NUR 2063/NUR2063 Final REVISED Final Exam Study Guide Patho Spring 202/22. (NUR2063)
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NUR 2063 (NUR2063)
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Rasmussen College
NUR 2063 Final REVISED Final Exam Study Guide Patho Spring 202/22.
NUR 2063/NUR2063 Final REVISED Final Exam Study Guide Patho Spring 202/22. (NUR2063)
nur 2063 final revised final exam study guide patho spring 20222
patho spring 20222
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Rasmussen College
NUR 2063 (NUR2063)
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Final Exam Concept Guide
Know the Etiology, Signs/Symptoms, Diagnosis/Diagnostics, Clinical Manifestation,
Risks, Treatment and Complications for the following:
Gastritis
Gastritis – inflammation of the stomach lining
Acute Gastritis – (just acquired) ingestion of toxins, alcohol, aspirin or other irritating
substances
Chronic- 2 months to become chronic
Triggers of Gastritis: Alcohol, caffeine, autoimmune disease, viral or bacteria
Chronic Gastritis: H Pylori is always a factor
H Pylori goes very deep in the lining of the stomach and It causes persistent inflammation
S/S: N/V – Anorexia- postcranial discomfort
Post Cranial Discomfort- after eating- goes away and come back 1-2 hrs
Gastritis- hematemesis- blood in the vomit- coffee brown color
Treatment: Treat H pylori treat GERD, change lifestyle, PPI
Peptic Ulcer Disease
Inflammation and ulceration in the stomach (acid and pepsin)
Gastric: stomach location
Duodenal: duodenal location
PUD is a complication of Gastritis
PUD is caused by aspirin, H pylori, Nsaids, Stress, Smoking
S/S Gastric N/V Anorexia Chest discomfort, asymptotic, Dyspepsia
Duodenal – normal weight
Biggest complication of PUD- GI bleeding due to Ulcer perforation- hole in the lining and
bleed
It is life-threatening if it keep bleeding (Anemic, electrolytes imbalance (losing volume)
Duodenal – Blood in the stool – black and tarry
Bleeding profusely-frank with cloth
Hematemesis- Bleeding in vomiting
Treatment: Cortery of perforation, treatment of H. pylori, PPI, Cessation of smoking
Ulcerative Colitis and Crohn’s the difference in the complications
Complication in UC Malnutrition – dehydration, increased risk factor of colon cancer
7-10 yrs, rarely in megacolon
Complication of Chron- Fistulas, perianal fissures, abscesses. The risk of colorectal cancer
Bowel Obstruction Manifestations
Obstructions in the jejunal area: Vomiting, dehydration, electrolyte depletion
Obstructions of the distal portion of the small bowl or ileum, dehydration to hypovolemic
schock
Obstructions of the colon: Massive gas distention
Blockage of the colon by a tumor is the most common cause of colonic obstruction and
perforation of the bowel wall adjacent to the tumor.
What percentage of the pancreas is dedicated to endocrine functions?
Only 5%
Pancreatic Cancer
Pancreatic Cancer – 2% of all cancers
Ranked 4th among death in all malignancies
Risk Factors; cigarette smoking, obesity
S/S; head: Jaundice, malabsorption, weight loss tail: Abd pain, nausea’
Hepatic Encephalopathy is due to?
Hepatic encephalopathy is a decline in brain function due to severe liver disease
,Hepatic encephalopathy is usually precipitated by certain well-defined clinical developments,
including hypokalemia, hyponatremia, alkalosis, hypoxia, hypercarbia, infection, use of sedatives,
GI hemorrhage, protein meal gorging, renal failure, and constipation. In some patients,
progressive liver failure leads to chronic encephalopathy without other exacerbating factors.
Hepatic encephalopathy is graded 1 to 4:
Grade 1: Confusion, subtle behavioral changes, no flap
Grade 2: Drowsy, clear behavioral changes, flap present
Grade 3: Stuporous but can follow commands, marked confusion, slurred speech, flap
present
Grade 4: Coma, no flap
Gastroesophageal Varices Management
- Initial treatment: Fluid resuscitation to stop bleeding
- Large bore intravenous lines are placed
- Admin of parenteral vitamin K and plasma, platelet infusion if thrombocytopenia is
present
- Octreotide acetate (synthetic analog) no more vasopressin 3-5 days
- Metoclopramide and B blockers
- Esophagogastroduodenoscopy EGD to determine site of bleeding
Difference between Diverticulosis and Diverticulitis
Diverticulosis (diverticular disease) presence of diverticula in the colon.
Diverticula are acquired herniations of the mucosa and submucosa through the muscular coat
of the colon
Diverticulosis The presence of one or more diverticula vs diverticulitis inflammation of one or
more diverticula
Kidney Disease- Assessment-CVA
Pain associated with intrarenal disorders are assessed by palpating or light percussion over
the costovertebral angle (CVA) posteriorly and is recorded as CVA tenderness. Pain is
transmitted to the spinal cord between T10 and L1
Kidney Cancer signs and symptoms
Benign renal neoplasm: S/S Hematuria and flank pain
Some may be asymptomatic until large
Renal cell carcinoma: Metastatic disease
Risk factors: smoking, obesity and hypertension
S/S CVA tenderness, hematuria, palpable mass
Dialysis- Benefits and Risks
Filter blood and rid the waist
Dialysis is the only therapeutic option for those with ESRD unable to obtain transplant
Each treatment of dialysis remove about 2/3 of the total body urea content
Dialysis maintain volume status
Prevent and treat acid-base and electrolyte disturbances
Prevent and treat uremia
Support nutritional needs.
Prevent and treat infection
Orevent and treat anemia
Improve quality of life
Lower mortalty and morbidity rates
Control pains
VS
RISKS
Electrolytes imbalance (potassium and sodium) -need to check hyper or hypo
, Low blood pressure (have to check vitals before and after)
Risk for infection
Long-term mobidity
Life threatening
Cardiovascular disease remained the most common cause of death in ESRD patient
Acute Kidney Injury- Three phases- Prodromal- Oliguric- Postoliguric
Prodomal Phase
- Normal or declining urine output
- Serum blood urea nitrogen (BUN) and creatine levels rise
Oliguric phase (10-14 days) range from 1 day to 8 weeks
- Oliguria – Small abnormal amount of urine
- Edema, Hypertension, Hypervolemia
- Distended neck veins, weight gain
- Crackles, possibly heart faily
- WBC and RBC in urine
- Protein in urine
- Hyperkalemka
- Volume overload
- Azotemia and uremia
- Metabolic acidosis
Postoliguric phase (5% recover)
- Fluid volume deficit
- Labs begin to normalize
- Polyuria – sodium waste
Acute Tubular Necrosis and the causes of Acute Tubular Necrosis
ATN is the result of tubular cell injury
- Ischemia: Exposure to nephrotoxic substances
- ½ of all cases of AKI
Nephrotoxins leading cause of ATN (aminoaglycosides, NSAIDS, amphotericin B, cisplatin,
tetracycline.
CI- AKI or Contrast-induced nephropathy
Cystitis- signs and symptoms
(inflammation of the bladder) no fever or flank pain If fever is present – Might be infection
(UTI)
Confusion
Cloudy urine
Frequency
Urgency
Dysuria
Intrarenal Kidney Injury- Toxic causes of
Box 28.1
Ty p e s o f A c u t e K i d n e y I n j u r y
Prerenal
• Absolute decrease in circulating volume
o • Hemorrhage
o • Dehydration
o • Burns
• Relative decrease in circulating volume
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