Final Flashcards
Glomerulus/GFR
GFR = how much blood is filtered per min
Normal GFR = 90mL/min or greater
Urea & creatinine excreted, water & electrolytes reabsorbed
Urinalysis categories
Color = clear, pale yellow
Specific Gravity = concentration of urine compared to water (water is 1) NORMAL IS ~1.02!
Osmolarity = particle concentration in urine
Hematuria = tea colored, pink, or red urine
WBC = should be none, if present -> infection (UTI, pyelonephritis)
Protein/glucose = should be None !
24hr urine test
Discard 1st urine, collect in orange jug, put on ice
restart if missed urine!
Creatinine
Breakdown of muscle present in urine
Normal = 0.6-1.20mg/dL
BUN
Normal = 6-20mg/dL
Acute Glomerulonephritis
Inflammation of glomerulus d/t immune response strep infection
occurs 14 days after infection!!
S&S:
- HTN (fluid retention)
- Positive for Strep
- facial/ orbital edema (fluid retention)
- Hematuria
- Elevated BUN/Cr
- Proteinuria
Nursing Interventions for Acute Glomerulonephritis
- Control BP (diuretics/ antiHTNs)
- Maintain fluid & electrolyte imbalances
- Strict I&O
- Monitor labs for electrolytes hypernatremia, hyperkalemia!!
- Low Na diet, limit protein intake
Nephrotic Syndrome
Damage to glomerulus cause leakage of A LOT OF PROTEIN in urine !
Can be d/t illness or med related
S&S:
- proteinuria >3g/day
- Foamy, frothy, dark urine
- hypoalbuminemia
- HLD
- Facial/orbital edema (no osmotic pressure)
Acute Kidney Injury (AKI)
Sudden, short term damage to kidney leads to abrupt loss of kidney function!
D/t decreased perfusion/CO (like in shock) or nephrotoxic meds
Pre-renal AKI
Injury BEFORE kidneys
Lack of perfusion (low CO), Volume depletion, impaired cardiac function, massive vasodilation
Intrarenal AKI
Injury WITHIN kidney
Nephrotic meds (NSAIDs), Glomerulonephritis, pyelonephritis, obstruction (kidney stones, blood clots)
Post-renal AKI
Injury AFTER kidney
Bladder retention, Urinary tract obstruction (BPH, stricture, foley kinked)
Phases of AKI - Initiation
Injury to kidney where S&S begin to appear
- oliguria
- fluid volume excess
- retaining H+ -> metabolic acidosis
- BP issues
Phases of AKI - Oliguric
- output is < 400mL/day
- Hyperkalemia
- Hyponatremia
- Hyperphosphatemia
- Hypocalcemia
- Increased BUN/Cr
- Edema
- Metabolic acidosis
Phases of AKI - Diuresis
EXCESSIVE urine output of 3-6L/day
Leads to hypokalemia!
Phases of AKI - Recovery
GFR returns to normal
Nursing interventions for AKI
- Identify & Tx cause
- maintain fluid balance MAP > 65
- Restore flow of urine if obstructed
- Assess for use of nephrotoxic meds (NSAIDs, certain abx)
- Monitor weight! daily weight AFTER 1st void!
1kg weight gain = 1 L fluid retention! - Fluid & Na restriction <1L/day, renal diet!
Chronic Kidney Disease (CKD)
Progressive, irreversible damage to the kidneys!
Body unable to maintain fluid, electrolyte, & metabolic balance
Risk Factors:
- DM
- HTN
- AKI (untreated or recurrent)
- Family hx
- Increased age
- Male > Female
CKD Stage 1
Damage w/ normal renal fx (GFR > 90) BUT proteinuria for longer than 3 months
CKD Stage 2
Damage w/ MILD loss of renal fx (GFR 60-89) w/ proteinuria > 3mo
CKD Stage 3
mild-severe loss of renal fx GFR 30-59
CKD Stage 4
SEVERE loss of renal fx GFR 15-29
Needs dialysis!
CKD Stage 5
ESRD! GFR < 15!
needs dialysis!
CKD S&S
- water retention d/t hypernatremia (edema, HF, HTN)
- metabolic acidosis (Iow pH, low bicarb)
- Anemia d/t no EPO
- Hyperphosphatemia & hypocalcemia -> tetany, seizures, weak bones, weak muscles
- Hyperkalemia -> arrhythmias! (Peaked T wave)
- odor of AMMONIA on breath, METALLIC taste in mouth!
- gray/bronze skin color
CKD Nursing Interventions/Tx
- daily weights (1 kg = 1 L retained)
- strict I&Os
- Safety seizure & fall precautions!
- Monitor anemia & electrolytes!
- monitor urine output
- low protein, fluid, Na, K , phosphorous diet!
Hemodialysis
Removes wastes & excess water from blood (replacing fx of the kidneys)
typically 3 days/wk for 3-5hrs per session
- Heparin admin to prevent clotting in tubing!
Dialysis disequilibrium syndrome (DDS)
Solutes are removed too quickly from the blood -> brain cells swell -> increased ICP -> cerebral edema -> AMS, confusion, death
Dialysis vascular access device - Temporary (Permacath)
- Double lumen large bore hemodialysis catheter
- Red cap = arterial blood, blue cap = venous blood
- inserted in internal jugular, subclavian, or femoral veins
- increased risk of infection
- used temporarily in AKI or as a bridge until permanent access
- ONLY used for dialysis, NO MEDS!
Dialysis vascular access device - AV fistula
- GOLD standard of permanent access!
- usually in forearm
- takes 4-6wks to mature!!
- No BPs or needle sticks on this arm!!
- Can palpate a bounding thrill
no lifting > 5lbs, no tight restrictive clothing on the arm
Dialysis vascular access device - AV graft
- synthetic graft material btwn artery & vein
- used when vessels are not suitable for fistula (scleroses, stenosed)
risk of infection, thrombosis!
Nursing management of hemodialysis pt
Before dialysis assess:
- fluid status
- VS
- fistula (feel thrill, auscultate bruit if not present alert MD!)
- Hold meds that cause LOW BP! (ACEs, ARBs, BBs, CCBs, diuretics, dilators, nitro)
- meds that will be dialyzed out (PCNs or cephs, digoxin, water soluble vits B, C, folic acid)
- Calcium and insulin
Peritoneal Dialysis
- Dialysate (Hypertonic fluid) introduced into peritoneal cavity via catheter
- fluid dwells in peritoneal cavity and then is drained via gravity
- removes toxins and wastes like urea, creatinine, metabolic wastes via diffusion & osmosis
-
slower than HD!
Before starting tx: - obtain weight
- warm fluid!
- must show they can lift 8L dialysate bag & understand how to access catheter!
Peritoneal Dialysis Complications
Peritonitis = fever, tachy, cloudy drainage (infection)
leakage = kink in catheter, coughing/emesis increases abd pressure
Bleeding = may occur 1-2 days after insertion or during menstruation
Incomplete recovery of fluid = put 8L in and should get 8L out!
If this happens:
- inspect catheter but DO NOT REPOSITION IT!
- turn pt on side to get full drainage
- can be d/t constipation
- alert MD if none of these methods work
Kidney Transplant
- indicated for ESRD
- can be from living donor or heartbeat only donor
Post-op: - antirejection meds for LIFE!
- Prevent infection (high risk d/t immunosuppressants)
- Assess for rejection! **increased WBCs, S&S of kidney failure, fever, tenderness over implanted kidney
- monitor urinary fx (large amount of urine immediately post op)
- continuing care = daily weights, I&Os at home, strict renal diet, infection control
Urolithiasis & Nephrolithiasis
- Stones/calculi formed in urinary system or kidneys respectively
- blood, minerals, wastes form the crystals
Causes: - consuming high amounts of purines, oxalates, salt, Ca/Vit D supplements
- hyperparathyroidism
- hypercalcemia
- hyperuricemia
- urine stasis
- low activity
Urolithiasis & Nephrolithiasis S&S + Diagnosis
- PAIN!!
- N/V
- Fever
- Cloudy, odorous urine
- urinary retention
- Hydronephrosis from urine backing up
Diagnosis:
- KUB = kidney ureter bladder X-ray
- US/CT
- Pyelogram , IVP dye (contra if renal failure)
- Urinalysis , assess for crystals/infection
Urolithiasis & Nephrolithiasis Tx
- pain management
- HIGH fluid intake 3-4L/day
- Monitor I&Os
- Strain urine!
- Prev education on staying hydrated!
- stones < 5mm usually pass on their own
For stones > 5mm:
Extracorporeal Shock Wave (ESWL) = noninvasive , shockwaves break up stone
percutaneous nephrolithotomy = invasive, stone removed by urologist
Nephrostomy tube = catheter placed in renal pelvis to drain urine until healed
Urethral trauma
- blunt force trauma to lower abd/pelvic region
- indwelling catheter contraindicated if blood at urinary meatus until tear is r/o
- can be caused by unintentional injury during Sx
- may cause fistula of ureter & vagina!
Bladder Trauma
Caused by pelvic fx or multiple blows to abd when bladder is full
** #1 S&S is gross hematuria**
Bladder Cancer
- tumors typically arise at base of bladder , involving ureteral orifices & bladder neck
- Dx w/ cystoscopy, CT, US
Tx: - transurethral resection of fulguration (cauterization)
- simple cystectomy or radical cystectomy
- chemo & radiation
Urinary diversions - Ileal conduit
- implanting ureters into loop of ileum led out to abd wall
- urine collected via ileostomy bag!
Urinary diversions - Cutaneous ureterostomy
- ureters detached from bladder & brought to abd wall
- stoma created, usually flush with skin or retracted
Urinary diversions - Indiana Pouch
Most common CONTINENT urinary diversion
- segment of ileum and cecum created to form reservoir for urine
- Pouch must be drained at regular intervals w/ catheter
- maintain aseptic technique and prevent urine from sitting on skin!
Stoma Care
- stoma should be pink/red and moist
- If stoma appears dusky, purple, brown, black = BAD, ischemia and/or necrosis!
- dusky color is superficial ischemia and outer layer of mucosa may slough off in several days
Pancreas Endocrine Fx
Islet of Langerhans produce: insulin, glucagon, somatostatin, pancreatic polypeptide
Pancreas Exocrine Fx
Acinar cells secrete digestive enzymes into pancreatic ducts -> flows through ampulla of vater (fusion of pancreatic & common bile duct) -> into duodenum where digestive enzymes ACTIVATE
Sphincter of oddi
Muscular valve that controls release of digestive enzymes and prev reflux of stomach contents into pancreas & bile duct
Acute Pancreatitis
Sudden inflammation of pancreas
- something triggered digestive enzymes to activate INSIDE pancreas -> high amylase & lipase in blood
- limited structural change, damage is reversible!!
- mainly caused by alcohol and gallstones
- can progress to pancreas digests itself -> tissue dies -> cyst/abscess of dead tissue forms -> can rupture/hemorrhage -> infection/sepsis!!
- Activated digestive enzymes can spread to surrounding organs and cause damage
Chronic Pancreatitis
Chronic inflammation of the pancreas
- IRREVERSIBLE damage to structure of pancreas
- fibrosis overtime and can’t produce digestive enzymes
- caused by YEARS of alcohol abuse! (Recurrent acute pancreatitis d/t alc)
- also caused by Cystic Fibrosis!
S&S of Acute Pancreatitis
- Abd pain worst when lying flat
- Sudden, v painful mid epigastric pain or LUQ + back
- Pain may start after eating greasy/high fat meal or alc!
- fever
- Tachy/hypotension
- N/V
- Hyperglycemia
- Cullen sign = bluish discoloration around belly button
- Grey Turner sign = bluish discoloration on flanks
S&S of Chronic Pancreatitis
- persistent, chronic epigastric pain! Or no pain d/t pancreas not producing any enzymes
- pain is worst after eating greasy/fatty meal or alc
- steatorrhea = oily/fatty stools d/t lack of pancreatic enzymes & bile
- Mass & swelling of abd
- weight loss d/t no enzymes to digest foods for nutrients
- Jaundice/dark urine = damage to common bile duct -> bile build up
- S&S of DM d/t no or inadequate insulin production
Nursing interventions for pancreatitis
- Rest pancreas = NPO until S&S subside then reintroduce food slowly (**liquids first)
- maintain IV hydration
- Pt edu on foods to avoid , eating low fat small meals
- NGT
- Monitor BGL
- Admin Pancreatic enzymes give RIGHT BEFORE meal, do NOT mix w/ alkaline foods like ice cream, pudding, milk, yogurt
- admin pain meds NO MORPHINE -> spasm of sphincter of oddi
- positioning to relieve pain = lean forward, sit up, NO SUPINE
- decrease acid secretion w/ PPIs, H2 blockers
Cholecystitis
Inflammation of gallbladder
Caused by Cholelithiasis or Acalculous
Cholelithiasis
Gall bladder stone obstructs bile duct -> increased pressure in gallbladder -> inflammation damages walls -> blood flow compromised -> death of organ
Risk Factors:
- Female > Male
- obese
- old age
- fam hx
- preg
Acalculous
Gallbladder not working, does not contract!
Risk Factors:
- high acuity pts
- post op
- severe illness (sepsis, burns, major trauma)
- TPN for long time (gallbladder not stimulated)
S&S of Cholecystitis
- N/V , bloating
- Fever
- epigastric abd pain that radiates to R shoulder esp after greasy meal!
- Murphy’s Sign = palpate under ribs on R side at mid clav line, have pt take a deep inhale, pt stops breathing in d/t pain of palpation
- steatorrhea
- jaundice
- dark brown urine
- clay colored stools
Nursing Interventions & Tx for Cholecystitis
“GALLBLADDER”
GI rest = NPO until recovered -> clear liquids
Analgesics & Antiemetics
Low fat, gas free foods
Large bore IV for hydration & electrolytes
Breathing in stopped (Murphy’s sign)
Labs = electrolytes, Bili, WBC, liver enzymes, pancreatic enzymes
Abx (IV)
Drain care
Deterioration = AMS, tachy, hypotension, high temp, high WBC count, worsening abd pain
ERCP = remove gallstones
Removal of gallbladder (cholecystectomy)
C Tube
Cholecystostomy tube placed thru abd wall into gallbladder
- indicated for pt that can’t have immediate cholecystectomy but infected bile needs to be removed
- keep collection bag at waist level to drain
- Empty & record drainage, not color
- monitor insertion site for infection
- flush per MD order to prevent blockage
T Tube
Works as a drain and for testing (dye injected into tube, X-ray taken to visualize stones)
- drainage bag kept at abdomen
- pt should be upright in semi-Fowler’s
- bile is harsh on skin, maintain integrity
- drainage should be < 500mL / day
- must have MD order to flush!
- may have MD order to clamp tube 1hr before & after meals so bile can enter duodenum to digest fats!
Hepatitis - Causes
- Meds
- Excessive Alc intake
- Illicit drugs
- Viruses (Hep A-E)
Hepatitis - Labs
- CMP for Liver Enzymes
- ALT (enzyme) = 7-56
- AST (enzyme) = 10-40
- Bilirubin = < 1 or 1.2
- Ammonia = 15-45 Lactulose admin for HIGH ammonia -> diarrhea
Hepatitis S&S
- May be asymptomatic
- Jaundice / dark urine
- N/V, stomach pain, loss of appetite
- Fever
- Fatigue
- Clay colored stool
- Arthralgia (joint pain)
Hepatitis A
- ACUTE ONLY no long term complications
- Fecal-Oral transmission
- Can be contagious for 2wks before S&S and contagious 1-3 wks after S&S subside
- Diagnosed by blood work for Anti-HAV abs!
- Anti-HAV IgM = active infection!
- Anti-HAV IgG = past infection or immunity from vaccine
- HANDWASHING for prevention!!
- Hep A Vaccine = 2 doses, 6 months apart
Hep A immunoglobulin can be given within 2wks of exposure for temporary passive immunity
Hepatitis B
-
Acute AND Chronic (leads to cirrhosis or liver cancer)
infants & young children at greatest risk for chronic! - Blood and bodily fluid transmission!
- Blood work for Hep B surface antigen , positive = current infection!
- Anti-HBs = recovered or immune
- Tx Chronic Hep-B with antiviral meds or interferon
- Prevent w/ handwashing, sharps precautions
- Vaccine for ALL INFANTS (3-4 doses 6-18mo course)
- All preg women tested , immunoglobulin give 12hrs post birth if POS
- Immunoglobulin given within 24hrs for all other exposures
Hepatitis C
- Acute AND Chronic!
- blood & bodily fluids transmission!
- Blood work for anti-HCV abs (ONLY FOR CHRONIC)
- Tx w/ antiviral meds
- Prevent w/ handwashing, sharps precautions, strict screening for blood transfusions & organ donors!
- NO VAX OR IMMUNOGLOBULIN THERAPY
Hepatitis D
- Acute AND Chronic
- Blood & bodily fluid transmission
- ONLY infects a person when they have HEP B!!
- Blood test for HDAg and anti-HDV
- Tx w/ antiviral meds or interferon
- Prevent w/ handwashing & sharps precautions
- Hep B vaccine to prevent development of Hep D!
no immunoglobulin for post exposure
Hepatitis E
- ACUTE ONLY!
- Fecal-Oral transmission!
- Blood test for HEV abs
- no Tx, rest & supportive for S&S
- prev w/ HANDWASHING!
- Use bottled water outside of US & cook meat thoroughly!
-
No Vax or IGs!
Can cause major complications in 3rd Tri of pregnancy!
“HEPATIS” for Nursing Edu/Management of Hepatitis
Handwashing
Eat low fat & high carb diet - helps w/ liver regeneration
Personal hygiene products NOT to be shared
Activty conservation - rest to heal liver
Toxic substances avoided - esp hepatoxic OTC like alc, sedatives, ASPARIN, Tylenol
Indiviual bathrooms
Small but freq meals - helps w/ nausea
pt should NOT cook for others until not infectious!
Kupffer Cells
Remove bacteria, debris, parasites, and old RBCs from blood entering liver
Hepatocytes
Produce bile, metabolize drugs/substances, store clotting factors, conjugate bilirubin, detox
Liver Fx - Metabolism
excess glucose synthesized and stored as glycogen!
in cirrhosis can’t synth glycogen -> hyperglycemia! And the reverse, can’t convert glycogen to glu -> hypoglycemia!
Liver Fx - storage
- Stores vit B12, A, E, D, K, minerals, Iron
- Bile is ESSENTIAL for absorption of fat soluble vitamins
Cirrhosis impairs bile prod -> decreased absorption & storage of fat sol vitamins
Liver Fx - Digestion
- Bilirubin in bile and stool
- Old RBCs removed by Kupffer cells break down Hgb to heme & globin
- Hepatocytes metabolize heme into Fe & bilirubin
- Bilirubin put into bile and excreted via stool
in cirrhosis Hepatocytes leak bili into the blood -> jaundice
Liver Fx - blood proteins
Produces albumin, fibrinogen, prothrombin
Cirrhosis
Liver disease that leads to scarring of liver
Causes:
- Viral infection of Hep B & C
- Alc consumption
- Fatty liver (obese, HLD, DM)
- Autoimmune disease (attacks liver)
- Bile duct issues (bile stays in liver & damages cells)
Compensated Cirrhosis S&S
- Typically asymp
- intermittent mild fever
- Ankle edema!
- Unexplained epistaxis
- Palmer erythema
- Vascular spider veins
- Splenomegaly
- Firm, enlarged liver
Decompensated Cirrhosis S&S
- Ascites
- Jaundice
- Muscle wasting & weight loss
- Continuous mild fever
- hypotension
- clubbing of fingers
- GI bleeding from esophageal varices
“THE LIVER IS SCARRED” Cirrhosis S&S
Tremors of hands (asterixis or hand flapping d/t increased toxins in blood
Hepatic foetor (late sign, pungent, sweet, musty smell to breath)
Eyes and skin yellow (jaundice)
Loss of appetite (spleen pushes on stomach)
Increased bili & ammonia
Varices (esophageal d/t increased pressure in portal vein)
Edema in legs (low albumin)
Reduced plts & WBCs
Itchy skin (toxins in blood)
Spider angiomas (chest, d/t increased estrogen in blood)
Splenomegaly & Stool clay colored
Confusion or Coma (high toxins & ammonia)
Ascites (low albumin)
Redness on palms (increased estrogen in blood)
Renal failure
Enlarged breasts in men (increased estrogen)
Deficient on vitamins (fat soluble vitamins)
Comp of Cirrhosis - Portal HTN
Portal v becomes narrowed d/t scar tissue in liver -> reduces blood flow to liver -> increased pressure in portal vein -> affects connected organs like spleen & GI structures (esophagus) -> varices!
Comp of Cirrhosis - Splenomegaly
Plts & WBCs are trapped in spleen d/t increased pressure in portal vein
Comp of Cirrhosis - Esophageal Varices
Increased pressure in portal vein causes vessels to become weak & rupture.
At risk of TOTAL BLEED OUT d/t low levels of clotting factors & plts!!
Comp of Cirrhosis - Fluid overload in Legs & Abdomen
Ascites -> risk of infection from bacteria in GI system (reduced WBCs from spleen sequestration)
Comp of Cirrhosis - Hepatic Encephalopathy
Liver unable to detoxify -> ammonia builds up & collects in brain -> AMS / Coma, neuromuscular problems, asterixis, hepatic foetor
Diagnosis of Cirrhosis
- Liver biopsy to see how much scarring present in liver
- Labs to evaluate liver enzymes (ALT/AST) , albumin, plt, & PT levels, Hep B & C titers, bili levels
Nursing Interventions or Cirrhosis & Tx
- monitor for BLEEDING! Limit invasive procedures & hold pressure at injection sites for 5mins or more!
- Monitor for esophageal varices by looking for dark-tarry stools, bloody emesis. Limit coughing, vomiting, drinking alc, constipation
- monitor reflexes & AMS
- monitor BGL
Tx: - liver transplant
- shunting Sx to alleviate Ascites
- Diuretics to remove excess fluid
- BB & Nitrates to help with portal HTN
- Admin blood products & Vit K to help w/ clotting
- Lactulose to decrease ammonia levels
- Paracentesis = removal of fluid from abd
Liver Transplant
Tx of choice for ESLD
- total Sx removal of diseased liver
Post op complications:
- bleeding
- infection (immunosuppressants)
- REJECTION
- Delayed graft fx
- Biliary leaks & obstruction
- Hepatic artery thrombosis
- Portal vein thrombosis
GI Bleeds
- type of bleed that occurs anywhere in digestive system
- may be d/t injury, infection, or inflammation
- sudden HEAVY bleeding is more immediately dangerous
- Upper GI bleed = anywhere above the ligament of Treitz (first part of Small intestine)
- Lower GI Bleed = anywhere below ligament of Treitz
GI Bleed - Angiodysplasia
Abnormal or enlarged blood vessel in the GI tract
GI Bleed - Benign Tumors or Cancer
May cause bleeding when they weaken lining of GI tract
GI Bleed - Colitis
Ulcers in large intestine may bleed! UC is an inflammatory bowel disease that can cause GI bleeding
GI Bleed - Colon Polyps
Can cause GI bleeding, some may be cancerous
GI Bleed - Diverticular disease
GI bleeding caused by small pouches that herniate outward, pushing against weak spots in colon wall
GI Bleed - Esophagitis
Lower esophageal sphincter is weak and stomach acid damages esophagus & causes bleeding
GI Bleed - Gastritis
If untreated leads to ulcers
GI Bleed - Mallory-Weiss tears
Caused by severe vomiting , a tear in mucous membrane at the junction of the esophagus and the stomach
GERD Complications - Esophagitis
direct effect of gastric acid on esophagus mucosa -> inflammation of esophagus
if severe, can cause serious bleeding!
GERD Complications - Resp irritation
Cough, bronchospasm, laryngospasm, cricopharyngeal spasm -> develop asthma, bronchitis, pneumonia
GERD Complications - Barrett’s Esophagus
Esophageal metaplasia
Normal squamous epithelium replaced w/ columnar epithelium
precancerous lesion!
MUST be monitored every 2-3yrs w/ endoscopy!
PPIs
Block ATPase that secretes HCl
Most common SE is headache
Long term/high doses increase risk of fxs of hip, wrist, spine
assoc w/ increased risk of C. Diff in hospitalized pts!
H2R Blockers
Cimetidine
Decreases conversion of pepsinogen to pepsin
- decreases secretion of HCl
- increases ulcer healing
- no common SEs
Antacids
Mylanta
Increase gastric pH by neutralizing HCl
Quick acting but short lived
Antacids
metoclopramide
Promotes gastric emptying = reduced risk of reflux
Peptic Ulcer Disease
Erosion of GI mucosa d/t digestive action of HCl and pepsin
Gastric ulcer = lower eso & stomach
Duodenal ulcer = duodenum
#1 cause of peptic ulcers is H. Pylori!!
Peptic Ulcer Disease Causes
H Pylori - produces urease -> inflammation
Asa/NSAIDs - inhibit prostaglandins that protect mucosa
Corticosteroids - decrease rate of mucosal cell renewal = decreased protection from HCl
Lifestyle - alc, caffeine, smoking, stress (increases HCl)
Gastric Ulcers
occurs in any portion of stomach or lower esophagus
less common
- affects F>M & older adults > 50yo
- pain HIGH in epigastrium (r/o MI)
- Occurs 30min-2hrs post meals
- Burning, gaseous feeling
- certain foods worse for pain like OJ, spicy, tomato sauce
Duodenal Ulcers
More common!
- seen at any age but especially increased 35-45yo
- Blood type O at increased risk!
- caused by H. Pylori in 90 to 95% of pts!!!
- Mid-epigastric pain beneath xyphoid process
- back pain if ulcer located in posterior duodenum
- PAIN 2-5hrs POST MEALS!!
- AWAKENING IN PAIN IS CLASSIC SIGN!!
- burning, cramp like pain that comes & goes `
Peptic Ulcer Complications - Hemorrhage
EMERGENCY
- d/t erosion of granulation tissue at base of ulcer during healing
- STOP BLEEDING -> bedside endoscopy to cauterize or OR
- Replace fluids (NS, LR)
- Blood products if needed
- Cerial CBCs
- Monitor VS (hemorrhage = hypoT, tachy)
- NGT for decompression
Peptic Ulcer Complications - Perforation
MOST LETHAL!
common in large penetrating duodenal ulcers that have not healed!
- d/t ulcer penetrating serosa w/ spillage of contents into peritoneal cavity -> peritonitis
- will have sudden, severe upper abd pain!
- Tachy w/ weak pulse
- Rigid, board like abd
- Shallow, rapid respirations
- Bowel sounds ABSENT
- N/V
- stop spillage into peritoneal cavity w/ NGT and/or Sx
- Abx for peritonitis! risk of septic shock!
Peptic Ulcer Complications - Gastric outlet obstruction
Ulcer -> histamine -> inflamm of pyloric sphincter -> food stuck in stomach
- pain worsens towards EOD as stomach fills
- pain relieved with belching & vomiting (emptying stomach)
- swelling in stomach & upper abd
- loud peristalsis (borborygmus)
- NGT for decompression
- Correct fluid & electrolyte imbalances
Tx of Peptic Ulcers
- multiple Abx used to eradicate H. Pylori infection
- usual Tx is 7-14 days or longer!!
- Dual therapy = ranitidine bismuth citrate w/ clarithromycin
- another option is Amox, calrithromycin, and omperazole
Sucralfate
- coats esophagus and stomach lining
- accelerates ulcer healing
- used for short term tx!
- given Q6h, NPO 1hr before/after, issues w/ pt compliance!
Billroth I
gastroduodenostomy
- partial gastrectomy w/ removal of distal 2/3 of stomach and anastomosis of gastric stump to duodenum!
Billroth II
gastrojejeunostomy
Partial gastrectomy w/ removal of distal 2/3 of stomach and anastomosis of gastric stump to jejunum!
Vagotomy
severing of vagus nerve
- vagus nerve innervates stomach and activates HCl prod
- partial vagotomy -> decreased innervation/stimulation to parietal cells -> decreased acid prod
- decreased gastric motility & gastric emptying
pyloroplasty done after vagotomy to enlarge pyloric sphincter and increase gastric emptying!
Dumping Syndrome
- direct result of Sx removal of large portion of stomach and/or pyloric sphincter
- stomach can’t control amount of gastric chyme entering SI -> a large bolus of hypertonic fluid enters SI
- fluid drawn into bowel lumen 15-30mins after eating
- acute weakness, sweating, palpitations, dizziness, cramps, intense urge to defecate!!
Postprandial hypoglycemia
variant of dumping syndrome
- uncontrolled gastric emptying -> bolus of fluid high in carbs in SI -> raises BGL -> excessive insulin release -> rebound hypoglycemia
- approx 2hrs post meals sweating, weakness, AMS, confusion, palpitations, tachy, anxiety
Peptic Ulcer Post Op care
- NGT for decompression
- observe aspirate for color, amount, odor
- color will be bright red first, darkening within 24hrs, yellow-green within 36-48HRS
- IV fluids
- Diet = small, DRY feedings, low carb, restrict sugar, mod protein/fat , LIMIT 4oz FLUID W/ MEALS, rest for 30mins post meals
Diarrhea
- freq loose/watery stools of > 200g/day
- causes can be drugs/abx, chemo
- Infectious agents: viral (rotavirus) , bacterial (salmonella, C. Diff) , Parasitic (giardia)
- electrolyte imbalances (hypokalemia, metabolic acidosis)
Diverticular Disease
- outpouching of bowel lining
- diverticulosis = multiple diverticulum
- most common in sigmoid colon but can happen anywhere
- May not have sig S&S
- crampy abd pain in LLQ relieved by flatus or BM
- alternating between constipation & diarrhea
- Prev w/ HIGH FIBER diet & adequate fluid intake
- Bulk lax like Metamucil
- anticholinergics relieve spasm
Diverticulitis
diverticula become infected & inflamed!
- can lead to abscesses
- can lead to scarring
- LOW FIBER DIET with active flares!
- broad spec abx
- increase fluids
- bedrest to decrease gastric motility
- may be NPO
- if it goes down to serous layer -> bleeding/hemorrhage -> perforation
Celiac Disease
- gluten sensitivity
- autoimmune response
- damage to SI from ingestion of rye, wheat, barely
- causes steatorrhea
pt must be careful w/ oats as often cross contamination
Lactose intolerance
- lack lactase -> can’t break down lactose
- diarrhea, cramping 30mins after ingestion
- can lead to osteoporosis (not absorbing Ca/Vit D in lactose containing prod)
IBS
- intermittent & recurrent abdominal pain
- constipation
- diarrhea
- belching
- STRESS plays a huge role
TX:
- 20g fiber / day
- avoid gas producing foods
- eliminate fructose & sorbitol
- probiotics may help
- anticholinergics
- stress management
- READ FOOD LABELS!
Inflammatory Bowel Disease (IBD)
encompasses Crohn’s & UC
- an autoimmune attack on intestinal tract
- chronic, recurrent widespread inflammation and tissue destruction
- periods of remission & exacerbation
- any age but peaks 15-25yo & white Jewish decent
- Diet high in seed oils and red meat may be triggers
- stress & smoking
- chronic NSAIDs use (inhibit prostaglandins that protect lining)
Crohn’s Disease
inflammation of ANY segment of GI tract
SKIP LESIONS! area of inflammation followed by non-inflamed tissue, then another spot of inflamm
- distal/terminal ileum and Cecum are the HIGHEST RISK area for the disease!
common to have B12 deficiency (soluble vitamins are absorbed in distal ileum)
S&S:
- diarrhea
- cramping, abd pain
- not as common is weight loss & rectal bleeding from inflammation
- fat malabsorption
Ulcerative Colitis (UC)
inflamm starts at rectum & ascends thru large intestine
- high incidence of occurence in rectum & sigmoid colon
- very severe flare up can go all the way to beginning of ascending colon
S&S
- diarrhea w/ LARGE fluid & electrolyte imbalances
- bloody diarrhea, several to 20x / day!!
- weight loss
- protein loss through stool
sometimes first S&S is skin rash
IBD Dx & Tx
- COLONOSCOPY gold standard for diagnosis
- Stool cultures for pus, blood, mucus
- Barium enema study, trans abd US, CT, MRI
TX - rest bowel
- control inflamm
- combat infection
- correct malnutrition / electrolyte imbalances
- alleviate stress
- immunosuppressants , corticosteroids
- biological anti-TNF MONITOR FOR ALLERGIC RXN!
DIET: - low fiber to decrease size of feces (pushing against colon walls)
- hot & cold foods eaten SLOWLY
- Liquid enteral feedings during acute exacerbations
Post Op care of Ileostomy
- when its new, stoma is very swollen and large
- as it heals it shrinks in size, wafer will have to be cut smaller
- when healed should be beefy red in color
- watch for skin breakdown for improperly fitting wafer
- purple, dusky stoma is BAD! Inspect, adjust wafer, contact MD
Intestinal Obstructions
Mechanical = adhesions, hernia, volvulus, intussusception, tumors
Non-mechanical = Paralytic ileus d/t Sx, anesthesia
Volvulus = twisted intestine
Intussusception = telescoping
DX
- abd X-ray
- barium enema (can also Tx)
- colonoscopy
- labs for CBC, electrolytes, BUN, amylase (increased in duo obstruction)
TX
- NGT to decompress
- NPO
- Correct fluid/electrolyte imbalance
- remove obstruction
Appendicitis
Acute inflammation/infection of appendix
pain precedes nausea
McBurney’s Point = halfway from ischial rim to belly button = rebound tenderness RLQ
Rovsing’s sign = palpate LLQ, pain in RLQ
DX w/ CT, CBC, UA
Sx = laparoscopic or traditional incision
Abdominal Trauma
Blunt/penetrating trauma to abd
- presents w/ guarding/splinting
- hard, distended abd
Cullen’s sign = periumbilical ecchymosis
- abd X-ray, CT
