sudden shift of fluid from the vascular compartment to the interstitial lumen. ANS dumping syndrome
  6. Dumping syndrome is usually managed very well with proper. ANS diet
  7. To manage dumping syndrome, an individual should eat frequent, meals, consume no , include high , and low.

ANS IBS

  1. Abnormal gastrointestinal permeability, motility, secretion, and sensitivity are associated with IBD/IBS. ANS IBS
  1. One of the main functions of the liver is the synthesis of. ANS amino acids
  2. All of the essential amino acids are obtained from. ANS food
  3. Within hepatocytes, amino acids are converted to carbohydrates by re- moval of (NH3). ANS ammonia
  4. The removal of ammonia from amino acids is called. ANS deamination
  5. Ammonia is converted to by the liver and passes into the blood to be excreted by the kidneys. ANS urea
  6. The plasma proteins, including a and and globulins are synthesized by the liver. ANS albumins, alpha, beta
  7. Any condition that disrupts the normal functioning of the liver, thus hepa- tocyte dysfunction, can cause. ANS hypoalbuminemia
  8. is an irreversible, inflammatory, fibrotic liver disease. ANS cirrhosis
  9. abuse and viral are the most common causes of cirrhosis. ANS al- cohol, hepatitis
  10. When fibrosis occurs in the liver, it obstructs biliary channels and blood
  1. Tachypnea and hypoxemia are indicative of when a patient presents with hypovolemia and systemic inflammatory response syndrome (SIRS). ANS - sepsis
  1. Transient can occur when glucagon is released from damaged A cells within pancreatic islets. ANS hyperglycemia
  2. Primary is attributed to excessive endometrial prostaglandin pro- duction. ANS dysmenorrhea
  3. Women with painful periods produce times as much prostaglandin F as asymptomatic women ANS 10
  4. Prostaglandin is a potent myometrial stimulant and vasoconstrictor.- ANS F
  5. Elevated levels of prostaglandins cause uterine , decreased blood flow to the , and increased - hypersensitivity, thus resulting in pain. ANS - hypercontractility, uterus, nerve
  6. Primary/secondary dysmenorrhea results from disorders such as en- dometriosis, endometritis, PID, obstructive uterine or vaginal anomalies, etc.- ANS secondary
  7. Uterine fibroids are called and are usually benign smooth muscle tumors in the myometrium. ANS leiomyomas
  8. Uterine fibroids are usually malignant/benign.