Test 3 (GI, Endocrine, DM, Neuro) Flashcards
Gastrectomy
partial or full removal of stomach. Complication = dumping syndrome (occurs 30 min after eating, group of vasomotor symptoms, vertigo, tachycardia, syncope, sweating, pallor, palpitations. Eat small meals, high protein, high fat, low carbs).
Colostomy/Stoma
healthy stoma is red, pink, moist & protrudes 1-3cm and ¾ width. Avoid heavy lifting/straining. 1-2wk usual activities. Monitor bleeding/infection.
GI @ high risk for…
infection, inflammation, autoimmune d/o, cancer, motility issues, structural/mechanical alterations
Functions of GI
secretion, digestion, absorption, motility, elimination
Aging changes w/ GI
atrophy of gastric mucosa (absorption malfunction), ↓ peristalsis (nerves dull w/ elimination), calcification of pancreatic vessels (distention/dilation fat absorption), immune system issues/GI flora dysfunction
Stomatitis
inflammation in the oral cavity. Disrupts a person’s ability to eat, talk, sleep. Affects mouth, gums, tongue, lips, palate, inner cheeks. Risk factors = women. Avoid any acidic foods or hard/crunchy foods.
Types: primary (noninfectious canker/aphthous sore - eroded tissue integrity causing pain, bleeding, and infection. Caused by coffee, citrus, gluten); secondary/systemic (virus, fungi, bacteria, thrush, cancer, lesions), candida, herpes simplex, traumatic ulcers.
Oral Tumors
Squamous cell carcinomas (most common. Occurs on lips, tongue, inner cheek, oropharynx. Red raised eroded lesions), Basal cell carcinomas (skin cancer, sun exposure), kaposi sarcoma (vascular painless tumor in mouth, tongue, gums, palate. Caused by AIDS).
Esophageal Tumors
squamous cell carcinoma (upper ⅔), adenocarcinoma (distal ⅓ - most common). High risk for metastasis w/ mucosa/lymph tissue to spread. Risk factors = ETOH, obesity, smoking, GERD. “silent tumor.” S/S = persistent and progressive dysphagia, obstruction, hoarseness, anorexia, regurgitation.
Oral cancer
S/S = bleeding from mouth, poor appetite/compromised nutritional status, difficulty chewing/swallowing, unplanned weight loss, thick/absent saliva, painless oral lesion that is red/raised/eroded, thickening or lump in cheek. Priority = gas exchange/airway management.
Sialadenitis
acute inflammation of the salivary gland. Affects parotid & submandibular glands. Cause = bacteria, virus, CMV, ↓ saliva production (oral, head, or neck radiation), systemic drugs (phenothiazines, tetracycline). Assessment = oral cavity, facial cranial nerves, fever/malaise. Treatment = underlying cause. Complications = abscess/systemic infection.
GERD
upper GI d/o where backflow of stomach contents into esophagus (regurgitation). Risk factors = obesity, H pylori, nutrition (coffee, caffeine, ETOH, citrus, tomatoes, chocolate), meds/lifestyle (smoking, CCB, anticholinergic, estrogen). S/S = asymptomatic (early), chest pain, burning, heartburn, sour stomach, morning hoarseness, odynophagia (painful swallowing). Complications = asthma, cough/wheezing, aspiration,), Barrett’s Esophagus (premalignant and risk of cancer. Epithelium causes resistance to acid/healing),, dental decay, cardiac disease (esophageal irritability), hemorrhage (varices), aspiration pneumonia. Interventions = balance nutrition, manage pain, drugs (antacids, H2 blockers, PPIs).
Hiatal Hernias
protrusions of the stomach through lining. Complications = volvulus (twisting), obstruction, strangulation (stricture), iron-deficient anemia, hemorrhage (rare). S/S = asymptomatic (early), GERD-like, worse pain after eating, dysphagia, supine is worse/fullness/breathless w/ meals. Diagnostic = barium swallow surgery (fluoroscopy). Interventions = non-surg (nutrition, lifestyle, PPI/GERD meds), surg (LNF - invasive surgery. Complications = bleeding, infection, DVT, respiratory. Post op - soft diet, PPI/H2 blockers, wound care).
Esophageal trauma
causes = blunt trauma, inhalation, surgery, seve vomiting, chemical burns w/ ingestions of caustic substances (acid - superficial mucosa affected, alkaline - deeper penetrating injury).
Gastritis
: Inflammation of the gastric mucosa (stomach lining). Prevention = balanced diet, regular exercise (maintains peristalsis which helps prevent gastric contents to irritate), stress reduction.
Acute Gastritis
ocal irritants causing the inflammation (thick red mucosa). Risk factors = bleeding and hemorrhage. Causes = long term NSAIDs, ETOH, coffee, caffeine, stress, smoking, drugs (steroids, aldosterone antagonists, SRIs). S/S = epigastric pain, dyspepsia, GI bleeding, hematemesis, melena. Diagnostic = EGD w/ biopsy. Interventions = treat symptoms, diet choices, drugs (PPI’s, H2 receptor antagonist, antacids), surgery (partial gastrectomy for major bleeding or severe ulcers)
Chronic Gastritis
chronic/systemic disorders causing the inflammation (patchy, diffuse). Risk factors = stomach cancer, bleeding, hemorrhage, CKD, inflammatory conditions. Causes = ETOh, smoking, radiation, chrons, uremia, surgery that ↑ acid production. Complications = pernicious anemia (vit B12), helicobacter pylori (type B gastritis). S/S = upper abdominal pain, anorexia, N/V, constant pain after eating. Diagnostic = EGD w/ biopsy, monitor DI tests w/ trends. Interventions = treat cause and symptoms, drugs (same as acute but may be lifelong).
Peptic Ulcer Disease
GI mucosal defenses become impaired and no protection from acid or pepsin. Causes = bacterial infection (H. pylori), long use of NSAIDs, family hx. S/S = upper GI bleeding (hematemesis, melena), ↓ H & H, ↓ BP, ↑ HR, weak pulse, acute confusion (OA), vertigo, dizziness, syncope. Complications = high risk (gastric ulcers, age), perforation (full thickness ulcer that erodes the GI wall splitting contents into peritoneal cavity. Tender, rigid abdomen - peritonitis. Untreated causes sepsis and hypovolemic shock), pyloric obstruction (caused by scarring, edema, inflammation, tumor. S/S = abdomen bloating, fullness pain, n/v), metabolic alkalosis (the loss of large quantities of gastric secretions), hypokalemia (from N/V or metabolic alkalosis). Diagnostic = CBC, H. pylori serum or stool test, stool antigen test, EDG. Interventions = manage acute/persistent pain, manage upper GI bleeding (priority. Fluid volume loss, blood loss, non surg - NG tube/lavage, surg - laparoscopy, gastrectomy, pyloroplasty), drugs (PPI, abx).
Gastric: Located in the antrum of the stomach. Inflammation of the mucosa. Causes = bacteria (transmission = oral to oral or fecal to oral).
Duodenal: most common w/ deep lesions. Located in upper portion of duodenum. High gastric secretion (excess acid w/ low pH). Causes = same as gastric.
Stress: stress of body no personal (acute gastric lesion). High mortality. Causes = sepsis, burns, head injury, trauma, untreated bacteria infection. Treatment = abx (clarithromycin, amoxicillin, tetracycline, metronidazole).
Gastric Cancer
Adenocarcinomas (abnormal mucosal cells in the lining of stomach), precancerous (gastritis & metaplasia - abnormal tissues). Risk factors = men and women > 50yo. 5 year survival rate d/t asymptomatic early. If untreated, metastasis to lymph w/ direct invasion to liver, pancreas, colon. Causes = H pylori, polyps, gastritis, anemia. S/S = early (dyspepsia, abdominal discomfort that can be relieved by antacids, feeling of fullness, epigastric/back/retrosternal pain), late (N/V, iron deficiency anemia, palpable epigastric mass, enlarged lymph, weakness/fatigue, progressive weight loss). Diagnostic = ↓ H&H, + guaiac stool, ↓ albumin, ↑ LFT). Treatment = radiation, chemo, surgery (tumor resection, gastrectomy), palliative (advanced).
Colorectal Cancer
cancer of large intestine and rectum. Risk factors = age, genetic, hx of Chrons or UC. Early diagnosis = highly curable. Causes = adenomatous polyps, smoking, ETOh, obesity, red mean and high fat diet (d/t high bile acid secretion and antibiotics in foods). Promotion = diagnostic screening, colonoscopy Q10 yr. S/S = rectal bleeding, change in stool, elimination habits, abdominal fullness/pain, anemia, weakness, weight loss, bloating, gas pain. Labs = guaiac stool test, fecal occult blood test, CEA, CBC. Diagnostic = CT, sigmoid/colonoscopy w/ biopsy. Interventions = pathology staging, chemo, radiation, removal of tumor/lymph nodes/colon resection.
Colorectal Cancer
cancer of large intestine and rectum. Risk factors = age, genetic, hx of Chrons or UC. Early diagnosis = highly curable. Causes = adenomatous polyps, smoking, ETOh, obesity, red mean and high fat diet (d/t high bile acid secretion and antibiotics in foods). Promotion = diagnostic screening, colonoscopy Q10 yr. S/S = rectal bleeding, change in stool, elimination habits, abdominal fullness/pain, anemia, weakness, weight loss, bloating, gas pain. Labs = guaiac stool test, fecal occult blood test, CEA, CBC. Diagnostic = CT, sigmoid/colonoscopy w/ biopsy. Interventions = pathology staging, chemo, radiation, removal of tumor/lymph nodes/colon resection.
IBS
(spastic/nervous colon) functional GI d/o that causes chronic/recurrent diarrhea, constipation, or abdominal pain. Causes = environmental/foods, hormonal, genetic, bacteria overgrowth, stress w/ mental illness. S/S = pain, wkns, bloating, diarrhea, constipation. Labs = CBC, albumin, ESR (inflammatory), stools for occult blood. Interventions = stress reduction, counseling. Drug = symptom control (bulk forming or antidiarrheals, probiotics, antidepressants, rifaximin, alosetron.
Obstructions
Blockage. All obstructions can lead to abdominal distention d/t contents accumulating at/above the area of obstruction (inability to absorb the contents & move waste. Peristalsis ↑ to move contents as compensatory rxn, bowel becomes edematous, plasma leaking into peritoneal cavity and fluid trapped in intestinal lumen). Complications = hypovolemic → hypovolemic shock (↓ blood volume), electrolyte imbalances, metabolic alkalosis (obstruction high in small interesting and lower tract causes loss in alkaline fluids), metabolic acidosis (obstruction at end of small interesting and lower tract causes loss in alkaline fluids). Untreated → AKI, bacterial peritonitis, blood flow complications (compartment syndrome). Assessment = Hx, hiccups, hypotn, could be peritonitis. Labs = no labs for obstruction. WBC could indicate strangulation/infarction/gangrene, increased H&H/BUN d/t dehydration. Diagnostic = CT, MRI, KUB, US, endoscopy, colonoscopy. Interventions = NPO, monitor, pain, NG tube (for bowel rest - salem sump w/ vent, assess Q4hr), surgery, prevent recurrence, bowel regimen, diet teaching, (high fiber foods, hydration, warm beverages to stimulate peristalsis).
Mechanical: bowel is physically blocked. Can be outside the intestine (adhesions), in the bowel wall (stricture in chrons), in intestinal lumen (tumors), hernias, can be intussusception/volvulus.. Risk factor = >60yo. Intervention = surgery (exploratory lap) —
Non-mechanical: paralytic ileus or functional obstruction. Post op ileus (POI - common by handling intestines during surgery) or intestinal ischemia (vascular insufficiency by arterial or venous thrombosis - mesenteric. Severe cases cause bowel infarction, gangrene, sepsis/shock). –
Small-bowel: abdominal discomfort or pain possibly accompanied by visible peristaltic waves in upper & middle abdomen. Upper or epigastric abdominal distention. Nausea and early, profuse vomiting (may contain fecal matter), obstipation, severe F/E imbalance, metabolic alkalosis. —
Large-bowel: intermittent lower abdominal cramping, lower abdominal distention, minimal or no vomiting, obstipation/ribbon like stools, no major f/e imbalance, metabolic acidosis.
Hemorrhoids
unnaturally swollen/distended veins in the anorectal region. Arterioles shunt blood to distended veins. Increase IAP, distended veins separate from smooth muscle resulting in prolapse of hemorrhoidal vessels. Can get blood clots w/in hemorrhoids. Causes = IAP from pregnancy, constipation w/ straining, obesity, HF, prolonged sitting/standing, weightlifting, strenuous activity. S/S = swelling, bleeding, prolapse/ bulging, bright red streaks of blood, rectal pain (thrombosed), itching, discharge. Interventions = treat symptoms/causes. Sitz bath, cold packs, topical anesthetics, high fiber/fluid diet, soft stools to avoid straining. Surgery = hemorrhoidectomy(for severe)
Types: Internal (above anal sphincter), external (below anal sphincter), prolapsed (thrombosed or inflammed, bleeding).
Appendicitis
acute inflammation of the vermiform appendix. Inflammation occurs where opening is obstructed leading to infection as bacteria enter the wall of the appendix. Causes = feces w/calcium deposits, mucous, salts. Complications = sepsis, peritonitis, gangrene. Labs=WBC >10-18K w/ L shift (immature WBC) or >20K if perforation of appendicitis. Diagnostic = US/CT. Intervention = pain control, appendectomy, lap or open surgery, education (abx, pain meds).
Peritonitis
acute inflammation and infection of the visceral/parietal peritoneum & endothelial lining of the abdominal cavity. Cause = contamination of peritoneal cavity by bacteria (e coli, strep, staphylococcus, pneumococcus, gonococcus) or chemicals (leakage of bile, pancreatic enzymes, gastric acid; perforation entry for appendicitis/diverticulitis/bowel segment, bowel obstruction, tumor, surgery complication, infection from peritoneal dialysis. S/S=rigid abd, abd pain, distended abd, N/V, anorexia, ↓ bowel tones, high fever, dehydration, tachycardia, ↓ urine output. Complications (if untreated) = fluid shift (↓ circulatory vol, hypovolemic shock), insufficient perfusion of kidneys (AKI w/ impaired F/E), septicemia (septic shock), ↑ abd pressure (IAP - respiratory distress). Labs = CBC, WBC (>20K w/ ↑ neutrophil), blood culture, gram -/+, renal labs (AKI/sepsis), ABG (metabolic acidosis/sepsis). Diagnostic = XR, US, CT. Interventions=monitor for septic shock (hypotn, tachycardia, fever, tachypnea, confusion), pain management, IV fluids, abx, O2, surgery (laparotomy, open abd surgery - identify cause and repair).
Gastroenteritis
very common health problem causes D/V r/t inflammation of mucous membranes of stomach/intestinal tract. Viral (more common) or bacterial. Assessment = travel, restaurant, camping, markets, raw/undercooked foods. Complications = (older adults) wkns, cardiac dysrhythmias, hypokalemia, hypovolemia. S/S = pale, diarrhea (blood, mucous), N/V, fever, abd pain/cramping, dehydration (late stage - poor skin turgor, fever, dry mucous membranes, orthostatic BP, hypotn, oliguria). Interventions = fluid replacement, oral replacement, IV fluids. Drugs = not recommended in early stage, loperamide( if cultures -), antinausea, abx (if bacterial).
Ulcerative Colitis
extensive (entire colon) disease that creates widespread chronic inflammation of the rectum and rectosigmoid colon. High risk for colorectal cancer. S/S = intestinal mucosa, edema, red, stool, mucous, blood, abd pain/distention, tachycardia, malaise, anorexia, anemia, fever, dehydration, severe (bloody stool w/ sm erosions/ulcers, abscess or tissue necrosis, edema could cause bowel obstruction), peritonitis/bowel perforation. Labs = WBC, ESR, CRP (inflammation), low Na/K/Cl (diarrhea) or CBC (blood loss). Diagnostic = MRE (enterorrhaphy) or upper endoscopy, colonoscopy. Interventions = managing diarrhea, monitor GI bleed, manage pain, nutrition therapy, drug therapy (aminosalicylates, glucocorticoids, antidiarrheals), surgical (optional, toxic megacolon, hemorrhage, bowel perforation, colorectal cancer), ileostomy (output is green, loose, dark, blood - may irritate skin more d/t bile salts and enzymes).
Ulcerative Colitis
extensive (entire colon) disease that creates widespread chronic inflammation of the rectum and rectosigmoid colon. High risk for colorectal cancer. S/S = intestinal mucosa, edema, red, stool, mucous, blood, abd pain/distention, tachycardia, malaise, anorexia, anemia, fever, dehydration, severe (bloody stool w/ sm erosions/ulcers, abscess or tissue necrosis, edema could cause bowel obstruction), peritonitis/bowel perforation. Labs = WBC, ESR, CRP (inflammation), low Na/K/Cl (diarrhea) or CBC (blood loss). Diagnostic = MRE (enterorrhaphy) or upper endoscopy, colonoscopy. Interventions = managing diarrhea, monitor GI bleed, manage pain, nutrition therapy, drug therapy (aminosalicylates, glucocorticoids, antidiarrheals), surgical (optional, toxic megacolon, hemorrhage, bowel perforation, colorectal cancer), ileostomy (output is green, loose, dark, blood - may irritate skin more d/t bile salts and enzymes).
Crohn’s
chronic inflammatory disease of the small intestines (occasionally large intestines). Recurrent, remissions, exacerbations. Fatty lining may cause fatty stools (steatorrhea). Cause = genetic, autoimmune, environmental. Risk factors = tobacco, stress, nutrition, jewish, young adults 15-35. S/S = diarrhea, anemia, hemorrhage, deep ulcers/fistular. Labs= anemia, vit B12 deficiency folic acid, CRP (inflammation abnormal if > 10), ESR (inflammation, abnormal if > 13), F/E balance (hypokalemia, hypomagnesemia). Diagnostic = XR, MRE. Interventions = symptom control, nutrition therapy (low residue, high calorie, avoid dairy/gluten), drug (azathioprine, mercaptopurine, methotrexate, glucocorticoid), surgical (laparoscopy - MIS, resection of diseased area or perforation/hemorrhage/obstruction/abscess/cancer)
Diverticular Disease
pouch-like herniations of the mucosa through the muscular wall in the small or lg intestine, usually in sigmoid colon. Is a weakness in the intestinal wall. Inflammation occurs w/ food, bacteria trapped and could perforate/abscess or peritonitis/GI bleeding.
Diverticulosis: presence of abnormal pouches (diverticula). Asymptomatic and undiagnosed except routine colonoscopy.
Diverticulitis: acute inflammation or infection of diverticula. S/S = fever, abd pain, nausea, LLQ, elimination changes, bleeding, distention. Labs = EBC, low CBC, stool studies for blood. Diagnostic = XR (free air), CT (abscess), US. Complications = peritonitis, rebound tenderness, sepsis, hypotn, hypovolemic shock. Interventions = pain control, drugs (metronidazole, sulfa, ciprofloxacin, IV fluids, avoid laxatives - motility issues), monitor for GI bleeding, surgery (if peritonitis, abscess, bowel obstruction, fistula, bleeding - colon resection - colostomy), education (high fiber diet, avoid gassy foods, avoid seeds, corn, veggies w/ seeds, nuts).
Celiac disease
a chronic inflammation of the small intestine mucosa that causes bowel wall atrophy, malabsorption, diarrhea. Multisystem autoimmune disease. Cause = genetic, immunologic, environmental factors. Severe = cancer, non-hodgkin’s lymphoma, gastric cancer. S/S = typical (anorexia, diarrhea, constipation, fatty stools, abd pain, bloating, distention, weight loss), atypical (osteoporosis, joint pain, anemia, migraine, epilepsy, infertility, autoimmune).
Parasitic infection
Lab = ↑ WBC, stool studies (O&P). Drugs = metronidazole/ paromomycin, amebicide
Cirrhosis
extensive, irreversible scarring of the liver, usually caused by hepatic inflammation and necrosis. Inflammation caused by toxins or disease w/ extensive degeneration/destruction of liver cells (hepatocytes). Liver nodules block bile ducts and blood flow → ↓ liver function over weeks to years. Scarring impairs cellular regulation leading to end stage liver disease. Cause = chronic alcoholisms, chronic viral hepatitis, bile duct disease, hepatitis B & C, age, obesity, DM, genetic (latinos). Types = post necrotic cirrhosis (viral hepatitis, drugs - isoniazid, flutamide), alcoholic cirrhosis, biliary cirrhosis (chronic biliary obstruction/autoimmune disease), nonalcoholic fatty liver disease. Assessment = hx (family, social, medical - abd surgery, blood transfusions, autoimmune, obesity, lipid panel, HF, respiratory d/o, liver injury, psychosocial - cognitive, personality changes, agitation, sleep patterns, emotional), physical (jaundice, icterus, itching, rashes, edema, ascites, fatigue, changes in weight, GI symptoms, nausea, abd pain, hernias (high risk), hepatomegaly, splenomegaly, neurologic function, girth measurements, asterixis (coarse tremors w/ flexion). Labs = abnormal liver function tests, AST, ALT, LDH, GGT, Alk phos, total bili, albumen, hyponatremia (ascites). Diagnostic = XR, CT, MRI, US, EGD. Priorities = fluid overload d/t third spacing of abd & peripheral fluid (ascites), potential for hemorrhage d/t portal HTN & subsequent GI varices, acute confusion & other cognitive changes d/t increased serum ammonia levels and/or alcohol withdrawal, pruritus d/t increased serum bilirubin and jaundice. Education = nutrition therapy, alcohol cessation, drug therapy (diuretic, K replacement, PPI; avoid OTC NSAIDs, tylenol, smoking drugs), psychosocial support.
Alcohol withdrawal s/s - tremors, jitters (6-8hrs after last drink), delirium tremens (DT), confusion, anxiety, odd behaviors, tachycardia, ↑ BP, sweaty.
Complications of cirrhosis
PORTAL HYPERTENSION: Increase in pressure within the portal vein < 5 mmHg. Obstruction/blockage of blood flow in portal vein causing splenomegaly. Veins in the esophagus, stomach, intestines, abdomen, and rectum dilate. Splenomegaly is from backup of blood into the spleen → enlarged spleen destroys platelets causing thrombocytopenia. Early sign of liver disease = low platelets.
ASCITES: Portal HTN causes ascites. A collection of free fluid within the peritoneal cavity caused by increased hydrostatic pressure from portal HTN. FLuid shifts from the vascular system to their spacing. Risk = hypovolemia & edema.
ESOPHAGEAL VARICES: Fragile thin walled esophageal veins gets distended from pressure. Portal HTN blood backs up from liver and enters esophageal and gastric veins. Life threatening medical emergency causing hypovolemic shock.
BILIARY OBSTRUCTION: genetic. Obstruction of the bile duct that leads to biliary cirrhosis. Production of bile is decreased which prevents clotting factors to produce prevention of vit K absorption. Cause = gallbladder disease or autoimmune disease.
HEPATIC ENCEPHALOPATHY: complex cognitive syndrome from liver failure and late cirrhosis. Shunts portal venous blood into central circulation so liver is bypassed. Labs = elevated ammonia > 45 (liver protein breakdown). S/S = early (confusion, mental status changes, mood, insomnia, speech difficulties), late (altered LOC, impaired thinking, neuromuscular problems).
JAUNDICE: yellow coloration of skin. Causes = hepatocellular disease liver cells cant excrete bilirubin, intrahepatic obstruction (edema, scarring on hepatic bile ducts interferes w/ excretion). Jaundice pts report itching excessively.
Managing fluid volume - preventing/managing hemorrhage r/t cirrhosis
nutrition (low sodium, IV supplements - thiamine, folate, MVT), drug (diuretics, oral potassium, IV abx), Paracentesis (invasive procedure to remove fluid), hemorrhage (prevent varices - beta blocker, vasoactive drugs, TIPS for severe esophageal varices), managing confusion (lactulose to remove excretion of ammonia in the flood for hepatic encephalopathy and pneumonia), manage itching.
Hepatitis
widespread inflammation and infection of the liver cells. Viral (acute or chronic). Risk factors = advanced age, chronic liver disease. Causes = environmental, liver injury from hepatotoxins, autoimmune. S/S = abd pain, yellow sclera, joint/muscle pain, diarrhea/constipation, light colored stools, dark urine, jaundice, fever, fatigue, n/v, itchy/dry skin. Labs = Hep A/B (lab test), Hep C/D/E (antibody titers), elevated liver tests (ALT, AST, Alk phos, bili). Diagnostic = liver biopsy, CT scan. Education = handwashing, community education.
Liver transplant
common procedure for end stage liver disease/liver failure. Cirrhosis is #1 reason for transplant. Transplant complications = acute graft rejection (tachycardia, fever, abd pain, jaundice), infection (prophylactic abx, immunosuppressants).
Functions of biliary system
secretes enzymes, promotes food digestion in the stomach & sm intestine, impairment in the biliary system impairs digestion leading to inadequate nutrition.
Cholecystitis
Inflammation of the gallbladder. Assessment = hx (nutrition, GI symptoms), physical (abd pain, atypical s/s w/ DM and age, rebound tenderness, jaundice, dark urine, icterus, steatorrhea, inflammation, fever, tachycardia, dehydration, pain triggered by meal, anorexia, dyspepsia, eructation, flatulence).
Acute cholecystitis
chemical irritation and inflammation from gallstones and calculi (from bile salts, cholesterol metabolisms, calcium, proteins. Mixed w. Mucous and viscous bile builds gallstones) that obstructs the cystic duct, gallbladder neck or common bile duct. How it happens = Gallbladder gets inflamed, bile is trapped & reabsorbed and irritates the gallbladder wall, bile-edema-gallbladder distension, impaired circulation, infection/inflammation/ischemia, tissue sloughing w/ necrosis/gangrene or gallbladder ruptures/perforates causing abscess/peritonitis (if severe). Labs = differential diagnosis to r/o other GI problems, WBC > 10k, elevated AST/LDH, amylase/lipase. Diagnostic = abd XR, US, HIDA scan, ERCP, MRI. Interventions = managing acute pain, non surg (prevention, diet controlled, high fiber, avoid fatty foods, acute (hydration, IV fluids, pain meds, abx), surg (procedure for breaking up gallstones like kidney stones - lithotripsy; lap chole).
Gallbladder complications: motility issues - lead to stone formation by delaying bile emptying and causes biliary stasis. Can be from a twist or kinking of GB neck or cystic duct or acalculous cholecystitis.
Gallstones: Causes = obesity, genetics (nutrition & genetic marker), high cholesterol, american indian, pregnancy, HRT decreasing bile emptying. Four F’s (female, fat, forty, fertile).
Chronic cholecystitis
recurrent episodes of cystic duct obstruction caused by chronic inflammation. Calculi present. GB becomes weak, fibrotic atrophy, decreased motility, deficient absorption. Causes = diet low in fat, vegetarian diet, pancreatitis, cholangitis (bile duct), back up bile (obstruction and jaundice).
Acute pancreatitis
serious and life threatening inflammation of the pancreas. 4 major patho processes = lipolysis (lipase enzyme), proteolysis (thrombus. gangrene), necrosis of blood vessels and inflammation (bleeding), mild involvement evidenced by edema & inflammation. Causes = ETOH, gallstones, obstructive pancreatitis, trauma, chole, gastrectomy. Complications = jaundice, pancreatic pseudocyst, hyperglycemia, pleural effusions, pulmonary failure, multisystem organ failure, ARDS, coagulation/hemorrhage (DIC, necrotic tissue), shock & hypovolemia (ARF), pancreatic infection, AKF, T2DM. S/S = inflammation, abd issues, jaundice, bowel tones, rigid abd. Labs = amylase, lipase, trypsin, elastase, glucose, bili, ALT, AST, CRP, leuko, BUN, triglycerides; Ca, Mg, platelets, albumin - decreased labs. Diagnostic = US, CT, XR, ERCP. Interventions = symptom control, nutrition therapy, IV therapy, NG tube, NPO, drug (PPI, H2 receptors, abx, antiemetics, ca or mg replacement), surgical (ERCP or lap chole).
Chronic Pancreatitis
Progressive, destructive disease of the pancreas that has remission and exacerbations. Inflammation w/ tissue fibrosis, pancreatic insufficiency, diminished organ function. S/S = intense abd pain, ascites, steatorrhea, jaundice, dark urine. Labs = increase amylase, lipase, bili, alk phos, glucose; decreased albumin. Diagnostic = ERCP, CT, MRI, US. Interventions = calories up to 4000/day to maintain weight, foods high in carbs/protein, avoid ETOH and high fat foods, drugs (pain, pancreatic enzymes, H2 blockers, PPIs, TPN/enteral feeding), Surgical (lap chole, sphincterotomy, partial resection, transplant)
Pancreatic Cancer
(adenocarcinoma/head of pancreas) rapid growing tumor w/ rapid mets to lymph & vascular systems. High risk pts = DM, cirrhosis, obesity, smoking, age, genetic, family hx, red meat intake. S/S: early asymptomatic, abd pain, clay stools, GI bleed, palpable mass, hepatomegaly, jaundice, weakness, weight loss. Venous thromboembolism is common complication. Labs = increase LFT, amylase, lipase, alk phos, bili. Genetic marker (CEA). Interventions = prevent tumor spread and decreasing symptoms, no cure, pain management, chemo and radiation, surgical (partial pancreatectomy, whipple)
Surgical complications: DM, hemorrhage, wound infection, bowel obstruction, intra-abd abscess. Whipple complications = hemorrhage, hypovolemia, MI, HF, thrombophlebitis, pulmonary complications (atelectasis, PNA, PE, ARDS, pulmonary edema), metabolic (renal failure), wound infection.
Type 1 DM
Insulin prod is absent d/t autoimmune pancreatic beta-cell destruction — susceptible genes, autoantigens, environmental factors, viruses, diet.
Type 2 DM
insulin resistance and decreased insulin secretion. Inability to suppress hepatic glucose production, impaired glucose uptake. Some beta cell dysfunction.
Indications for testing ppl for T2DM = BMI > 25, first degree relative w/ DM, physically inactive, high-risk ethnic population, gave birth to baby weighing > 9# or had gestational diabetes, A1C>5.7%
S/S of DM
fatigue, 3P’s (polyuria, polydipsia, polyphagia), recent infections, skin injuries, changes in vision, sensory changes
Screening for DM
Korean/Vietnam vet (exposure to agent orange, digoxin), recommended for pts > 45yr
Metabolic syndrome
simultaneous presence of metabolic factors that increase risk for developing T2DM and CVD. (abdominal obesity, hyperglycemia, HTN, hyperlipidemia, HDL < 40/50
Absence of Insulin
glucose regulation requires insulin to move glucose into many tissues. Lack of production or a problem w/ insulin use at cell receptors. The absence of insulin causes glucose to build up in the blood causing hyperglycemia - disturb f/e balance (leads to polyuria, polydipsia, polyphagia). Insulin secreted daily in a two step manner (low level secretion during fasting - basal insulin secretion; two phase release after eating - prandial - an early burst of insulin secretion occurs within 10 min of eating, followed by an increasing release that lasts until BG level returns to normal)
Insulin stimulators
Stimulate insulin release from pancreatic beta cells. Used for pts who are still able to produce insulin (functioning pancreas). Include sulfonylureas (glipizide), meglitinide analogs (repaglinide). Education = s/s of hypoglycemia, take w/ or just before meals to prevent hypoglycemia
Biguanides: (Metformin)
lower BG by inhibiting liver glucose production, decreasing intestinal absorption of glucose and increasing insulin sensitivity (on cells). Education = no ETOH, must be stopped b4 using contrast agents and not started again for 48hr after testing d/t increased risk for kidney damage and lactic acidosis. Administer w/ meals to minimize GI effects. May cause hypoglycemia if combined w/ sulfonylurea.
Insulin Sensitizers (thiazolidinediones (TZDs or glitazones))
Increase cellular use of glucose, which lowers BG. Black box warning - serious side effects - heart related deaths. Education = weigh daily (report 2lbs in one day or 4-5lbs in one week). Report vision changes immediately. Weight gain and peripheral edema are common.
Incretin Mimetics (GLP-1 Agonist) (Dulaglutide):
reduces liver glucose production and delays gastric emptying. Can cause hypoglycemia when used w/ insulin, sulfonylureas or meglitinides. Education = s/s of hypoglycemia, how to inject (SQ), report persistent abd pain/nausea, read pens carefully (some ER is only ejected weekly).
Dipeptidyl peptidase-4 (DPP-4) Inhibitors (Alogliptin)
breaks down natural gut hormones (GLP-1 & GIP). Works w/ body’s insulin. Reduces BG levels by delaying gastric emptying. Education = hypoglycemia, report a rash/persistent abd pain/dyspnea on exertion/cough esp when lying down. Associated w/ HF.
Sodium-Glucose Cotransport Inhibitors (SGLT2) (Canagliflozin)
glucose is excreted in urine rather than moved back into blood. Education = hypoglycemia, dehydration, hyponatremia, UTI, genital yeast infection, report any swelling/tenderness/redness or genitals or perineal skin.
Insulin therapy
For T1 and T2(when other measures fail). Timing = for rapid onset give within 10 min before or after mealtime; regular insulin give 20-30 min prior to mealtime
Education for DM
BG monitoring - teach to assess BG frequently for these situations: s/s of hypo/hyperglycemia, periods of illness or stress, b4 of after exercise, gastroparesis, adjustment of meds, pregnancy.
Nutrition - RDN. Consider cultural background, financial status, lifestyle. No alcohol.
Exercise - improves glycemic control. Decreased mortality and improved A1C. Exercise a min of 50 min 3x/week. Can cause hypoglycemia in T1DM. May need carbs during workout.
The diabetic foot - inspect feet daily. Wash daily in lukewarm water (use thermometer), mild soap, dry thoroughly. Apply fragrance free moisturizer to top and bottom of feet but avoid between toes. Clean cotton socks daily. Breathable shoes. Trim nails straight across, smooth w/ emery board.
Reducing risk for kidney disease - BG control, ACE or ARB, annual kidney function eval, cholesterol management, avoid nephrotoxic agents, smoking cessation.
Sick day rules = Notify HCP that you are ill. Monitor BG at least Q4hrs. Test urine for ketones when BG > 240. Continue to take insulin or other antidiabetic agents. Prevent dehydration (drink 8-12 oz sugar free liq every hr you are awake). Call diabetes HCP if: persistent N/V, BG elevation after 2 supplemental doses of insulin, high temp or increasing fever (fever > 24 hr).
Hypoglycemia
Cold and clammy need some candy. Cool, clammy, sweaty, anxious, nervous, irritable, confusion, seizure, coma, wkns, double/blurred vision, hunger, tachycardia, palpitations.
15-15 rule
Hyperglycemia
hot and dry = sugar high. Warm, dry, vasodilated skin, s/s of dehydration, rapid/deep respirations, rotten fruity breath, abd cramps, N/V, BG >250.
Dawn phenomenon: abnormal early morning hyperglycemia. Interventions = additional insulin at 10pm instead of evening meal. Avoid carbs b4 bedtime, increase evening exercise, increase protein intake. Do not skip breakfast.
Somogyi Phenomenon: begins as hypoglycemic episode overnight. Body has a hormonal response that causes hyperglycemia. Caused by excess insulin &/or inadequate calorie intake with insulin therapy
Diagnosis dawn or somogyi phenomenon = check BG around 2 or 3 am for several nights in a row. Write down other contributing factors. Discuss findings w/ PCP.
Diabetic ketoacidosis
Complications of DM characterized by uncontrolled hyperglycemia, metabolic acidosis, and increased prod of ketones. Wide anion gap (Cl, bicarb, Na); When gap closes that’s when pt no longer in DKA. Most common precipitating factor is infection. S/S=dehydration w/ electrolyte loss, polyuria, polydipsia, polyphagia, rotting citrus fruit odor to breath, vomiting, abd pain, dehydration, wkns, confusion, shock, coma. Interventions=BG management, f/e, drug therapy.
Hyperglycemic-hyperosmolar state
Hyperosmolar state caused by hyperglycemia. Caused by sustained osmotic diuresis leading to extremely high BG levels. Differs from DKS in that ketone levels are absent or low and BG levels are much higher (BG may exceed 600; blood osmol may exceed 320). Interventions = fluid replacement (.5NS or NS if shock or severe hypotn. Infused at 1L/hr. Assess hourly for s/s of cerebral edema).
Macrovascular (Chronic complications of DM)
CVD: treatment = aggressive management of HTN, hyperglycemia, hyperlipidemia.
Cerebrovascular disease: high risk of stroke. Increases likelihood of severe carotid atherosclerosis
Reduced immunity: combination of vascular changes & hyperglycemia reduces immunity. Infections become serious more quickly. (WBC don’t like to swim in a sugary environment).
Microvascular(Chronic complications of DM)
Eye & Vision: diabetic retinopathy (r/t blocked retinal blood vessels and cause them to leak, leading to retinal hypoxia), blindness, sensory perception, cataracts, open angle glaucoma –
Diabetic peripheral neuropathy: progressive deterioration of nerve function. Damage causes pain at first, followed by loss of sensation. Onset slow. Damage to nerve fibers in ANS. ANS also affects bowels, bladder, etc (can cause incontinence). –
Diabetic autonomic neuropathy: cardiovascular autonomic neuropathy (CAN). Orthostatic hypotn, syncope. D/T failure of heart & arteries to respond to position changes by increasing HR & vascular tone. Can affect entire GI system (gastroparesis). Loss of normal sweating, skin temp regulation. Dry, thinning skin. Skin cracks and fissures. —
Diabetic nephropathy: changes in the kidney. Leading cause of ESRD. Causes progressive albumin excretion and declining GFR. —
Sexual dysfunction: d/t damage to both nerve and vascular tissue. Made worse by poorly controlled BG. —
Cognitive dysfunction: DM increases risk for developing all types of dementia. D/T neuron damage, brain atrophy, cognitive impairment. Frequent and more severe in longer duration DM. Increase complications of neuropathy and retinopathy.
Overview of endocrine system
Glands works w/ CNS & PNS to secrete hormones. Important roles in homeostasis = metabolism, nutrition, elimination, temperature, f/e balance, growth, reproduction
Endocrine Changes w/ Aging
Decreased ADH production (urine more dilute and may not concentrate when fluid intake low. Offer fluids Q2hr if no restrictions), decreased ovarian production of estrogen (decreased bone density, skin is thinner/drier), decreased glucose tolerance (weight gain, elevating fasting BG, slow wound healing), decreased general metabolism (poor cold tolerance, HR & BP decreased).
Hypopituitarism
deficiency of one or more pituitary hormones (anterior). Causes = diseases of pituitary gland, diseases of hypothalamus, tumors, malnutrition or rapid loss of body fat, head trauma, infection, radiation or surgery or the head/brain, AIDS. Interventions = management focuses on replacement of all deficient hormones. Replace deficient hormones (hydrocortisone, levothyroxine, testosterone, estradiol, injections of GH). Treat tumors if present.
Anterior Pituitary Hormones & Symptoms - Growth Hormone (GH; Somatotropin) (changes in body composition - increased fat mass, decreased lean body mass); Thyroid Stimulating Hormone (TSH; Thyrotropin)(bradycardia, cold intolerance, constipation, facial puffiness - treat w/ levo); Adrenocorticotropic Hormone (ACTH; Corticotropin)(most life-threatening)(Mild = fatigue, anorexia, weight loss, hypogly. Moderate = postural hypotn, tachycardia. Severe = vascular collapse leading to death. Treat w/ steroid); Follicle-Stimulating Hormone (FSH) & Luteinizing Hormone (LH)(women - ovarian hypofunction effects estrogen. Men - testicular hypofunction effects testosterone); Prolactin (PRL) (inability to lactate after delivery. Not a treatment).
Panhypopituitarism: all anterior pituitary hormones are decreased.
Hyperpituitarism
Hormone oversecretion that occurs w/ anterior pituitary tumors or tissue hyperplasia (overgrowth of tissue). Genetic considerations. Usually diagnosed in 30-50yrs. Assessment = ask about changes in hat/glove/ring/shoe size, fatigue, backache, joint pain, headaches, vision changes, sexual dysfunction (esp r/t PRL). Interventions = drug (bromocriptine and cabergoline - inhibit release of GH & PRL), radiation therapy (gamma knife surgery is painless treatment that delivers highly focused radiation to tumors and lesions of the brain), surgical hypophysectomy (along w/ tumor removal is most common treatment - decreases hormone levels, releives headaches, and may reverse changes in sexual functioning. Post op = monitor neuro, assess postnasal drip, elevate HOB, avoid coughing, hormone replacement, avoid bending, avoid straining at stool/constipation, avoid brushing teeth.
Pituitary adenoma: a benign tumor that’s classified by the hormone secreted. As an adenoma gets larger and compresses brain tissue, neurologic changes & endocrine problems may occur. Assess vision changes, headache, and increased ICP.
Acromegaly: Side effect of hyperpituitarism. Overproduction of GH in adults. Gradual w/ slow progression. Irreversible if not detected early. Enlargement of face, hands, feet. Skeletal thickness, hypertrophy of skin. Enlargement of many organs such as liver and heart. Usually caused by pituitary adenoma.
Diabetes Insipidus (DI)
decreased release of ADH. Water loss is caused by either an ADH deficiency or an inability of the kidneys to respond to ADH. Leads to excretion of lg vol of dilute urine, changes in f/e balance. Assessment = onset may be slow or abrupt and can occur at any age. Ask about polyuria, nocturia, polydipsia. Ask about amnt of fluid intake and color of urine (very dilute w/ SG <1.005 and usually unable to concentrate). Symptoms of dehydration and hypovolemia may develop quickly if urinary losses are not continuously replaced. Increase in frequency of urination and excessive thirst. Diagnosis = dehydration and hypertonic saline tests, 24hr fluid I&O (DI considered if urine output is more than 4L during this period and is greater than the volume ingested). Interventions = desmopressin (synthetic form of vasopressin and replaces ADH), drink fluid in amount = to urine output, monitor fluid overload, teach that polyuria and polydipsia indicate need for another dose of desmopressin, weigh daily.
Idiopathic - destruction of hypothalamic nuclei (autoimmune)
Neurogenic - tumors in or near the hypothalamus or pituitary gland. Head trauma, infection, brain surgery.
Nephrogenic - failure in the kidneys response to ADH. A severe kidney injury can reduce the ability of the kidney tubules to respond to ADH.
Drug related DI- caused by lithium carbonate (a drug used to treat bipolar disorder) and demeclocycline (a tetracycline)
Syndrome of Inappropriate ADH (SIADH)
Problem in which ADH/vasopressin is secreted even when plasma osmolarity is low or normal. Water is inappropriately retained by the kidneys causing dilutional hyponatremia. Results in water retention and fluid overload. Occurs w/ many conditions (cancer therapy, pulmonary infection/impairment, specific drugs - opioids, NSAIDs, antiseizure, antipsychotics, cytotoxic). Assessment = medical hx, recent head trauma, TB, cerebrovascular disease, cancer, meds, decrease in sodium levels (hyponatremia). Interventions = treat cause. Restrict fluid intake, replace sodium, promote excretion of water w/ loop diuretic or tolvaptan (causes effective water diuresis w/o significant loss of electrolytes in the urine. Black box warning - rapid increase in serum sodium level > 12 in 24 hrs. It can cause CNS demyelination that can lead to serious complications and death), vasopressin receptor antagonist (vaptans).
Adrenal Gland Hypofunction
Slow but progressive development. Inadequate secretion of ACTh may cause a decrease in production of steroid hormone. Dysfunction of the hypothalamic pituitary control mechanism or direct problems of adrenal gland tissue. Adrenal crisis can occur gradually or rapidly w/ stress. Adrenal gland hormones = Sugar (glococorticoids), Salt (mineralcorticoids), Sex (androgens).
Acute adrenal insufficiency (addisonian/adrenal crisis): progressive hypofunction of adrenal cortex. Often occurs in response to a stressful event. Life threatening d/t falling Na levels w/ rapid rising K levels. Severe hypotn will occur from hypovolemia that occurs w/ loss of aldosterone. Need for cortisol and aldosterone is greater than bodys supply. S/S = profound weakness, severe pain (abd, back, legs), peripheral vascular collapse, azotemia (build up of nitrogenous products). Diagnostic = serum electrolytes, salivary cortisol levels, fasting BG (can lead to hypoglycemia d/t ↓ gluconeogenesis), ↑BUN, ACTH stimulation testing. Interventions = rapid infusion of NS or D5 in NS, Hydrocortisone or dexamethasone IV bolus, continuous hydrocortisone sodium IV infusion for 8hr, hyperkalemia management, hyponatremia management.
Addison’s disease: S/S = weakness, fatigue, orthostatic hypotn, hyperpigmentation, N/V/D, dehydration
Hypercortisolism (Cushings)
excess secretion of cortisol from adrenal cortex. Most common cause = glucocorticoid therapy. S/S = moon face, buffalo hump, truncal obesity, weight gain, increased appetite, osteoporosis, emotional instability (mood swings, irritability, new onset confusion), immune changes (from corticosteroids). Labs = blood/salivary/urine cortisol levels, plasma ACTH (high in disease low in syndrome), dexamethasone suppression testing, imaging (MRI, CT, arteriography - lesions of adrenal or pituitary glands). Priority = fluid volume overload d/t hormone induced H2O & Na retention, potential for injury d/t skin thinning/poor wound healing/bone density loss, potential for infection d/t hormone induced reduced immunity. Interventions = prevent fluid overload, monitor Q2hr, fluid restriction, prevent skin breakdown, encourage high protein and potassium diet, restore f/e balance, prevent infection, drug (steroidogenesis inhibitors - ketoconazole)
Cushing Disease: caused by problems from excess pituitary production of ACTH, usually d/t pituitary adenoma.
Cushing Syndrome: cluster of clinical abnormalities caused by chronic high blood levels of cortisol or corticosteroids. S/S = moon face, buffalo hum, very slender distal extremities and fingers.
Hypothyroidism
Reduced or absent hormone secretion from thyroid gland. Results in whole-body decreased metabolism from inadequate cellular regulation. Onset gradual and undramatic. S/S = weight gain, compare activity or today to one year ago, increased sleeping, generalized weakness, anorexia, muscle aches, constipation, cold intolerance, goiter. Labs = T3 & T4 levels, TSH. Priorities = ↓ gas exchange & oxygenation d/t ↓ energy, obesity, muscle weakness, fatigue; Hypotn & ↓ perfusion d/t ↓ HR from ↓ myocardial metabolism; potential for complication of myxedema coma. Interventions = improve gas exchange, prevent hypotn, prevent myxedema coma, thyroid hormone replacement (levothyroxine - take on empty stomach), education (wear medical alert bracelet, lifelong drugs, eat high fiber diet, prevent constipation, fiber supplements may interfere)
Myxedema Coma: Hypothyroid crisis.. Serious complication of untreated or poorly treated hypothyroidism. Dangerously ↓ cardiopulmonary & neurologic functioning. Can lead to respiratory failure
Hyperthyroidism
Excessive thyroid hormone secretion from thyroid gland. Increases metabolism in all body organs. Can be temporary or permanent depending on the cause. S/S = tachycardia, dysrhythmias, rapid/shallow respirations, heat intolerance, blurred/double vision, wide-eyed or startled appearance, diaphoresis, weight loss, emotional instability (wide mood swings, irritability, ↓ attention span, manic behavior, hyperactivity). Labs = T3, T4, TSH, TRAbs, thyroid scan, radioactive iodine uptake, ultrasonography, ECG (SVT, AF, dysrhythmias, PVCs). Interventions = reduce stimulation, promote comfort, drug (antithyroid - methimazole, iodine preparations, beta-adrenergic blocking - propranolol), radioactive iodine therapy (destroy thyroid), total/subtotal thyroidectomy (complications = hemorrhage, respiratory distress - keep emergency tracheostomy equipment at bedside, hypocalcemia, tetany, laryngeal nerve damage, thyroid storm - fever, tachycardia, systolic HTN, thyroid crisis, eye & vision problems, suture line pressure, hoarseness, stridor).
Graves disease
autoimmune disorder that occurs after an episode of thyroid inflammation. More common in women. Hyperthyroidism symptoms. Exophthalmos. Pretibial myxedema. Associated w/ other autoimmune d/o (DM, RA). Autosomal recessive w/ sex limitation to females.
Thyroiditis
inflammation of thyroid. 3 types. (1) acute thyroiditis caused by bacterial invasion of thyroid gland (pain, neck tenderness, malaise, fever, dysphagia. Treat w/ abx). (2) subacute caused by viral infection after a cold or URI (fever, chills, dysphagia, muscle and joint pain). (3) chronic - Hashimoto - triggered by bacterial or viral infection (selective thyroid tissue destruction, dysphagia, painless enlargement of the gland).
Thyroid cancer
papillary, follicular, medullary, and anaplastic. Painless lump or nodule in thyroid gland. Additional s/s depend on presence and location of metastasis. Treatment = radiation, ablative amounts of radioactive iodine therapy, total thyroidectomy. Patient has hypothyroidism after treatment of cancer
Hypoparathyroidism
Parathyroid glands maintain calcium & phosphate balance. Parathyroid function decreased and serum calcium levels cannot be maintained. Hypocalcemia develops, serum phosphorus increases. Rare disorder. Assessment = any surgeries that could damage parathyroid glands, serious neck injury. S/S = mild tingling/numbness, muscle tetany (hypocalcemia), severe muscle cramps, spasms, seizures, mental changes, bands or pits around teeth. Diagnostic = EEG, blood tests (Ca, Ph, Mg, Vit D, cAMP), CT. Interventions = correct hypocalcemia, vit D deficiency, hypomagnesemia. Long term therapy for Vit D (oral erogocalifeol), education (eat foods high in Ca but low in Ph - avoid milk, yogurt, processed cheese d/t high Ph content, wear medical alert, teach that therapy for hypocalcemia is lifelong)
Hyperparathyroidism
Parathyroid secretion of parathyroid hormone is increased, resulting in hyperglycemia & hypophosphatemia. Exact trigger is unknown in primary hyperparathyroidism. Benign tumor and CKD cause secondary hyperparathyroidism. Assessment = r/t effects of excessive PTH or effects of hypercalcemia.Ask about bone fractures, arthritis, recent weight loss, GI problems, physiological stress, radiation treatment of head/neck. Assess for waxy pallor of skin. Assess for bone deformities in extremities and back. Labs = serum PTH, Ca, Ph, urine cAMP, XR (if kidney stones, Ca deposit, bone lesions). Interventions = diuretic and hydration therapies, drug (cinacalcet - excretes Ca - monitor for hypocalcemia), monitor cardiac function, prevent injury, surgical (parathyroidectomy).
CNS
Brain & spinal cord. Regulation & function of the NS & systemic system. Reflex activity & transmits impulses to and from the brain
Frontal Lobe
primary motor area, speech center, behavior, cognition, judgment, reasoning, concentration
Parietal Lobe
spatial perception, taste impulses
Temporal Lobe
auditory center, memory, language
Occipital Lobe
visual center
Medulla
cardiac/respiratory center, cranial nerves 9, 10, 12 (portion of 7,8)
Pons
cardiac/respiratory center, cranial nerves 5, 6, 7, 8
Midbrain
cerebral aqueduct, cranial nerve 3, 4
Autonomic Nervous System (ANS):
component of the PNS that regulates involuntary physiologic processes including HR, BP, respiration, digestion, & sexual arousal. It contains three anatomically distinct divisions (sympathetic, parasympathetic, enteric)
CN1
Olfactory - Sensory
Sense of smell
CN2
Optic - Sensory
Vision
CN3
Oculomotor - Motor
Eye movements; pupillary constriction and accommodation, muscle of upper eyelid
CN4
Trochlear - Motor
Eye movements; intorsion, downward gaze
CN5
Trigeminal - Sensor & Motor
Somatic sensation from face, mouth, cornea; muscles of mastication
CN6
Abducens - Motor
Eye movements (abduction or lateral movements)
CN7
Facial Nerve - Sensory & Motor
Controls muscles of facial expression; taste from anterior tongue; lacrimal and salivary glands
CN8
Vestibulocochlear - Sensory
Hearing & sense of balance
CN9
Glossopharyngeal - Sensory & Motor
Sensation from posterior tongue and pharynx; taste from posterior tongue; carotid baroreceptors and chemoreceptors; salivary gland
CN10
Vagus - Sensory & Motor
Uvula and swallowing
CN11
Spinal Accessory - Motor
Shoulder and neck muscles
CN12
Hypoglassal - Motor
Movements of tongue
Neuro Changes w/ Aging
slower cognition (provide sufficient time to respond), memory loss (reinforce repetition, memory aids), ↓ sensory perception (remind, instruct, aids), pain perception (describe pain, variables), sleep patterns (schedule and circadian), altered balance & coordination (move slow, positions slow, handrails), ↑ infection risk (monitor closely), ↓ or change in mental status, mobility/sensory changes, brain weight/capacity, atrophy & vascular changes.
Neuro Assessment - Mental Status
consciousness (awareness of surroundings, LOC, alert, lethargic, stuporous, coma), cognition (test of memory/attention that require verbal or written ability, orientation, onset of symptoms - may need to ask family for baseline).
Neuro Assessment - Motor Function
bservation (tremors, movements, strength, grips), cerebral motor/brain stem (eyes closed, arms or legs up/out & watch for drift), reflex activity (asymmetry - may indicate disease or injury, DTR, babinski sign - upgoing toes is abnormal & may be caused by drug or ETOH intox, post seizure, MS, liver disease)(hyper-reflexes could indicate damage to brain or upper SC; hypo-reflexes could indicate damage to lower SC or NM diseases).
Neuro Assessment - Sensory Function
changes in pain, temp, pain perception, touch sensory. Acute spinal injury. Cerebellar function (fine motor coordination), neuro testing/tasks (run heel of one foot down shin, hands palm up then rapid palm down, touch finger to nose w/ eyes closed), gait and equilibrium testing
Neuro Assessment - Psychosocial Function
neurological disease or injury is life changing. Depression, fear, anxiety.
Neuro Assessment - Lab Assessment
abnormal labs can cause neurologic-type symptoms. Hypoglycemia, hyponatremia, f/e imbalances, low CBC, abnormal ABGs, albumin
Neuro Assessment - Diagnostic Assessment
XR, CT, MRI, US, EEG, EMG, Cerebral Angiography(Provides images of blood vessels in and around the brain. Aneurysms, TBI, tumors, occlusions. Post op = bleeding, ice to area, extremely straight, pressure dressing for 2 hrs), lumbar puncture/spinal tap.
Decortication
abnormal motor movement of arms, wrist, fingers are flexed/internal rotation, flexion of legs
Decerebration
abnormal mvmnt w/ rigidity by extension of arms, legs, pronation or arms, flexed feel, bowed body. 10% survival rate w/ posturing. Represents dysfunction of brainstem
Glasgow coma scale
Used to establish baseline or trends. Change in LOC is 1st sign of near deterioration. 2 or more point change is significant w/ immediate intervention
Eye Opening
(4) spontaneous (3) to sound (2) to pain (1) never
Motor response
(6) obeys commands (5) localizes pain (4) normal flexion withdrawal (3) abnormal flexion (2) extension (1) none
Verbal Response
(5) orientated (4) confused conversation (3) inappropriate words (2) incomprehensible sounds (1) none
Trigeminal Neuralgia
persistent, painful debilitating d/o that involves CN5 (trigeminal nerve). Women>men. Cause = unknown. May be r/t facial trauma, dental procedures, or vascular compression
Bell’s Palsy
paralysis of facial muscles. Can’t close eye or wrinkle forehead. Tearing d/t eye droop. Cause = viral illness, HSV, mono, flu.
Dementia
general term for progressive loss of brain function and impaired cognition. Chronic confused state or syndrome. Not a normal part of aging. Affects the ability to learn new info, impairs language, judgment, behaviors (early), functional ability decreases w/ motor complications (late).
Vascular dementia
multi-infarct dementia, stroke, or vascular d/o. Risk factors = Male >65yo. Cause = ↓ blood flow to parts of the brain (ischemia). Comorbidities = DM, CAD, HTN. Management = risk factor/prevention, safety, behavior.
Alzheimers
common type of dementia. Accelerated changes of the brain. Microcirculation changes/plaques and degeneration vascularly. Cognitive decline, progressive. Risk factors = female, TBI, > 65yo, veterans, PTSD, lifestyle.. Cause = genetic, environment. Assessment = Hx (AD or delirium from other cause. Family hx, subtle changes, onset, duration, progression), physical (neuro, progress not always typical). Labs = none, genetic testing, CSF for amyloid. Diagnostic = CT, MRI/MRA, MMSE, MoCA. Priorities = ↓ memory & cognition d/t neuronal changes, potential for injury/falls d/t wandering or immobility, potential for elder abuse by caregivers. Interventions = ↑ quality of life, safety, behavior management, interaction, PT, OT, ADL progression and self care focus, family care/support, drugs (help w/ symptoms - psychotropic drugs - abilify, haldol, seroquel, risperdal - cause drowsiness, confusion, unsteady, shaking), quiet and nonstimulating environment, communication strategies (dont lie, yes/no answers, reading or written notes/instructions, simple short steps, simple gestures, limit choices, calm quiet manner in speaking).
Stages: Stage 1 (early/mild 1-4 yr progression - short term memory, independent in ADL, mild impaired cognition, forgets names, loses things, stress), Stage 2 (moderate 2-3yr progression; 6-7yr from initial signs - impairment in cognition, money issues, driving & getting lost, wandering, insomnia, depressed, help w/ some ADLs), Stage 3 (severe - completely incapacitate, total dependence in ADLs, loss of mobility, tremors, verbal minimal, agnosia or object recognition).
Huntington Disease
a rare hereditary d/o that is characterized by progressive dementia & choreiform (rapid, jerky mvmnts) in limbs, trunk, and facial muscles.Gradual decline over 15yrs. Cognitive and neuromuscular. Cause = genetics (50/50 chance), autosomal dominant trait. Incolces dopamine imbalance (dopamine is essential for control of coordinated mvmnt). Interventions = safety, fall risk, supportive care, behavior, ADL help.
Parkinson Disease
progressive neurodegenerative disease that is one of the most common neurologic d/o in OA. Risk factors = Men > 50yo. Cause = primary (unknown), secondary (trauma, tumor). Gradual steady decline 10-20yrs. Cognition & mobility. S/S = tremor, muscle rigidity, bradykinesia (slow) or akinesia (no movement & postural instability), late (cognition, dementia, psychosis). Assessment = hx (time, progression, behavior changes, resting tremor, fatigue), physical (classic symptoms -stages). Labs = none specific, CSF (decreased dopamine). Diagnostic = MRI, neurologist. Interventions = promote mobility (exercise/mvmnt program, prevent falls), managing cognitive dysfunction (safety & quality of life), surgical (stereotactic pallidotomy, deep brain stimulation), home education (symptom control, resources, care team, palliative, respite, hospice), drugs (dopamine agonist for 1st 3-5yrs of diagnosis - pramipexol, ropinirole, apomorphine - can cause drowsiness & hypotn — CNS agents - decarboxylase inhibitor, levodopa, levodopa-carbidopa - improves motor function, take on empty stomach, may cause dyskinesia or involuntary mvmnts — MAOIs zelapar, azilect, safinamide - used for early & mild symptoms — take meds b4 meals, avoid foods w/ tyramine, cured meats, or cheeses , red wine can cause HA or HTN. medical marijuana).
Stages: 1 (initial - unilateral limb mvmnt, minimal wkns, hand/arm trembling), 2 (mild - bilateral limb involvement, masklike face, slow shuffling gait), 3 (moderate - postural instability, increased gait disturbances), 4 (severe - akinesia, rigidity), 5 (compete ADL dependence).
Migraine Headache
common clinical syndrome characterized by recurrent episodic attacks of head pain. Risk factor = women, depression, seizures, stroke. Cause = unknown. Neurogenic process w/ cerebral vasodilation. Triggers = caffeine, red wine, MSG, environmental, stress, weather changes. S/S = throbbing, unilateral head pain, n/v, photophobia, sound, head mvmnt pain, lasts 4-72 hrs. Assessment = neuro assessment. Interventions = preventative meds (NSAIDs, beta blocker - propranolol, Ca channel blocker - verapamil, antiepileptic - topiramate), abortive therapy (symptomatology therapy during acute phase - alleviate pain at onset of aura or early headache. Mild = APAP, NSAIDs, caffeine tablets. Severe = Triptans/Sumatriptan - may cause chest pain, flushed, hot, tingling. Caution w/ CAD, CVA, HTN, PVD, SSRI, St John wort), other drugs (lasmiditan, cafergot).
Migraine headache w/ aura - classic migraine. Aura = sensation visual, smell, minutes to hrs prior to headache.
Common migraine - migraines without aura.
Simple migraine - visual, light, spots.
Complex migraine - numbness, aphasia, weakness, confusion, drowsy.
Atypical or status migrainosus - lasts > 72 hrs. Neuro symptoms > 7 days.
Seizures
abnormal, sudden, excessive, uncontrolled electrical discharge of neurons within the brain that may change LOC, motor, sensory, & behavior. New onset seizures may be r/t HTN, CAD, DM, CVA, dementia, or brain injury. Memory loss is common after seizureCause = primary (unknown or tumor), secondary (metabolic d/o, fever, stroke, head injury, CAD, illicit drugs, stress, caffeine, foods, chemicals, ETOH). Assessment = hx, physical (time, duration, injury, meds/drugs, seizure hx, head injury/trauma). Diagnostic = EEG, CT, MRI, no labs. Interventions = drugs (antiepileptic - dilantin, cerebyx, tegretol, lamictal, depakote, gabapentin - may cause leukopenia, liver dysfunction - warfarin is drug-drug interaction, avoid grapefruit bc it increases drug toxicity, close therapeutic monitoring), common to be cyanotic w/ generalized seizures (put on O2 post seizure), surgical (VNS)
Tonic-Clonic or Grand Mal: 2-5 min w/ tonic phase (stiff or rigid) then clonic (jerking movement). Tongue biting & incontinence is common. Postictal period after seizure. Fatigue, confusion, lethargy up to 1hr post seizure.
Myoclonic seizures: brief jerking/stiffening of extremities. Few seconds w/ unilateral or bilateral mvmnt
Atonic seizures (akinetic): sudden loss of muscle tone, injury w/ sudden fall.
Partial seizures (Focal/Local): complex (syncope, LOC, older adults), or simple (aura, smell, pain, one-sided).
Psychomotor seizures: epileptic.
Status Epilepticus: Emergency. Seizure lasting > 5min or repeated over 30min. Causes = sudden withdrawal of antiepileptic drugs, infection, acute alcohol or drug withdrawal, head trauma, cerebral edema, metabolic disturbances. If untreated = hypoxia, hypotn, cardiac dysrhythmias, metabolic acidosis, RF, brain damage. Priorities = safety, airway, oxygen, IV, RRT. Interventions = drugs (lorazepam IV or diazepam IV or PR. 2-4mg over 2min x2. Dilantin IV/fosphenytoin 100-150mg IV), home education (meds, diet, rest, stress, lab levels).
Epilepsy
chronic d/o in which repeated unprovoked seizure activity. Cause = genetic, head trauma, infections. S/S = confusion, staring spell, LOC, jerking mvmnts suddenly, fear, anxiety. Meds = antiseizure. No cure.
Meningitis
infection of the meninges of the brain & spinal cord. Organisms in CNS-CSF that spread to cranial or spinal nerves. May lead to ICP (blockage in blood flow/CSF), thrombus or clot formation. Cause = bacterial or viral, cancer, drugs (NSAIDs, abx). Prevention = vaccine. S/S = LOC, disorientation, confusion, photophobia, nystagmus, motor response (normal if early, hemiplegia or CN if late), memory changes, headaches, myalgia, N/V, fever, tachycardia, red macular rash (w/ meningococcal meningitis), nuchal rigidity (stiff neck). Assessment = neuro (GCS, LOC, vascular Q4 hrs). Diagnosis differentiation = encephalitis (infection), hydrocephalus (excessive CSF - altered LOC, incontinence). Labs = CBC, electrolytes, blood/CSF cultures (gram stain, cell count, protein). Diagnostic = XR, CT, MRI (ICP or brain abscess). Interventions = drugs (bacterial = broad spectrum abx, increase ICP = mannitol, steroids, AED, NM exposure = rifampin, cipro, ceftriaxone), lumbar puncture/spinal tap, isolate based on bacterial precautions, treat like bacterial unless otherwise specified.
Viral: most common type. No organisms in CSF. Cryptococcus neoformans (fungus w/ HIV/AIDS). Enterovirus, HSV-2, varicella, mumps, HIV.
Bacterial: Strep pneumococcal, neisseria meningococcal (NM - very life threatening <24 hr survival. . Causes = crowded living, college dorms, military barracks, high population).
Hernia
Weakness in abdominal muscle wall segment of bowel or other abdominal structure protrudes. Cause = congenital or acquired muscle weakness, obesity, pregnancy, heavy lifting. Interventions = truss/pad/firm material over hernia w/ belt, surgical repair/herniorrhaphy (avoid cough, straining, lifting).
Classifications: Reduction (moves back and forth with gentle pressure. Pops out when pt is flat), irreducible/incarcerated (cant be pushed back), strangulated (Ischemia/obstruction in bowel loop. Can lead to necrosis, sepsis, perforation. s/s = distention, n/v, pain, fever, tachycardia).
Multiple Sclerosis (MS)
chronic disease caused by immune, genetic and infection factors. MS affects the myelin & nerve fibers of brain and spinal cord causing demyelination. Risk factors = genetic, women, 20-50yo, cold climates. S/S = muscle weakness, muscle spasms, fatigue, tremors w/ activity, numbness/tingling, ataxia - if exacerbated - stress, fatigue, over exertion, temperature extremes. Labs = CSF. Diagnostic = MRI (confirmed MS if >2 separate areas of plaque on brain or spinal cord. Priorities = immunity, mobility, visual acuity, cognition. Interventions = avoid large crowds, exercise program (not rigorous), rehab, assist w/ organization (calendars, messages, lists, structured environment), drugs (to treat and control progression & symptoms - antiinflammatory, muscle relaxants, chemo), alternative meds (acupuncture, marijuana, rest & activity).
Relapsing remitting MS
most common type of MS. Symptoms develop & resolve in a few weeks-months w/ return to baseline
Primary progressive
Type of MS. Steady and gradual neurologic deterioration w/ remission of symptoms. Progressive disability w/ no acute attacks. Age onset 40-60yo
Secondary progressive
Type of MS. relapsing-remitting than later progressive steadily. Late stage of relapsing-remitting.
Progressive relapsing
Type of MS. frequent relapses w/ partial recovery but not back to baseline. Uncommon. Progression, symptoms, and deterioration over 2-3 years
MS vs ALS
MS
Definition: Chronic disease caused by immune, genetic, and infection factors. Impacts myelin sheath and nerve fibers. Affects brain/spinal cord.
Neuro changes: Mental status change, bowel/bladder problems
Affects: Women, 20-50yo
Symptoms:Fatigue, paresthesia, ataxia gait, muscle spasms/spasticity.
Progression: Depends on type
ALS
Definition: Progressive neurodegenerative disease that affects neurons in the brain and spinal cord. Progressive muscle wasting leads to paralysis.
Neuro changes: Mental status change, bowel/bladder problems
Affects: Men, 40-60yo
Symptoms: Fatigue, muscle atrophy, weakness, abnormal reflexes, stiff gait
Progression: 100% fatal
Spinal Cord Injury (SCI):
Sudden traumatic blow to the spine that fractures, dislocates, crushes, or compresses. Prevention = seatbelts, hempets, padding, impaired driving, shallow diving. Damage to spinal cord causes neurologic deficits. Assessment = Hx,ABCs!, monitor VS, assess lowest neurologic segment that is intact/normal function, DTRs, respiratory (breathing problems r/t respiratory muscle use - C spine), cardiovascular (above T7 injury - decreased HR/BP/Temp and cardiac dysrhythmias), spastic(above T7)/Flaccid (below T7) bowel or bladder. Complications = internal bleeding, hemorrhage, paralytic ileus, prolonged immobility, DVT risk, pressure sores, osteopenia w/ high risk fractures. Priorities = respiratory distress/failure, cardiovascular instability, secondary SCI, mobility and sensory perception. Interventions = airway management!, critical lung assessment (Q2-4 hrs), intubation, tracheostomy, IV fluids, monitor for neurogenic shock, treat bradycardia (atropine), treat hypotension (dopamine), neuro assessment, motor/sensory eval, pain scale, VS hourly, spinal immobilization/stabilization (reduction of fracture/unstable spine to prevent further damage), turn 1-2 hr, bowel or bladder injury, drugs (PPI for stress ulcers, muscle relaxants, pain), surgery (C spine = wiring, spinal fusion; T-L spine = steel/metal rods. Post op complications = bleeding, infection, subtle neurological changes, sensory/motor trends, neurogenic shock).
Complete: spinal cord has been damaged in a way that eliminates all innervation below the level of injury
Incomplete: SCI that allow some function or movement below the level of injury
Spinal shock: temporary loss of motor, sensory, reflex, and autonomic function < 48hrs. May be temporarily caused by inflammation or edema.
Autonomic dysreflexia: high level SCI w/ sudden, massive uninhibited reflex discharge from visceral stimuli. Severe HTN (stroke), keep HOB elevated.
5 primary mechanisms w/ SCI:
hyperflexion (a sudden forceful acceleration or movement of the head forward, extreme flexion of neck. Head on collision, driving accident, fall landing on butt), hyperextension (head is accelerated backward. Stretches and tears ligament. Rear-ended or fall w/ chin struck), axial loading/vertical compression injury (caused by driving accidents, fall on butt, jump landing on feet, osteoporosis, falls), excessive rotation (turning head beyond normal range), penetrating trauma (speed of objects causing injury).
5 secondary mechanisms w/ SCI
mortality is high in SCI due to secondary complications. Hemorrhage, ischemia, hypovolemia, impair tissue perfusion/neurogenic shock, local edema (cord ischemia). Can also cause infection, pneumonia, septicemia.
Traumatic brain injury (TBI)
amage to the brain from an external mechanical force. Temporary or permanent impairment in cognition, mobility, and sensory perception depending on severity. Risk factors = men, sports, military. Can be either mild, moderate, or severe. Mild (blow to head, confusion, no evidence of brain damage - dazed, stunned, LOC < 30 min, HA, NV, gain, dizziness, visual problems that resolve w/ time, emotional, sleep), Moderate (LOC, brain injury seen on MRI/CT, amnesia < 24 hrs), Severe (GCS 3-8, focal or diffuse damage to brain, tissue damage, edema, necrosis. S/S = non resolved mild TBI symptoms plus permanent cognitive findings, sleep disturbances, emotional change). Cause = fall, MVC. Complications = hypotn & hypoxia (shock, respiratory failure, asphyxiation, loss of airway, cerebral edema), increased ICP (poor cerebral perfusion, ischemia, edema) , untreated ICP (brainstem herniation, irreversible brain damage, death), hemorrhage (brain hematoma - epidural or subdural), brain herniation (increased ICP, shifts away from lesion, ischemia, edema), hydrocephalus (abnormal increase in CSF volume. Impaired reabsorption of CSF, blockage of outflow from brain ventricular system from tumor, edema, debris, lesion, hematoma). Assessment = ICP, cushings, GCS, LOC, visual/sensory/motor eval. Priorities = perfusion, cognition, sensory perception, mobility. Interventions = close monitoring of ICP, neuro assessment, symptom control, VS trends, therapeutic cooling, determine brain death (coma/LOC, core body temp, normal BP, neuro assessment unchanged, EEG, cerebral CTA/US), drugs (mannitol - osmotic diuretic to treat cerebral edema by pulling water out of the extracellular space of edema brain tissue; furosemide; fentanyl - caution w/ LOC, decrease pain, anxiety, agitation; propofol - sedation, decrease ICP, agitation).
Primary: time of injury and results from physical force caused by blunt/penetrating force. S/S = impair cognition, memory or thinking process, and headache. Many different types — Focal brain injury (localized damage to a specific area or brain - MVC, gunshot, penetrating wound), Diffuse brain injury (generalized damage throughout many areas of brain - shaking or strong rotation of head), open TBI (skull fracture or pierced through skull), closed (skull bone intact, damage to brain tissue d/t increased ICP), concussion (mild TBI - traumatic injury to the brain caused by a blow/fall to head w/ or w/o LOC).
Secondary: injury/process that occurs after the initial injury. Caused from hypoxia, hypotension, edema, ICP.
Post concussion syndrome: secondary injury from mild TBI. S/S = HA, impaired cognition, dizziness, N/V. Lasts weeks - months.
Hemorrhage after TBI: 3 major types. Epidural (arterial bleeding between dura and inner skill. Cause = temporal bone fracture. S/S = alert or altered LOC), subdural (venous bleeding into the space beneath the dura and arachnoid. Acute or chronic SDH. S/S = headache, paresis, confusion, seizures, LOC), intracerebral hemorrhage (Accumulation of blood within the brain tissue by tearin of sm arteries & veins).
Brain Tumors
can concur anywhere within the brain structures. Can be benign, malignant, metastatic, cerebral, primary, secondary. Assessment = hx, physical, neuro. S/S = headaches, NV, seizuers, impaired sensory perception, dizziness, balance, weakness, speech). Interventions = radiation, chemo, drugs (analgesics, dexamethasone for cerebral edema, phenytoin for seizures, PPI for gastric acid decreased and stress ulcers), surgery (craniotomy - complications = ICP; management = neuro status, periorbital edema, elevate HOB to 30 degrees, dressing and bleeding monitoring, ABCs).
Primary: originates within the CNS, rarely spreads
Secondary: metastasis from other areas of the body (lung, breast, kidney, GI tract)
Intracranial pressure (ICP)
Normal = 10-15 mmHg. Increasing = LOC, HA, NV, aphasia, abnormal posturing, cushings. Interventions = HOB elevated, oxygen, limit stimuli, airway, photophobia, VS trends, close monitoring or temperature.
Cushing’s triad
very late sign of increased ICP. HTN, wide pulse pressure, bradycardia.
Transient Ischemic Attack (TIA):
temporary neurologic dysfunction resulting from a brief interruption in cerebral blood flow. Causes = carotid stenosis is a hardening & narrowing of the carotid artery w/ decreased blood flow to brain. Risk factors = atherosclerotic plaque buildup, atrial fibrillation. S/S = vision changes (blurred, diplopia, hemianopia, tunnel), mobility (weakness, facial droop, arm/leg weakness, hand grip weakness, ataxia, gait, balance, ability to walk), sensory (numbness, vertigo). Assessment = ABCD (age, BP, clinical TIA, duration), NIHHS. Labs/diagnostic = coagulation, PT, PTT, INR, lipids, EKG, EEG, CT, MRI, MRA. Interventions = drug (antiplatelet, aspirin, clopidogrel, antihtn, hyperglycemia drugs), keep glucose levels between 100-180, MIS surgery to remove plaque (carotid artery stent/perfusion to brain), lifestyle changes (diet, mobility, smoking, stress).
Stroke
“brain attack.: Interruption of perfusion to any part of the brain resulting in cell death (infarction). Infarction can happen in minutes causing impaired blood flow. Blood flow is important for removal of metabolic waste. Non-affected side causes edema, obstruction, shift w/ blood/mass/lesion/edema. Increased ICP. Risk factors = lifestyle (diet, income, healthcare access, compliance, smoking, obesity, HTN, DM, lipids/cholesterol, drugs, ETOH, BCP), genetic. Health promotion = ABCS - aspirin use when appropriate, BP control, cholesterol management, smoking cessation. Complications of clots = AF, MI, PE, DVT, heart murmur, HTN, cardiac dysrhythmias. S/S = sudden onset of confusion, aphasia, unilateral numbness/weakness, vision changes, dizziness, headache, gait, balance, note that s/s can look differently depending on the area of brain affected. Assessment = cognition, neuro, NIHHS, ataxia, rule out hypoxia and hypoglycemia. Labs = elevated H&H, elevated WBC, elevated glucose. Get stat coag labs for potential thrombolytics (PT, INR, aPTT). Diagnostic = CT, MRI, US). Priorities = perfusion, decreased mobility, aphasia, weakness, sensory perception. Interventions = ischemic stroke therapy (Fibrinolytic to improve blood flow), alteplase 90mg over 1 hr (contraindicated w/ HTN crisis, hx of stroke, DM, active bleeding), carotid stenting, NPO pending swallow eval, speech therapy, diet, self care, monitor for DVT/PE, manage ICP, drugs (antiplatelets, anticoagulants, calcium BB, stool softeners, pain management, antianxiety, cholesterol/statin meds), promote effective communication.
Types of strokes
Acute ischemic stroke
Thrombotic: Clot that causes decreased blood flow. Risks = HTN, atherosclerosis, TIA Cause = atherosclerosis in intracranial or extracranial arteries. S/S= intermittent & gradual onset, headache, speech, visual changes, confusion. Duration of symptoms = improvement over weeks to months (some permanent damage)
Embolic: dislodged clot that breaks off from one area and travels to cerebral arteries. Risks = CAD, TIA. S/S = abrupt and sudden onset, paralysis, aphasia. Duration of symptoms = Rapid improvement w/ treatment.
Hemorrhagic: vessel integrity is interrupted, and bleeding occurs into the brain tissue or subarachnoid space. Onset = abrupt. LOC = stupor, lethargy, coma. Cause = HTN crisis, cocaine. S/S = headache, seizure, permanent neuro deficits.
Subarachnoid hemorrhage (SAH): bleeding in the brain in the space between pia mater (meninges/layer covering brain). Cause = ruptured aneurysm or arteriovenous malformation (AFM). S/S = sudden onset of headache, N/V, photophobia, LOC.
Aphasia
loss of ability to understand or express speech. 4 types. Expressive aphasia (difficulty w/ speaking & writing), receptive aphasia (difficulty understanding words that are written or spoken, made up words), mixed aphasia (combo of difficulty understanding words, speech, and hard to read or write), global aphasia (profound speech or language problem, limited garbled speech or no speech).
