NUR 425 Test 1 Notes PDF

**NUR 425 -- Test 1 Notes** **[Week 1: Digestive System ]** **[Gastroesophageal reflux disease ]** - Syndrome characterized by reflux of gastric contents into lower esophagus - Affects 1/6 canadians - Can be normal -- happens after large/fatty meals - When it's more pervasive GERD...

**NUR 425 -- Test 1 Notes** **[Week 1: Digestive System ]** **[Gastroesophageal reflux disease ]** - Syndrome characterized by reflux of gastric contents into lower esophagus - Affects 1/6 canadians - Can be normal -- happens after large/fatty meals - When it's more pervasive GERD **GERD** - The lower esophageal sphincter (LES) is a ring of muscle at the bottom of the esophagus that acts like a valve between the esophagus and stomach - Incompetent LES allows stomach content to reflux back into the esophagus **Predisposing conditions** - Lower esophageal sphincter (LES) dysfunction stomach acid able to flow back into esophagus - Impaired esophageal motility allows some acid to remain longer in the esophagus - May be d/t neuro conditions, inflammation, meds - In diabetes -- damage to vagus nerve (responsible for controlling esophageal muscles) - Vagus nerve can be impaired by opioids - Delayed gastric emptying if stomach is not able to empty quick enough, there is inc vol and inc pressure - Can be caused by high bp meds, antidepressants, opioids - Increased intra-abdominal pressure pregnancy, obesity, chronic coughing can push stomach contents higher up into esophagus - Hiatal hernia upper part of stomach pushes into diaphragm into chest cavity, disrupting normal pressure barrier b/w stomach and esophagus which will facilitate reflux - Often seen in age-related changes Diaphragm can weaken as ppl age -- makes it easier for stomach to push up into diaphragm - Lifestyle factors and diet - Foods that decrease LES pressure chocolates, etc. - Anticholinergic meds - Pregnant women at inc risk d/t hormone change (progesterone relaxes smooth muscle) **Pathogenesis** - Number of factors that contribute to development of GERD - Defective mucosal defence: esophagus has defence mechanisms to protect it from stomach acid - Esophagus has mucus secreting glands that protects against gastric acid - Reflux, infections, meds, etc. can cause these defence mechanisms to become ineffective - Reflux of gastric contents: something like lying down after large meal can cause this - Small intestine reflux of bile: when bile refluxes into stomach, it can go into esophagus and cause inflammation and damage to esophageal lining - Caused by damage to pyloric valve (separates stomach from duodenum), surgeries (especially anything around the stomach or gall bladder) - LES dysfunction: *refer to above* - Delayed gastric emptying: *refer to above* - Impaired esophageal motility: *refer to above* **Pathophysiology** - Regurgitation of acid contents from stomach into the esophagus esophageal irritation & inflammation; may see corrosion of the mucosa - *Esophagus cannot withstand prolonged exposure to stomach acid* - *In addition to stomach acid, gastric enzymes can further contribute to the damage being caused to esophageal lining* **Clinical Manifestations** - Heartburn (pyrosis): burning sensation in chest or upper central abdo - Need to consider cardiac cause of symptoms -- rule out cardiac issue first - Mild symptoms: occurs once a week - May have respiratory symptoms -- wheezing, coughing, dyspnea - Regurgitation - Early satiety, bloating, N&V - Dysphagia (difficulty swallowing), odynophagia (painful swallowing) **Complications** - **Esophagitis:** inflammation of esophagus - Frequent complication/can lead o other complications - **Dysphagia:** difficulty swallowing - Secondary to esophageal strictures; occurs from esophagitis - Strictures can form overtime when repeated exposure to stomach acid, scar tissue forms in esophagus which can narrow esophagus - **Barrett's esophagus**: esophagitis + esophageal ulceration = changes to esophageal lining - Squamous mucosa gradually replaced by columnar epithelium - Inc risk of esophageal cancer - **Respiratory complications** - **Dental erosion:** may lead to diagnosis of GERD **Evaluation** - **Symptoms** - **Medical Hx:** frequency, duration, diet, lifestyle, meds, previous surgeries - **Diagnostics:** barium swallow, paper endoscopy, biopsy/cytology, esophageal manometry, pH monitoring, radionuclide tests - **Barium swallow:** protrusion of the stomach - **Biopsy/cytology:** Barrett's esophagus - **Manometry:** measure pressure in the esophagus and in LES pH monitoring - *Normal pH around LES is 4-6 (if higher indicates GI problem)* - **Radionuclide:** location/movement of things in the esophagus **How to manage GERD** - Avoiding foods that lead to symptoms -- eating small, frequent meals may be helpful - Losing weight may improve symptoms by decreasing intra-abdominal pressure - Elevating HOB 10-15 cm to promote esophageal emptying - Stopping smoking -- nicotine relaxes LES and irritates and decreases saliva production - Avoiding alcohol -- alcohol impairs peristalsis, promotes acid secretion, affects LES - **Nutrition management** - Avoiding high fat foods: associated with dec LES pressure - Avoiding chocolate, peppermint, caffeine: decrease LES pressure - Avoiding dairy products: associated with inc gastric acid secretion - **Pharmacotherapy** - Antacids -- first line PRN - H2R (Histamine-2-Receptor) blockers decrease acid production -- reduce Cl- release - Proton pump inhibitors **[Peptic Ulcer Disease]** **PUD: Defensive vs Aggressive Factors** +-----------------------------------+-----------------------------------+ | **Aggressive Factors** | **Defensive Factors** | +===================================+===================================+ | **Helicobacter Pylori:** releases | Protect stomach & duodenum from | | a toxin that destroys gastric & | self-digestion: | | duodenal mucosa, reducing the | | | epithelium's resistance to | **Mucus:** forms protective | | acid/pepsin | barrier against attack by acid & | | | pepsin | | **NSAIDs:** inhibit the | | | biosynthesis of prostaglandins; | **Bicarbonate:** neutralizes H+ | | can also irritate the mucosa | ions | | directly | | | | **Blood flow:** maintains mucosal | | **Gastric acid:** can cause | integrity; dec blood flow causes | | direct injury; activates pepsin | local ischemia & cell injury | | | | | **Pepsin:** can cause direct | **Prostaglandins:** stimulate | | injury | secretion of mucus & bicarb, | | | promote vasodilation & suppress | | **Smoking:** may contribute by | gastric acid secretion | | accelerating gastric acid | | | emptying and reduced secretion of | | | bicarbonate | | +-----------------------------------+-----------------------------------+ **Risk Factors of PUD** - **H. Pylori** - Most common cause (but not all ppl with H. pylori will develop PUD) - Secretes an enzyme called urease that creates a protective barrier around the bacteria, which makes it harder to eradicate - Urease generates ammonia in the mucous layer which damages the mucosa and creates a condition of chronic inflammation - This inflammation also makes the mucosa more vulnerable to other noxious substances - Risk factor for gastric carcinoma - If presented with PUD, test for H. Pylori and eradicate - **NSAIDs** (non-steroid anti-inflammatory drugs) - second most common cause - includes aspirin - **Steroids** - **Cytotoxic drugs** - Examples: chemotherapy, agents used in treatment of rheumatoid arthritis - **Alcohol, smoking & drug use** - **Diet** - **Genetics** - Examples: blood group O at increased risk - **Chronic diseases** - **Psychological stress** - **Age** - A viscous cycle that lead to worsening erosions and damage to blood vessels **Clinical Manifestations** **Pain** **Gastric** **Duodenal** ----------------- ----------------------------------------------------------------------------- ----------------------------------------------------------------------------------------- **Location** High in the epigastrium Mid-epigastric region, possibly back **Description** Burning or gassy Burning or cramp-like **Timing** Occurs about 1-2 hours after eating, but can also occur on an empty stomach Usually occurs 2-4 hours after meals. Often occurs at night. May be relieved by eating. **Complications** - **Hemorrhage** - Most common - May present with hematemesis (vomiting blood) or melena (tarry stool) - Signs: tacky & hypo, pale & clammy, dec RBC, altered LOC - **Perforation** - Sudden onset of abdominal pain, Abdomen is rigid, board-like, Tachycardia, Shallow, rapid respirations - **Peritonitis and septic shock** - Tachycardia & hypo, Threads pulse, Cold and clammy, Altered LOC - **Gastric outlet obstruction** - early satiety, bloating, N&V, epigastric pain after eating, weight loss - obstruction can be caused by edema, spasms, etc. **Evaluation** - endoscopy & biopsy (biopsy can identify H. pylori) - urea breath test (can detect H. pylori) - stool antigen test (can detect H. pylori) - Note: prior to testing for H. pylori, ideally PPI therapy should be stopped 1-2 weeks - Barium studies -- lack accuracy - Swallowing barium and x-ray to visual stomach and duodenum - Labs: CBC, LFTs, amylase, fecal occult blood - CBC -- may be increased WBC d/t ulcers, dec RBC - Liver Function Tests -- rule out other diseases - Amylase -- lipase (pancreatic enzyme) -- elevated can be pancreatitis (can mimic peptic ulcer signs) - Fecal occult blood for bleeding ulcers **How to manage PUD** - Treat the underlying cause (e.g. H. pylori, discontinue NSAIDs) - In addition to pharmacotherapy: - Adequate rest - Dietary changes may be needed - Smoking cessation -- smoking irritates mucosa, delays healing - Complete healing (with pharmacotherapy) may take 3-9 weeks - **Pharmacotherapy: antacids** - Short-lasting relief of heartburn - Work by neutralizing hydrochloric acid - Taken 1-3 hours after meals and at bedtime - Not beneficial with moderate-severe symptoms - Examples: aluminum hydroxide, calcium carbonate, magnesium hydroxide - Avoid magnesium preparations with renal insufficiency -- inc risk of electrolyte imbalance and kidney failure - Antacids may interfere with absorption of many medications -- check timing - **H2R blockers** - Block the action of histamine on the histamine2 receptors of the parietal cells - This decreases the secretion of hydrochloric acid by the stomach - Decreases conversion of pepsinogen to pepsin, and helps ulcer healing - Examples: cimetidine, famotidine - Cimetidine is used less often due to multiple side effects & drug interactions - **Proton pump inhibitors (PPIs)** - Gastric proton pump is made up of H+/K+/ATPase - Hydrogen ion, potassium ion, adenosine triphosphate enzyme - This gastric proton pump is in the parietal cells of the stomach, and is needed to produce hydrochloric acid - PPIs block this pump - Most effective drug for suppressing gastric acid secretion - Examples: Lansoprazole, omeprazole, pantoprazole - Treatment should be limited to 4-8 wks - However, there are patients who require long-term therapy - Adverse effects: incl, dec absorption of calcium & magnesium, inc risk of C. diff, vitamin B12 and iron malabsorption - drug interactions: can dec levels of anticoagulants, dec absorption of protease inhibitors (for HIV) - **Treatment of H. Pylori** - **Triple medication therapy:** Proton pump inhibitor, amoxicillin, clarithromycin - **Quadruple medication therapy:** PPI, Bismuth subsalicylate, Tetracycline, Metronidazole (created to maximize eradication of H. pylori) - **Other anti ulcer medications** - **Sucralfate:** forms a barrier over the erosion that protects against gastric acids, enzymes and bile salts - this protective barrier promotes healing - can decrease absorption of other drugs - **Misoprostol:** used with NSAIDs to prevent ulcers - Contraindicated in pregnancy -- causes uterine contraction and leads to miscarriages (also used in abortions) **[Biliary disorders: Cholelithiasis & Cholecystitis ]** - Cholelithiasis - Refers to stones in the gallbladder - Most common disorder of the biliary system - Cholecystitis - Inflammation of the gallbladder - Usually associated with cholelithiasis - Store 30-60 ml of bile concentrated as water is being absorbed by cells of gall bladder -- contract to force the bile to the duodenum after eating **Gallstones** - Can form if the bile being stored has: - Too much cholesterol - Too much bilirubin - Not enough bile salts - Bile hardens into small hardened deposit or stones - No direct reasoning - Suspect of high cholesterol and abnormal metabolism - Most stones are made of cholesterol **Cholelithiasis** - Most individuals with cholelithiasis are asymptomatic - Obstruction can cause spasms (biliary colic) - Obstruction of common bile duct may cause: - - Bleeding tendencies - Clay-coloured stools - Dark amber urine - Inability to tolerate foods that are fatty - Jaundice - Pruritus - Steatorrhea (fatty stools bc no bile to absorb dietary fats) - - Malabsorption of vitamin K (important for clotting) -- bc bile is important for absorption of fat (and fat soluble vitamin, aka Vit K) - Bile gives stool its colour - Pruritus (itchiness) bc of build up of bilirubin **Cholecystitis (inflammation of the gall bladder)** - Most commonly associated with gallstones or biliary sludge - Often caused when gallstones are blocking the gallbladder -- biliary sludge can contribute - Symptoms range from none to severe - Clinical manifestations - Indigestion - Acute pain at RUQ, may radiate to right shoulder and scapula (d/t phrenic nerve from diaphragm to neck) - May have positive Murphy's sign on exam -- pt has pain on palpation around gallbladder area, they abruptly stop breathing - Nausea & vomiting -- d/t inflammation in gallbladder, severe pain, or obstruction - Fever -- d/t inflammation or infection (not common) **Evaluation** - **Ultrasound** - **ERCP** (endoscopic retrograde cholangiopancreatography): used to diagnose conditions of the bile duct and pancreas; flexible tube w endoscope and camera is inserted to visualize and sometimes treat blockages - **Labs**: - bilirubin (high bili jaundice) - LFTs -- assess liver function and detect any abnormalities + elevated liver enzymes , - CBC (to assess for leukocytosis) -- look for signs of infection and inflammation **Cholelithiasis management** - Laparoscopic cholecystectomy: most commonly used for symptomatic cholelithiasis - Extracorporeal shock-wave lithotripsy -- using high energy sound waves to break up the stones. Can be painful. Once broken up, the stones can pass on their own through biliary system - ERCP: can remove stones - Medications - Ursodeoxycholic acid (Ursodiol) can be used to dissolve stones - For pts who can't tolerate or undergo surgery, and prevents gallstones long term - Pain management key part of management - **For acute cholecystitis:** - Admission to hospital & placed on bed rest - Pain management - If vomiting, N/G suction, NPO & IV fluids - Broad-spectrum parenteral antibiotics - The definitive treatment is a cholecystectomy (timing depends on risk factors) - **For chronic cholecystitis:** - Laparoscopic cholecystectomy -- to prevent symptom recurrence and further complications - Conservative interventions (e.g. low-fat diet, weight reduction, anticholinergics, pain meds & antacids) **[Acute Pancreatitis ]** - **Pancreas** secretes enzymes to help **digestion** (lipase, amylase, trypsin) - *Important for breaking down fats, carbs, and proteins* - *Also important for producing insulin and glucagon*  - Other causes include trauma, infection, post-op complications, medications **Pancreatic enzymes** - Pancreatic enzymes are **inactive** when they are secreted into the duodenum - Inactive secretion prevents enzymes from digesting the pancreas itself - They are only **activated once they reach the duodenum** - In pancreatitis, the enzymes return to the pancreas in their **activated** form and cause **auto digestion of the pancreas** - Enzymes include: trypsin, phospholipids A2, and elastase - Can cause severe inflammation leading to necrosis and bleeding - Gallstone can travel and block ampulla of voter block pancreatic enzymes' exit back up into pancreas, becoming activated within pancreas **Pancreatitis: Alcohol use disorder** - Pathophysiology is not completely understood - Binge drinking increases the release of pancreatic enzymes and plays a role in the activation of the enzymes - Chronic alcohol use though to possibly lead to formation of protein plugs that block pancreatic ducts **Clinical manifestations of pancreatitis** - LUQ, mid-epigastric pain that can radiate to the back (worse with eating) - Typically sudden onset - Abdo tenderness with muscle guarding - N&V - Weakness - Fever, leukocytosis - Jaundice, if there is obstruction of the bile duct - Shock secondary to hemorrhage - Grey-turner's sign: ecchymosis in the flanks, discolouration of the flank (retroperitoneal hemorrhage) - Cullen's sign: peri-umbilical ecchymosis, jaundice or necrosis around the umbilical signs of pancreatitis - Both are associated with hemorrhagic pancreatitis -- worry about bleeding -- severe pancreatitis + poor prognosis **Autodigestion of pancreas --** pancreatic enzymes digest the pancreas itself - Inflammation - Vascular damage - Necrosis - Formation of pseudocyst within the pancreas (which are collections of leaked pancreatic fluids) -- as a result of inflammation and damage that's happening **Complication** **Pseudocyst** **Abscess** ------------------------------- ---------------------------------------------------------------------------------------- ------------------------------------------------------------------------- **Description** Accumulation of fluid, pancreatic enzymes, tissue debris, inflammatory exudate Infected pseudocyst, associated with extensive necrosis in the pancreas **Clinical manifestations** Abdominal pain, palpable mass, N&V Abdo pain, abdo mass, high fever, leukocytosis **Course without management** May resolve spontaneously or perforate (leading to peritonitis) May rupture or perforate into other organs **Management** Watchful waiting (if small and asymptomatic); drainage (if larger or causing symptoms) Requires surgical drainage **Evaluation** - **Labs:** - **amylase, lipase** - **key indicators for acute pancreatitis: lipase is more specific for acute -- will remain elevated longer** - **LFTs, bilirubin** - **Assess liver involvement and potentially bile duct obstruction** - **Calcium** - **Hypocalcemia can be assoc with acute pancreatitis** - **Imaging:** abdo U/S, CT scan (to check extent of inflammation and damages) **Management** - Supportive care - Ensuring hydration - Pain management - Treatment of shock if present - Bowel rest to decrease enzyme secretion: NP, use of NG suction - Monitoring for infection - Treating cause if indicated (gallstones) - Nutrition therapy - May require enteral feeds (via jejunal feeding tube or TPN) - When food is allowed -- small, frequent meals, high carbohydrate **[REVIEW QUESTIONS WEEK 1]** 1. Where is the antrum of the stomach located? a. Near the esophagus b. In the middle of the stomach c. **Near the pylorus** d. In the duodenum 2. Where is bile released during digestion? e. **Duodenum** f. Esophagus g. Stomach h. Large intestine 3. What is the name of the sphincter that separates the esophagus from the stomach? i. Pyloric sphincter j. **Lower esophageal sphincter** k. Ileocecal valve l. Urethral sphincter 4. The most common site for peptic ulcers is? m. **Duodenum** n. Antrum (of the stomach) o. Fundus (of the stomach) p. Esophagus 5. What is the most common complication of PUD? q. Esophageal stricture r. **Hemorrhage** s. Perforation t. Pyloric obstruction 6. GERD is a result of: u. Excessive production of hydrochloric acid v. **A zone of low pressure of the LES** w. Presence of H. pylori in the esophagus x. Reverse muscular peristalsis of the esophagus 7. In managing the symptoms with GERD, the nurse should assign the highest priority to which of the following interventions? y. Decrease daily intake of vegetables and water, and ambulate frequently z. Drink coffee diluted with milk at each meal, and remain in an upright position for 30 mins a. **Eat small, frequent meals, and remain in an upright position for at least 30 mins after eating** b. Avoid over-the-counter drugs that have antacids in them 8. The most common cause of duodenal ulcers is: c. Hypersecretion of gastric acid d. Hyposecretion of pepsin e. **H. pylori** f. E. Coli 9. A client with cholelithiasis has a gallstone lodged in the common bile duct. When assessing this client, the nurse expects to note: g. **Yellow sclerae** h. Light amber urine i. Circumoral pallor j. Black, tarry stools 10. Which of the following best describes Murphy's sign? k. Periumbilical ecchymosis exists l. On deep palpation and release, pain is elicited m. **On deep palpation, pain is elicited and breathing stops** n. Abdominal muscles are tightened in anticipation of palpation 11. Which of the following is a common clinical manifestation of acute pancreatitis? o. Right lower quadrant pain p. **Mid-epigastric pain radiating to the back** q. Pain relieved by eating r. Chronic cough 12. Which laboratory test is most specific for diagnosing acute pancreatitis? s. Serum amylase t. **Serum lipase** u. Liver function tests v. Complete blood count (CBC) 13. What is the preferred initial imaging modality for evaluating suspected acute pancreatitis? w. MRI x. **Abdominal ultrasound** y. Chest x-ray z. PET scan **[Week 2: Digestive System ]** **Blood supply -- 2 sources** (ensure liver is receiving continuous supply of blood) - Hepatic artery - 500 ml/min of oxygenated blood - 30% of liver's blood supply - Hepatic portal vein - 1000 ml/min of partly oxygenated blood - 70% of liver's blood supply, plus rich supply of nutrients, toxins, drugs from stomach, small and large intestines, pancreas and spleen **Portal venous system** - The portal venous system refers to a system of veins that come from the stomach, bowel, spleen and pancreas to the portal vein - The portal vein then breaks off into smaller blood vessels and travels through the liver **Main functions of the liver** - Blood filtration and detoxification - Metabolism (carbohydrate, lipid and protein) - Bile production - Storage (vitamin, minerals, glycogen) - Synthesis (hormones, proteins) - Immune function **[Hepatitis ]** Viral hepatitis Acute/Chronic Type of virus ----------------- ------------------ --------------- A Acute RNA B Acute or chronic DNA C RNA D E Acute - Widespread inflammation of liver tissue - Hepatitis virus destroys hepatocytes (liver cells) - Large numbers destroyed in acute infection, causing necrosis - Impairment of normal liver functions, including - Protein metabolism - Blood coagulation (synthesis of coagulation factors) - Synthesis of albumin - Production of bile **Antigen-antibody immune complex** - Antigen -- hepatitis virus - Antibodies -- protective proteins created by the immune system (important for detection and screening of hepatitis) - Antigen-antibody complex initiates the immune response & activates the complement system **Acute phase** - Can be asymptomatic - Manifestations: anorexia, n&v, malaise, fatigue, h/a, low-grade fever, arthralgias, skin rash, RUQ discomfort - Sense of taste can change - Possible physical exam findings: - Hepatomegaly (RUQ), lymphadenopathy - Jaundice - Icteric (jaundice is present), anicteric or non-icteric (no jaundice) **Acute vs Chronic Hepatitis Clinical Manifestations** +-----------------------------------+-----------------------------------+ | **Acute** | **Chronic** | +===================================+===================================+ | - Altered taste and smell | - Fatigue | | | | | - Anorexia | - Hepatomegaly | | | | | - Arthralgias | - Malaise | | | | | - Dark urine | - Myalgia and arthralgia | | | | | - Fatigue | - Easy bruising | | | | | - Low-grade fever | - Palmar erythema | | | | | - Headache | - Spider angiomas | | | | | - Hepatomegaly | - Splenomegaly | | | | | - Jaundice | | | | | | - Clay-coloured stools | | | | | | - Malaise | | | | | | - Nausea & vomiting | | | | | | - Pruritis | | | | | | - RUQ tenderness | | | | | | - Splenomegaly | | | | | | - Weight loss | | +-----------------------------------+-----------------------------------+ **Bilirubin** - Bilirubin is created when the spleen breaks down old & damaged RBCs (RBC heme + globin bilirubin) - Orange yellow pigment, produced from normal breakdown of RBCs (gives bile its colour) - Unconj. bilirubin (bound to albumin), iron and proteins then travel from the spleen to the liver - Unconjugated = indirect - Unconjugated is converted to conjugated (aka direct) bilirubin in the liver makes it water soluble and allow it to be excreted in bile - Liver processes bilirubin (makes it conjugated/soluble), which allows it to be excreted in bile **Bilirubin metabolism** - Bilirubin metabolism happens in the liver - Normally the liver creates bile from bilirubin and other waste products - Bile normally moves through the bile ducts, into the gallbladder and the small intestine to help digestion - If liver doesn't synthesize enough albumin, bile can't get where it needs to go buildup of bilirubin in liver jaundice **Clinical manifestations of increased levels of bilirubin** - Jaundice: bilirubin gets deposited in the skin and sclera - Pruritis (itchiness): bile salts accumulate beneath the skin - Dak amber urine: bilirubin is being excreted by the kidneys - Clay-coloured or white stool that is floating: lack of bilirubin in stool, high fat content of stool  - Diagnostic tests - Serological -- identifies specific antibodies and antigens (ex. Hepatitis B surface antigen = HBsAg - Liver enzymes - ALT -- elevated levels indicate liver cell injury or inflammation - More specific marker bc found more primarily in liver - AST -- found in other tissues - ALP -- found in liver and other areas - GGT -- also in bile ducts and other organs -- marker for damage to bile duct - Important function of livers -- synthesizing albumin, clotting factors and bilirubin - In hepatitis -- decreased albumin bc not able to synthesize albumin effectively - Bilirubin -- inc bc can't conjugate or clear it out - INR/prothrombin time -- inc bc blood will take longer to clot if we don't have enough clotting factors - Usually only concerned when 2-3x above the normal liver **Hepatitis A** - Cause: hepatitis A virus (HAV) - Typically acute, self-limiting (resolves on its own) - Route of transmission: oral-fecal route (contaminated food/water) - Most infectious during 2 weeks **before** symptoms develop - Viral serological tests: - Anti-HAV IgM means acute hepatitis -- antibody to HAV immunoglobulin M - IgM is first responder short lived recent new infection - Anti-HAV IgG means past infection, or vaccination -- antibody to HAV immunoglobulin G - IgG, produced later in infection process - provides long term immunity - Elevation in IgM recently infected - Elevation in IgM and IgG may be infected few weeks ago - Elevation in IgG infected a long time ago - Acute symptoms in adults, but typically not in children - No specific treatment - Management is focused on relief of symptoms hydration, resting, avoid alcohol - Recovery gives lifelong immunity - Vaccine available (e.g. Havrix) **Hepatitis B** - Cause: Hepatitis B Virus (HBV) - Route of transmission: exposure to blood or blood products (parenteral or mucosal), sexual contact, perinatal transmission - Infectious before symptoms appear, may be asymptomatic - Infant born to an HBV-infected person needs to receive first dose of vaccination and immunoglobulins within 12 hours of birth - If not, infant will have acute infection (which typically is asymptomatic) and 90% will develop chronic infection - Management focuses on symptom relief and education to prevent transmission - Antiviral therapy may be needed **Hepatitis B: selected viral serologic tests** - **HBsAg:** Hepatitis B surface antigen -- indicates infection, and if present after 6 months indicates chronic infection - **Anti-HBs**: antibody to hepatitis B surface antigen -- indicates immunity, either from past infection or vaccination - **HBV DNA** -- indicates viral load (measures how much is in you) - this is a DNA type of virus so it is a good marker for active Hep B virus replication - not important for diagnosis, but important for ongoing management and treatment - if treatment is effective viral load will dec **Hepatitis B pharmacotherapy** - to reduce viral load, slow the rate of disease progression, prevent long-term complications (such as cirrhosis, liver cancer) - Indicated for patients who are having a severe acute course, persistent symptoms - Pegylated-interferon alfa (old treatment) rarely used since advent of oral antiviral therapy - Nucleoside analogues are oral antiviral agents (newer form of treatment that is more common now) - Work by inhibiting viral DNA replication - Agents include *entecavir & tenofovir* - Nucleoside analogues have very rare but possible AE of severe hepatomegaly & lactic acidosis - **Tenofovir:** possible AE of nephrotoxicity - **Entecavir:** contraindicated in pregnancy **Hepatitis B Vaccine** - Hep B only -- Energix-B, Recombivax - Hep A & B -- Twinrix - Vaccines contain hep B surface antigen (HBsAg) - Usually given 3 doses: at 0, 1, and 6 months **Hepatitis C** - Cause: hepatitis C virus (HCV) - Route of transmission: exposure to blood or blood products (parenteral or mucosal), sexual contact, perinatal transmission (like Hep B) - Infectious 1-2 weeks before symptoms appear and can be asymptomatic - **Anti-HCV:** antibody to hepatitis C virus -- indicates past or current infection - **HCV RNA --** viral load, confirms whether disease is active - There are 6 diff genotypes of HCV -- the different genotypes are important in determining treatment plans and predicting how diseases will progress **Hepatitis C pharmacotherapy** - Evidence that more than 50% of people with acute hepatitis C will clear infection spontaneously, however early treatment is recommended to prevent complications - Indicated for people with acute and chronic HCV infection - Goal: cure HCV infection **Direct-acting antiviral agents (DAAs)** - Direct-acting antiviral agents (DAAs) were introduced in 2011 - **DAAs** are medications that work by interfering with RNA replication of the HCV - These drugs target specific steps in HCV replication (4 categories of drugs) - Protease inhibitors work by inhibiting viral protease, which is needed for RNA replication of HCV - AE can include hepatic injury, severe rashes, photosensitivity - NS5A inhibitors inhibit the protein NS5A that is needed for RNA replication and assembly of HCV - NS5B nucleoside polymerase inhibitors (NPIs) - NS5B non-nucleoside polymerase inhibitors (NNPIs) - NS5B inhibitors (NPIs and NNPIs) inhibit the protein NS5B that is needed for RNA replication of HCV - Common AE of all are headache & fatigue - Used in children older than 3 years - Not recommended during pregnancy - These agents are used in combo to dec developing viral resistance - 12 week course of therapy is typical - Need to check response to agents by checking HCV RNA (viral load) at 12 weeks after the end of therapy - Interferon alpha and ribavirin in combination are rarely (if ever) used since advent of DAAs - Ribavirin may be used with DAAs - Common side effects include: anemia, fatigue, H/A, nausea, insomnia - AE include hemolytic anemia, teratogenic effects **Hepatitis D** - Cause: Hepatitis D virus (HDV) - Hep D can only cause infection if Hep B is present - Route of transmission is same as hep B - Treatment of acute HDV is mostly supportive - Chronic cases may require treatment with pegylated interferon alpha - Flu-like symptoms occur in up to 90% of patients, other side effects include fatigue, anorexia, nausea, diarrhea, weight loss, hair loss, bone marrow suppression **Hepatitis E** - Cause: hepatitis E virus (HEV) - Route of transmission is oral-fecal - Zoonotic: may be transmitted from animals to humans - Outbreaks typically associated w contaminated water supply - Treatment is mostly supportive; disease is usually mild and self-limiting - Chronic disease usually occurs in immunocompromised patients; treatments may include ribavirin **[Cirrhosis ]** - Chronic progressive disease characterized by fibrosis (development of scar tissue) and inflammation - Fibrosis occurs when the cells try to regenerate, but the regeneration is disorganized - Results in an overgrowth of new, fibrous connective tissue which distorts the normal structure of the liver's lobules - Effects liver structure and function - Gold standard: biopsy to look at cells, but often can diagnose with basic U/S bc of how different the appearance is - **Final stage of liver disease** - Can be prevented! **Causes of cirrhosis** - Cirrhosis is the final state of chronic liver disease - Chronic viral hepatitis -- hep B and C can become chronic (not all) - Alcohol (excessive use) -- alcohol has a direct, hepatoxic effect that causes cell necrosis & fatty infiltration in the liver - Non-alcoholic fatty liver disease -- characterized by too much fat being stored in liver cells (i.e. obesity, type 2 diabetes, high cholesterol) - Genetic diseases - liver congestion associated with heart failure **Pathophysiology of cirrhosis** - key changes that happen during cirrhosis - tissue that isn't well perfumed and damaged can lead to reduced blood flow to the liver ---\> ischemia and necrosis - body will try to replace those cells but will replace with scar tissue - when it is replaced, liver loses functionality - fibrous tissue can form nodules ---\> hallmark for cirrhosis - nodules can further disrupt normal architecture of the liver - damage ---\> impaired blood flow ---\> decreased function d/t irregular cell growth, lack of nutrition, and hypoxia **Clinical manifestations of cirrhosis** - **compensated** - liver is still able to function normally - often is undetected - may have abdo pain, non-specific signs & symptoms - want to do routine tests like LFTs - **decompensated** - liver is not functioning normally - illustrated by tests of liver function: low albumin, high bilirubin, inc INR - clinical signs & symptoms of liver disease -- i.e. jaundice (common), as cites, hepatic encephalopathy - our focus will be on decompensated cirrhosis **Clinical manifestations of cirrhosis: Endocrine disturbances** - one of the functions of the liver is to metabolize estrogen & testosterone (maintains hormonal balance) - if the liver function is impaired, then the body will accumulate estrogen - increase in estrogen can cause gynecomastia (in males), palmar erythema, spider angiomas, amenorrhea in younger women and vaginal bleeding in older women - gynecomastia: an increase in the amount of breast gland tissue in males - palmar erythema: rare condition that makes your palms red; they may also feel warm - spider angioma: collection of blood vessels under the surface of your skin (red to purple) - amenorrhea: absence of menstruation - in addition, a decrease in testosterone (not enough protein to bind to) can cause impotence and testicular atrophy **Portal hypertension** - fibrosis and changes to the blood vessels in the liver due to cirrhosis leads to resistance to blood flow within the portal venous system - this causes portal HTN, which is abnormally high BP in the portal venous system - most complications of cirrhosis are related to portal HTN - esophageal & gastric varices -- swollen blood vessels in the upper gastrointestinal tract that can cause bleeding -- caused by blockage in blood flow to liver - ascites -- condition that occurs when fluid collects in spaces in your belly (can be painful) - hepatic encephalopathy -- potentially reversible; characterized by a range of neuropsychiatric and neuromuscular abnormalities resulting from the buildup of toxic substances in the bloodstream ---\> impacting brain function - hepatorenal syndrome - multi organ condition of acute kidney injury -- pts with this condition prevent with s&s of liver failure and oliguria - Decrease of pressure in portal venous system will prevent complications - When you have a lot of pressure developing the body will try to bypass the high pressure areas - New vessels can reform to get blood around the liver - This circulation can lead to development of esophageal varices (most common type), gastric varices, and hemorrhoids - Prominent veins in abdo can be a sign of this **Esophageal & gastric varices** - Varices are enlarged, tortuous veins (large and winding d/t inc pressure in the venous system) - Esophageal & gastric varices can rupture & bleed - May see hematemesis (vomiting blood) or melena (more common for gastric) - Bleeding esophageal varies are an emergency **Management of varices** - Avoidance of irritants: ASA, NSAIDs - NSAIDs can irritate stomach lining - Non-selective beta-blocker agents may be used to prevent bleeding, such as propranolol - Reduces portal venous pressure by decreasing the C/O - Bleeding varices need treatment with medication and endoscopic therapy - Initial management: hemodynamics stabilization - Medications: octreotide or vasopressin, used to reduce blood flow - Octreotide used more often, fewer adverse effects - Endoscopy - Sclerotherapy (done with endoscopy) -- injecting solution in varices that causes clotting - Variceal ligation (this is use of elastic bands to tie off the vessels that are bleeding) - Compression of the varices with an inflatable tube or balloon (balloon tamponade) -- temporary control but applies direct pressure until we can do more definitive treatment such as sclerotherapy or ligation - Shunting procedure - Interventional radiology to create a shunt from the portal vein to the inferior vena cava (done as last step) ---\> transjugular intrahepatic portosystemic shunt (TIPS) - Radiologist inserts stent in jugular to liver - Imaging used to visualize it and guide it down to where it has to go - Stent created a channel between portal vein and hepatic vein, and allows blood flow to bypass liver and go into systemic circulation - Minimally invasive - But detoxification issue -- one of key functions of liver is to filter out ammonia and other toxins from blood ---\> can lead to complications (last resort) **Peripheral edema** - Swelling of the tissues (lower extremities) because of fluid accumulation - Decreased oncotic pressure - Oncotic pressure is pressure exerted by proteins - Largest protein exerting this pressure is albumin - In cirrhosis we have reduced oncotic pressure which can allow fluid to leak from vasculature into tissues - Portal hypertension -- increased pressure in portal vein pushing fluid out of vasculature into other areas **[Ascites]** - The accumulation of serous fluid in the peritoneal cavity - Serous fluid fills the body's cavities, it is typically a thin, watery, pale yellow, transparent fluid - There are several factors that lead to ascites, and 3 important factors are - Portal hypertension - Hypoalbuminemia - Hyperaldosteronism **Pathophysiology of ascites** - **Portal hypertension:** increased pressure in the portal venous system pushes proteins from the blood vessels into the lymphatic space, but lymphatic drainage is impaired, and protein & water leak into the peritoneal cavity - **Hypoalbuminemia:** the decreased synthesis of albumin means that there is decreased colloidal oncotic pressure - fluid accumulates in the interstitial spaces and leaks into the peritoneal cavity - **Hyperaldosteronism** - Damaged hepatocytes stop metabolizing aldosterone - Aldosterone accumulates, and aldosterone stimulates the kidneys to increase water & sodium reabsorption - If the CO is decreased, there is activation of the renin-angiotensin-aldosterone-system which leads to an inc in anti-diuretic hormone, which leads to additional water retention **Clinical manifestations of Ascites** - Abdo distension with weight gain - Umbilicus can be everted - Abdominal striae with distended abdominal wall veins - Signs of dehydration -- all the fluid is going into the peritoneal space, not where it needs to be in vasculature space **Management of Ascites** - Assessment & monitoring - Vitals, abdominal girth, fluid balance, electrolytes, albumin - Be aware of respiratory distress -- peritoneal cavity may be pushing up on the lungs ---\> poor lung expansion - Have these pts sit upright to help with lung expansion and breathing - Measure abdominal girth -- daily weights to see if retaining fluid - Sodium restriction - Limit sodium to 2 grams/day can help reduce fluid retention - Diuretic therapy - Increase sodium excretion - Combination of drugs is typically used that work at different. Sites of the nephron (i.e. spironolactone and furosemide) - Paracentesis - Catheter is used to remove fluid from the abdominal cavity - Generally only done to relieve symptoms -- relief is temporary - Remove 1-2 L of fluid at a time and see how patients are coping. While they are doing this, pts can lose 10-30 g of protein - Risk of infection is there - In addition to removing fluid, they will send it to be analyzed to determine cause of ascites - Number of hematological conditions can stem - Cirrhosis leads to scaring of liver which increases pressure which causes blood to backup to spleen and other organs - Backup of blood leads to engorged organs (splenomegaly -- engorged spleen) - Large spleen can trap and destroy more blood cells than normal at a faster rate ---\> anemia (RBC, leukopenia (WBC), thrombocytopenia (Plts) - With thrombocytopenia -- liver function is impaired which can exacerbate thrombocytopenia **Hematological conditions** - Decreased clotting factors - In advanced cirrhosis, the liver is unable to produce prothrombin and other factors needed for blood clotting - Signs & symptoms include increased bleeding - Epistaxis: nosebleed - Purpura and petechiae - Petechiae: tiny red dots caused by broken blood vessels (type of purpura) - Purpura: larger spots that are between 4-10 mm in diameter, they are caused by small blood vessels leaking blood under the skin - Easy bruising - Gingival bleeding  **[Hepatic encephalopathy ]** - This is a serious complication of cirrhosis - protein digestion in small intestines -- once absorbed, amino acids transported to liver - production of ammonia from intestine ---\> converts to urea by normal healthy liver - clinical signs of hepatic encephalopathy: liver is not able to detoxify NH3 ---\> accumulation ---\> crosses BBB **Clinical manifestations of Hepatic Encephalopathy** - - **Early signs** - Emotionally labeled (highs and lows) - Apathy - Irritability, agitation - Memory loss - Drowsiness, insomnia - Slows slurred speech - Impaired judgment - **Late signs** - Confusion - Asterixis (flapping tremors) -- caused by nerve damage; brief, irregular, involuntary jerking movements in the muscles (usually fingers and wrists - Fetor hepaticus -- "breath of the dead" -- sweet, musty or like a combination of rotten eggs and garlic **Management of hepatic encephalopathy** - Goal is to reduce ammonia formation by decreasing the amount of ammonia formed in the intestines - Lactulose (osmotic laxative) is used to prevent ammonia absorption (lactulose can be administered PO, NG, or via retention enema) - Lactulose traps the ammonia in the intestine and the laxative action expels it - If patient does not respond to lactulose, rifaximin (antibiotic) can be added to reduce production of ammonia by targeting gut bacteria that produces it **[Hepatorenal syndrome ]** - This is renal failure with advancing azotemia, oliguria and intractable ascites - Azotemia: nitrogenous waste (urea/creatinine) accumulation - Results bc of dec blood volume to kidneys secondary to portal HTN - In patients with cirrhosis, it is typically seen following diuretic therapy, gastrointestinal hemorrhage, or paracentesis - Creatinine will be elevated - Liver transplantation will reverse the kidney failure -- dialysis may be helpful - Often times pts are resistant to treatment ---\> overworking the kidney following ascites treatment - Certain meds may be helpful to shunt off blood: vasodilators **[Cirrhosis: diagnostic tests ]** - LFTs (AST, ALT, GGT) are increased - Decreased albumin - PT and INR prolonged - Increased bilirubin (hyperbilirubinemia) - CBC: thrombocytopenia, leukopenia, anemia - Liver biopsy: to identify liver cell changes (not necessary with clinical manifestations of cirrhosis) (gold standard) - Ultrasound - Can identify changes in liver size, shape, texture; assess degree of fibrosis (scarring) - Identify complications (i.e. ascites, splenomegaly) - Evaluate presence/severity of portal hypertension **Cirrhosis: management** - Medications: no specific med therapy for cirrhosis, but used to treat underlying cause (e.g. antivirals for hepatitis), or symptoms (e.g. antacids for gastric discomfort) and complications (i.e. diuretics for ascites) - Lifestyle changes (i.e. avoid alcohol, healthy diet, exercise) - Vitamins & nutritional supplements may be needed - Diet: high in calories, high in carbohydrates, moderate to low levels of fat - Sodium restriction with ascites & peripheral edema - Procedures (i.e. paracentesis, TIPS) - Regular monitoring (e.g. blood tests, imaging, endoscopies) - Liver transplant **Review Questions** 1. Which of the following proteins is primarily synthesized by the liver? a. Insulin b. Hemoglobin c. **Albumin** d. Immunoglobulins 2. Which of the following statements correctly describes the blood supply to the liver? e. the hepatic artery provides most of the liver's blood supply f. **the hepatic portal vein provides most of the liver's blood supply** g. all of the blood supply to the liver comes from the hepatic artery h. the hepatic artery and the hepatic portal vein each provide 50% of the liver's blood supply 3. which of the following substances is primarily detoxified by the liver? i. Bilirubin j. Creatinine k. **Ammonia** *(forms urea)* l. Lactate 4. Which of the following clinical manifestations is most characteristic of chronic hepatitis? m. Dark urine n. Jaundice o. **Palmar erythema** p. Nausea and vomiting 5. Which of the following classes of medications is commonly used in treatment of chronic hepatitis B? q. Nucleotide analogs r. Protease inhibitors s. NS5A inhibitors t. **Nucleoside analogs** 6. Which of the following hepatitis viruses are preventable through vaccination in Canada? u. Hep A & B v. **Hep A, B and D** w. Hep A, B, C, and D x. Hep A & D 7. Hepatic fat accumulation is seen in which form of cirrhosis? y. Biliary cirrhosis z. Hepatitis-C related cirrhosis a. Postnecrotic cirrhosis b. **Alcoholic cirrhosis** 8. The most common clinical manifestation of portal HTN is \_\_\_\_\_\_\_\_ bleeding c. Rectal d. Duodenal e. **Esophageal** f. Intestinal 9. Which of the following is a key management strategy for managing cirrhosis? g. High-fat diet to improve energy levels h. Regular use of broad-spectrum antibiotics to prevent infections i. **Diuretics and sodium restriction to manage ascites** j. Routine administration of corticosteroids to reduce liver **[Week 3: Increased intracranial pressure, TBI & stroke]** **Increased intracranial pressure** - There are 3 components of the cranium - Brain tissue (makes up most of the content) - Blood - Cerebrospinal fluid (CSF) - Normally, the volume of these 3 components is stable and intracranial pressure is within normal limits - If there is any change to the volume of any of the 3 components, this will change the intracranial pressure **Regulating and maintaining ICP** - Normal ICP: under usual conditions, the balance among brain tissue, blood and CSF maintain the ICP (normal range 3-15 mmHg) - Modified monro-kellie doctrine - Describes a dynamic equilibrium in the skull - If the volume of one component increases, another must decrease to maintain total intracranial volume - If one component's volume increases without a corresponding dec in another, ICP rises - *Anything above 20 = increased pressure* - *Kids are more resistant to higher pressure bc of sutures, skulls are not as rigid, and have different soft parts* **Factors that can affect ICP** - Changes in: - Blood pressure - Cardiac function ---\> increase venous pressure ---\> can cause changes - Intra-abdominal and intra-thoracic pressure - Body position -- lying flat can inc pressure, upright can reduce - Temperature (hyperthermic ---\> inc cerebral blood flow ---\> inc ICP) - Blood gases, particularly CO2 (inc CO2 = inc ICP) - Degree to which these factors increase or decrease ICP depends on the ability of the brain to accommodate to the changes **Regulating and maintaining ICP** - Compliance -- the ability of the brain to adapt to increases in ICP - Normal compensatory mechanisms - Displacement of CSF into the spinal canal - Reduction of blood volume -- this alters brain metabolism and eventually leads to hypoxia and ischemia - Brain tissue can shift or compress (but has limited ability to do this) - If compensatory mechanisms fail, this leads to: - Increased ICP - Neuronal compression (displacement and herniation of brain tissue) - Ischemia (sustained ICP ---\> neurocompression ---\> herniation ---\> ischemia) - Herniation = medical emergency - Herniation occurs really late in ICP inc - This is last thing that may happen and is potentially fatal **Cerebral blood flow** - The brain uses 25% of body's oxygen and 25% of body's glucose - Doesn't have the ability to store O2 and glucose so we have to have adequate blood flow to ensure functioning - If we have any disruption in cerebral blood flow it can lead to significant neuro deficits **Autoregulation** - Ability of the brain to maintain cerebral blood flow to meet metabolic needs - Cerebral blood vessels can dilate or constrict to ensure the brain received enough blood - Does not work in cases of severe hypotension or severe hypertension - If mean arterial pressure is less than 50 mmHg or greater than 150 mmHg **Other factors affecting cerebral blood flow** - CO2 -- important one - Increasing levels of CO2 will cause increasing vasodilation bc body will attempt to increase cerebral blood flow - Decreased levels --\> vasoconstriction - Low levels of oxygen -- body will cause cerebrodilation form ore blood flow into brain - If oxygen levels are really high -- cerebrovascular vasoconstriction - Acidosis: high level of hydrogen ion = dilation. Low levels = constriction - Regulation to ensure we have adequate perfusion **But what if it doesn't work?** - Switch to anaerobic metabolism ---\> producing lactic acid ---\> H+ ---\> increase vasodilation ---\> loss of autoregulation **Cerebral hemodynamics** - **Cerebral perfusion pressure (CPP):** amount of blood flow from the systemic circulation needed to maintain adequate blood flow to brain tissue - **Normal CPP is 70-100 mmHg** - **Minimum CPP of 50-60 mmHg** is needed for adequate perfusion - **CPP \< 50 mmHg** ---\> cerebral ischemia - **Mean arterial pressure (MAP):** the avg pressure during the cardiac cycle - **MAP = DBP + 1/3 (SBP-DBP)** or [ **SBP + 2(DBP)**] *(no questions on calculating MAP)* - 70-110 mmHg - CPP = MAP -- ICP - Understand that diastolic pressure is longer in terms of length of cardiac cycle - MAP has to balance ICP out -- if ICP is stable but MAP decreases = problems with perfusion ---\> dec perfusion to brain **Pressure-volume curve** *(not asked to draw on test)* - Intracranial compliance is the change in volume per unit change in pressure - Compliance refers to the ability of the volume of brain tissue, blood and CSF to accommodate change in volume - Curve has 4 stages from high compliance to low compliance - Small changes in volume ---\> high compliance = no change in ICP - At 4, any increase in volume can lead to extreme changes in pressure (increase) **Causes of Increased ICP** - Brain tissue - Brain tumour ---\> growth in brain tissue - Contusion ---\> leads to swelling - Abscess ---\> can increase tissue volume - Edema - Blood - Hemorrhages ---\> accumulation of blood in spaces - Hematoma ---\> pool of mostly clotted blood in an organ, tissue, or body space - Metabolic and physiological factors -- hypoxia, hyper cap is, lying flat - CSF - Hydrocephalus -- excess CSF within brain ventricle - Brain tumour that affects CSF ---\> tumour can obstruct flow or stimulate production of CSF or disrupt areas in brain where CSF is being absorbed **Cerebral Edema** - Contributes to increased ICP, as fluid accumulates in the extra vascular spaces of brain tissue - Many causes (e.g. lesions, tumours, hemorrhages, infections) - Three types of cerebral edema - Vasogenic (most common): blood-brain barrier is disrupted, causing fluid to leak from blood vessels into the surrounding brain tissue; primarily affects the white matter o the brain - Cytotoxic: brain cells swell d/t the accumulation of fluid inside the cells ---\> inc risk for stroke - Interstitial: CSF leaks from the ventricles into the surrounding brain tissue - Associated with conditions like hydrocephalus or meningitis **Clinical manifestations of increased ICP** - Earliest indicator is change of LOC - Changes in VS are caused by pressure on the thalamus, hypothalamus, pons and medulla - Cushing's triad is associated with increased ICP - *Abnormal resp patterns* - *Bradycardia with full bounding pulse* - *Increased SBP with widening pulse pressure* - Seeing all 3 signs in cushing's triad = not good +-----------------------+-----------------------+-----------------------+ | **Early signs --** | **Late Signs --** | **Terminal signs --** | | compensatory | compensatory | decompensation | | mechanisms intact | mechanisms failing | | +=======================+=======================+=======================+ | **Altered LOC | **dec LOC (stupor)** | **Coma** | | (confusion, | | | | restlessness)** | - Unilateral or | - Bilaterally fixed | | | bilateral | and dilated | | - Unilateral pupil | pupillary | pupils | | change in size, | changes: size, | | | equality, and/or | equality and/or | - Respiratory | | reactivity | reactivity | arrest | | | | | | - Altered resp | - Ineffective | - Absence of motor | | pattern | breathing pattern | response | | (bradypnea, or | (Cheyne-Stokes | (flaccid) | | irregular) | respirations) | | | | | | | - Unilateral | - Abnormal motor | | | hemiparesis | response | | | (one-sided muscle | (decorticate or | | | weakness) | decerebrate | | | | posturing) | | +-----------------------+-----------------------+-----------------------+ | **Variable signs** | - HTN with widened | | | | pulse pressure | | | - Focal findings | | | | (e.g. speech | - Bradycardia | | | difficulty, | | | | visual | - Hyperthermia | | | disturbances) | | | | | | | | - Papilledema | | | | (swollen optic | | | | nerve) | | | | | | | | - Vomiting | | | | | | | | - Headache | | | | | | | | - Seizures | | | +-----------------------+-----------------------+-----------------------+ **Cerebral herniation** - Life threatening complication - Brain tissue can shift downwards from the skull into the brainstem, and pressure can force the cerebellum and brain stem downward through the foramen magnum (hole in the base of the skull where brain connects to spinal cord) - Signs: unilateral, fixed dilated pupil; Cushing's triad **Diagnostic tests** - Goal is to identify the underlying cause - CT scan -- x-rays to see brain injury, bleeding, tumours etc. - MRI -- takes very long, not good for emergencies - Provides good picture, good for brain tumour identification, stroke, etc. - CTA/MRA -- computed tomography angiography & magnetic resonance angiography - Non-invasive imaging that provides detailed info about blood vessels - Measurement of intracranial pressure (neuro-monitoring in ICU) **Management** - Monitoring (vitals, electrolytes, ICP, brain tissue oxygenation) - Decrease environmental stimuli (can inc ICP) - Positioning can help to reduce ICP include by improving venous drainage: - Elevation of HOB at 30 degrees - Maintaining the head and neck in alignment - Avoiding flexion at the hip - Surgical intervention if required -- decompressive craniotomy, evacuating hematomas - Medications (e.g. sedatives, mannitol) - Mannitol is an osmotic diuretic that moves fluid from the extravascular space into the blood (intravascular space) - Given via IV - Need to monitor fluids and electrolytes - Sedatives: dec metabolic need, vasodilator, dec agitation of pt - Nutritional therapy - Early nutrition after TBI can improve pt outcomes - Ideally started within 5 days of injury - Can use tube feeds or TPN **Glasgow Coma Scale (GCS)** - GCS is standardized way to assess pt's LOC - 3 areas corresponded to the definition of coma as: - Inability to speak - Inability to obey commands - Inability to open eyes to verbal/painful stimuli - 3 indicators - Eye opening - Best verbal response - Best motor response - Conditions that render GCS invalid - Nonverbal pt (may be dementia) - Baby - If condition doesn't allow us to assess them using the parameters - Language barrier - Trauma -- eyes swollen or trauma to face - Blind pts - Prior paralysis - A: abnormal flexion of extremities -- damage to both sides of cerebral hemisphere - Brain injury above level of brain stem - Better prognosis than B - B: abnormal extension of extremities -- more severe damage to brainstem - Poorer prognosis **[Traumatic brain injury ]** - Scalp lacerations -- bleeding, watch for infection and extent of injury - Skull fractures -- simple, basilar, depressed, etc. - Head trauma -- general term for any head injuries (e.g. bruising, hematoma, concussion) - Leading cause is car accidents, driving under influence - Males, young adults under 30 are most likely to be affected **Basilar Skull Fracture** - Key signs and symptoms - Periorbital edema and ecchymosis -- raccoon eyes, bleeding under skin deep down - Postauricular ecchymosis -- battle's sign -- bruising ver the mastoid process - Rhinorrhea -- CSF comes out of nose - Otorrhea -- CSF out of ear - Serious head trauma **Testing fluid for CSF** - Use gauze and apply to liquid -- see clear yellowish ring around spot of blood = halo sign - Suggests leak of CSF **Traumatic brain injury** - Categorized as diffuse (generalized) or focal (localized) - Mild: GCS 13-15 - Moderate: GCS 9-12 - Severe: GCS 3-8 (lowest GCS score is 3 -- can have score lower than 3 if unable to assess) **Diffuse brain injury** - Involves multiple areas of the brain - Major cause: sports - Concussion - Mild concussion - Post-concussion syndrome - Chronic traumatic encephalopathy - Diffuse axonal injury -- rapid acceleration/severe force causing injury - Some damage along the axons - Very serious implications **Concussion** - Jarring injury of the brain -- results in a disturbance of cerebral function; aka mild traumatic brain injury (mTBI) - Only one symptom (e.g. dizzy, nausea, H/A) following a head injury is needed for diagnosis - Sport concussion assessment tool: SCAT-5 - Signs and symptoms include: H/A, weakness, dizziness, vomiting, nausea, lack of coordination, difficulty balancing - Treatment = bed rest (physical and mental), followed by a slow transition to light activity - **Red flags (indicate severe concussion):** neck pain or tenderness, double vision, weakness or tingling/burning in arms or legs + severe or increasing headache, seizure or convulsion, loss of consciousness, deteriorating conscious state, vomiting, increasingly restless, agitated or combative **Post-concussion syndrome** **Chronic traumatic encephalopathy** ---------------------------------------------------------------------------------------------------- ---------------------------------------------------- Can occur 2 weeks to 2 moths post concussion From repeated concussions H/A, lethargy, personality changes, behaviour changes, changes to attention, dec short-term memory Progressive brain disease, development of dementia **Diffuse axonal injury (DAI)** - With DAI, there is shearing, tearing or stretching of axons - Can occur w mild, mod, or severe brain injury - Develops 12-24 hours post-brain injury - Signs: decreased LOC, inc ICP, cerebral edema **Focal brain injury** - Mild to severe, localized to the injured area - Lacerations involve tearing of brain tissue -- occurs with skull fractures & penetrating injuries - Contusion is a bruising of brain tissue - Associated with skull fractures - May develop with hemorrhage, infarction, and edema - Coup & contrecoup injury **Review of Brain Anatomy** - Brain is protected by the skull, CSF, and 3 membranes called the meninges - Dura mater = outermost layer of protection - Tough, fibrous, and leather-like tissue - Arachnoid mater = middle protective layer - Thin, delicate, fibrous membrane - Pia mater = innermost protective layer of connective tissue **Epidural hematoma** - Results from bleeding between the dura mater and the skull (epidural space) - Most caused by arterial bleeding and are an emergency - Venous epidural hematomas are less common and develop slowly - Typically, person becomes unconscious, has moment of lucidity, and then dec LOC - Pt will need rapid surgical intervention to remove hematoma to relieve pressure on the brain **Subdural hematoma** - Results from bleeding between dura mater and arachnoid mater - Usually caused by brain and brain blood vessel injury - Typically venous bleeding - Can be acute, subacute, or chronic - Symptoms: dec LOC, confusion, lethargy - Symptoms can take weeks to develop **Intracerebral hematoma & subarachnoid hemorrhage** **Intracerebral hematoma** **Subarachnoid hemorrhage** --------------------------------------------------------------------------------------------------------------------------------- --------------------------------------------------------------------------------------- Bleeding within the brain tissue itself Bleeding between arachnoid mater and pia mater Can be a result of trauma, ruptured cerebral aneurysm, arteriovenous malformation, or hypertensive injury to blood vessel walls Can be result of trauma, ruptured cerebral aneurysm, or an arteriovenous malformation **Cerebral hemorrhage: clinical manifestations** - Depend on type of hemorrhage - Common manifestations include: changes in LOC, H/A, N&V +-----------------+-----------------+-----------------+-----------------+ | **Epidural | **Subdural | **Subarachnoid | **Intracerebral | | hematoma** | hematoma** | hematoma** | hematoma** | +=================+=================+=================+=================+ | -may present w | -acute | -sudden onset | -h/a, vomiting, | | initial LOC, a | presentation is | severe h/a | dec LOC | | lucid interval, | similar to | "worst ever"; | | | followed by | epidural | associated | -neuro signs | | rapid | hematoma | symptoms incl: | vary w location | | deterioration | | brief LOC, | of hemorrhage | | (H/A, vomiting, | -chronic -- | vomiting, neck | | | drowsiness, | more insidious | pain or | | | confusion, | (h/a, | stiffness | | | aphasia, | light-headed, | | | | seizure, | cognitive | -signs of | | | hemiparesis) | impairment, | meninges | | | | apathy, | irritation/infl | | | -signs of inc | somnolence, | ammation | | | ICP | occasional | (nuchal | | | | seizures); | rigidity, | | | | symptoms may | photophobia, | | | | not appear till | blurred vision, | | | | wks later | irritability, | | | | | restlessness, | | | | | low-grade | | | | | fever); | | | | | positive kermit | | | | | sign, positive | | | | | Brudzinski sign | | +-----------------+-----------------+-----------------+-----------------+ **Management** - Specific to cause; focus on cessation of bleeding and controlling ICP - Diagnostic tests similar to those for pts with inc ICP - Always do neck x-ray to assess for assoc C-spine injury (head injury can cause C-spine injury) - Often requires ICU or specialized care - Large subdural and epidural hematomas may req surgery **[Stroke ]** - Referred to as cerebral vascular accident (CVA) - Stroke is the leading cause of disability and 3^rd^ leading cause of death in Canada - Risk factors include: - HTN and type 2 diabetes - CVD - A fib - Valvular disease - Oral contraceptive use in certain conditions - Hypertensive and smokers - Use with migraines inc risk for stroke **Transient ischemic attacks** - Episodes where neurological deficits occur for up to one hour - Considered to be a warning sign of an ischemic stroke - Signs and symptoms depend on the location of the affected artery - Include unilateral weakness or numbness, diplopia (double vision), sudden confusion, loss of balance, and speech deficits (slurring words) **Ischemic stroke** - Occurs when there is an obstruction to arterial blood flow to the brain which causes ischemia and can lead to death of brain tissue (infarction) - **Thrombotic stroke** - Usually due to atherosclerosis and inflammatory processes that damage the walls of blood vessels in the brain - Plts and fibrin stick to the damaged blood vessel wall and forms a clot - Risk factors: HTN and diabetes - **Embolic stroke** - Occurs when embolus lodges in and occludes cerebral artery - Sources of emboli include blood clot or other debris (i.e. fat, tumour) - Risk factors: A fib, endocarditis, valvular heart disease **Hemorrhagic strokes** - Primary cause of an intracerebral hemorrhage is chronic HTN - Weaken blood vessels OT -- can lead to rupture and bleeding - Intracerebral hemorrhages are also caused by trauma, coagulation disorders and cocaine use (cocaine use assoc. w severe HTN) - Subarachnoid hemorrhages are caused by ruptured cerebral aneurysms or arteriovenous malformations **Clinical manifestations of stroke** - Similar between ischemic and hemorrhagic stroke - S&s will depend on the location of the stroke - Clinical manifestations include - Hemiparesis -- weakness on one side of body - Hemiplegia -- paralysis on one side of body - Dysphagia -- difficulty swallowing - Dizziness - Ataxia -- lack of muscle coordination ---\> inc falls risk - Sensory deficits - Inc ICP and development of cerebral edema more common w hemorrhagic stroke, but can occur w ischemic stroke **Left-brain damage** - Paralyzed right side: hemiplegia - Impaired speech-language (aphasias) - Impaired right-left discrimination - Slow performance, cautious - Aware of deficits: depression, anxiety - Impaired comprehension related to language, math **Right-brain damage** - Paralyzed left side: hemiplegia - Left-sided neglect - Spatial-perceptual deficits - Tends to deny or minimize problems - Rapid performance, short attention span - Impulsive; safety problems - Impaired judgment - Impaired time concepts **Evaluation of stroke** - CT or MRI of head used for diagnosis - CT scan = easier to access and faster - Either can indicate the size & location of stroke and differentiate b/w ischemic and hemorrhagic - CTA -- allows for visualization of cerebral blood vessels - Identify blockages, aneurysms, or arterial malformations - Cerebral angiography -- more detailed images of blood vessels **Stroke: prevention** - Control of HTN, DM, and treatment of underlying cardiac issues (i.e. AF) - Lifestyle mods (i.e. quit smoking, exercise, limit alchol, etc) - Med therapy (in patients with previous transient ischemic attacks (TIA)) - Antiplatelets - Aspirin (ASA): antiplatelet drug - Inhibits cycle-oxygenate, the enzyme req to help plts create thromboxane - Thromboxane plays key role in pat aggregation - Clopidogrel (placid) - Inhibits plt aggregation - Works by inhibiting P2Y12 receptor on plts which prevents pat aggregation - Effects are not reversible, meaning that effects lasts 7-10 days after last dose - Can be given w aspirin - Surgical therapy (e.g. transluminal angioplasty) - Treat narrow or blocked arteries of the brain -- good for ppl w large areas of atherosclerosis which can lead to full blockage **Stroke: Acute Care** - Manage ABCs, maintain cerebral oxygenation - Manage fluid and electrolyte balance - Restore cerebral blood flow (ischemic stroke) -- thrombolytic therapy - Present and manage complications (i.e. bleeding, cerebral edema, stroke recurrence, aspiration) - Surgical therapy - Ischemic stroke: endovascular tx can be used to remove the clot - Hemorrhagic stroke: may need surgery to evacuate the hematoma - Aneurysms can be treated by clipping of the aneurysm in the operation room or coiling of the aneurysm in interventional radiology - Rehabilitation **Medication summary** +-----------------------------------+-----------------------------------+ | **Drug** | **Use/Nursing Considerations** | +===================================+===================================+ | Thrombolytics (alteplase \[tPA\]) | Used to dissolve blood clots | | | during an acute ischemic stroke. | | | Most effective when administered | | | within 3-4.5 hours of onset | | | | | | Monitor closely for signs of | | | bleeding | | | | | | Perform frequent neuro vitals | +-----------------------------------+-----------------------------------+ | Antiplatelets (ASA, clopidogrel) | Helps prevent blood clots | | | | | | Pts should be taught to recognize | | | signs of bleeding | | | | | | Meds should be taken exactly as | | | prescribed | | | | | | Avoid taking with NSAIDs (inc | | | risk of bleeding) | +-----------------------------------+-----------------------------------+ | Anticoagulants (warfarin | Prevent clots from forming | | \[Coumadin\], Apizaban | | | \[Eliquis\]) | Patients should be taught to | | | recognize signs of bleeding | | | | | | Meds should be taken exactly as | | | prescribed | | | | | | Warfarin is a Vit K antagonists | | | and requires regular blood | | | monitoring (INR 2-3) | | | | | | Warfarin interacts w a wide range | | | of meds, supplements and foods | | | (which can inc/dec its | | | anticoagulant effect) | | | | | | Apixaban is a DOAC (direct oral | | | anticoagulant) and can also | | | interact w various meds | +-----------------------------------+-----------------------------------+ | Other meds (e.g. statins, | Used to manage risk factors nano | | antihypertensives) | prevent stroke (e.g. high | | | cholesterol, high bp) | +-----------------------------------+-----------------------------------+ **Review Questions** 1. Which cranial nerve is responsible for pupil constriction? a. Cranial nerve II b. **Cranial nerve III** c. Cranial nerve IV d. Cranial nerve VI 2. Which layer of the meninges is the innermost and closely adheres to the surface of the brain? e. Dura mater f. Arachnoid mater g. **Pia mater** h. Epidural space 3. What is the primary effect of increased levels of CO2 on cerebral blood vessels? i. Vasoconstriction j. **Vasodilation** k. No effect l. Inc blood viscosity 4. What is the earliest indicator of increased ICP? m. **Change in level of consciousness (LOC)** n. Headache o. Vomiting p. Seizures 5. Which ocular change is considered an emergency and indicates potential brain herniation in a patient with increased ICP? q. Blurred vision r. Diplopia (double vision) s. **Fixed, dilated pupil** t. Sluggish response to light 6. A nurse is assessing a pt using the GSC. The pt opens their eyes only in response to pain, makes incomprehensible sounds, and withdraws from pain. What is the pt's GCS score? u. 6 v. 7 w. **8** x. 9 - Note: 2(eyes) + 2 (verbal) + 4 (pain) = 8 = intubate (threshold for intubation) 7. A nurse is caring for a pt with post concussion syndrome (PCS). Which of the following are common symptoms associated with this condition? (SATA) y. Long-term memory loss z. **Persistent headache** a. **Difficulty concentrating** b. **Sensitivity to light and noise** 8. A patient presents with a head injury and a period of lucidity followed by a rapid decline in consciousness. Which type of hematoma is most likely? c. Subdural hematoma d. **Epidural hematoma** e. Intracerebral hematoma f. Subarachnoid hemorrhage 9. Which type of brain injury is characterized by widespread damage to the brain's white matter, particularly the axons? g. Concussion h. Epidural hematoma i. **Diffuse axonal injury (DAI)** j. Subarachnoid hemorrhage 10. A nurse is caring for a patient w a suspected transient ischemic attack (TIA). Which of the following symptoms should the nurse expect to find? k. Persistent headache l. **Unilateral weakness** m. Hemiplegia n. Fixed and dilated pupils 11. A nurse is assessing a pt with right-brain damage following a stroke. Which of the following findings is most likely? o. **Impaired speech and language** p. Right-sided neglect q. Impulsive behaviour r. Slow and cautious performance 12. A pt is prescribed Clopidogrel (Plavix) for stroke prevention. Which statement by the pt indicates need for further teaching? s. "I will take this medication to prevent my platelets from clumping together" t. "the effects of this medication will last for about a week after I stop taking it" u. "I can take this medication with aspirin if my doctor advises" v. **"I can stop taking this medication whenever I feel better"**