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Adult health exam 3
oncology, metabolic disorders, GI, transfusions
| Question | Answer |
|---|---|
| Primary components of whole blood | Erythrocytes → RBC’s Platelets Plasma Leukocytes rarely used |
| A single unit of blood contains ____ ml of blood and ___ ml of an anticoagulant | A single unit of blood contains 450 ml of blood and 50 ml of an anticoagulant |
| Homologous (Allogenic) transfusions | Most common When pt gets blood from someone they do not know → unknown donor |
| Autologous transfusions | Pts own blood is collected for future transfusions in advance of procedures Mostly used for orthopedic surgery Any blood not used must be discarded |
| Autologous transfusions advantages | Prevention of viral infections from another donors blood |
| Autologous transfusions requirements | Must have a hematocrit within a normal range to start Must be donated 4-6 weeks in advance in procedure, 1-2 times a week and stop within 72 hours before surgery → pts put on iron supplements |
| Blood Salvage transfusions | self salvage Type of autotransfusion done in emer/OR/trauma used with jehovah witness Equipment to collect blood lost during surgery blood cleaned, filtered, returned to pt as IV infus Cant store b/c bacteria cant be completely removed from blood |
| Directed Donor transfusions | People donate to specific pt Red cross against - donations based on idea of altruism (donating b/c it is the right thing to do) Often done because pt is afraid of getting disease from transfusion → however, not necessarily safer to use people you know |
| Artificial Blood transfusions | Not available Armed services is experimenting |
| Criteria for Blood Donation… | Healthy 17 years or older (<17 parent consent) 110 lbs weight Hgb 12.5 g/dl women 13.5g/dl men Temp<99.6F (37.5) Systolic BP 80-180 and diastolic 50-100 |
| amount of blood in our bodies | 10 pints |
| PRBCs can be stored for | 42 days (@ 4C or 39.2) |
| Platelets stored for | 5 days (room temp, agitated to avoid clumping) Involves apheresis machine during donation Takes longer to donate than donating pint of blood → so less donors for platelets When pts get platelets, they usually get 5-6 units |
| fresh Frozen Plasma (FFP) frozen stored for | 1 year (frozen immediately) FFP has clotting factors Frozen immediately to maintain the activity of the clotting factors Plasma is further pooled and processed into blood derivatives such as albumin, immunoglobulin, factor VIII and factor IX |
| Complications associated with blood donation bleeding | Laceration of vein or excessive tourniquet pressure |
| Complications associated with blood donation Fainting | d/t emotional factors → seeing blood Vaso vagal response to seeing blood Prolonged fasting before donation Pts may experience hypotension or syncope |
| Hematocrit & Hemoglobin normal range | Ballpark Hct: 35-45% with women and 40-50% with men Hgb: 12-15 gm/dl with Men slightly higher 3: 1 Ratio…Hct to Hgb |
| Platelet Count normal range | 150 K to 350 K(thousand) |
| Why transfuse platelets? | Platelets transfused usually with thrombocytopenia → low platelet count → risk pf bleeding Transfusing clotting factors(FFP) → FFP to start cascade of clotting Pts with liver disease or cirrhosis may need clotting factors because liver makes clot fact |
| clotting factors what to monitor | PT 9-11 seconds INR 1 second PTT 25-35 seconds |
| why do we transfuse PRBC | increased O2 carrying capacity of blood or to replace blood loss Active bleed |
| symptoms requiring PRBC transfusion if HCT <25% | Feeling tired No energy Tachycardia Low BP SOB pallor |
| why do we transfuse platelets | increase thrombocytes |
| why do we transfuse FFP | increase clotting factors |
| Febrile transfusion reaction | Temperature increase of >2 degrees F from start of transfusion Do full set of vitals at start of transfusion If this happens, nurse must stop transfusion and work pt up for transfusion reaction |
| Allergic transfusion reaction | urticaria, pruritus, flushing |
| Hemolytic transfusion reaction | fever & chills, low back pain, SOB, weezing, feelings of doom, chest pain, dark urine(d/t lysis of RBC) Most serious |
| TACO | transfusion associated circulatory overload an occur when blood is transfused too quickly → hypervolemia can occur |
| Signs of fluid overload include | Dyspnea → related to pulmonary edema Tachycardia Orthopnea Increased BP Anxiety |
| Transfusion-related acute lung injury(TRIALI) | Usually occurs with transfusions of platelets or plasma Human leukocyte antigen (HLA) or human neutrophil antigen(HNA) involved S&S SOB Acute onset hypoxia can be fatal |
| PRBC usual transfusion rate | Usually transfuse at rate of 250-375 ml/1-3 hours |
| Indirect Coombs | Coombs test when you mix donor and recipient blood and check for reaction test good for 48 hours→ must be typed and cross-matched again if more than 48 hours because people are always changing → may get new allergy, etc. new type/cross every 48-72 hrs |
| what guage do we hang blood with | 22 gauge tubing |
| how long can blood run for | 4 hours max |
| transfusion when to take vitals | Take first set of vitals at start of transfusion Ask pt about symptoms → itching, trouble breathing, SOB Take vitals at end of 15 minutes |
| Expected Results for PRBC transfusions for each unit transfused | Increase of 3% Hct and 1 gm Hgb for each unit of PRBC Draw the blood 2-4 hours after transfusion NOT earlier → any earlier will not show change in HCT Is HCT and hgb trending in right direction |
| signs of a reaction | Fever: an increase in T of 2 degrees F or more Assess for Itching, rash, flushed face & chest Chills, Rash, Back pain, “feel funny,” wheezing, chest pain, tachycardia, hypotension |
| what to do when there is a febrile reaction | STOP the blood Take down blood & IV tubing→ flush the line→ then replace it with new IV tubing and NS → take vitals→ call the doctor dminister tylenol and benadryl 30 minutes before subsequent transfusions |
| what to do when there is a allergic reaction | STOP the blood Take down blood & IV tubing→ flush the line→ then replace it with new IV tubing and NS → take vitals→ call the doctor administer benadryl 30 minutes prior to next transfusion |
| what to do when there is a hemolytic reaction | STOP the blood Take down blood & IV tubing→ flush the line→ then replace it with new IV tubing and NS → take vitals→ call the doctor give fluid bolus, maybe epinephrine and lasix to clear everything through the kidney |
| When to transfuse platelets | Platelet count is < 20,000 OR Platelet count is < 50,000 and patient is bleeding |
| platelet transfusion expected response | Increase of 5000 to 10,000 units per unit of platelets |
| FFP transfusion expected response | decreased INR, PT, PTT |
| Achalasia | When there is absent or ineffective peristalsis of the distal esophagus → failure of esophageal sphincter to relax in response to swallowing with gradually increasing dilation of the esophagus in the upper chest |
| causes of achalasia | Scar tissue Chronic reflux that can change the cell structure in esophagus |
| Pathophysiology of achalasia | Spasm of LES and dilation of lower esophagus |
| Symptoms of achalasia | Dysphagia→ difficulty swallowing May feel like heartburn(pyrosis), pain, potential for aspiration(pts can vomit but can't swallow), may have reflux related chest pain Pain aspiration |
| achalasia nursing interventions | Educ – eat slow(chew well), fluids w/meal to wash food down Assess for comps of surgs → education on procedure, (tubes, etc.) Potential comps include… Perf/nicking of the esophagus → watch for bleed, vomiting blood Evaluate for dysphasia |
| achalasia diagnosis | X-ray Studies Barium swallow CT Scan Endoscopy Manometry |
| Barium swallow | Pt NPO 6 hours before test White chalky substance Pts put on tilt table, swallows barium, then are tilted as x-rays are taken sees flow of barium and where its getting stuck Barium causes constipation → drink water eat more fiber |
| Manometry | To measure pressure in esophagus → tube with pressure sensors inserted into esophagus usually through nose Helps confirm diagnosis is stricture or narrowing is seen on images |
| tucking the chin helps... | prevent aspiration |
| achalasia treatment | Pneumatic dilation Surgery Botox |
| Pneumatic dilation | Guidewire inserted and then dilator(ballon) is passed through guidewire and is blown up when in the narrow area → blows up and builds pressure to dilate narrowed area Can be done on outpatient basis or patient may be admitted if pt is at risk for comps |
| Botox for achalasia | Injected into quadrants of esophagus via endoscopy Inhibits contraction of smooth muscle disadvantage→ must go quarterly (every 3-4 months) for this to be effective |
| Nutcracker esophagus | Excessive contractions in the smooth muscle of the esophagus and the stomach(tightening or spasm of smooth muscle of stomach and intestine) |
| Nutcracker esophagus S&S | Dysphagia Chest pain Odynophagia → pain with swallowing in chest |
| Nutcracker esophagus treatment | Nitrates (nitroglycerin SL) Calcium channel blockers (verapamil) Meds help relax muscles of the esophagus and stomach |
| Sliding hiatal (type 1 or diaphragmatic) | Muscle weakening in esophageal hiatus→ supports in lower portion of esophagus loosen and portion of stomach can rise up through hiatus and sit on top |
| Sliding hiatal (type 1 or diaphragmatic) S&S | Heartburn (pyrosis) Regurgitation (vomiting) Chest pain Dysphagia Belching |
| Paraesophageal (type 2) | Fundus and/or portions of stomachs greater curvature slide through the esophageal hiatus and into thorax |
| Paraesophageal (type 2) S&S | Feeling of fullness after eating → stomach is smaller b/c portion of stomach is herniated Breathlessness after eating Feeling of suffocation Chest pain that mimics angina Worsening of manifestations in a recumbent position |
| Volvulus | Twisting of herniated part of stomach Can cause ischemia and necrosis Can also occur in intestine |
| Paraesophageal (type 2) complications | volvulus Anemia may occur - If obstruction, then could be oozing or bleeding→ gastric mucosa itself can be engorged and ooze blood → anemia |
| hiatial hernia diagnosis | Barium Swallow with Flouroscopy EGD(Esophagogastroduodenostomy) Chest CT scan |
| EGD(Esophagogastroduodenostomy) | Endoscopy where tube with camera is inserted through esophagus into the stomach and then into the duodenum Takes a look at all the segments to try to see where the problem is Also called an upper GI endoscopy |
| hiatial hernia Nursing interventions | Frequent small feeds Edu pt not to recline for 1 hour after eating Edu to elevate HOB Try to do more conservative interventions before surgery like medications, small meals, more fluids → if opt does not respond then surgery may be needed |
| hiatial hernia surgical interventions | nissen fundoplication surgery Surgeon goes in and wraps and then sutures gastric fundus around the esophagus → lowers esophageal sphincter area to below the diaphragm so the stomach can no longer herniate |
| hiatial hernia pre-op interventions | Small feedings with fluid Pts with hernia should not lay down after eating → Worse heartburn elevate HOB with 4-8 inch blocks |
| hiatial hernia post-op interventions | NG tube care Elevate HOB Incentive spirometer turn, cough, and deep breathe Pain medication Assess for dysphagia Antacids mobility simethicone for gas Assess respiratory status Monitor/treat complications: abdominal bloat syndrome Diet/meds |
| hiatial hernia post-op NG tube care | so stomach not distended and pulls on sutures Monitor drainage/secretions make sure NG is patent Mouth care bowel sounds no irrigation of NG |
| Gastro-esophageal Reflux Disease (GERD) | Inflammation of esophageal and gastric tissue → can be r/t chronic reflux of stomach or duodenum acids → can cause changes in tissue over time → can cause dysplasia(change in structure of tissue) in esophagus, which can be a precursor to a malignancy |
| GERD causes | Increase in production of gastric acid Decrease in emptying of gastric contents Decrease in pressure of lower esophageal sphincter which allows acid and foods to rise and go into the sphincter into the distal esophagus |
| GERD risk factors | Obesity → when overweight, pt is putting extra pressure on diaphragm and creates pressure that weakens the tissues → reflux Sedentary lifestyle |
| GERD patho | Incompetent LES Hiatal Hernia |
| GERD symptoms | Dyspepsia (indigestion, Heartburn) Dysphagia(difficulty swallowing) Pyrosis (burning sensation in esophagus) Odynophagia (painful swallowing) Reflux Esophagitis Eructation(burping) Water brash (hypersalivation) N&V Unexpected weight loss |
| GERD complications | Esophageal strictures Barrett’s Esophagus Bronchospasm Aspiration |
| Barrett’s Esophagus | Change in cell structure in esophagus → more column shape rather than square shape Premalignant condition → can become esophageal cancer Dysplasia is abnormal cell → not cancer, but may become cancer Mucosa becomes red and inflamed as opposed to pink |
| Barrett’s Esophagus Treatment | Long term PPI → PPI usually not taken for more than 3 weeks, but long term PPI is less risk than cancer Monitor weight F/u endoscopy q 6 months Photodynamic therapy → ablation(killing) to remove barrett's esophagus tissues and dysplasia Esophagectomy |
| Factors that exacerbate GERD | Recumbent Position → should wait 2 hours after eating before laying down Avoid Large Meals Alcohol Caffeine Nicotine Mint Carbonated beverages Acidic foods and beverages |
| GERD diagnosis | endoscopy |
| GERD treatment | Proton Pump Inhibitors (PPI) H2 Blockers Antacids PRN(H2 receptor antagonists) Prokinetic agents (GI stimulants) Antinausea meds Elevate HOB Lifestyle Changes |
| PPI for GERD | Reduce production of hydrochloric acid which reduces chance of reflux Give before meals |
| H2 blockers for GERD | Reduce production of hydrochloric acid Don’t give at same time as a PPI Pepsin, zantac, tagamet Long duration → 6-10 hours as opposed to 1-2 hours with antacids |
| Prokinetic agents (GI stimulants) for GERD | accelerate gastric emptying → GI stimulants → increase gastric motility |
| Esophageal Cancer risk factors | Smoking Barrett's esophagus GERD Excessive alcohol |
| Esophageal Cancer Symptoms | Dysphagia Reflux Weight loss (r/t dysphagia/reflux, tumor chems decrease appetite) Sensation of mass in throat Painful swallowing Substernal chest pain/fullness Regurgitation of undigested food, foul breath, hiccups obstruction as the tumor grows |
| Esophageal Cancer Diagnosis | Barium Swallow with UGI Series EGD w/biopsy and brushing CT scan, PET scan (to look for metastatic disease) PET shows glucose uptake To let oncologist know if cancer has spreas Endoscopic U/S (detect spread to lymph) |
| Esophageal Cancer Treatment | Early stage – cure often not diagnosed until late stage Often late stage – symptom management (surgery, radiation, chemo or combination) Radiation to shrink tumor Chem: Cisplatin, 5FU → to treat systemic disease Surg 5-6 weeks after chemo/radiation |
| Pre-op Esophagectomy Nutritional management | These pts will lose weight so must get them protein, PEG, JT tube to help nut stat before surg mon caloric intake - need high caloric, high protein intake, increase weight, PEG/JT may be used for 2-3 weeks prior to surgery to improve nutritional status |
| Patient Education preoperatively Esophagectomy | Post-op NGT with suction possible Chest Tube d/t mult incisions in chest TPN b/c pt having major surgery - not enteral → do not use gut Gastric Intubation place in a Fowler’s position to prevent reflux, may be abdominal and neck incisions |
| Transthoracic and Transhiatal esophagogastrectomy | Taking out esophagus and stretch stomach so upper portion of esophagus is connected to the stomach 6 hour surgery |
| colon interposition | Taking piece of colon and connects to upper esophagus Radical, only for otherwise healthy clients after a period of nutritional support, high mortality rate, high risk of chyme leaks at sites of resection |
| Postop Esophagectomy Issues respiratory | Risk of Atelectasis, PNA, Pulmonary Edema Assess for fever, dyspnea, crackles Turn cough and deep breathe hourly HOB in fowlers to prevent reflux and aspiration May have chest tube if thoracic approach used |
| Postop Esophagectomy Issues pain | Assess for fever, elevated WBC Is incision site infected Is there drainage→ is it purulent or clear? |
| Anastomotic Leak | Leak at where upper esophagus and stomach or colon is now attached → leak can start to come out of incision Initially will see drainage is bloody and then green colored |
| S&S of an anastomotic leak | Fever SOB Dyspnea (difficulty breathing) Tachypnea Chest pain Gastric contents or saliva coming out of the neck incision |
| Postop Esophagectomy Issues bleeding | Likely to be a GI bleed Monitor NG tube drainage → if bright red or brown, then likely a hemorrhage Melena(bloody stool) → black tarry stool if bleeding in stomach or below(like duodenum → this is digested blood) Monitor H&H |
| Postop Esophagectomy Issues aspiration | Pt in fowlers when feeding begins 6 small meals daily |
| Postop Esophagectomy Issues nutrition | NPO for 7-14 days Fed with TPN When NG tube is d/c’ed watch patients weight, check albumin levels, check for peripheral edema |
| Gastritis | Inflammation of gastric of stomach mucosa Disruption of protective mucosal barrier Secretes bicarbonate and mucous Damage by HCL acid, pepsin |
| Gastritis risk factors | Alcohol Smoking NSAIDS, ASA, Corticosteroids Helicobacter Pylori infection (H pylori) Physiological Stress |
| Gastritis symptoms | Pain Nausea/Vomiting → vomiting blood Upper GI bleed Can get superficial ulcers that can lead to hemorrhage |
| Gastritis diagnostics | EGD →mucosa is edematous and hyperemic H pylori C13 urea breath test serum anti-H pylori antibodies IgG(blood test) H+H→ these patients will become anemia d/t hypemic state of stomach |
| Gastritis treatment | Treat H pylori Administer PPI Eliminate causative factors Teach about bland diet if they eat a spicy food diet |
| Triple Therapy for H. pylori | 2 antibiotics and a PPI Amoxicillin Clarithromycin (Biaxin®) PPI 10-14 day course Pt symptoms should dissipate after treating H. Pylori |
| quadruple Therapy for H. pylori | 2 antibiotics, PPI, and bismuth PPI Tetracycline Metronidazole (Flagyl®) Bismuth → not really understood why bismuth is toxic to H. Pylori but it is |
| Peptic ulcer disease | Complete erosion of GI mucosa Esophagus, stomach, or duodenum ulcer can occur |
| Gastric Ulcers | Pain aggravated by food Highly associated with NSAIDS Pain L of the midline/ upper epigastrium |
| Duodenal Ulcers | Pain between meals Relieved with food/antacids Pain R of epigastrium More common in males People with blood Type O are more likely to have duodenal ulcers |
| Stress Ulcers | Transient ischemia associated with hypotension, burns, trauma etc. |
| Gastric Ulcers symptoms | Reflux of blood if a bleeding ulcer→ hematemesis Weight loss HCL → normal or hyposecretion Pain ½ hour to 1 hour after meals Vomiting Eating increases pain |
| Duodenal Ulcers symptoms | Bleeding in stool if a bleeding ulcer since it is below sphincter → melena Pain 2-3 hours after meals Food decreases pain |
| Stress Ulcers symptoms | Physiological stress shock Cushing's ulcer→ brain injury Curling's ulcer → extensive burns → will prophylactically treat burn victims with medication to prevent ulcer formation |
| Peptic ulcer disease risk factors | Medication H Pylori ETOH Tobacco (smoking) Zollinger-Ellison Syndrome NOT food associated Stress, anxiety, gram negative bacteria ingested in food, chronic use of NSAIDS |
| PUD S&S | Dull gnawing pain Burning in midepigastric area Heartburn Vomiting gero less liklely to have pain |
| PUD Diagnostics | Barium study Endoscopy → EGD Biopsy of ulcer H pylori IgG(blood test) H Pylori breath test CBC, CMP, Amylase Lipase(pancreatic enzymes) |
| PUD treatment | depending on cause PPI Sucralfate (Carafate®) H Pylori therapy Lifestyle modification Surgery (Rare) if needed |
| complications of PUD | Upper GI Bleed Perforation Gastric outlet obstruction(GOO) |
| Upper GI Bleed symptoms | Hematemesis Coffee ground emesis Melena Syncope, dizziness Anemia |
| Upper GI Bleed managment | Vital Signs Labs Fluid Replacement Transfusions CVP Monitoring (central venous pressure monitoring) H+H Every 6 Hours Urine Output Supplemental O2 Prep for Endoscopy → to diagnose Medications surgery recumbant position to perfuse brain |
| Intra-arterial vasopressin (ADH) | Effective for patients with gastric hemorrhage Catheter is introduced into superior or inferior mesenteric artery and the ADH is administered |
| PPI for upper GI bleed | Decrease splanchnic blood flow and acid secretion |
| Saline lavage | washing out body cavity → to remove clots or acids |
| Perforation S&S | Abdominal pain Fever Chills sepsis/septic shock Sudden severe pain radiating to shoulder Board-like abdomen Absence of bowel sounds |
| Perforation Treatment | Antibiotics Surgery |
| Perforation Post-operative nursing care | Broad Spectrum Antibiotics NPO NGT to decompress the stomach Management of incision and drains IV fluids/ fluid balance/ electrolytes Pain→ medication Prevention of complications |
| Gastric outlet obstruction(GOO) | Obstruction of the pyloric sphincter Scarring from chronic reflux can be cause of GOO |
| Gastric outlet obstruction(GOO) S&S | Vomiting → obstruction of sphincter so food won't go anywhere |
| Gastric outlet obstruction(GOO) treatment | NG tube Replace Fluids/Lytes Surgery if fails to resolve |
| Billroth I (gastroduodenostomy) | Partial gastrectomy with anastomosis to duodenum Removal of lower portion of the stomach and small portion of duodenum are removed Remaining duodenum is then anastamized to the stomach |
| Billroth II (gastrojejunostomy) | Partial gastrectomy with anastomosis to jejunum Removal of lower portion of stomach which is then anastomosis to jejunum Duodenal stump remains |
| Vagotomy | Severing of branches of vagus nerve |
| Gastric cancer Dietary risk factors | Smoked, salted or pickled foods Diet low in fruits/vegetables |
| Gastric cancer risk factors | Chronic inflammation of stomach H. pylori infection (or chronic PUD related to H. Pylori) Pernicious anemia Smoking Gastric ulcers and polyps Previous subtotal gastrectomy Genetics Hx of GERD or barrett's esophagus diet risk factors |
| Gastric cancer Diagnostics and treatment | EGD w/biopsy Id polyp seen, may remove it If tumor seen, will biopsy it CT scan Surgery for resection of tumor or palliative treatment (chemo) Billroth I Billroth II Ofr partial or total removal of the stomach(gastrectomy) |
| Gastric cancer | Pain management Respiratory management Potential for Injury r/t abdominal distension amb bleeding or leak Ileus F/E management Reducing anxiety → always an issues with patients having major surgery nutrition Risk of DVT psychosocial support |
| Gastric cancer Complications | Dumping syndrome Reflux gastritis Delayed gastric emptying Post-Prandial Hypoglycemia Drop in glucose after dumping syndrome Post-Prandial Hypoglycemia, Vit deficiencies: B12, Folic Acid, iron, calcium, vitamin D |
| dumping syndrome | Physiologic response when there is a rapid emptying of gastric contents into the jejunum so if less of stomach present or no stomach, then bolus of food goes very quickly to jejunum |
| dumping syndrome patho | Hyperosmolar bolus enters intestine fluid shift to jejunum from vasculature to decrease [con] of food → body's attempt to make food iso With all the fluid pulled out of vascular, pt will become hypovolemic (s&s d/t hypovolemia) hypotension and diarrhea |
| dumping syndrome symptoms | Weakness Dizziness hypotension Vertigo Diaphoresis Tachycardia Heart palpitation Abdominal cramping Diarhea Occurs 15-30 minutes after eating Epigastric fullness Self-limiting body adjusts over time |
| dumping syndrome treatment | Isotonic fluids No stomach, so no intrinsic factor made→ will need long term B12 injections |
| dumping syndrome pt education | Small frequent meals No fluids with meals Avoid concentrated carbs(high carb like bread, potatoes) Low carb, low fat, high protein diet Semirecumbent position with meals to slow food(do not want gravity to take over) → do not put in high fowlers |
| Duodenal cancer | Often not discovered until metastasis occurs → why pts get endoscopy after certain age → often not discovered until symptoms occur |
| Duodenal cancer symptoms | Can be asymptomatic or w/intermittent pain Occult bleeding, blood in stool Sustained weight loss N&V |
| Duodenal cancer N&V complications | Dehydration Electrolyte Imbalances Alkalosis → because vomiting gastric acid Aspiration risk |
| Duodenal cancer N&V nursing assessment | Character of emesis→ color, volume Precipitating factors → are they vomiting after they eat or certain foods Associated symptoms/other symptoms Fluid/Electrolyte balance |
| Duodenal cancer N&V treatment | Address underlying cause Antiemetics If one antiemetic doesn't work, can try another Monitor electrolytes |
| Duodenal cancer N&V medications | Phenothiazines: Prochlorprazine (Compazine) Prokinetic agent: Metoclopromide (Reglan) Antihistamine: Promethazine (Phenergan) Serotonin 5HT3 Receptor Antagonist: Ondanseton (Zofran) |
| liver functions | Storage: glucose, vitamins B12, D, K, copper, & FE Degradation: insulin, bilirubin, ammonia, drugs Metabolism: carbs, lipids Synthesis: albumin, coag factors, CRP, hormones, pro-hormones, proteins, non-essential amino acids |
| ALT normal range | 22-29 for males, 19-25 for females |
| AST normal range | 10–40 in males, 9-32 in females |
| Alkaline phosphatase normal range | 45 – 115 in males, 30 – 100 in females |
| Bilirubin total normal range | 0.0 – 1.0 mg/dL |
| Bilirubin direct | 0.0 – 0.4 mg/dL |
| Serum albumin | 3.3 – 5.0 g/dL |
| AST | present in the liver and other organs including cardiac muscle, skeletal muscle, kidneys and brains, |
| ALT | present primarily in the liver making it a more specific marker of hepatocellular injury Elevated ALT should be assessed for underlying liver disease |
| serum Alkaline phosphatase | derived from liver and bones, liver source can be confirmed with comparison to other lab results, lalso raises in third trimester of pregnancy |
| acute hepatitis patho | Virus targets hepatocytes In acute phase many hepatocytes destroyed→ liver-related dysfunctions→ Affects detoxification/processing of drugs, hormones, metabolites→ effects bile productions, coag, blood glucose reg, protein reg |
| Chronic hepatitis patho | insidious→ symptoms develop slowly persistent and continual destruction of infected hepatocytes Scar tissue develops→ fibrous tissue is not functioning tissue, so less functioning tissue→ Fibrosis & compromised function → Cirrhosis & liver failure |
| hepatitis Systemic effects | Antigen & antibody complexes circulate Immune complexes activate the complement system Cause rash, angioedema, arthritis, fever, malaise Cryoglobinemia(abnormal proteins in the blood), glomerulonephritis, vasculitis, involvement of other organs |
| Acute Hepatitis S&S | asymptomatic if symptoms, lethargy, nausea, vomiting, skin rashes, diarrhea, constipation, malaise, fatigue, myalgias, arthralgias, RUQ tenderness Anorexia, loss of appetite → May have decreased sense of smell & decreased appetite |
| Acute Hepatitis physical exam | Hepatomegaly(enlargement of liver) lymphadenopathy(enlargement of lymph nodes) abdominal tenderness May have splenomegaly jaundice, bilirubinuria pruritis |
| acture hepatitis maximal period of infectivity | acute phase |
| Chronic Hepatitis S&S | Anemia, coagulation problems(easy bleeding, bruising), spider angiomas, palmar erythema, gynecomastia(enlargement of breast especially in men) May have spleen, liver, or cervical lymph node enlargement |
| hepatitis Risk factors for progression to cirrhosis | Male sex Alcohol use Concomitant fatty liver disease Excess iron deposition in the liver → often caused by hemochromatosis |
| treatment for acute hepatitis | No specific treatment Supportive treatment reduces metabolic demands on liver & promotes regeneration Avoid alcohol Notify contacts on transmission May use antihistamines for itching(benadryl) & antiemetics for nausea(Zofran) |
| HAV transmission | Transmitted fecal-oral route or sexual transmission Incubation of 28 days but can range from 15-50 days |
| HAV S&S | Abrupt onset n/v, anorexia, fever, malaise, abdo pain later dark urine(bilirubinuria), pale stools Progresses to jaundice and pruritis which peaks in 2 weeks n/v, anorexia, fever, malaise, abdominal pain will go away from jaundice starts |
| HAV treatment | No specific treatment Supportive care, caution with medications that are metabolized by liver or those that can cause liver damage Primary prevention with vaccination is goal |
| HAV prevention | Preventable with vaccination, infection causes lifelong immunity In children can give 2 dose series starting at 12 months If somebody is infected, provided life long immunity One dose antigen vaccine often used with outbreaks |
| HAV prophyaxis | HAIG given 1-2 weeks post exposure or pre-travel gives immunity for 2-3 months |
| HAV outcome | Recovery can take 2-3 months, occasionally as long as 6 months may relapse within 6 months |
| HAV physical exam | jaundice, hepatomegaly, RUQ tenderness, possibly splenomegaly, skin rash, arthralgias |
| HAV labs | elevated LFTs Diagnosed with presence of serum IgM anti-HAV antibodies → detectable from symptom onset and peak in acute phase and remain detectable for 3-6 months anti-HAV IgG antibodies→ pt now immune anti-HAV IgM antibodies→ current infection |
| HAV risk factors | People who use drugs (injection and non-injection) People experiencing unstable housing or extreme poverty Men who have sex with men People who are or recently were incarcerated People with chronic liver disease(cirrhosis, hepatitis B, hepatitis C) |
| HBV transmission | Blood-borne pathogen can cause acute or chronic hepatitis Detected in almost every bodily fluid→ blood → lower levels found in semen, vaginal secretions, saliva Can survive in the environment up to 7 days Incubation period lasts 1-4 months |
| HBV S&S | Acute: approx 70% have subclinical illness(meaning they don't have symptoms and it is self-limiting) If symptomatic: anorexia, nausea, jaundice, RUQ discomfort, rash, arthralgias Can ast 1-3 months Prolonged fatigue |
| HBV treatment | supportive care for acute HBV antivirals, interferon |
| HBV prevention | universal vaccination of infants and those who have not received it 3 dose series→ 1 at birth, 2 one month after birth, 3rd 6 months after 1st dose Must start whole series again if you do not get 3rd dose 6 months after 1st |
| HBV prophyaxis | immnune globlin (HBIG) within 24 hours of exposure |
| HBV outcome | may be severe, carrier state possible, increased risk of chronic hepatitis, cirrosis, liver cancer |
| HBV labs | elevated ALT and AST (ALT > AST) Serum bilirubin remains normal Labs return to normal in 1-4 months Elevated ALT for more than 6 months means person is progressing to chronic HBV |
| HBV immunity labs | HBsAg: surface antigen → indicates presence of virus Anti-HBs: antibody to surface antigen→ indicates immunity Can do titer for Anti-HBs to determine that pt either has been vaxed/was infected and now immune |
| HBV antivirals | Long-term antiviral therapy (Tenofivir, Entecavir) → end in “-vir” |
| HBV interferon | naturally occurring immune protein made by body during infection respond to pathos injection weekly for 48 weeks side effects: flu-like symps, depression, bone marrow suppression(monitor CBC and LFT every 4-6 weeks) Monitor CBC & LFTs every 4-6 weeks |
| HCV transmission | Blood-borne pathogen can cause acute and/or chronic infection Injection drug use Men who have sex with men Needle stick exposure |
| HCV S&S | similar to HBV but less severe rash, arthralgias |
| HCV treatment | Drug regimen is complicated → lots of factors involved Chronic HCV Goal: eradicate virus and prevent complication Administer direct acting-antiviral block proteins needed for HCV replication Usually 12 week regime |
| HCV prophyaxis | no post exposure prophyaxis |
| HCV prevention | no vaccine |
| HCV outcome | frequent occurence of liver disease and carrier state increased risk of liver cancer |
| HCV labs | elevated ALT/AST HCV viral load measurable 1-2 weeks after inoculation Anti-HCV antibody indicates presence of HCV in body, nonspecific to infection stage or immunity Antibodies dont provide immunity |
| cirrosis | End stage of liver disease Extensive degeneration and destruction of liver cells→ replaced by scar tissue(fibrosis which is not functional) Fibrosis, regenerative nodules form |
| cirrosis patho | Liver cells try to regenerate but the process is disorganized Abnormal blood vessel & bile duct architecture Overgrowth of new and fibrous connective tissue distorts structure Lobules of irregular size & shape Impeded blood flow |
| cirrosis early S&S | few symptoms May be fatigued, may have enlarged liver Labs will usually be normal → body can compensate |
| cirrosis late S&S | Jaundice, periph edema, ascites, Spider angioma, Palmar eythrocemia, Thrombo/leukopenia, anem, epistax, purpura, peticehea, gum bleed, heavy menses, gynecomastia, loss of axil/pub hair, testicular atrophy, impotence, libido loss, anovulation, Perip neurop |
| cirrosis labs | Initially LFTs elevated due to release from inflamed liver cells At end stage AST & ALT may return to normal d/t death and loss of hepatocytes Low albumin High serum bilirubin & globulin Prolonged PT |
| cirrosis diagnostics | Ultrasound→ not diagnosis but can look at nodes, examine liver Biopsy → diagnostic |
| cirrosis complications | Peripheral edema Hepatorenal syndrome Abdominal ascites Hepatic encephalopathy Portal hypertension |
| cirrosis Treatment | TIPS Na restriction ballon tamponade if bleed lactulose transplant |
| TIPS | Transjuglar Intrahepatic Portosystemic Shunt Nonsurgical placement of shunt between systemic & portal venous system to redirect portal blood flow Helps reduce portal venous pressure & decompresses varices(no need for side roads) |
| cirrosis Na restriction | 2g or less per day |
| Paracentesis | nserting catheter into peritoneal cavity to withdrawal of fluid from peritoneal cavity Done with severe ascites causing pain, pressure, and/or difficulty breathing not relieved with diuretics |
| Lactulose | given PO or via enema bright orange, sticky medication will make pt have BM traps ammonia in gut and reduces formation in intestines→ expels ammonia through feces Antibiotics (Rifamixin) - If not responding to lactulose |
| cirrosis Magnesium sulfate | To correct mag levels that may be off d/t liver dysfunction |
| Octreotide (Sandostatin) or vasopressin | to control variceal bleeding with cirrosis |
| Functions of the pancreas | Exocrine function for digestion Produce enzymes Trypsin and chymotrypsin → digest protein Amylase → digest carbs Lipase→ digest fats Endocrine function for blood sugar regulation Islet cells create and release insulin and glucagon |
| Acute Pancreatitis | Acute inflammation of the pancreas Spillage of pancreatic enzymes into surrounding pancreatic tissue cause autodigestion of pancreas → severe pain |
| Acute Pancreatitis patho | Inciting event: gallstones, alc abuse, hypercalcemia → Abnormal activation of digestive enzymes (trypsinogen→normally converted to trypsin in duodenum)→converted while still in pancreas → activation of enzymes in pancreas→ digestion of pancreatic tissue |
| Acute Pancreatitis S&S | Abdominal pain Nausea, vomiting, low grade fever Leukocytosis Hypotension, tachycardia, jaundice, abdominal tenderness & guarding Bowel sounds decreased or absent crackles ecchymosis on flanks & periumbilical Cullen’s & Grey Turner’s Signs |
| Acute Pancreatitis labs | Serum amylase & lipase elevated→Amylases rises early, stays 24-72h→Lipase helps to differentiate acute pancreatitis from other causes of elevated amylase CBC: leukocytosis hypocalcemia liver enzymes, blood glucose, serum triglycerides, electrolytes |
| Acute Pancreatitis diagnosics | labs CT imaging→ to check for causes of abdominal inflammation ERCP: Endoscopic Retrograde Cholangio-Pancreatography |
| Cullen’s sign | bloody exudates from inflammation Deep hemorrhagic pancreatic → usually deeper purple than grey cullen Occurs 2-3 days after onset of patho |
| Grey Turner’s Sign | ecchymosis on flank Severe acute necrotizing pancreatitis Can be a/w other retroperitoneal bleeding |
| Abdominal pain in pancreatitis description | O: sudden L: LUQ, radiates to back D: steady & continuous C: severe, deep, piercing A: eating R: not relieved by vomiting T: mild relief over time, but as autodigestion of pancreas worsens, so will pain |
| ERCP: Endoscopic Retrograde Cholangio-Pancreatography | Upper endos→views liv, galblad, panc NPO x4 h, VS, CMP, CBC, coag pan base in proc, can pass instru through→do surg Consc sedation→pt NPO after proc until gag reflex returns High risk pts→clear liq 1st day post-op→reg diet mon for infect, vitals |
| Pancreatic pseudocyst | ccumulation of fluid, pancreatic enzymes, tissue debris, & inflammatory exudate → around wall next to pancreas |
| Pancreatic pseudocyst labs/diagnostics/risks | Serum amylase will be elevated Evaluate with CT, MRI, or endoscopic ultrasound Usually resolve spontaneously within few weeks Risk of perforation of cyst→ can lead to peritonitis or rupture into stomach or duodenum |
| Pancreatic pseudocyst treatment | surgical drainage, percutaneous catheter drainage, endoscopic drainage |
| Pancreatic abscess | infection of pseudocyst Will cause extensive necrosis into pancreas Upper abdominal pain, abdominal mass, high fever, leukocytosis Requires prompt surgical drainage d/t risk of sepsis |
| Antacids for Acute Pancreatitis | To neutralize gastric secretions and decrease production of pancreatic enzymes and bicarbonate |
| PPI for Acute Pancreatitis | Decrease acid secretion |
| antispasmodics for Acute Pancreatitis | Like dicyclomine To decrease vagal stimulation, motility, allow pancreas outflow |
| Carbonic anhydrase inhibitor | To decrease volume and bicarb concentration of pancreas secretion for Acute Pancreatitis |
| Acute Pancreatitis diet | start with small, frequent meals If reports pain with meals, or note increase abdominal girth, increase serum amylase, or lipase stop meals and reevaluate Provide high-carbohydrate, low-protein, and low fat diet as tolerated |
| Chronic Pancreatitis | Continuous, prolonged, inflammatory, and fibrosing process of pancreas Pancreas progressively destroyed & replaced with fibrotic tissue Strictures and calcifications may form Over time, pancreas cannot function properly |
| Chronic Pancreatitis Causes | Chronic alcohol use, gallstones, tumor, pseudocysts, trauma, acute pancreatitis Chronic systemic disease(lupus), autoimmune pancreatitis, cystic fibrosis Idiopathic(no identifiable cause) |
| Chronic Pancreatitis Complications | Pseudocyst, Pseudoaneurysm Bile duct or duodenal obstruction Ascites or pleural effusion Splenic vein thrombosis Pancreatic cancer |
| Chronic Pancreatitis S&S | Abdominal pain→Episodic with recurrent attacks→LUQ, heavy, gnawing/burning/cramp like, not relieved w/ food/antacids S&S of pancreatic insufficiency→Malabsorption with wt loss, constipation, mild jaundice w/ dark urine, steatorrhea, diarrhea, diabetes |
| Chronic Pancreatitis Diagnostic testing | Serum amylase & lipase→may be normal to slightly elevated if lot of fibrotic tissue and little functional tissue left Bilirubin, alk phos, & ESR(non specific indicator of inflammation in body) elevated May do stool sample for fecal fat content ERCP |
| Alcohol Use Disorder | Leads to many cases of acute pancreatitis Impaired ability to stop or control alcohol use → interferes with everyday functioning Mental health disorder |
| CAGE questions | Cut down: Have you ever felt you needed to cut down on drinking Annoyed: Have people annoyed you by criticizing your drinking Guilt: Have you felt guilty about drinking Eye-opener: Have you ever felt you needed a drink first thing in the morning |
| CIWA-Ar Tool | to assess for alcohol withdrawal looks at symptoms and each is graded on scale from not present to severe |
| Alcohol Use Disorder treatment | Treatment of phenobarbital or ativan based on CIWA score |
| Chronic Pancreatitis nutrition | small, frequent meals, low in fat Avoid alcohol, smoking, caffeinated beverages Pancreatic enzyme replacement: Pancrelipase (Pancrease) |
| Pancrelipase (Pancrease) | Contains amylase, lipase, trypsin to replace deficient enzymes Enteric coated to prevent breakdown/activation by gastric acid Pt given pancrelipase with each meal Monitor for steatorrhea to determine effectiveness of enzymes→ less fat if working |
| Gallbladder functions | Stores bile, releases to help with digestion especially of fat |
| Risk factors for cholelithiasis and cholecystitis | Female, multiparous, overweight, over age 40 Hormone treatments→ sometimes done in post menopausal women for symptomatic relief, contraceptive, or meds for transgender transition Men over age 50, overweight |
| Cholelithiasis | stones in the gallbladder → gallstones |
| Cholelithiasis Pathophysiology | Balance that keeps Cholesterol, bile salts, calcium in solution precipitate into stones Cause not fully understood→infection, estrogen Hormonal changes(pregnancy)→delayed emptying of gallbladder→ bile stasis → which can precipitate and cause stone |
| Cholelithiasis S&S | asymptomatic if stones are small enough Crescendo-like pain tachycardia, diaphoresis, prostration Pain attacks→last 1-6 hours Can be precipitated by high fat meal RUQ tenderness r/t inflammation caused by stone dark colored urine w/ obstruction |
| Cholecystitis | inflammation of the gallbladder |
| Cholecystitis patho | Most often a/w obstruction by gallstones or biliary sludge imflammation |
| Cholecystitis Initial symptoms | indigestion and acute pain in RUQ Pain may radiate to R shoulder and scapula |
| Cholecystitis S&S | Nausea & vomiting, restlessness, diaphoresis Inflammation causes leukocytosis, fever |
| Cholecystitis physical findings | RUQ or epigastrium tenderness, abdominal rigidity |
| chronic Cholecystitis S&S | can develop fat intolerance, dyspepsia, heartburn, flatulence over time |
| Diagnostic studies for cholelithiasis and cholecystitis | Ultrasound→ to visualize gallbladder, look for gallstones ERCP percutaneous transhepatic cholangiography Labs |
| Percutaneous transhepatic cholangiography | Inserting needle through skin directly into gallbladder ducts→ injecting contrast material and getting CT to evaluate for duct blockage |
| cholelithiasis and cholecystitis labs | CBC→look for leukocytosis(increased WBC) Serum enzymes(alkaline, phosphatase, ALT, AST), direct & indirect bilirubin level, urinary bilirubin(may be increased if there is obstruction) Serum amylase if pancreatic involvement |
| Subphrenic abscess | Accumulation of infected fluid between diaphragm, liver, and spleen |
| Cholangitis | Inflammation of biliary ducts |
| Fistulas | Chronic pipe like ulcer that can connect gallbladder with biliary tree or even extend into colon |
| ursodeoxycholic and chenodeoxycholic | Bile acids medications To dissolves tones |
| Transhepatic biliary catheter | Used preoperatively for biliary obstruction or for palliative care in inoperative cases(symptomatic relief) Catheter inserted percutaneously Cleanse skin around catheter→ bile acid is irritating to skin Observe for bile leakage around site |
| cholelithiasis and cholecystitis nutrition | Smaller, frequent meals with some fat(to promote gallbladder emptying) Low in saturated fats and high in fiber & calcium Avoid rapid weight loss s/p lap chole: liquids post-op and small meals for next few days Amount of fat depends on pt tolerance |
| Absolute neutrophil count(ANC) → normal range | 3000-7000 (3K-7K cells/mm3) |
| Mild neutropenia is ANC of ... | 1500 |
| Moderate neutropenia is ANC of... | 1000-1500 |
| Severe neutropenia is ANC of... | 500-1000 |
| Neutrophils | mature WBC→ also called segs → < 50-70% |
| Bands | immature WBC |
| ANC formula | WBC count x (% neutrophils + % bands) |
| Neupogen | Growth factor Injection given to promote growth of WBC or neutrophils |
| Angiogenesis | tumors can secrete tumor angiogenesis factor (TAF) → which helps promote growth of blood vessels so cells can break off into blood and lymph system and spread |
| Fibronectin in cancer | decreased fibronectin cells adhere loosely together → risk of cells breaking off(easier to travel) → increased risk of metastasis |
| Pleomorphism | large nucleus relative to cell size |
| alopecia | hair loss related to treatment of cancer |
| nadir | lowest point of white blood cell depression after therapy that has toxic effects on the bone marrow |
| cancer grading grade 1 | degree→ low grade Character → well-differentiated (structure and function still like parent cell) |
| cancer grading grade II | degree→ Intermediate grade character→ moderately differentiated |
| cancer grading grade III | degree→ high grade character→ poorly differentiated |
| cancer grading grade IV | degree→ anaplastic character→ anaplastic |
| staging TNM Tx | tumor cannot be adequately assessed |
| staging TNM T0 | no evidence of primary tumor |
| staging TNM Tis | carcinoma in situ (precancerous but treated as if they are cancerous because these tumors will go on to be cancerous) |
| staging TNM T1-4 | progressive increase in tumor size or involvement |
| staging TNM Nx | regional lymph node cannot be assessed |
| staging TNM N0 | no evidence of regional node metastasis |
| staging TNM N1-3 | increasing involvement of regional lymph nodes |
| staging TNM Mx | not assessed |
| staging TNM M0 | no distant metastasis → chance of cure way higher than if there was spread |
| staging TNM M1 | distant metastasis present specify sites → required more systemic treatment |
| Cryosurgery | instilling liquid nitrogen into the tumor through a probe, e.g. skin cancer |
| Chemosurgery | using corrosive paste with multiple frozen sections to ensure complete removal of tumor.. |
| .Mohs skin surgery | chemosurgery usually to remove cancerous skin lesion in area where they want to keep area as much intact as possible (ears, face) look for clean margin before removing next layer |
| Laser surgery | using a laser beam to resect tumor or raise temperature of tumor cells, destroys cells…e.g. liver tumors |
| Laparoscopic surgery | performing surgery through two small incisions…e.g. lung cancer |
| tamoxifen (NolvadexTM) | anti-estrogen drug for estrogen-receptor positive breast tumors(timor grows in presence of estrogen) After pt treated for estrogen positive cancer→ they will be on tamoxifen for 5-10 years to reduce incidence of recurrence |
| WBC reach nadir in | 7-14 days |
| RBC reach nadir in | may takes weeks to reach nadir(because RBC have longer lives) |
| doxorubicin and daunorubicin | chemo therapies with greater risk of cardiac side effects can cause CHF, Arrhythmias such as sinus tachycardia and PVC’s |
| Dexrazotane (Zinecard) | given to reduce heart damage associated with cardiotoxic chemo (specifically doxorubicin and daunorubicin) |
| Mucositis and stomatitis | inflammation and sores(red, open sores) in pt mouth |
| Magic Mouthwash | contains Lidocaine, maalox, diphenhydramine(benadryl) Helps to numb sores (GI impairment in cancer-stomatitis) Sores get so bad, pt has trouble/pain when eating |
| Palifermin | stimulates epithelial cells Drug given prophylactically→reduces mucositis/stomatitis Given when pt is having bone marrow or stem cell transplant and all chemo that goes along with it → because pt can have terrible mucositis and stomatitis following |
| Dysgeusia | changes in taste of food→ says everything taste like cardboard, metallic |
| chemo drugs that cause alopecia | Adriamycin, 5FU, cisplatin tend to cause alopecia |
| sentinel node | Dye is injected and shows which lymph node receives the most lymph drainage→ that lymph node is the sentinel node |
| breast cancer staging → stage I | tumor < 2cm, no nodes, no mets (metastasis) |
| breast cancer staging → stage II | 2-5 cm, 0-1 nodes, no mets |
| breast cancer staging → stage II | > 5cm, no nodes OR < 2cm with nodes, no mets OR 2-5 cm with nodes no mets |
| breast cancer staging → stage IV | any size, nodes and mets |
| TRAM | Transverse rectus abdominis muscle (TRAM) flap → use abdominal muscle for reconstruction → more complex and longer recovery form than tissue expander procedure |
| DIEP | Deep Inferior Epigastric Perforator (DIEP) flap → more popular→ skin and tissue taken but no muscle taken from abdomen Assess adequate blood flow after any graft |
| frozen shoulder | pt tends to guard area and they do not move shoulder so joint has limited ROM Teach exercises to move joint→ passively then actively |
Created by:
Linds4321