Acute Exam #3 Study Guide PDF
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This is a study guide covering various acute conditions and their management. The notes cover topics such as acute kidney injury, bowel obstruction, acute pancreatitis, DKA, HHS and hypoglycemia and liver diseases. It reviews relevant pathophysiology, manifestations, and treatment options.
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What causes What complications Assessments Interventions for complications Class Kahoot BUN: Cr → 25:1 = pre and postrenal Hemolytic Uremic Syndrome - Comes from E. Coli - Blood transfusion for anemia, monitoring for dehydration, fluid and electrolyte balance management,...
What causes What complications Assessments Interventions for complications Class Kahoot BUN: Cr → 25:1 = pre and postrenal Hemolytic Uremic Syndrome - Comes from E. Coli - Blood transfusion for anemia, monitoring for dehydration, fluid and electrolyte balance management, renal dialysis if indicated Pyelonephritis→ start e antibiotic - Start tx while awaiting culture results and sensitivity data Which lab finding characterizes nephrotic syndrome - Proteinuria greater than 3.5 g/L in a 24 hr urine collection Nephrotic syndrome manifestations - Proteinuria, hypoalbuminemia, hyperlipidemia, edema Diet mod for pt with nephrotic syndrome experiencing significant edema - High-protein, low-sodium diet Nephrotic syndrome common complication: CKD Pt diagnosed w/ pyelonephritis. Clinical manifestation to expect: - Vomiting and flank pain - Fever and chills Pt w hx of recurrent UTIs prescribed antibiotics for an active infection. - Potential complication: fungal infections Dietary management for nephrotic syndrome: - Limit protein intake if kidney function is severely impaired - Restrict fluid intake if edema is significant Videos Burns: https://www.youtube.com/watch?v=h4wvoWA702s Appendicitis: https://www.youtube.com/watch?v=r9amif1DQMc&t=303s Bowel Obstruction: https://www.youtube.com/watch?v=sBm12CkNtAo Peritonitis: https://www.youtube.com/watch?v=COKb-Vf9FMY Pyloric Stenosis: https://www.youtube.com/watch?v=XHt0qrfy1Oc&t=29s Intussusception: https://www.youtube.com/watch?v=YOeuI0R_BbU Pancreatitis: https://www.youtube.com/watch?v=0v1PwN03hwc Cirrhosis- Varices: https://www.youtube.com/watch?v=LMFFJjAlENQ&t=9s Esophageal Varices: https://www.youtube.com/watch?v=1f-9ZT16Emo DKA vs HHS: https://www.youtube.com/watch?v=99KimaS6tTU WEEK 7: Acute Kidney Injury - Risk Factors: age >65 y.o., HF, nephrotoxic meds (iodine, NSAIDs, -mycins, ACEI, cocaine, heroin, herbal remedies) - Prerenal: involves no direct damage to kidney tissues. - Decreased renal perfusion= drop in GFR - Decreased blood flow to kidneys - Common causes: hemorrhage (hypovolemia), burns, HF, dehydration, vasodilation, GI losses (vomiting/diarrhea) - Prerenal azotemia- BUN: Cr >20:1 and low urine sodium (20) and Cr (>1.2), Decreased GFR (1.030) - Diuretic (1-3 weeks) - osmotic diuresis u.o. Up to 5L/day - Hypovolemia - Hypotension - Hypokalemia (bradycardia and decreased LOC) - May experience type 1-3 cardiac blocks - BUN and Cr start to normalize - Recovery (Months-Years) - GFR increases - BUN and Cr levels plateau then decrease - Decreased edema - Normalization of fluid/electrolyte balance Labs: - Normal: - GFR: >/= 90 mL/min - BUN: 7-20 mg/dL - Cr: 0.6-1.2 mg/dL - BUN/Cr: 10-15:1 - Urine Sodium: 20-40 mEq/L - FeNa: 1-2% - Serum Sodium: 135-145 mEq/L - Serum Potassium: 3.5-5.0 mEq/L - Prerenal: - GFR: decreased (low perfusion) - BUN: elevated - Cr: elevated - BUN/Cr: >20:1, high BUN - Urine Sodium: 20:1 (high) early, then low - Urine Sodium: variable (low early, high later) - FeNa: Variable - Serum Sodium: Variable (often normal or low) - Serum Potassium:: elevated (especially with prolonged obstruction) Diagnostics: - 20:1 BUN:Cr Ratio: Suggests prerenal AKI – the kidneys conserve creatinine while urea rises with hypovolemia. - Muddy Brown Casts: Indicative of acute tubular necrosis – common in intrarenal AKI. - Elevated Cr w/ Normal UA: May suggest early postrenal obstruction or prerenal without tubular damage. - Decreased GFR w/ Normal BUN: Possible chronic kidney disease or early AKI. - Key Points: Renal ultrasound is the first-line imaging; KUB x-ray, CT urogram; FeNa 2% in ATN. Assess for urine sediment and casts. Dialysis - Hemodialysis (HD): Removes waste quickly; used in both AKI and CKD. Requires vascular access. Rapid fluid shifts may cause hypotension. Intermittent 3-4 hr runs. At hospital or dialysis center - Peritoneal Dialysis (PD): Intermittent over 3-4 hr. Instill dialysate into peritoneal space and drain after sitting for 3-4 hr. Draining takes about 10 minutes. Can be done at home. Uses peritoneal membrane. Risk for peritonitis and protein loss. Have to be stable Risks: - Peritonitis: Rigid Board-Like Abdomen. Acute abdominal pain, distention, fever, shallowing breathing d/t pain (and diaphragmatic pressure), altered mental status, shock - Abdominal Compartment Syndrome (abdominal HTN that restricts ventilation and can lead to respiratory failure. High pressure in abdomen and decreased Cardiac output can lead to AKI. and inflammation of other organs such as pancreas and liver) - Hyperglycemia - CRRT: Ideal for unstable ICU clients. Continuous filtration prevents hypotension and allows gentle fluid/electrolyte correction. Used until no longer needing it. - Key Points: Indications for dialysis: volume overload, hyperkalemia, acidosis, BUN >120, toxins, pericarditis, encephalopathy. AEIOU mnemonic Indications for Dialysis Tx- - A: Acidosis - E: Electrolyte Imbalances (hyperkalemia) - I: Intoxicants (ingestion or overdose of medications/drugs) - O: Overload of fluid (causing HF) - U: Uremia (urine in blood–leads to encephalitis/pericarditis →infections) - Best for Unstable Client: CRRT due to gradual solute/fluid removal. Urinary Tract Infections - Infection anywhere in the urinary tract - Manifestations: dysuria, frequency, urgency, cloudy urine Pyelonephritis/ Kidney Infection - UTI that specifically affects the kidneys. - Manifestations: fever, chills, N/V, flank pain (costavertebral angle tenderness) - Hallmark signs= flank pain and N/V Glomerulonephritis –STREP - Patho: a kidney condition that involves damage/inflammation to the glomeruli. Inflammation of glomeruli = “leaking” = RBCs in urine = mild protein - Less protein in urine and tea colored urine - 1. Immune system creates an antigen antibody complex = inflamed glomeruli - Post strep infection (positive ASO titer) – 14 days post infection – Pediatric 2 -10yrs old - HTN - Antigen ASO titer - Decreased GFR (decr Urine) - Swelling face (edema) - Tea colored urine - Recent strep - Elevated labs (incr BUN and Cr) - Proteinuria (mild) - Main Nursing concern: - Monitor vitals + Blood Pressure - Anti-HTN and Diuretics - Monitor I’s&O’s and Potassium - Relapse not common - Teach to monitor child for sore throat- strep - Etiology, R/F, causes: - Streptococcal infection of the throat (strep throat) or skin (impetigo). Hereditary diseases. Immune diseases such as SLE. Diabetes. HTN. Vasculitis (inflammation of the blood vessels). Viruses (HIV, Hep B, and Hep C). Endocarditis (infection of the heart valves). - Manifestations - Diluted tea color urine, Foamy Urine - Flank pain (back/vertebral pain) - Hematuria – a lot/visible to naked eye - Oliguria, Dysuria - Treatment - Treat underlying cause - Controlling BP is most important - Dialysis - Medications - Diuretics - Immunosuppressants (not typical) - Antihypertensive’s (CCB or ACE inhibitors: Beta blockers not good for children) - Sodium and water restriction - Potassium, phosphorus, magnesium restriction - Take calcium supplements - Maintain a healthy weight through diet and exercise - Physiotherapy tx : Breathing exercise, endurance training, Lymphatic massage to reduce edema - Complications: Acute kidney failure/CKD, nephrotic syndrome, electrolyte imbalances, pulmonary edema, CHF d/t fluid overload - Hemolytic Uremic Syndrome - Patho: Triad→ hemolytic anemia, thrombocytopenia, acute kidney injury (d/t damage to small blood vessels in the kidneys) - Causes: - Typical: most common… infection with STEC (shiga toxin-producing e.coli) - Atypical: genetic or r/t immune system problems - Sx: - Bloody diarrhea - Abd pain - Vomiting - Progresses to: pale skin or jaundice, bruising or petechiae, decreased urine output, swelling - Nursing Management: Supportive care - Fluids, BP regulation, acid/base balance, blood transfusions, kidney support (dialysis, if needed) - Avoid antibiotics - Eculizumab - Immunosuppressive medication that causes an increased risk for meningococcal infection, so a vaccine is recommended. Nephrotic Syndrome - Patho: Increased glomerular permeability, loss of plasma proteins (albumin), reduced plasma oncotic pressure, edema - Reduced oncotic pressure is caused by hypoproteinemia (low plasma protein levels, especially albumin), which leads to fluid shifting from the blood vessels into the surrounding tissues, resulting in edema (swelling). Fluid leaves blood vessels and goes into surrounding tissues - Changes in glomeruli = leaking = MASSIVE Protein - Hallmark Sx: Lots of protein in urine (proteinuria), dark and frothy (tea/ cola color) - Proteinuria, hypoalbuminemia, hyperlipidemia, oedema (around eyes, legs, labia = Anasarca = Massive edema) - SWOLLEN CHILD - Cause: Congenital, primary or idiopathic, secondary - Unknown changes to glomeruli. Other causes = SLE, DM, HF = peds 2:10 - Low ASO titer (not caused by Strep) - Main Nursing Concern: - Monitor I’s&O’s + fluid state - Diuretics - IV albumin - Corticosteroids - Diet = decrease sodium, fluids and protein - Medical Management - Steroid therapy (ie prednisone) at least 4-6 wks - Antacid to prevent gastric complication - Antibiotic therapy - Diuretics (Furosemide or Spironolactone) - Potassium Supplement - Albumin Infusion – in case of massive edema - Colloids: Maybe blood transfusion or plasma depending on hypoalbuminemia - Immunosuppressant drugs ie methotrexate - DIET = high protein, low sodium - protein rich (unless advanced disease state), sodium restricted (esp. when edema present), If decreased salt intake doesn’t help edema may need a water restriction as well. - High calorie, carbohydrate, and protein. Be mindful with low fats for elevated triglycerides during flare ups. WEEK 8: Burn Injuries - Burn Degree/Type - Superficial partial thickness (first degree) = epidermis and portion of the dermis may be injured = blisters: wet, blanching erythema (Ie red, blanchable, blisters and swelling over 24-hrs) - Deep partial thickness (second degree) = epidermis and dermis = fluid filled vesicles red shiny and possibly wet, severe pain, and edema.. Starting to get into nerves, starting to lose sensation - Full thickness (third degree) = destruction of all skin elements and local nerve endings= Coagulation necrosis present, surgery required… Dry, waxy, white or black/brown charred leather hard skin. Insensitivity to pain - Manifestation: - High potassium– cells are getting destroyed and potassium is getting released to be circulating in the blood - Give calcium gluconate first to lower potassium and stabilize heart membrane - Hyponatremia + hypovolemia → sodium follows water - Hypovolemia, decreased CO, edema, decreased circulating blood volume, hyponatremia, hyperkalemia, hypothermia - Management: warm room (80-85F), provide warm IVF and blood product, minimize exposure, cool guard should be provided, lighting - Early fluid resuscitation required for burns >20% of body surface - Potential Complications: acute respiratory failure, distributive shock, acute renal failure, compartment syndrome - Tx: - Escharotomy- used to tx full thickness burns by creating incisions… performed to release pressure, facilitate circulation, and allow healing - Skin grafting- remove healthy skin from one area of the body and moving it to a different place on the body. - Preventing Contractures: PT and OT to achieve full ROM, psychological/psychiatric referral for help coping, stretching exercises, pressure garment - Estimating TBSA (Rule of 9’s) adds up to 100% - Head = 9% - Ant./ Post. = 4.5% each - Arms = 18% combined - L ant./post. R ant./post. = 4.5% each - Anterior Chest + Abdomen = 18% - Ant. Chest = 9% - Ant. Abdomen/belly = 9% - Posterior Chest + Abdomen = 18% - Post. Chest = 9% - Post. Abdomen/belly = 9% - Legs = 36% combined - L ant./post. R ant./post. = 9% each - Groin = 1% - Fluid resuscitation/Parkland Formula - 4ml x kg of body weight x % of body burned - Day 1: ½ of Parkland Formula in first 8 hrs, then ¼ in the next 8hrs and then last ¼ in the last 8 hr Adult GI - Appendicitis - Patho: Caused by luminal blockage in the appendix - Distention, venous engorgement, and accumulation of mucous and bacteria - If left untreated, can lead to gangrene perforation(rupture) and peritonitis - Sx: dull periumbilical pain- RLQ (McBurney’s Point), N/V, anorexia, low grade fever, rebound tenderness + guarding (Positive Rovsing sign) - Tx: appendectomy (laprascopic or open appendectomy procedure), antibiotics and IVF started before surgery - If ruptured or signs of peritonitis or abscess, giving IVF and antibiotics 6-8 hr before surgery to help reduce the possibility of dehydration and sepsis - Keep PT NPO Bowel Obstructions - Simple obstruction: allows blood supply but blockage of intestinal content - Strangulated obstruction: cuts of blood supply - Accumulation of fluids/gas leads to distention - Increased intraluminal pressure from the proximal distention leads to ischemia which can cause perforation - Risk of sepsis and hypovolemic shock Small Bowel Obstruction Clinical Manifestations: colicky pain, vomiting (bilious), no stool Often adhesions - S/SX: Colicky abdominal pain (sudden pain, comes in waves lasting 4-5 min each), N/V, Constipation, Abdominal distention, Hyperactive BS - - Abdominal exam: empty bladder (1), Lay supine (2), Assess for distention and symmetry (3), Auscultate (4), Percussion (5), Palpate (6) Large Bowel obstruction Often cancer Clinical Manifestations: cramping, distention, obstipation (chronic constipation that is characterized by the inability to pass stool despite a strong urge), late vomiting Signs of dehydration and sepsis Tx: NPO, NG tube for decompression, bowel rest, IVF and electrolyte correction, or surgery WEEK 9: - Cleft Lip - Repair at 3-6 months - Feed by bottle with special nipple and a wide base, squeeze cheeks together to create a tighter seal, and sit upright - Post-Surgery: use petroleum jelly, elbow immobilizers to avoid interaction with site, avoid pacifiers, avoid sucking by using syringe post-op - Cleft Palate - Repair at 9-12 months - Feed by bottle with 1 way flow valve, burp frequently to decrease air, and sit upright - Post-Surgery: use petroleum jelly, elbow immobilizers to avoid interaction with site, avoid pacifiers, avoid sucking by using syringe post-op - Pyloric Stenosis - Patho: muscle at the outlet of the stomach, called the pylorus, thickens and narrows, causing a blockage that prevents food from passing into the small intestine. This thickened muscle obstructs the flow of stomach contents, leading to forceful vomiting, dehydration, and malnutrition - S/Sx: - Severe projectile nonbilious vomiting (especially after eating) - Olive-shaped mass in RUQ - Persistent hunger even right after vomiting - Stomach contractions (wavelike contractions- peristalsis of upper abdomen) - Dehydration – sunken fontanels, hypotension, decreased tear production - Changes in BM- constipation - Weight Loss - At risk for metabolic alkalosis d/t losing stomach acid - Intussusception - Patho: one section of the intestine folds into the part next to it, causing a bowel obstruction… "telescoping"... decreased blood flow that is trapped between intestine layers can lead to bowel strangulation that can result in gangrene, sepsis, shock, and death - S/Sx: - Severe abrupt abdominal pain (Fetal position- knees to chest) - Currant jelly stool= contains blood + mucus - Sausage shaped mass- palpable in RUQ - Vomiting, lethargy, wt. loss - Dx + Tx: air enema - Operative: resection of dead bowel and joining of healthy bowel Acute Pancreatitis - Thinking about food increases salivation which causes more pain - Manifestations, what is going on, why are they NPO, why are they in pain, what diet should they be on - Patho: Acute inflammation of pancreas. Spillage of pancreatic enzymes into surrounding tissue causes auto-digestion (Lipase) & severe pain = pancreas is eating itself - Causes: gallstones, alcoholism, hyperlipidemia, drug reactions, pancreatic cancer, infections - Varying severity- mild (edema in pancreas) to severe (ischemia that leads to necrotize) - Hemorrhage d/t rupture of pseudoaneurysms in necrotizing pancreatitis. - Manifestations: - Severe LUQ or midepigastric pain- may radiate to back - Eating/digesting worsens pain - Sudden, severe pain - Discomfort when lying back - Abdominal distention - SOB, DOE, Pulmonary edema - Paralytic ileus - Jaundice - N/V, Fever, Leukocytosis - Hypotension + Tachycardia - Turner’s & Cullen sign = sign of internal hemorrhage/external bruising - Hypocalcemia- tetany/carpal spasm (Trousseau’s sign) - Steatorrhea= foul smelling, fatty stools (sign of liver distress) - Hypokalemia/Hyperkalemia - Complications: - SEPSIS - Pseudocyst lead to abscess, pulmonary complications, CV complications, hypocalcemia (Tetany) → Chvostek and Trousseaus signs - Labs: - Increased amylase, lipase, triglycerides, glucose, liver enzymes, WBC - Decreased calcium - Dx: CT scan - WHY NPO- What aggravates Pancreatitis - Any stimulation of saliva- must be strict NPO, no ice chips - Thoughts of food – Digestion in general - Fatty foods or Acidic foods - Treatment: Supportive Care - Monitor and replace electrolytes (ie Calcium Gluconate for low Ca) - Strict NPO, oral care - NG suction - Fat restricted diet, Pancrelipase at meals - Maintain adequate ventilation (ABC’s) - IVF’s – aggressive hydration (LR, Albumin) - Pain relief- PCA pump, Ketorolac IVP (monitor Kidneys) - PPI (Pantoprazole)- decrease stomach activity - Reduce pancreatic secretions - Surgical drain placement Surgical Therapy - ERCP plus endoscopic sphincterotomy (specific to obstruction, to allow drainage) - Laparoscopic cholecystectomy - Percutaneous drainage - Most belly surgeries you’ll place an NG tube- WHY? - Decrease the risk of aspiration if you suction out contents - Bowel rest, decompression, med administration McBurney’s point, cullens sign, murphy’s sign, gray turner - McBurney’s point= RLQ abdominal pain (also think rebound tenderness) - Sign of appendicitis - Cullens sign= Bruise surrounding the umbilicus - Sign of pancreatitis - Gray Turner= bruise at LLQ/ side of abdomen… back/ flank pain - Sign of pancreatitis - Murphy’s sign= URQ pain/just below ribcage - Sign of inflamed gallbladder Liver Complications - Esophageal varices - What's going to kill them? What is it developed from? - Patho: Weakening of the veins in the wall of the esophagus… dilated veins in lower esophagus - Causes: Portal Hypertension (Liver HTN d/t an obstruction), Cirrhosis scarring that obstructs blood flow to liver - S/sx: Esophageal bleeding, vomiting w blood, bloody stools, decreased BP, Increased HR, (BLEEDING) - WHAT CAN KILL YOU → BLOOD LOSS - Treatment (prevent bleeding & rupture + reduce portal pressure) - Bleeding= stabilize pt. manage airway - Blood products- FFP, pRBCs - Stop the bleeding= balloon tamponade- applies pressure - Vitamin K= to promote clotting - PPI= to reduce stomach acid and reduce irritation to varices (Pantoprazole) - Lactulose and Rifaximin= to manage encephalopathy, get ammonia out of body - Vasopressors= Norepi, vasopressin, Somatostatin (Octreotide) - Others: Avoid alcohol, NSAID, ASA, No Tylenol, EGD to screen - Beta Blockers: propranolol & nadolol to reduce portal HTN… spontaneous bleeding and risk of death… DO NOT GIVE IF ACTIVELY BLEEDING - Liver Disease- Cirrhosis - Patho: extensive damage to liver cells which are replaced by fibrosis and regenerative nodules… liver cells try to regenerate but the process is disorganized and leads to formation of scar tissue. - Causes: HCV infection, NASH, ETOH induced liver disease - Clinical Manifestations: - Early: often asymptomatic, may experience fatigue and hepatomegaly - Late: jaundice, edema, ascites, and larger systemic problems due to the livers ability synthesize proteins and regulate bodily functions. - Complications: Portal HTN → leads to esophageal and gastric varices… also ascites, encephalopathy, and hepatorenal syndrome (liver failure that causes kidney failure due to decreased blood flow to kidneys) - Ascites - Patho: Accumulation of fluid in peritoneal cavity - Cause: Typically by portal HTN associated with cirrhosis - Complications: abdominal distention, hernia, hydrothorax (fluid accumulates in the pleural space causing difficulty breathing) - Tx: Sodium restriction, diuretics, paracentesis - Acute Liver Failure - Patho: rapid onset of severe liver dysfunction with no Hx of liver disease - Cause: Commonly drug toxicity (Acetaminophen) - S/Sx: jaundice, coagulation problems, encephalopathy DKA - Hyperglycemia (>250), ketosis (+ urine ketones), and acidosis (pH600 that causes severe osmotic diuresis, leading to fluid volume deficit - Complication: Seizure, shock, coma, death - Hallmark Signs: polydipsia/polyuria and extreme dehydration - hypotension/tachycardia - Dry mucous membranes - Tx: IVF NaCl - Once insulin therapy has brought CBG to