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NUR 430  Exam 3 SG GI Disorders: (20 questions) Acute GI Bleeding/Stress Erosive Syndrome Understand difference between GI bleed & PUD  Gastric mucosal resistance disruption is caused by ↑d acid production & ↓d mucosal blood flow that results in ischemia & degeneration of mucosal lining  PUD o Breakdown of protective mechanisms causing autodigestion of stomach & intestine leading to damaged blood vessels & bleeding  Caused by ↑d gastric acid production & high h. pylori &/or NSAIDs  To treat H. Pylori, need anti-ulcer & antibiotics  SMRD o Occurs w ↑ acid production & poor perfusion of mucosal lining (  mucosal blood flow)  Seen often in pts requiring MV or have burns, sepsis, surgery, acute neuro disease & severe trauma  Pain, bleeding, ↓d CO, low BP, tachycardia  Management  prevention (PPI, H2)  Goals  ↑d acid production, more acidic pH Patho GI o Types of GI Hemorrhage  PUD, SMRD  Esophageal varices d/t portal HTN  Often get form cirrhosis of liver from alcoholism  This is where blood is backed up & causes a rupture in esophagus o Patho  Acute, massive bleeding  hypovolemic shock, initiation of shock response, & devel of MODs, if left untreated  Most common cause of death is exacerbation of underlying disease, not intractable hypovolemic shock  Hypovolemic Shock  hemorrhage (loss of O2 carrying RBCs) & hypovolemia  loss of circulating or intravascular Vol  ↓ venous return  ↓ preload  ↓d SV & CO  ↓ MAP Common S/S GI  Hematemesis (in upper GI bleeds)  vomiting blood; from a source above duodenojejunal junction o Bright red or coffee ground appearance  Hematochezia bright red stools (in lower GI bleeds)  Melenadigested blood from an upper GI bleed o Purple, clumpy, red  Losing whole blood thus Hgb & Hct many not ↓ for many hrs  Pale & cool skin, ↓d peripheral pulses, flat jugular veins  Hypovolemic s/s Hypotension, tachycardia, ↓d urine output  Resp alkalosis, ↓ CVP & PAWP Medical Management GI  ↓ gastric acidity & support gastric mucosal defense mechanisms  Identify at risk pts & manage m o Give prophylactic agents Antacids, H2 blockers, Cytoprotective agents, PPI o Vasopressin If GI bleed d/t liver, intraarterial infusion to  portal blood flow & pressure  Priorities for GI Hemorrhage

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o Airway protection, Fluid Resuscitation, Stop bleeding, Determine underlying cause Stabilization o Crystalloids, blood, need several IV sites (large bore?) o Intubate to prevent aspiration; O2 rapy to  O2 delivery & improve tissue perfusion Control bleeding o Use of saline for gastric lavage (helps place pressure against raw areas of stomach in hopes it will help slow bleeding down) o Endoscopy for exploratory measures need to configure where bleed is located w/in GI tract

Remember classes of antiulcer drugs, ir use & side effects  Antacids o Act as a base -> ↓ pH o Neutralize stomach acid o Admin 1-3H after meals & at bedtime  H2 blockers o Block release of acid into stomach o Reversible, just blocks acid secretion (doesn’t bind) o End in “tidine” o Ex Pepsin  Cytoprotective agents Sucralfate (Carafate) o Forms a protective coating around ulcer o Give 1H b4 eating (on empty stomach) o ↓s absorption of or drugs give separately by 2H  PPI o Bind irreversibly, blocks acid production  Vasopressin (normal occurring body chemical – ADH from pituitary) o Helps retain some fluid in kidney naturally to prevent dehydration o In high doses, it acts as a vasoconstrictor  ↓ blood flow overall to GI tract ↓s blood leaving GI tract to portal circulation  Helps slow bleeding down Nursing Interventions GI  SRMD o Gastric pH should be between 3.5-4.5 o Monitor color & type of emesis & stools  Vol Replacement o Need 2 large diameter IV cater peripheral IV sites (possibly more than 2 if hemorrhage)  Need to administer Vol replacement! (initial priority) o Hemodynamic stability isotonic solutions (NS, LR)  Control bleeding o Saline for gastric lavage  Maintain surveillance of complications o Monitor for signs of perforation Severe pain, fever, leukocytosis, & tachycardia  Positioning for hypotension pts o Trunk flat, legs up, head & shoulders above chest  Assessment / monitor o Assess Q15M until shock is controlled o LOC, pulse, BP, CVP, RR, O2 sat, skin color, urine output, SvO2  NPO  NG tube for active bleeding, gastric lavage, ↓ risk for aspiration 

Common nursing diagnoses for GI bleeding

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o Deficit fluid Vol r/t absolute loss o ↓d CO r/t alterations in preload o Risk for aspiration o Imbalanced nutrition: less than body requires r/t lack of exogenous nutrients &  metabolic demands o Risk for infection o Powerlessness Be able to identify & evaluate pt outcomes of medical & nursing care o Treatment Goals  Maintaining O2 Sat at 95% or higher  ABGs w/in normal range  Maintenance of urine output > 30 mL/hr  Maintenance of MAP w/in 10mmHg of baseline

Acute Pancreatitis Know definition of acute pancreatitis  Acute inflammation of pancreas that produces exocrine & endocrine dysfunction that may also involve surrounding tissues &/or remote organ systems  Etiology Biliary disease (gallstones) & alcoholism plus less common causes  Not chronic; happens all of a sudden Patho- particularly autodigestion, massive inflammatory response, inflammatory mediator spread, hypovolemia d/t third spacing, & systemic effects  Autodigestion Inactive digestive enzymes become prematurely activated w/in pancreas itself  Inflammatory Mediator Spread o Enzymes become activated through obstruction, damage, alterations in secretory processes of acinar cells, infection, ischemia, &/or or unknown factors o Trypsin becomes activated first & initiates auto-digestion process by triggering secretion of protein enzymes including lipase  Trypsin in lungs breaks down alveoli o  cap. permeability d/t mediators = fluid leakage = edema & hypovolemia  Hypovolemia d/t 3rd Spacing [relative] o Triggers secretion of proteolytic enzymes such as kallikrein, chymotrypsin, elastase, phospholipase A, & lipase  Release of kallikrein & chymotrypsin result in  cap mem permeability o Albumin  in pancreatitis (& liver problems) o Elastase, most harmful b/c it dissolves elastic fibers of blood vessels & ducts leading to hemorrhage  breaks down protein (muscle wasting) o Or enzymes digest phospholipids of cell membrane causing severe pancreatic necrosis; lipase goes into damaged tissue & into circulation w/ fat necrosis of pancreas & surrounding tissues Common S/S: Cullen’s sign, Grey Turner’s sign, Kehr’s sign, rebound tenderness  acute pancreatitis  Mild to severe pain twisting knife-like sensation that radiates to low dorsal region back, epigastric to midabdominal pain that can be mild & tolerate to severe & incapacitating o Acute onset of abd pain is hallmark SX!  N/V from pain, hypoactive bowel sounds, abd. tenderness, guarding, distension  Kehr’s sign  referred pain to left shoulder; from spleen or irritation of diaphragm from bile of or material in peritoneum  Seek comfort by leaning forward or lying down w knee drawn up (fetal position)  Hypovolemic Shock Fever, diaphoresis, weakness, tachypnea, hypotension, tachycard  If pancreatic hemorrhage: (retroperitoneal bleed) o Grey Turner: blue-gray discoloration of flank  abdomen cavity bleed

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Cullen: discoloration of umbilical region  abdominal wall bleed

Abnormal Lab Findings acute pancreatitis  Elevated serum amylase, isoamylase, lipase, urine amylase (digestive enzymes) o Amylase is present in or body tissues & disorders; excreted in urine  Clearance ↑s w/ acute pancreatitis & may only be  for 3-5 days  Elevatedtriglycerides, glucose (give insulin), WBC, CRP  ↓d Ca, Mg, K+, albumin (if albumin low  calcium low too normally), bicarb o Albumin lost d/t  cap permeability o Mg direct relationship w/ Ca so give calcium & albumin  Elevatedbilirubin & liver enzymes  ABGs Hypoxemia & metabolic acidosis Diagnostic Results/Testing acute pancreatitis  Abdominal ultrasound for gallstones  Contrast-Enhanced CT scan gold standard Medical Management Goals & Treatments acute pancreatitis  Interventions o IV crystalloids & colloids to prevent relative hypovolemic shock & maintain hemodynamic stability  Colloids – albumin (prevents/treats 3rd spacing edema)  Isotonic first to expand intravascular space, n hypertonic (3%NS) o Enteral feedings soon as possible (NPO)  May need TPN if not orally fed in 2 days o Correcting Metabolic Alterations/Replacing Electrolytes  Ca, K+, Mg & albumin replacement  If hyperglycemic, exogenous insulin may be given o O2 rapy Nursing management goals & interventions  acute pancreatitis o Minimize pancreatic stimulation  Provide bed rest  Carefully consider food & fluids NPO!  Avoid NGT unless gastric distention or aspiration risk (vomiting)  Only NG suction if persistent vomiting, obstruction, or gastric distention o Provide comfort & emotional support  Morphine for pain management  Position knee to chest  Relaxation techniques o Monitor complications in all body systems & organs (especially lung & kidney)  Hypovolemic Shock  From 3rd spacing, vasodilation &  cap permeability  Lungs (ARDS)  First problem will be lungs; ARDs 1st sign b/c fluid shift/pulmonary edema o Monitor pulse ox, RR status, hypoxemia, PE, atelectasis  Kidney (AKI)  Mediators- if intravascular Vol is low for a long time, RAAS happens  GI Hemorrhage  stress response from SRMD & varies (alcoholics) o How do we know it worked? Pain , amylase & lipase ↓ing, WBC normal, tolerating feedings 

ND Acute Pain, DFV,  CO, ineffective breathing patterns, imbalanced nutrition: less than body requirements

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Acute Liver Failure Know definition of acute liver failure  Severe acute liver cell dysfunction, coagulopathy, & hepatic encephalopathy  MEDICAL EMERGENCY  Occurs in pts w/o existing liver disease  Etiology: o Infections, drugs, toxins, direct injury to liver (stabbing), hypoperfusion, metabolic disorders, & surgery Patho acute liver failure  Develops over 1-3 weeks (happens quick!)  Followed by hepatic encephalopathy w/in 8 weeks in a pt w previous healthy liver o Usually less n 2 weeks  Cause is massive necrosis of hepatocytes  Results in: o Impaired bilirubin conjugation  Jaundice o ↓d production of clotting factors o ↓d glucose synsis  hypoglycemia o ↓d lactate clearance  metabolic acidosis o ↓ metabolism of carbs, proteins, & glucose  Imbalances o Hypoalbuminemia, F&E imbalances, Acute portal HTN  All cause ascites  Encephalopathy will develop because of inability to detoxify substances in blood, pus, fluid w high ammonia  Complications o Cerebral edema &  ICP develops as a result of breakdown of BBB & astrocyte swelling o Systemic complications -> ARDS, aspiration pneumonia, acute renal failure Common abnormal lab findings  acute liver failure  Elevated serum bilirubin, AST, alkaline phosphate  Elevated serum ammonia (needs to be reduced ASAP)  ↓d albumin, plasmin, plasminogen, platelets o If cerebral encephalopathy develops, give albumin  ↑d PTT!!! (40 to 80 seconds above control), platelets   ABGs  Resp alkalosis &/or metabolic acidosis; abnormal pH  Asterixis (unique in liver failure)** o Tremor of hand when wrist is extended; hepatic encephalopathy; pretty bad liver failure!  S/S o HA, hyperventilation, jaundice, mental status changes, palmar eryma, spider nevi, bruises, edema o Monitor for asterixis (liver flap) &  LOC Hepatic Encephalopathy Stages  I Euphoria vs depression, mild confusion, slurred speech, disordered sleep, slight asterixis, normal ekg  IILethargy, moderate confusion, marked asterixis, abnormal EKG  III marked confusion, incoherent speech, sleepy but arousable, asterixis present, abnormal EKG  IV Coma, responsive n nonresponsive to painful stimuli, asterixis absent, abnormal EKG Medical Management Goals & Interventions  Hepatic Encephalopathy  Admin Lactulose creates an acidic environment that  bacterial growth; traps ammonia & has a laxative effect that promotes expulsion  Neomycin  ↓s bacterial flora of colon; aids in  ammonia formation by  bacterial action on protein in feces thus  amount of ammonia released  Prevent bleeding particularly SRES, need prophylaxis

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Antibiotic prophylaxis peritonitis; risk for infection If pt develops active bleeding give Vitamin K to promote clotting Cerebral edema -> ICP monitoring, Mannitol Intubation & MV w Vasoactive meds Liver transplant!!

Nursing Management Goals & Interventions, such as injury protection to protect for bleeding, surveillance of complications, restraining versus sedation  Injury Protection o Padded side rails, bed alarms, call light w/in reach o Monitor LOC & pt frequently  Maintain Surveillance of Complications o If neurological condition worsens, watch for Resp complications, need O2 sats  Continuous pulse ox monitoring & ABG analysis o Perform thorough neurological assessment at least q1h  Restraining vs Sedation o Use of benzos & or sedatives is discouraged b/c of “masking” of neurological changes & y go thru liver o Pt may be extremely agitated & combative so restraints may be necessary to keep pt safe  Be able to identify & evaluate pt outcomes of medical & nursing care  Indicators that pt getting better  Improvement of LOC, ↓ AST/ALT, less risk for bleeding Common ND  ↓d intracranial adaptive capacity, ineffective breathing pattern, ineffective renal tissue perfusion,  CO, impaired gas exchange, risk for infection Abdominal Trauma Know mechanisms of injury  Blunt trauma o MVCs, falls, & assaults  more fatal o Side injuries, pedestrians  Penetrating trauma o Knives or bullets; unpredictable o Liver, spleen, diaphragm, & colon  Life-threatening conditions: o Hemorrhage o Hollow viscous perforation w peritonitis (possible sepsis) Assessments ABD trauma o Signs of bleeding  Cullen sign  discoloration of umbilical region  abdominal wall bleed  Grey-Turner sign  blue-gray discoloration of flank  abdomen cavity bleed o may indicate retroperitoneal bleed or pancreatic injury  Distended abdomen, hematoma in flank area o Or S/S  Rebound tenderness  Rigidity, friction rubs over spleen  peritoneal inflammation  Kehr sign (to L shoulder)  Acute pain in tip of shoulder d/t blood in peritoneal cavity when person is lying down & legs elevated  Classic sign of ruptured spleen

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 Subcutaneous emphysema on abdomen (ruptured colon) Diagnosis  ABD trauma  Ultrasound (FAST) o bedside ultrasound to test for blood around heart or abdomen if pt unstable  Abd CT Scan  if pt is hemodynamically stable & re is time  Peritoneal lavage for frank blood  if positive, re is trauma in abd  NGT  to decompress stomach & contents can be checked for blood  Urinary Cater  bloody urine Treatment: such as damage control surgery, measurement of intra-abdominal pressures  ABCs, manage bleeding  Damage Control Surgery o Initial operation (laparotomy)  duration kept short  Reasons: hypormia & coagulopathy in a pt who is hemodynamically unstable, inability to control bleeding by direct pressure or inability to close abdomen b/c of massive edema (belly left open) o ICU Resuscitation  aggressive resuscitation & correct hypormia, coagulopathy & acidosis  Coagulation factors & platelets, rewarming, vent support, ID injury o Definitive re-operation  pack removal & definitive repair  Measurement of Intraabdominal Pressures o Measure thru bladder cater after inj 50-100mL of NS; monitor q2-4h  Compartment Syndrome o End-organ dysfunction caused by intraabdominal HTN; ↑d pressure causes  blood flow leading to ischemia & necrosis  S/S  CO &UO, PVR, peak pulm. Pressures, hypoxia o Measure intrabdominal pressures  Measure through bladder cater to detect onset of HTN o Surgical decompression if pressures > 20-25mm o Intraabdominal HTN is a IAP > 12mm o IAP of 20-25  surgical decompression  Likely will return w/ open abdomen w/ sterile perforated sheet clipped w/ vacuum tubing or closed suctioning o Likely will return after surgery w an open abdomen Specific Organ Injury, its effects, & its treatment  Liver o Diagnosis  abdominal CT o Bleeding can be severe, can lead to hypovolemic shock, ↓ CO  Monitor! o Need fluid resuscitation o Need platelets, FFP, cryoprecipitate  Monitor pt’s response to medical rapies  Spleen o Most common organ injured by blunt abdomen trauma o Try to avoid removal; if hemodynamically unstable may need splenectomy  Requires pneumonia vaccine after surgery to promote immunity against bacteria  Intestinal o Surgical interventions are usually required in presence of multiple findings on CT scan  Unexplained free fluid, bowel wall thickening, mesenteric hematoma o May cause peritonitis  from intestinal contents leaking into peritoneum o Need repair or resection

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Genitourinary Injuries Consider GU injury when:  Any penetrating injury to torso  Pelvic fracture, blunt trauma to flank  Lower abd, or perineum, genital swelling or discoloration  Blood at urethral meatus  Hematuria after caterization  Difficulty w urination Common Assessments GU injury  Renal o Flank bruising, gross hematuria, tenderness over flank & lower abd o CT scan  Bladder o Most are from pelvic fractures o Lower abdomen bruising, distension, & pain o Retrograde urethrogram Common nursing diagnoses & ir primary interventions GU injury  Nursing Diagnosis: o Ineffective tissue perfusion o Pain o Risk for infection o Risk for deficit fluid Vol  Primary Interventions: o Assess for hemorrhage o Maintain fluid & electrolyte balance o Maintain drain & tube patency; may need to irrigate to clear clots o Monitor urinary output frequently o If extraperitoneal rupture  manage w/ cater & antibiotics Neurologic Disorders (30 Questions) Understand categories of consciousness  Descending states: ( determine cause of coma  Thiamine  Glucose  Naloxone (Narcan) o Assess:  Motor function  Pupil responses  Resp responses o Diagnostics:  CT scans or MRI  Check for ICP first n lumbar puncture* Differences between structural & metabolic comas o Slide 7 on PowerPoint o Metabolic coma has better prognosis than structural lesion coma

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Medical Management goals & treatments o Identify & treat underlying cause of coma o Support vital functions  ABCs + cervical neck stabilization o Prevent furr neurologic deterioration o Administer thiamine, glucose, or Narcan if cause of coma is not obvious o Make decisions jointly w family

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Nursing Management & Interventions o Support all body functions  skin care, toileting, positioning (30º), ROM, feeding o Eye Care  Instilling saline or methyl cellulose lubricating drops  Taping eyelids shut o Initiate rehab measures o Coma stimulation rapy once hemodynamic stable & no intracranial HTN  Stimuli must be meaningful**  Recorded spouse, family or friends voice  Music, photographs, faces, spices, perfumes, rubbing lotion  Start w only one stimuli  Consider exposing pt 10-30 minutes a session, 2-4 times/day  Monitor neurologic status & or VS during stimulation o Nutritional rapy o Maintain surveillance for complications

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Nursing Diagnosis o Ineffective airway clearance, ineffective breathing pattern, imbalance nutrition, compromised family coping

Persistent Vegetative State (PVS) [need to get most of this from course packet]  Know definitions o State of unconsciousness in which wakefulness is present, but awareness is lacking  Eyes are open, blinking, swallowing but not aware & no purposeful movements  cannot follow demands  Family education is important! o Unconsciousness in which sleep-wake cycles & complete or partial hypothalamic & brain stem automatic function are present, but complete unawareness of self & surrounding environment b/c of absence of any ascertainable cerebral cortical function o Considered persistent when present for 3 months or more after acute traumatic or nontraumatic brain injury, metabolic or degenerative disorders & developmental malformati...