Nurs 232 Exam 2

Stomach Anatomy Review

• parietal cells secrete hydrochloric acid in the stomach

• chief cells secrete pepsinogen

• bile secreted from the liver

• digestive enzymes released from accessory organs

• vitamin B12 needed to form RBCs & DNA

• alpha cells produce glucagon

• beta cells produce insulin (along w/ delta & F cells)

Thrush

treated aggressively & rapidly w/ Nystatin or IV Fluconazole

Pathophysio of GERD

• occurs as a result of backward flow of stomach contents into the esophagus, which overtime leads to disease; symptoms are caused by exposing the esophageal mucosa to the irritants from the stomach/duodenum

• most common cause of GERD is the excessive relaxation of the LES (lower esophageal sphincter)

• upper sphincter prevents excess air

• lower sphincter prevents backflow of contents

• Reglan given to increase motility while also providing anti-nausea

• stomach acid pH = 1.5 - 2.0/3.5

• distal esophageal pH = 6.0 - 7.0

• increased wt leads to greater intra-abdominal pressure

• NG tube heavily impacts the lower esophageal sphincter

Inflamed Esophagus

esophagus is injured by being bathed in gastric acid & pepsin; s/sx: dental caries, asthmatic, hoarse voice; chronic inflammation leads to hyperemia, erosions, laryngitis

Key Features of GERD

dyspepsia (indigestion), regurgitation, hoarseness, hypersalivation, dysphagia, odynophagia (painful swallowing), epigastric pain, generalized abd pain, belching, flatulence, nausea, pyrosis (heartburn), globus (feeling smth in back throat), pharyngitis, dental caries, atypical chest pain

Diagnostic Assessments for GERD

Barium swallow test, pH monitoring exam, upper endoscopy (aka EGD), gastric emptying study

Assessment of GERD

nauseous, pain, green stuff on toothbrush, pregnant, wt around abd, coughing wheezing @ night, globulus

Clinical Problems for GERD

potential for compromised nutrition status, acute pain d/t reflux of gastric contents (tx: meds to control the acid)

Interventions for GERD

nutrition, smoking, ETOH, positioning, pressure, medication, lifestyle changes

Antacids

give 1-2hrs after meals, don’t give w/ other drugs within 1-2hrs (interferes w/ absorption)

Histamine Blockers

depress the production of hydrochloric acid, reach peak blood levels in 1-3hrs; Four H2 blockers → Tagamet, Zantac, Axid, Pepcid

Proton Pump Inhibitor

blocks acid, can be increased to twice a day if once a day isn’t effective, taper off; Protonix needs to be reconstituted when given IV, not tolerated well w/ other drugs → flush 10mL first & another 10mL after

Gastritis

• inflammation of gastric mucosa; pain, dyspepsia, vomiting blood

• stomach is relatively free from disease, affected by PUD, gastritis, & cancer

Gastric ulcers

in stomach, pyloric sphincter is malfunctioning, back diffusion process is malfunctioning

Duodenal ulcers

in duodenum, increased secretion of gastric acid & increased stomach emptying, pH levels in duodenum are low for an extended period of time

Stress ulcer

in stomach or other location, main manifestation is bleeding/hemorrhage (frank red blood), gastric erosion

Complications of PUD

hemorrhage, perforation (BIG SICK → surgical emergency), pyloric obstruction (acid is staying in the stomach), intractable disease

Etiology of PUD

• H. pylori, NSAIDs, corticosteroids, Theophylline, caffeina, radiation therapy

• H. pylori: ABx → clarithromycin & amoxicillin, Omeprazole (PPI)

Clinical problems & interventions for PUD

• pain & potential for upper GI bleeding

• interventions: drug therapy, nutrition, managing upper GIB, NGT placement & lavage, endoscopic therapy, surgical management

• PUD drug therapy purposes: pain relief, heal the ulceration, eliminate H. pylori infection, prevent recurrence

Key features of upper GIB

bright red vomitus, melena, low H/H, hypotension, tachycardia, syncope, dizziness

OPQRST

Origin, Palliate/Provoke, Quality, Region, Severity, Timing

Liver (receives 1200mL of blood/minute)

• storage: iron, copper; vitamins A, D, & E; & water-soluble vitamin B12; also stores glycogen for release when body is hypoglycemic

• protection: phagocytic Kupffer cells engluf harmful bacteria & anemic RBCs; liver also detoxifies potentially harmful compounds (drugs, alcohol)

• metabolism: breaks down protein, amino acids, & produces bile; liver can regenerate

Cirrhosis

• extensive, irreversible scarring of the liver

• caused by chronic rxn to hepatic inflammation & necrosis

• impairs cellular regulation through degeneration & damage to hepatocytes

• nodules block bile ducts & normal flow throughout the liver

• LFTs (liver fxn test) elevated

• Lactulose → helps w/ BM to remove NH3 (ammonia) & be mentally clear

• higher the ammonia → less interactive pt will be

• ALP, ALT (most specific to liver), AST

• ascites: buildup of fluid in abd

• common causes: ETOH abuse, chronic viral hepatitis, NASH, bile duct disease, genetics

• Hepatitis C (viral) is the leading cause of cirrhosis & liver cancer (veterans are at high risk for hepatitis C)

Common complications of Cirrhosis

• Portal Hypertension (increase in pressure within the portal vein, >5mmHg)

• Ascites/Jaundice: fluid fills abd cavity, decreased albumin → 3rd spacing

• Encephalopathy: cognitive syndrome caused by liver failure & cirrhosis

• Esophageal Varices: esophageal veins become distended & tortuous from increased pressure (portal hypertension)

• Coagulopathy: decreased prothrombin production, splenomegaly destroys platelets (thrombocytopenia)

• Hepatorenal Syndrome: affects kidneys & manifested by → oliguria (<500mL/day), elevated BUN & creatinine, increased urine osmolality

4 Stages of Encephalopathy

• Stage 1: impaired thinking, behavior changes, fatigue, slurred speech

• Stage 2: mental confusion, disorientation, asterixis (hand flapping)

• Stage 3: marked mental confusion, stuporous, hyperreflexia, asterixis

• Stage 4: unarousable, no asterixis, positive Babinski sign, muscle rigidity, fetor hapticus (liver breath - musty, sweet odor)

• *avoid high protein diet → protein breaks down into ammonia

Tx for Encephalopathy

• Lactulose: promotes excretion of ammonia in the stool, increase osmotic pressure to draw fluid into the colon, prevents absorption of ammonia in the colon (target BM 3-5 per day)

• Rifaximin (Xifaxan): poorly absorbed abx thought to reduce ammonia production (changes urine to orange)

Assessment of Liver

• jaundice, pruritis

• rashes, lesions, spider angiomas

• abd ascites, edema of extremities & scrotum

• vitamin deficiency

• bleeding

• fatigue, significant wt changes, GI symptoms

Labs & Imaging Liver

• ALP, ALT (liver specific), AST, LDH (will always be elevated)

• Serum proteins (increase in acute LD, decrease in chronic LD, decreased albumin in severe LD)

• Creatinine (increased levels w/ hepatorenal syndrome)

• Bilirubin increased in both blood & urine)

• NH3, PT/INR (NH3 increased, PT/INR prolonged)

Priority Problems Liver

• fluid overload b/c of ascites

• potential for hemorrhage d/t portal hypertension & GI varices

• confusion & cognitive changes d/t increased ammonia levels

• pruritus d/t increased bilirubin & jaundice; head to toe itching → bleeding

Cirrhosis Interventions

• nutrition: low sodium diet, high carb, moderate fat

• drugs: avoid all OTC drugs; thiamine (energy production), multivitamin, folate (cell growth & repair), diuretics + albumin

• No ETOH

Hepatitis A

fecal-oral, *poop transmitted*

Hepatitis B

vaccine available; sex, needles, blood; HBV virus

Hepatitis C

blood, needles, tattoo

Hepatitis D

needs HBV; parenteral & sexual contracts

Hepatitis E

waterborne, international travel, fecal contamination of food/water; *poop transmitted*

Hepatitis

• widespread inflammation of the liver

• tenfovir, entecavir, glecaprevir, grazoprevir

• S/sx: N/V, fatigue, fever, dark urine, pruritus, jaundice, abd painn

Peritonitis

• acute inflammation/infection of the peritoneum & endothelial lining

• gangrene & sepsis can occur within 24-36 hrs (life-threatening + emergency surgery), perforation may develop within 24hrs but risk rises rapidly after 48 hrs

• mortality rate of 20% in post-op pts

• bacteria floating around in abd cavity

• normal bowel fluid is 7-8L/day

Peritonitis Assessment

• cardinal signs: abd pain, rebound tenderness, distention

• other signs: abd rigidity, high fever, tachycardia, hypoactive bowel sounds

• when bacteria present, the body tries to wall off the infection → increased vascular dilation & increased capillary permeability, this allows transport of leukocytes & phagocytosis; if left unchecked, 3rd spacing continues & body can go into hypovolemic shock → inadequate kidney perfusion

Appendicitis

• S/sx: epigastric/abd pain, anorexia; McBurney’s point

• risk of perforation → can lead to peritonitis/sepsis; gangrene & sepsis occur 24-36hr

• do not give laxatives/enemas or apply heat

Interventions for Peritonitis & Appendicitis

• prepare for OR: broad-spectrum abx, NGT, labs, CT scan, NPO

• surgery: laparoscopy (tiny incision), exploratory laparoscopy (wash out), open abdomen (abthera)

• pain control: IV opiates (give the good stuff!!)

• positioning: semi-Fowlers

Gastroenteritis

• inflammation of GI tract caused by viral (more common), bacterial or parasitic infections

• leads to increased intestinal secretions & motility, resulting in diarrhea & vomiting

Norovirus

• leading foodborne disease (November - April)

• fecal-oral route (respiratory if vomitus)

• incubation 48hr

• contaminated food

Gastroenteritis Assessment

• recent travel

• dining out: within 24-36hr, raw food

• S/sx: N/V, abd cramps, diarrhea, hypotension

Gastroenteritis Interventions

• oral rehydration therapy (pedialyte, sports drinks)

• loperamide (imodium): anti-diarrheal

• Abx

• skin care: bidet, barrier cream, avoid harsh wiping

• leakage: pads

Ulcerative Colitis

affects the colon’s mucosal lining causing continuous inflammation; 10-20 liquid bloody stools/day; complications: hemorrhage, nutritional deficiencies; 25-35% need for surgery, intestinal mucosa becomes hyperemic (increased blood flow, edematous & reddened)

Crohn’s Disease

patchy inflammation through all layers of the bowel, 5-6 loose nonbloody stools/day; complications: fistulas, nutritional deficiencies; 65-75% need for surgery; most common affected site is the terminal ileum; s/sx: abd pain, joint pain, fever, anemia

Interventions for UC & CD

• drugs, assess skin, nutrition, surgery

• Aminosalicylates (anti-inflammatory), Glucocorticoids, Anti-diarrheal, Immunomodulators

Cholecystitis

inflammation of the gallbladder; RF: female, diet w/ high fats, low calorie, low protein, & obesity; affects many adults commonly in affluent countries

• s/sx: abd pain, N/V, Murphy sign, clay-colored stool, jaundice, dark urine; Dx: increased WBC, ALP, AST, LDH, bilirubin; amylase distinguishes b/w cholecystitis & pancreatitis (elevation points to pancreatitis), ERCP or MRCP

Gallstones

5 F’s: female, forty, fat, fertile, family hx

Cholangitis

inflammation of common bile duct

Acalculous Cholecystitis

inflammation w/o gallstones, typically associated w/ biliary stasis; can be r/t sepsis, trauma, MODS, hypovolemia, major abd surgery, long-term total parenteral nutrition

Acute Cholecystitis

calculous (more common) & acalculous, inflammation caused by obstruction or reduced blood flow, trapped bile = chemical irritant to gallbladder wall; impaired circulation, edema, distention of gallbladder; tissue sloughing & necrosis

Chronic Cholecystitis

repeated episodes of cystic duct obstruction w/ or w/o stones, inflammation, decreased motility of bile; complications → pancreatitis & cholangitis; jaundice & icterus more common w/ chronic cholecystitis; w/ obstructive jaundice, excess bile accumulates → results in clay-colored stools, dark urine, pain, pruritus

Acute Pancreatitis

• s/sx: acute, severe abd pain, “boring” pain through body front back, signs of shock (massive hemorrhage), jaundice, vital sign changes

• dx: labs (amylase, lipase, ALT)

• etiology: I GET SMASHED (Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion stings, Hypercalcemia & Hypertriglycermidemia, ERCP, Drugs)

• clinical problem: wt loss & inadequate nutrition, hemodynamic stability, severe pain

Undernutrition (pt does not or cannot consumer calories & protein)

• Marasmus: body fat & protein are wasted, serum proteins are often preserved

• Kwashiorkor: lack of protein quantity & adequate calories; body wt is more normal & serum protein are low, risk for ascites & pedal edema

• Complications: decreased CO, cold intolerance, malabsorption, increased risk for infectious disease, poor wound healing, muscle wasting, weakness, substance misuse, reduced vital capacity (resp.)

• S/Sx: alopecia, dry/scaling skin, muscle wasting, edema, cardiac dysrhythmias

• Priority Problem: wt loss d/t inability to access, ingest, or digest food or absorb nutrients; labs (decreased): albumin, cholesterol, hemoglobin, hematocrit

Obesity

• WC better predictor of CAD than BMI

• Hormones: Leptin, Resistin, Ghrelin

• Complications: DM, CAD, hypertension, OSA, cholelithiasis (gallstones)

• Monogenic: caused by a single gene

• Syndromic: associated w/ other phenotypes

• Oligogenic: d/t the absence of a certain phenotype

• Polygenic: caused by a cumulative effect of numerous genes

Communicate w/ RESPECT

Rapport, Environment, Safe, Privacy, Encourage, Compassion, Tact

Hypothyroidism

• Primary patho: destruction of thyroid tissue, decreased synthesis of thyroid hormone; Hashimoto thyroiditis = most common cause in US, or part of having the thyroid removed

• Secondary patho: congenital pituitary defects, pituitary tumors, trauma, infections, infarc

• S/Sx: Hypo - slows down functioning; hypoventilation, constipation, decreased metabolic rate (wt gain), slow/slurred speech; major complication → myxedema coma

• Diagnostic/Labs: pt hx → Hashimoto thyroiditis, medication use (lithium amiodarone), or prior tx for hyperthyroidism; T3 & T4 levels are low; TSH is high in primary hypothyroidism, can be normal to low in secondary hypothyroidism

• Meds: Levothyroxine (Synthroid) → taken on an empty stomach, 30-60 min prior to a meal, take alone w/ no other meds

• Occurs most often in women age 30-60

Hyperthyroidism

• Pathophysio: excessive thyroid hormone secretion, excess hormones causes systems to speed up

• Causes: Grave’s disease, iodine deficiency, Levothyroxine excess

• affects women age 20-40 more than men

• S/Sx: STEPN’ WIDE → Sweating, Tremor, Enlarged thyroid, Palpitations, Nervousness, Wt loss, Intolerance to heat, Diarrhea, Exophthalmos

• Diagnostic/Labs: assess for goiter, T3 & T4 elevated, TSH elevated (secondary/tertiary hyperthyroidism) or decreased (Graves disease)

• 6 Ps of Thyroid Storm: Propanolol, Propylthiouracil (PTU), Prednisone, Potassium iodide, Plenty of fluids, Pyretic control

• Meds: Methimazole, PTU (pregnant pts), Iodine (short-term), Radioactive iodine

Parathyroid glands

maintains calcium & phosphorus balance; PTH acts on kidneys → increases reabsorption of calcium & increased phosphorus excretion

Hypoparathyroidism

• fxn of parathyroid is decreased, serum calcium can’t be maintained

• causes: thyroidectomy or surgery or radiation

• Labs: decreased calcium (9-10.5), decreased magnesium (1.3-2.1), increased phosphorus (2.5-4.5)

• results in hypocalcemia

• S/Sx: Trousseau & Chvostek signs, tingling, numbness, irritability of muscles, heart failure

• Tx: calcium supplements w/ vitamin D

Hyperparathyroidism

• hypercalcemia & hypophosphatemia

• Causes: vitamin D deficiency, CKD, cancer, drug therapy

• excessive PTH increases bone resorption by decreasing osteoblast (builders) activity & increased osteoclast (demolition) activity

• S/Sx: bone fractures, wt loss, arthritis, psychological distress

• balance calcium levels to aovid renal calculi formation

• Tx: cinacalcet (decrease PTH production), biphosphonates (decrease calcium levels), IV hydration, telemetry