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GI study session
Pancreatitis, ischemic bowel, GI bleed, and liver disease
| Question | Answer |
|---|---|
| What are causes of chronic hepatic failure? | Cirrhosis (alcoholic, postnecrotic, biliary, cardiac), chronic active hepatitis, hepatic vein thrombosis. |
| What are causes of fulminant hepatic failure? | Infection ( heptitis virus, herpes simplex, cytomegalovirus, adenoviruses), Toxins (mushroom poisoning), drug reaction ( acetaminophen overdose, NSAIDS, amiodarone), Ischemia ( cardiac failure, hepatic vascular occlusions, HTN). |
| What are the pathophysiologic alterations seen in fulminant hepatic failure? | Cerebral edema, Hypoglycemia, Lactic acidosis, Hypokalemia, and Hyponatremia. |
| What are the pathophysiologic alterations seen in chronic hepatic failure? | Portal HTN, Vasular spiders (angioma), Overall poor health, and Hypoalbuminemia. |
| What are S/S of fulminant hepatic failure? | Headache, dizziness, jaundice, vomiting, altered mental status, encephalopathy, hypotension, tachycardia, arrhythmias, tachypnea, spider nevi, elevated temperature, and asterixis (liver flap). |
| What are S/S of chronic hepatic failure? | Malnourished, malaise, weakness, fatigue, weight loss, anorexia, easy bruising, vascular spiders, palmar erythema, ascites, peripheral edema, asterixis, flushed extremities with clubbing and cyanosis, gynecomastia, splenomegaly. |
| What are the S/S of Grade I encephalopathy? | Euphoric, occasionally depressed, fluctuant mild confusion, slowness of mentation and affect, untidy, slurred speech, reversal of sleep pattern, may have asterixis alone. |
| What are the S/S of Grade II encephalopathy? | Accentuation of I, drowsy, inappropriate behaviour, possible to hold conversation. |
| What are the S/S of Grade III encephalopathy? | Sleeps most of the time but is rousable, unable to converse coherently. May be manifest as extreme agitation or irritability with violence to self/others. |
| What are the S/S of Grade IV encephalopathy? | Unrousable, may respond to noxious stimuli? |
| What are interventions for fulminant hepatic failure? | Reduce and monitor cerebral edema, monitor for hepatic encephalopathy, control and monitor for hypoglycemia, monitor for coagulopathy and bleeding, monitor BP and CO, monitor for hepato-renal failure, monitor for infection,monitor for respiratory failure. |
| What are interventions for chronic renal failure? | Monitor for encephalopathy,improve nutrition,monitor for coagulopathy, monitor/prevent infection, reduce portal HTN, control/prevent bleeding from varices, monitor to reduce ascites,monitor liver function test,prepare for liver transplant if needed. |
| Name some medications used to treat fuliminant and chronic hepatic failure? | Osmotic diuretics, laxatives,aminoglycoside, vitamin replacement, blood replacement, histamine 2 receptor antagonists, bartiburates, inotropic agents, K-sparing diuretics, loop diuretics, volume expanders, antidote for acetaminophen (mucomyst). |
| What are some nursing diagnosis for fulminantand chronic hepatic failure? | Altered thought process, high risk for injury, altered tissue perfusion:hepato-renal, fluid volume excess or deficit, altered nutrition: less than body requirements, risk for impaired skin integrity. Prevent: MODS and Cerebral Edema. |
| What are some lab findings with fulminant and chronic hepatic failure? | Hypoglycemia(fulminant), hyperglycemia(chronic), decreased K, Na, Ph, BUN, platelet, albumin. Increased Ptt, PT, bilirubin, ammonia, lactic acid, FSP/FDP(fulminant). + hepatitis screen. Metabolic acidosis(fulminant), metabolic acidosis/alkalosis(chronic). |
| What are some diagnostic test for fulminant and chronic hepatic failure? | EEG(decreased frequency), ECG(increased rate, arrhythmias), CX(pulmonary edema, lobar collapse, ARDS), Biopsy, hepatic ultrasonography, CBF, and cerebral oxygen consumption. |
| Peptic ulceration occurs when protective mechanisms cease to functions. The two main causes of peptic ulceration include: | Glycoproteins on the surface of the of the epithelium and gastric blood flow, Nonsteroidal anti-inflammatory drugs and bacterial action of Helicobacter pylori, Bicarbonate secretions and prostaglandins, Glycoproteins and bicarbonate secretions, |
| Acute upper gastrointestinal hemorrhage occurs from the sudden onset of bleeding from lesions in which of the following organs? | Stomach duodenum jejunum, Duodenum jejunum ileum, Ileum jejunum colon, Esophagus stomach duodenum |
| Acute GI hemorrhage results in hypovolemic shock, initiation of the shock response and the development of multiple organ dysfunction syndrome if left untreated. Which of the following are more closely associated with lower GI tract hemorrhage? | Inflammatory bowel disease hemorrhoids trauma, Mallory Weiss tear stress-related erosive syndrome neoplasm, Peptic ulcer disease esophagogastric varices esophagitis, Aortoentric fistula Angiodysplasia Aneurism |
| The presence of blood in the GI tract results in increased peristalsis and diarrhea. Hematochezia | Has the appearance of coffee grounds, Is black, tarry or dark red stool, Is blood vomited from a source above the duodenojujunal junction, Is bright red stool |
| Peptic ulceration occurs when protective mechanisms cease to functions. The two main causes of peptic ulceration include: | Nonsteroidal anti-inflammatory drugs and bacterial action of Helicobacter pylori |
| Acute upper gastrointestinal hemorrhage occurs from the sudden onset of bleeding from lesions in which of the following organs? | Esophagus, stomach, duodenum |
| Acute GI hemorrhage results in hypovolemic shock, initiation of the shock response and the development of multiple organ dysfunction syndrome if left untreated. What are some cause closely associated with lower GI tract hemorrhage? | Diverticulosis, angiodysplasia, neoplasm Inflammatory bowel disease, trauma, infectious colitis, radiation colitis, ischemia, aortoenteric fistula, hemorrhoids |
| The presence of blood in the GI tract results in increased peristalsis and diarrhea. Hematochezia is? | Bright red stool which occurs from a massive lower GI hemorrhage |
| Lab tests can help to determine the extent of GI bleeding. As whole blood is lost, plasma and red blood cells are lost in the same proportion. It may take _______for the patient’s hemoglobin level and hematocrit values to decrease. | 24-72 hours |
| Progressive shock state may result in cardiac and vasomotor failure, intravascular clotting, increased capillary permeability acidosis and death. Greater than 40% total loss of blood amounts to? | >2000cc of blood loss |
| Depend on the rate and amount of blood loss and the coexistence of other diseases, patients with anemia may experience 10-15% loss of total blood volume. This percent of blood loss initiates sympathetic reflexes and represents a volume of? | 500-700cc of blood |
| The loss of 750-1500cc of blood stimulates baroreceptor reflexes and CNS ischemic responses causing arterial and venous constriction and stimulating cardiac activity. This amount of blood loss represents a? | 15-30% loss of blood |
| A 30-40% loss of total blood volume initiates angiotensin and vasopressin compensatory mechanisms resulting in constriction of blood vessels and retention of Na and H2O. A 30-40% loss of blood represents a volume of? | 1500-2000cc of blood |
| There are various diagnostic tests available to isolate and treat the source of a GI bleed. What procedure is used to identify specific bleeding vessels? | Mesenteric arteriography |
| Abdominal assessment includes inspection, auscultation, percussion and then palpation. When auscultating the abdomen of a patient with a suspected GI bleed what kind of bowel sounds will be heard? | hypoactive |
| A patient diagnosed with a lower GI bleed is being given an administration of crystalloids to restore adequate circulating blood volume to prevent shock. Treatment with crystalloids would include: | Lactated Ringers and 0.9% NaCl |
| What causes an ischemic bowel? | It is an acute or chronic, arterial or venous disorder that is caused by an occlusion or narrowing of the mesenteric vessels which decreases the perfusion and delivery of oxygen to the intestinal tissue which causes necrosis of the bowel wall. |
| What is some predisposing factors concerning ischemic bowel disorders? | Superior mesenteric artery embolus, SMA thrombosis, nonocclusive mesenteric ischemia, mesenteric venous thrombosis, intestinal adhesions, SMO, or chronic heart disease. |
| What does the degree of the intestinal damage depend on in ischemic bowel? | Metabolic needs of the tissue, Amount of collateral circulation, Number of mesenteric vessels involved, Length of time of compromised blood flow, Overall condition of systemic circulation, and Response of the vascular bed to hypoperfusion. |
| What are the subjective assessment findings in an ischemic bowel disorder? | Pain that will vary in severity, location and nature, Weight loss with fear of eating, Nausea, and Vomiting. |
| What are the objective assessment findings in an ischemic bowel disorder? | Diarrhea or constipation, Abdominal distention, Cachexia, Ascites, Mental confusion, Tachypnea, cool, pale, clammy skin, Abdominal guarding with tenderness, and Absent or hyperactive bowel sounds. |
| What are some lab tests that will assist in supporting the diagnosis of ischemic bowels? | Increased WBC with a left shift, Increased HCT/Hgb, Metabolic acidosis, and Increased amylase, phosphate, lactate, SGOT/SGPT. |
| What are the diagnostic tests that will assist in supporting the diagnosis of ischemic bowels? | Abdominal x-ray, Arteriography of the aorta and mesenteric branches, Barium enema, CT of abdomen, Colonoscopy, and Esophagogastroduodenoscopy (EGD). |
| How fast must a diagnosis of ischemic bowel and treatment be started to ensure a 60% survival rate? | Diagnosis and treatment must be started within the first 24 hours of onset to ensure a 60% survival rate. The survival rate drops to less than 30% if the treatment is started later than 24 hours. |
| What interventions can be done to assist in correcting the underlying injury associated with ischemic bowels? | PTCA, Thrombolytic agents, Heparin, Catheter embolectomy, Resection of infarcted bowel, NG to low intermittent suction (LIS), crystalloids and colloids, antibiotics, and Foley with hourly outputs. |
| What medications can be administered to those patients with an ischemic bowel? | Crystalloid solution: LR and NS, Colloid solutions: albumin (5% - 25%), Antibiotics: Mefoxin, Cleocin (clindamycin), Garamycin (gentamycin), Vasodilator: Papaverine hydrochloride, Thrombolytics: Streptokinase, and Anticoagulants: Heparin. |
| What are some nursing diagnoses associated with an ischemic bowel? | Acute pain, Fluid Volume Deficit, Risk for infection, and Risk for injury. |
| What are the causes of acute pancreatitis? | gallstones, prolonged alcohol intake, abdominal surgery, trauma, hyperlipidemia, hypercalcemia, organ transplantation, peptic ulcer, outflow obstruction, pregnancy,hereditary, hypoperfusion of the pancreas, drug or chemical induced. |
| What are the pancreas enzymes? | Trypsin, Phospolipase A2, Elastase. |
| What are S/S of acute pancreatitis? | Mild-severe epigastric or periumbilical pain, N/V, anxiety, intense localized epigastric tenderness to deep palpation, hypotension, grey turners sign, cullens sign, tachycardia, tachypnea, oliguria, crackles, atelectasis, pleural effusion. |
| What are most common lab test to to tell function of the liver? | Amylase and Lipase |
| What are other lab test may be completed? | AST, Alkaline Phosphatase, LDH< bilirubin, blood sugar, Ca, albumin, Hgb, Hct, WBC, BUN, c-reative protein, urine amylase, creatinine clearance ration, isoenzyme, immunreactive trysinogen/trypsin, ST. |
| What test will be conducted to show acute pancreatitis? | CT with contrast MRI |
| What are the 5 Ranson's prognostic sign documented on admission? | Hct decrease >10%,BUN increase >5, Serum Ca <8, PaO2 <60, Base deficit >4, and Estimated fluid sequestration >6L. |
| True or False:Mortality increase with the number of negative signs. | False, Mortalitly increases with the number of positiv signs. |
| True or False: If <2 signs are postive, the mortality rate is <5%, If >2 are postive mortality is 15 to 20%? | False< If <3 signs are positive, the mortality rate is <5%, If >3 are postive mortality is 15 to 20% |
| What is the drug therapy choice for acute pancreatitis? | Opiod analgesic (NO MORPHINE), Colloid solutions, crystalloid solutions, histamine-2 receptor antagonist, antibiotics, anatacids, PT. is NPO s long as amylase and lipase are high. |
| What is the reason for not ging Morphine to a pt. with acute pancreatitis? | It causes the sphincter of Odi to spasm |
| What type of die would a pt. with acute pancreatitis be on once the lipase and amylase levels are under control? | Diet low in fat and residue. |
| What are some nursing diagonsis for acute Pancreatits? | Pain, Fluid Volume Deficit or Excess, Diarrhea, Constipation, Altered Nutrition less than body requirements, Altered Peripheral Tissue Perfusion, hight risk for Impaired Skin Integrity, risk for Impaired gas exchange, high risk for Injury |
| What life-threatening conditions are you trying to keep a pt. with acute pancreatitis from developing? | ARDS, hemorrhagic shock, DIC, Acute Renal Failure, Septic Shock, MODS. |
| What the term used to describe bruising around the flanks? | Grey Turner sign |
| What is the term used to describe ecchymoses of the umbilical region? | Cullen's sign. |
Created by:
IUeast
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