Module 4: GI - Chronic Liver Disease PDF

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AdequateAwe9942

Uploaded by AdequateAwe9942

FSU College of Nursing

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liver disease cirrhosis GI medical notes

Summary

This document provides a detailed overview of module 4, focusing on gastrointestinal (GI) conditions, specifically cirrhosis. It covers the pathology, symptoms, complications, and management strategies related to this condition. The document also briefly touches upon GERD.

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module 4: GI cirrhosis ○ patho: end-stage degeneration & destruction of liver cells causes physical changes to the liver causes: chronic hepatitis C and alcohol induced liver disease ○ symptoms: early symptoms are min...

module 4: GI cirrhosis ○ patho: end-stage degeneration & destruction of liver cells causes physical changes to the liver causes: chronic hepatitis C and alcohol induced liver disease ○ symptoms: early symptoms are minimal, they are most often noticed late jaundice, small areas of bleeding into the skin, palmar erythema, hirsutism, hemorrhoids, spider angiomas edema thrombocytopenia, peripheral neuropathy, ascites & esophageal varices changes in mental responsiveness & memory ○ complications: decompensated cirrhosis: major complications portal hypertension: increased venous pressure ○ engorges the spleen ○ can cause esophageal & gastric varices, which are enlarged veins symptoms: bloody/coffee ground emesis, dark stools, rectal bleeding, paleness ESOPHAGEAL ARE THE MOST-LIFE THREATENING COMPLICATION if patient bleeds, they will be ICU, intubated, and on a ventilator stabilize with either endoscopic variceal ligation (putting a band around it to fall off), sclerotherapy, or balloon tamponade ○ balloon tamponade: have to be intubated & sedated; keep scissors at bedside, airway suctioning give vasopressin or octreotide for vasoconstriction peripheral edema abdominal ascites ○ serous fluid build up in abdominal cavity ○ caused by portal hypertension or hypoalbuminemia (caused by poor protein intake) ○ risk of infection hepatic encephalopathy ○ neurotoxic effects of ammonia, which the liver is not able to convert to urea when damaged ○ crosses the blood brian barrier & causes mental status changes, sleep disturbances, hyperventilation, coma, flapping tremors, musty/sweet breath, and inability to construct simple figures ○ assess neuro states Q2h, minimize constipation, encourage fluids hepatorenal syndrome ○ renal failure d/t cirrhosis ○ liver failure causes high waste products & nitrogen in the blood as well as decreased urine output ○ portal hypertension occurs, causing renal vasoconstriction ○ diagnostics: liver enzyme tests, total protein (albumin), serum bilirubin, cholesterol liver biopsy (the best) ultrasound to evaluate liver structure & scarring ○ management: goal - slow progression of cirrhosis & prevent further complications rest, B complex vitamins, avoid alcohol, avoid ASA, tylenol, and NSAIDS (esophageal bleeding) can give albumin to absorb fluid (in ascites) can give diuretics sodium restriction tolvaptan (diuretic that excretes ONLY free water & not electrolytes) max time for use is 30 days transjugular intrahepatic portosystemic shunt (helps fluid move to decrease ascites) ○ nutrition therapy 3k calories high in carbs & protein protein supplements low sodium diet for ascites & edema lactulose (causes a significant amount of diarrhea, will excrete ammonia) GERD ○ patho: weak lower esophageal sphincter that does not properly handle stomach acid, leading to a chronic syndrome of mucosal damage ○ risk factors: obesity, smoking, poor diet (large meals), pregnancy, hiatal hernia, beta & calcium blockers ○ symptoms: heartburn upset stomach regurgitation chronic cough ○ complications: esophagitis (inflammation of esophagus d/t regurgitation) causing scar tissue or dysphasia barrett’s esophagus: makes cells more resistant to stomach acid, but can lead to malignant tumors dental erosions cough, hoarseness, bronchospasm, laryngospasms ○ diagnostics: main is H&P upper endoscopy with biopsy (for barrett’s esophagus) should be done annually to ensure it has not progressed esophagogram (for hiatal hernia) pH monitoring using a catheter into the stomach ○ medications: goal - inhibit acid secretion, increase gastric emptying, protect stomach lining antacids caution in older adults, cirrhosis, HTN, renal histamine receptor antagonists (pepsin & famotidine) PPIs (omeprazole) first line drugs take on an empty stomach long-term use can cause bone fractures (lower calcium absorption) prokinetics (metoclopramide) used in gastroparesis (slow stomach emptying) CNS and EPS symptoms ○ surgical management: laparoscopic nissen fundoplication: wrap part of the stomach around the esophagus to give the lower esophageal sphincter more support ○ lifestyle changes & therapy: smaller, more frequent meals stay upright 2-3 hours after eating weight loss avoid citric/acidic/spicy foods, carbonated drinks, coffee, chocolate, alcohol, peppermint chewing gum may help relieve some symptoms hiatal hernia ○ pathophysiology: structural changes that increase intraabdominal pressure type 1 (sliding): most common part of the stomach herniates upwards, allowing acids to enter the esophagus symptoms: heartburn, regurgitation, chest pain, belching, dysphagia type 2 (rolling): more dangerous stomach moves below diaphragm stomach can become strangled (medical emergency) full or breathless after eating, symptoms worsen when lying flat, NO REFLUX ○ symptoms: can be asymptomatic, if there are symptoms they are similar to GERD ○ complications: GERD, esophagitis, ulcers, hemorrhage, strangulation, aspiration, stenosis (narrowing of the esophagus) ○ diagnostics: barium swallow can make patients very constipated, stools will be gray & white for 3 days endoscopy manometry measures pressure & muscle activity when a patient swallows ○ management: similar meds & therapy to GERD surgery: herniotomy (excision) herniorrhaphy (closure) fundoplication IBD - chronic recurrent inflammation of the intestinal tract ○ crohn’s disease: inflammation from mouth to anus skip lesions: normal tissue between areas of inflammation strictures & lesions can penetrate the intestine symptoms: non-bloody diarrhea crampy abdominal pain (RLQ) weight loss & rectal bleeding not common ○ ulcerative colitis: ulceration of the colonic mucosa (rectum & sigmoid) from colon to cecum symptoms: frequent diarrhea with blood & mucus ○ diarrhea w/ large fluid & electrolyte loss cramping abdominal pain dehydration weight loss anemia feeling the need to use the bathroom ○ diagnostics: H&P CBC, electrolytes, albumin, inflammatory markers stool studies (to make sure there is nothing different causing it) double contrast barium enema study (identify abnormal mucosa patterns) CT MRI colonoscopy or sigmoidoscopy colonoscopy: ○ low fiber or clear liquid diet for 1-3 days prior to clear out colon can commonly cause nausea & vomiting ○ laxative solution the day prior ○ abdominal cramping common ○ NPO 4-6 hours before test capsule endoscopy (crohn’s) assess small intestine for mucosal integrity & inflammation ○ management: primary goal - bowel rest to control inflammation medications: aminosalicylates (sulfasalazine) ○ helps to achieve remission and maintain it ○ better for ulcerative colitis but works for both ○ causes yellow-ish skin + urine, makes more sensitive to sunlight glucocorticoids ○ can cause osteoporosis (will need calcium supplements) antimicrobials immunomodulators nutrition: malnutrition & dehydration are common during acute flare ups use enteral feedings food diary smoking cessation experiment with fiber levels (high can cause diarrhea, pain, and gas) surgical: ulcerative colitis: surgery is curative ○ total proctocolectomy with either ileal pouch or permanent ileostomy crohn’s disease: surgery treats complications ○ resect diseased sections ○ can cause short bowel syndrome IBS ○ pathophysiology: functional disorder of the intestines ○ risk factors: GI motility, hypersensitivity, intestinal inflammation, psychosocial dysfunction, gluten sensitivity ○ symptoms: intermittent abdominal pain altered bowel habits LLQ pain with relief after defecation abdominal distention, anorexia, excessive flatulence, dyspepsia, belching nausea & increased pain associated with meals ○ diagnostics: based on symptoms & criteria recurrent ab pain on average at least 1 day in the week for the last 3 months, associated with at least 2 of these things: ○ related to defecation ○ associated with change in frequency of stool ○ associated with change in form of stool ○ management: medications: goals - control spasm, minimize diarrhea, promoting peristalsis symptom-based treatment cognitive behavior therapy surgical: nutrition & lifestyle: food diary high fiber diet peppermint, fennel, ginger avoid triggering foods (wheat/gluten, dairy, fried & fatty foods, caffeine, carbonated drinks, bean, chocolate, alcohol) 8-10 cups of water daily regular exercise adequate sleep (7-8 hours) smoking cessation hemorrhoids ○ pathophysiology: increased anal pressure & weak connective tissue cause downward displacement & dilation of veins ○ risk factors: pregnancy, constipation, straining, diarrhea, heavy lifting, prolonged standing & sitting, obesity, ascites ○ symptoms & types: internal: above internal sphincter bleeding w/ defecation, pain, prolapse diagnosis: digital examination, anoscopy, sigmoidoscopy external: below external sphincter reddish blue color, itching, burning, edema diagnosis: visual inspection & digital examination ○ complications: infection, pain, urinary retention, fecal impaction, sphincter damage, bleeding, abscess formation ○ medications: ointments, creams, suppositories impregnated pads anesthetics stool softeners astringents (witch hazel) shrink them relieve itching, stinging, and burning by cooling the area sitz baths NO ice packs ○ surgical treatment: for thrombosed (full of blood and painful) hemorrhoids: rubber band ligation coagulation ○ necrosis & scarring of the hemorrhoid cryosurgery ○ freezing of the hemorrhoid, very painful hemorrhoidectomy ○ excising the entire vein & hemorrhoid ○ big concern is infection & healing closing it helps with pain but increases risk for infection ○ nutrition therapy: high-fiber diet & increased fluids diverticulosis & diverticulitis ○ diverticulosis: asymptomatic diverticular disease some cramps, bloating, and constipation ○ diverticulitis: inflammatory stage of diverticulosis tenderness on palpation in LLQ abdominal pain decreased bowel sounds, N/V, distension systemic signs of infection rectal pain ○ pathophysiology: chronic low fiber diet, weaker colon wall ○ risk factors: obesity, inactivity, smoking, excess alcohol use, NSAIDS use ○ complications: bleeding seek care! abscess give antibiotics drain via catheter (if severe) perforation caused by infection peritonitis leakage from perforation site MEDICAL EMERGENCY intestinal obstruction scarring from infection MEDICAL EMERGENCY ○ diagnostics: CBC colonoscopy or sigmoidoscopy abdominal ultrasound CT of abdomen or pelvis digital rectal exam (physical exam) ○ management: prevention: high fiber & decreased fat/red-meat diet ○ add fiber supplements physical activity (not weight lifting) lack of restrictive clothing, bending, vomiting, and lifting acute diverticulitis: goal - bowel rest & reducing inflammation clear liquids, bed rest, analgesia hospital admission (if severe) recurrent diverticulitis: surgical resection or temporary colostomy module 5: neuro parkinson’s patho symptoms medication interventions - progressive neurological TRAP: tremors at rest, - antiparkinsonian drugs - encourage independence disease (no cure) rigidity, akinesia, postural (levodopa with carbidopa) as much as possible - ACh & dopamine imbalance instability that level out the - optimize well-being d/t loss of basal ganglia cells - akinesia can also cause neurotransmitters - chemicals & drugs can bradykinesia and dyskinesia - give on empty stomach, cause - sleep disorders, pain, report uncontrolled urinary retention, ED, movements, monitor for memory changes, dyskinesia! constipation - decrease B6 intake - late symptoms: reduced arm swinging, shuffling gait, OH, dyskinesia, slow speech CVA dementia & alzheimer’s alzheimer’s is a type of dementia! dementia is the overarching decline in cognitive ability patho symptoms diagnostics interventions dementia irreversible - short-term memory goes first - mini-mental state avoid stimulants deterioration of - difficulty with communication, focus, reasoning, exam cognition or visual perception - EEG - psychosis (hallucinations, delusions, paranoia) - worsened by alcohol or medical disorders alzheimer’s combo of aging, - reading difficulty, poor direction, poor judgment - mini-mental state avoid stimulants family hx, cardio, - misplacing belongings exam head trauma - visual changes - CT or MRI - difficulty communicating - PET scan - lab tests multiple sclerosis patho symptoms diagnostics medication interventions plaques or lesions on - can be slow/gradual 2 inflammatory - immunomodulators the spinal cord or rapid demyelinating lesions - - infection, smoking, - periods of in 2 different locations immunosuppressants pregnancy, poor health remissions & within the CNS - glucocorticoids exacerbations (prednisone & - blurred vision, methylprednisolone) red-green distortion - physical, - extremity muscle occupational, and weakness & lack of speech therapy balance - psyllium for bowel - dysarthria, ataxia, dysfunction nystagmus - gabapentin for - spastic bowel & neuropathic bladder - painful intercourse - STM loss myasthenia gravis patho symptoms diagnostics medication interventions autoimmune - can first show as - AChR antibodies - pyridostigmine: complications: neuromuscular disorder ocular issues present in blood improves - myasthenic crisis: - antibodies go after (drooping eyelids), will - EMG test - neuromuscular muscle weakness skeletal muscle lead into generalized decreased response transmission around the lungs & receptors - skeletal muscle to stimulation – initial choice of resp failure d/t - can be weakness starting in - chest CT routinely treatment infection exacerbated/caused by face and moves to to evaluate for a – given at the same – give IV IG (calms rheumatoid arthritis extremities mediastinum tumor time every day down the immune medication - muscles become - neostigmine: system) exhausted by the end shorter-acting version - cholinergic crisis: of the day - removing the taking too much MG thymus gland can be medication & causing helpful for symptoms bradycardia, sweating, (it produces small pupils antibodies) – stop the medication trigeminal neuralgia patho symptoms diagnostics medication interventions - vascular compression - type 1: severe, - history, physical, - antiseizure meds - evaluate the degree of the trigeminal nerve excruciating episodes neuro exams (type 1) (block the of pain & effects on - affects sensory & of stabbing pain; facial nerve from firing) lifestyle motor branches of the twitching/grimacing, -do not - discuss use of CNS facial sensory loss, suddenly complimentary trigger zone that discontinue alternative medicine requires light touch, - take w/food, - easy to chew food aggravating stimuli but not milk mild in temperature & (hot/cold air, yawning, - avoid ETOH spice eating, brushing teeth) - urine may - meticulous oral - type 2: facial pain of look pink/red hygiene & semiannual spontaneous onset - avoid OTC dental visits with >50% constant meds - protective eye shield pain - tricyclic - use of an electric antidepressants (type razor 1) - analgesics/opioids (type 2) GBS gradual blocking of sensation patho symptoms diagnostics medication interventions - autoimmune disease - generalized - EMG - watch for blood clots attacking the PNS weakness - lumbar puncture & DVT - lower motor neuron - motor neuropathy (will have an elevated - pain management disorder - areflexia CSF protein level) - distal limb paresthesias - facial & oropharyngeal weakness - dysphagia - facial palsy - flaccid bladder/bowel ALS no muscle nourishment patho symptoms diagnostics medication interventions - brain cannot control - gradually weakening - MRI of neck, brain, - riluzole and - normal things for muscle movement muscles & atrophy spinal cord rule out edaravone when a patient is - paralyzed with other dx - riluzole: reduces essentially bedbound sensations intact - EMG: nerve damage to motor and cannot move - slurred speech, conduction neurons muscle cramping, - muscle biopsy - edaravone: fatigue of extremities - myelogram neuroprotective - hyperreflexia - baclofen for muscle - difficulty swallowing cramps - upper motor neuron - stool softeners damage causing - CNS stimulants for spasticity fatigue - lower motor neuron - tricyclic damage causing antidepressants for flaccidity excessive saliva, pain, depression - PT and OT - trach & vent if needed (resp infection is most fatal complication) module 6: renal urinary incontinence & retention patho diagnostics medication interventions UI involuntary loss of urine - focused history, - based on type of DRIP: physical exam, incontinence delirium, dehydration urinalysis - surgery to restricted mobility, rectal - PVR tighten pelvic impaction - urinalysis & urine floor infection, inflammation culture - clean polyuria, polypharmacy - bladder scan intermittent cath UR inability to empty bladder - bladder scan - anticholinergics - scheduled voiding d/t obstruction, neuro - urinalysis to improve - double voiding impairment, detrusor muscle - PVR storage capacity - intermittent/indwelling cannot contract (diabetes, - cath over distension), infection, alpha-adrenergic - acute: emergency, lean renal stones, pregnancy blockers to towards indwelling cath reduce resistance - if unable to void: drink (flomax) caffeinated drinks to - surgery to increase urgency, warm remove baths/showers obstruction (TURP) or increase muscle strength (sacral neuromodulation) - types of urinary incontinence: - stress (increased pressures on the bladder) - common in women w/weak pelvic floor, post menopause - common in men after prostate surgery - treatments: pelvic floor exercise, surgery - urge (overactive bladder) - abnormal contractions causing the strong urge to pee followed by leakage - treatments; anticholinergics, absorbent products - mixed (stress+urge) - high abdominal pressure + overactivity - overflow - decreased contractility/bladder obstruction - treatments: catheter, alpha blockers - functional (d/t age or physical mobility) - unable to get to the bathroom in time - treatment: modify environment, better timing, better clothing, adaptive equipment - types of urinary retention - acute urinary retention: - complete inability to pass urine; medical emergency! - empty bladder with cath - get post void residual - chronic urinary retention: - incomplete emptying despite urination - normal post void residual 50-75 mL - more than 200 is further evaluation polycystic kidney disease ○ caused by renal cysts that become enlarged and awaken the disease ○ symptoms: htn, hematuria, pain/heaviness in back/side/abdomen, abdominal swelling cerebral aneurysms, cysts in liver or other organs, diverticulosis frequent UTIs ○ diagnostics: family history!! it is genetic urinalysis (will show blood and/or bacteria) BUN, creatinine, electrolytes, urine culture ultrasound ○ treatment: no cure! will lead to CKD tolvaptan for acute rapid cases prevent/treat the UTIs nephrectomy dialysis & kidney transplant genetic counseling ○ interventions: renal diet (if impaired function) low protein, potassium, magnesium, phosphorus control HTN fluid restriction (if renal failure) avoid NSAIDS chronic kidney disease ○ progressive, irreversible loss of kidney function diabetes & hypertension are leading causes ○ symptoms: edema (fluid retention) loss of appetite, nausea, anorexia, GI bleed fatigue dry skin muscle cramps foamy urine increased frequency of urination stages: 1 - kidney damage with normal renal function 2 - mild reduction of renal function 3 - GFR reduction of less than 60 4 - severe reduction 5 - renal failure metabolic acidosis cannot excrete excess acid fluid & electrolyte imbalances hypermagnesemia hyperkalemia (most serious disorder!) ○ acute: IV glucose and insulin kayexalate for cation exchange (sodium instead) ○ dialysis is most effective hyponatremia or hyper hypocalcemia chronic anemia personality & behavioral changes hyperglycemia & hyperinsulinemia (no insulin excretion occurring with kidney damage) ○ diagnostics: persistent proteinuria GFR < 60 urinalysis, creatinine clearance, serum creatinine, BUN as GFR decreases, BUN and serum creatinine increase renal ultrasound, CT scan ○ treatment: manage diabetes & hypertension ACEs and ARBs (with caution, as they can increase K+) prevent cardiovascular disease calcium & vitamin D supplements iron supplementation (anemia) correct electrolyte imbalances protein, sodium, fluid, potassium, phosphate restriction diet adjust existing drug dosing for renal impairment end-stage renal disease ○ dialysis ○ corrects fluid/electrolyte imbalances & removes waste products in kidney failure ○ started when: uremia (amount of waste in the urine) can’t be treated conservatively and/or GFR is less than 15 metabolic acidosis volume overload severe hyperkalemia ○ types: peritoneal fill, dwell, and drain multiple times a day dextrose is most often used for ultrafiltration very simple, home-based, not super strict diet ○ sodium & water restriction monitor abdominal girth & outflow complications: ○ site infection which can lead to peritonitis monitor for: fever, rebound ab tenderness, cloudy outflow, n/v ○ d/v, distension (use antibiotics) ○ hernias (d/t increased ab pressure) ○ lower back problems (increased pressure) ○ bleeding d/t initial catheter placement or active bleeding intraperitoneally ○ decreased lung expansion d/t atelectasis or pneumonia (elevate HOB, reposition, breathing exercises) ○ protein loss (monitor nutrition) hemodialysis filters out excess fluid & waste from the blood and returns clean blood ○ requires rapid blood flow and access to a large blood vessel ○ 3-4 hours a day 3x weekly complications: ○ hypotension (d/t hypovolemia, decreased cardiac output, vision changes, chest pain, light-headed, nausea) treatment: decrease volume of fluid removal & IV NSS ○ muscle cramps (d/t hypovolemia, low BP, increased ultrafiltration) treatment: decrease ultrafiltration & IV fluids ○ loss of blood (d/t blood not being rinsed, accidental tube separation, rupture, heparin) treatment: rinse all blood, avoid excess heparin ○ hepatitis (usually C, sometimes B, d/t infection) ○ disequilibrium syndrome occurs often in new clients, caused by rapid removal of solutes n/v, seizure, heart attack ○ sepsis, shock, depression, non-adherence always assess fluid status before (weight, BP, peripheral edema, heart & lung sounds) ○ the difference between weight from last post & current pre determines how much fluid will be removed assess vascular access & temp before during dialysis assess vitals q 30-60 mins daily weights monitor labs before, during, and after: BUN, creatinine, CBC HOLD MEDS LIKE HTN UNTIL AFTER TREATMENT protein restriction/reduction cirrhosis: - symptoms: jaundice, palmar erythema, spider angiomas, thrombocytopenia (decreased platelets, increased bleeding), ascites, gastric & esophageal varices, edema, peripheral neuropathy - treatment: - increased protein & carb diet, protein supplements - diuretics for edema - lactulose for hepatic encephalopathy - draining fluid for abdominal ascites - complications: - hepatic encephalopathy - liver cannot change ammonia to urea, causing buildup of ammonia in body, goes past blood brain barrier - symptoms: inability to construct simple figures, flapping hand tremors, sweet/musty breath, coma, sleeping issues - q2h neuro checks, lactulose - hepatorenal syndrome - gastric/esophageal varices - caused by portal hypertension dilating veins - esophageal is serious! - if bleeding occurs, p.t. must be ventilated, intubated, and in the ICU - treat with sclerotherapy, balloon tamponade, or rubber band ligation - abdominal ascites - caused by portal hypertension or hypoalbuminemia - serous fluid build up in the abdomen, risk for infection - portal hypertension - causes splenomegaly & varices & ascites - diagnostics: - liver biopsy! - serum albumin, liver enzymes, CBC - ultrasound for scarring - teaching; - avoid nsaids, asa, alcohol, vitamin B6 GERD meds: PPI (omeprazole), H2 receptor antagonists (pepsin), antacids, prokinetics crohn's: - symptoms: RLQ pain, diarrhea, weight loss - treatment: - glucocorticoids, aminosalicylates (first choice! work better for UC but still helpful), antimicrobials - symptomatic surgery of removing the infected parts (can lead to short bowel syndrome) - diagnostics: - capsule endoscopy - colonoscopy (not as common) - labs (CBC, albumin) - patient teaching: - experiment with fiber levels UC: - symptoms: LLQ pain, bloody diarrhea, dehydration, tenesmus, anemia, weight loss - treatment: - same as crohn’s - diagnostics: - same as crohn’s - double contrast barium enema study diverticulitis: - symptoms: systemic signs of infection, LLQ pain, tenderness on palpation, rectal pain - treatment: - antibiotics, analgesics, clear diet - diagnostics: - CT of pelvis/ abdomen - CBC, albumin - colonoscopy - prevention: - regular exercise (no weight lifting or straining) - high-fiber, low-fat & red meat diet MS: - demyelination of the CNS - symptoms: - nystagmus, dysarthria, tremors - urinary retention/constipation - ataxia - muscle weakness - diagnostics: - CSF increased protein - treatment: - glucocorticoids (prednisone & methylprednisolone) - PT, ST, OT MG - grave muscle weakness - autoimmune; stopping neuromuscular junction transmission - symptoms: - strong muscles in AM, weak as day goes on - overall weakness throughout body - can start off as drooping eyelids and will eventually become general MG - diagnostics: - AChR antibodies in blood - EMG conduction test - CT of thymus gland as it may be causing the tumors - treatment: - immunomodulators - thymus gland removal - pyridostigmine or neostigmine (improve neuromuscular transmission) - take at the same time every day! GBS - d/t infection (gastroenteritis) - diagnostic: - EMG - CSF - treatment: - IV immunoglobulins - heparin if blood clots occur trigeminal neuralgia: - vascular compression of trigeminal nerve - symptoms: - T1: episodic sharp pain d/t aggravating factors - T2: constant pain - diagnostic: - H&P, neuro exam - treatment: - T1: antiseizure meds & tricyclic antidepressants - help with the upset neurotransmitter balance - T2: opioids & analgesics - teaching: - semiannual dentist visits, CHG mouthwash, non-abrasive toothbrush - easy to chew foods - shave with electric razor - do not abruptly stop meds - pink/reddish-brown urine normal for antiseizure meds - take with meals - do not take OTCs ALS - no muscle nourishment - symptoms: paralysis w/ sensation, facial slurring & slow speech, no muscle movement - diagnostic: - EMG - H&P - treatment: - riluzole & edaravone that protect the neurons

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