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Liver Diseases

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Largest gland in body Highly vascular with four lobes RUQ abdomen CHEMICAL FACTORY**Stores nutrients and transforms checmicals for use secrets a large amount of substance and detoxs;

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Major functions Liver: risk group? Diet required?

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Regulates the metabolism of carbohydrates, fats & proteins; GLUCOSE nutrients, vitamins, minerals & iron Removes old RBCS Metabolic detoxification (drugs, hormones & foreign substances) Deactivation of clotting factors (people with liver disease don't clot well) Manufactures, secretes & stores bile; Produces bile salts for fat digestion: gall stones may block duct (*RISK GROUP: female, fat, 40; must be on low fat diet)* Synthesizes cholesterol & produces triglycerides Ammonia conversion=very neurotoxic when ammonia builds up; neuropathies

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Gallbladder Functions

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Storage = stores bile if GB is blocked perhaps by stone, a t-tube connected to a drainage bag is placed. If tube becomes blocked the patient will have yellowing of the sclera; T tube (not draining) ? Asssess sclera, pain, bili levels, abdomen swelling, then call MD Surgery can be open or laparoscopic, done for pain, usually due to blockage of CBD by gallstones or tumor If GB removed=low fat diet

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Liver Disease

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Statistics=more common men, African American; complications easily lead to death Pathophysiology Esophageal Varices: out pouched, thin wall, fragile and prone to rupture=esophageal bleed - hepatocellular: viral, alcohol, cellular - cholestatic=obstructive Chronic state can easily become acute Womens liver seem to be more sensitive to alcoh

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Liver Failure (2) which patient medication is important to know

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- Fulminant: acute - Acute on Chronic: loss most of their liver function and have an acute exacerbation ***must know the pain killers they take that is toxic to liver

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Causes Liver Disease (5) primary liver toxin?

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Bacterial /Viral infection (hepatitis) Toxins=PRIMARY TOXIN IS AMMONIA (effect of ammonia=Ascites: pressure from liver shifts into abdomen and all over the body Medications (acetaminophen) Malnutrition Alcoholism

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Hepatocytes respond to irritants by; results?

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Replacing glycogen stores with lipids & causes: Fatty liver Inflammatory cells Fibrotic liver Hepepatocytes replaced with fibrotic tissue

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Key Work Up (7): reason for renal function study?

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CBC, Electrolytes Liver enzymes (AST/ALT), Liver biopsy Renal function studies (some drugs that help with ascites may effect renal) Coagulation studies (PT/INR) CT (clots?) with contrast & MRI=structure Endoscopy & Ultrasound (ascites) Chest X-RAY (pleural effusions)

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Liver Function Tests (5)

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-Lactic dehydrogenage (LDH)=not as specific to liver disease -Serum Amino Transaminases: more specific than LDH -SGOT (AST) & SGPT (ALT)= enzymes -Serum albumin/protein=will be liver in liver pt. which leads to ascites; cannot keep fluid in vascular space -Alkaline phosphatase, Bilirubin, Ammonia=elevated (damage)

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Care of patient with Liver Biopsy: must have what? special instructions

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Before Procedure, Explain procedure *Check PT/ PTT (will be low=risk for bleeding)*, Check consent, Check vitals NPO 4-8 hours before Type & cross match Have patient void Position patient: pillow under rib cage; *must have a COOPERATIVE patient!!!* Inserted at 6th-7th rib; breath in, hold it and aspirated tissue

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Liver Biopsy Post Op + contraindications**check complication?

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Position patient: Lie on RIGHT side, avoid sudden movements Check vitals q 10-20 min. REPORT: bleeding at the site, elevated temp, shock, severe pain Contraindications to Biopsy: Thrombocytopenia, prolonged PT Peritonitis, massive ascites Uncooperative patient Complication

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Clinical Manifestations (STUDY CHART) ****

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Cardiovascular Gastrointestinal Hematologic Integumentary Neurological Reproductive Jaundice

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Fibrotic liver

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Increases portal vein pressure Esophageal varices: HALF will develop and a third will have rupture=Increases risk for bleeding Cannot metabolize sex hormones

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Jaundice (4)

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1. Hemolytic=(incompatible RBC) can affect the brain stem; RBCs lyse=high bili (babies) 2. Hepatocellular Jaundice (sometimes reversible)=infection, toxicity, cirrhosis; Normal amounts of bili not cleared from blood 3. Obstructive=gallstone/tumor; bile is forced back into liver, *Stool will be light or clay colored: bile not getting into GI system bc is blocked; stool not darkened; Bile reabsorbed through blood=darkens skin, sclera, MM; Urine will be frothy, dark, orange* 4. Hereditary Hyperbilirubin

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Cirrhosis & Patho

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=chronic liver disease characterized by destruction of normal liver cells; replaced by fibrous connective tissue Pathophysiology: Liver becomes fatty and enlarges (hepatomegaly)and scar tissue replaces normal tissue. Hepatomegaly leads to abdominal discomfort & SOB due to compression of diaphragm

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Causes of Cirrhosis (6): which gender at risk?

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Alcoholic cirrhosis Biliary cirrhosis Chronic inflammation from hepatitis B&C Inhrited: Cystic fibrosis (mucus) or Wilson's disease (connective tissue) *these pts may get alcoholic cirrhosis more easily if drinking* Exposure to hepatotoxins Chronic severe right CHF (more of a chance fluid building and backing up into liver) Womens liver is more sensitive & *Very large portion of liver has to be damaged for compensation*

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Assessment of Cirrhotic Patient

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Family history, ETOH history (HOW MUCH how long), Exposure to toxins (work hx, meds) Bleeding/Bruising (deact of clotting) Less alert, jaundice, mental changes (unable to breakdown ammonia/bili) gynecomastia, testicular atrophy (cant metabolize sex hormones) ^abdominal girth, ascites (fluid shift) epigastric/URQ pain (hepatomegaly) OTHER: anorexia/weight loss, Fetor hepaticus, peripheral neuropathy, palmar erythema, prutitus, flatus, N&V, diarrhea, spider nevi, ankle edema

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Clinical Manifestations (Early)***

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Anorexia Dyspepsia (upset stomach), N & V, Changes in bowel habits, a lot gas Pain Ankle edema *Liver gets fatty and firm=Glissons Capsule forms around the liver and is hard covering*

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Clinical Manifestations (Later)

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Portal HTN and Ascites Vitamin Deficiencies (lack of bile to absorb fat soluble vits) Anemia (fatigued) Skin lesions: bile salts accumulate and they scratch them causes bruises/open lesions Jaundice Peripheral edema, Palmar erythema Ammonia causing neurological toxic manifestations (Coma )

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Nursing Plan & Interventions Cirrhosis: Monitor

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Vitals & neuro status, sclera & MM for jaundice Electrolytes, Albumin, & LFT's, Ammonia, & clotting factors I&O, daily weight

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Nursing Care to Give: Cirrhosis

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-IV: fluids, FFP (fresh frozen plasma to replace fluid and decrease leakage of fluid out of the vascular system bc pulls back in; decrease abdomen enlargement) -Skin care: bile salt build up: warm water and emmolient to remove bile salts; pressure mattress & turn frequently -Elevate legs to decrease edema & observe for pulmonary edema -Avoid injections if possible, small gauge needles, & maintain pressure on sites for 5 minutes

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Nursing Plan & Interventions Cirrhosis

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Assess for injury risk; Pad the side rails in case they have DTs; Watch for signs of ETOH withdrawal Eliminate causative agent (ETOH, hepatotoxins) Rest (bedrest to decrease O2 demands) If coughing up sputum and there is blood, may indicate varices rupture Monitor abdominal girth Prevent straining with stool softeners & high fibers

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Diet For Liver Patient

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Teach about diet restrictions/precautions Low protein, low sodium (200-500mg), low fat, HIGH carb Vitamin supplements: A and B complex, C, K

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Nursing Diagnosis

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Fluid volume excess related to: fluid shift Potential for injury: abnormal clotting factors Pain Ineffective breathing pattern: pressure on diaphragm Altered nutrition, less than body requirements Potential for infection Alteration in Skin Integrity: bile salts

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Goals

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Relief of discomfort Avoid complications Return to as normal lifestyle as possible Support groups

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Portal Hypertension: occurs in?

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(advanced cirrhosis) fibrotic liver affects blood flow from the intestines and abdominal organs to the liver causing obstruction through the portal vein = increase BP; To compensate for ^ pressure in the portal system collateral circulation develops

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Clinical Manifestations Increasing BP in Portal Vein + treatment***

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=Varices & Ascites Medication Treatment of Ascites -Diuretics: Aldactone(potassium sparing)***(diuretic of choice; bc it does NOT cause potassium level loss; will try to avoid Lasix diuretics and use this); Lasix -Laculose (Cephulac)= increases BM frequency in order to get rid of toxins (ammonia); may give NG tube if unconscious - Albumin=IV infusion to help draw the fluid back into vascular space

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Management of Portal Hypertension

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Prevent gastroesphageal varices & hemorrhage Antihypertensive drugs; Neomycin***=used to reduce bacteria in GI tract (will reduce production of ammonia) Low sodium diet Nursing Management: Monitor Labs, Assessment for GI bleeding & emergent care

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Treatment of Ascites what is the nursing care?

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Paracentesis: draw out fluid out of the abdomen; small incision is made in abdominal wall; end of the needle inserted into peritoneum Helps with breathing issues SOB Before: must be able to sit, After: gauze pad on the site: BIGGEST S/E HYPOTENSION

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Treatment of Ascites: TIPS hi risk for?

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Redirects fluid away from liver to relieve portal HTN Procedure = connects portal vein to hepatic vein; Extra channel created to shunt blood Mechanism = done through access of jugular vein and threading catheter into liver with radiology assistance Nursing Management = watch for bleeding monitor vital signs, labs, I&O, watch for signs of encephalopathy, *high complication rate of infection and blockage*

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Goals of Treatment

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Decrease fluid retention->Sodium balance Decrease ammonia levels Lasix =last resort to reduce fluid Salt poor albumin=IVM infusion draw fluid from tissues

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Hepatic Encephalopathy(HE)& Hepatic Coma(HC)***REC sure signs?

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Definition: Incidence Pathophysiology: ammonia build up crosses BBB *flapping hand sign and increase disorientation are sure signs*

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Clinical Manifestations HE Early (4)

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Minor mental changes: Slight confusion & mood alteration Minor motor disturbances: *Reflexes(hyper)* Patient unkempt Sleep/wake pattern disturbances *(awake during night/sleep during day)*

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Clinical Manifestations HE Later

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Mental: Completely disoriented Motor: Hand writing changes (smaller), Reflexes(disappear and limbs flaccid) Asterixis(flap sign) Sleep: Difficult to awaken Fector hepaticus cut grass breath

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Assessment & Diagnosis: HE/HC what will EEG look like

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EEG=brain wave slower and less amplitude, Serum ammonia elevated Check handwriting progression daily Observe for seizures *35% of Cirrhosis patients die in hepatic coma

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Medical Management HE/HC: why glucose?****

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lactulose(Cephulac) + rifampin (Rifaximin) better outcome; Enemas to decrease ammonia IV Glucose Administer antibiotics Neomycin (rectal), Diuretics Monitor Electrolyte imbalances *K (d/t diuretics) Protein restricted diet (breaks down in ammonia) Neuro & mental assessment, I&O, & body weight daily & VS q4hrs

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Nursing Management

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Safe environment Monitor for complications Encourage deep breathing Communicate/teach family

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Bleeding Esophageal Varices

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Life threatening rupture; bleeding fr torturous vein from lower esophagus may extend into stomach Varicose veins Distal esophagus

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Bleeding Esophageal Varices (BEV)

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Overview=collateral vessels developed due to increased press causes thin, torturous, not flexible vessels=easily ruptures Mortality: 45-50% first one, with each bleed mortality increases

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BEV Risks & Contributing Factors

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Risks: Portal HTN, muscular strain from heavy lifting, strains with stool, sneezing/coughing/vomiting, rough food Contributing factors: salicylates

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Increased risk factors for Variceal Hemmorage (2)

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1. Initial hemorrage: Large variceal >5mm, Portal hypertension >12mm/hg, More severe cirrhosis 2. Recurrent hemorrage (all of the above plus the following) Severity of initial bleed, Age over 60, Renal failure, Active alcoholism, Bacterial infection

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Bleeding Esophageal Varices Clinical Manifestation

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Hematemesis, Melena Decrease/marked change in mental status S/S of shock (cool clammy skin, hypotension, tachycardia) *consider an emergency*

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Hematemesis (BEV) Nursing Care (5)

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Frequent VS with transfer to ICU Turn patient on side, high fowlers Protect airway, Yankauer suction (prevent aspiration) + Oxygen through non rebreather mask Transfuse 2 units PRBC Bolus of Octreotide (sandostatin)

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Bleeding Esophageal Varices Diagnostics

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Endoscopy: Done in OR/Radiology Dept. Hepatoportography Celiac Angiography Blood work: CBC & chemistry with lytes, LFTs, BUN, PT *put pressure on the site*

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Providing Hemodynamic Support (3): when to treat with endoscopy?

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Blood & Saline Treat coagulopathy Reduce portal pressure *once hemostasis is achieved treat with endoscopy procedures*

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Management Goals BEV

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Transfer to ICU, Control Bleeding Neuro checks, continuous VS Foley, Intubate, Suction, O2 IV fluids, Blood Products (Prepare for PA/Central venous catheter placement)

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Nonsurgical Management in BEV is ____?

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Preferred due to high mortality associated with emergency surgery to control bleeding d/t poor condition of these patients

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Pharmacologic Therapy BEV (3)*****

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Octreotide + nitro (Sandostatin)=constrict vessels to bleed less but nitro keeps vessel in heart open *S/E: orthostatic change, palpitations, nausea* Vasopressin (Pitressin) + nitroglycerin Beta blockers (Corgard)=reduce bp

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Pharmacologic Therapy Specific Situations* (5)

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Acetaminophen overdose=Treat with N-acetycysteine Valptoate overdose =Treat with carnitine Elevated ammonia levels =Treat with lactulose Stress ulcer prophylaxis =Histamine2-receptorblockers Active hemorrhage=FFP

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Nonsurgical Treatments BEV (2)

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Definitive treatment for active bleeding (to prevent bleed); Done under sedation 1. Endoscopic variceal ligation (EVL): banding; causes throbmbosis and necrosis to destroy varices 2. Endoscopic injection sclerotherapy (EIS): inject material that hardens the area

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Nonsurgical Treatments BEV + Complications

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Both are performed using conscious sedation Two nurses need to be present one to monitor the pt at all times, one to assist the gastroenterologist. Complication: Bleeding ulcers, esophageal perforation strictures, pleural effusion, aspiration pneumonia, bacterial peritonitis

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Salvage Therapy: TIPS Placement when it is done?

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*DONE ON SECOND MAJOR BLEED* shunt performed by an interventional radiologist; Decreases pressure long term Used when other treatment has failed Goal is to effect cure/improve quality of life

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TIPS: Monitoring & Comps

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Complications: enphalopathy, liver failure, Increase death compared with endoscopy tx Monitor for bleeding Serumn ammonia, loc

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Balloon Tamponade

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pressure is exerted on the bleeding varicies by a double balloon tamponade. Stengtaken-Blakemore Tube This tube has 4 openings each with a special purpose.

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Balloon Tamponade REC****

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Gastric aspiration Esophageal aspiration Inflation of gastric balloon Inflation & deflation of esophageal balloon

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Balloon Tamponade Complications**

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Whenever there is a tube in patient worry about aspiration pneumonia 60-70 need EVS/EVL afterwards

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Liver Cancer Types (3)

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*Hepatocellular carcinoma*=not resectable due to rapid nature & growth Choliangiocellullar carcinoma (CCC)=resectable; limited to one area of the liver Combined Can be malignant/benign Common in African countries due to hepatitis; Hepatic cancer may not be primary site *most common site of metastasis is LIVER*

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Causes Liver Cancer (4)

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Cirrhosis Hep B & C Toxins Cigarettes

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Diagnosing Liver Ca: tumor markers?

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Clinical S/S, history Blood work; Tumor Marker: AFP elevated; CEA: elevated (if + does not confirm liver cancer but there IS malignancy somewhere) Biopsy/laparoscopy

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Clinical Manifestations Liver Cancer

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Abdominal pain Jaundice only if bile duct occluded Ascites if cells in peritoneal space Anorexia (unexplained)->Weight loss Anemia->Loss of strength

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Management Liver Cancer (2)

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-Radiation Therapy (Percutaneous placement of a high-intensity source for interstitial radiation) -IV/intra-arterial injection of antibodies tagged with radioactive isotopes attacking tumor associated antigens

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Chemotherapy Liver Cancer

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Systemic chemo therapy; Implantable pump to deliver high-concentration chemo through the hepatic artery; clot the tumor's blood vessels=cut off blood supply to tumor

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Percutaneous Biliary Drainage + nursing care

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=bypass biliary ducts obstructed by liver ca in pts with inoperable tumors/poor surgical risks Nursing care: *several days post placement catheter is open to external drainage* Watch:fever/chills, sepsis, leakage of bile, hemorrhage, reobstruction, increase pain, pressure, pruritis, jaundice

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New Non Surgical Modalities (5)

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Hyperthermia=heated laser directly to tumor; spare surrounding tissue Radio Frequency Thermal Ablation=two small incision + electric zaps Embolization=block the tumor blood supply US guided injection=alcohol injected to promote dehydration of tumor Immunotherapy=cell specific

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Surgery Liver Cancer: most common ?

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Lobotomy *most common* Local Ablation Liver transplants=less chance of rejection; liver also regenerates within 6 mo. if lobe is removed Nursing care r/t extensive thoracic & abdominal incisions, risk of metabolic, respiratory complications

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Pancreatic Cancer

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Dx late bc vague early signs=hard to detect Risk factors: First degree relative, 65-79 (common older), smokers. Red meat, hx cirrhosis, chronic pancreatitis, DM Patho: most at head of pancreas; sxs r/t loss of pancreatic tissue=referred pain to shoulder & back; STEATOrrhea, trouble controlling blood sugar

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Clinical Manifestations Pancreatic Ca

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-Rapid & profound weight loss (not getting nutrients) -Pain & Jaundice (bile duct @ head) in 80% of patients -Left upper & mid-abdominal pain radiates to the back, more severe at night, sudden, severe, deep, piercing & continuous *RADIATING SHOULDER PAIN* -Meals often aggravate epigastric pain -S/S of insulin deficiency=Glycosuria, hyperglycemia

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Diagnostics Pancreatitis (5)

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CT, CECT (Contrasted enhanced CT): 85-90%accurate ERCP: gold standard; can reveal stones, Tumors, strictures: npo 6 HRS, IV access, dye used may cause discomfort, may feel flushed/need to urinate Ultrasound, EUS (endoscopic US)=US with biopsy GTT

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Stages of Pancreatic Cancer (3)

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Resectable Locally Advanced Unresectable=may relieve pressure but cannot take any more tumor cells Metastatic

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Treatment Pancreatic Cancer + preop care

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Radiation & Chemo including IORT (treatment in OR) Pre op: Correct clotting disorders, Treat anemia TPN & Blood (usually NPO and have TPN WITHOUT fats)

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Surgical Treatment for Tumors of the head of the pancreas

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Pancreatoduodenectomy "Whipple Procedure": redirecting the pancreatic enzyme directly into the Jejunum (allows bile and enzymes to flow into jejunum) after procedure: major surgery in ICU

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Whipple Procedure Post OP

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Semi fowlers; intubated but come off quickly; NPO + TPN with insulin coverage, NG tube with suction (continuous suction to relieve pressure at suture line) 4 parts removed: GB, Distal portion of stomach, Head of pancreas Duodenum (GSPD)

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Nursing Management Pancreatic Cancer: watch for?

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Symptomatic & supportive (Medication) Psychological Nutritional support Watch for bleeding Facilitate grieving End of life issue: hospice

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A & P Pancreas

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Endocrine & exocrine, Divided into head, tail & body Functional units: Islets of Langerhans Acinar cells=produces hormones, juices, chemicals=digests food via enzymes

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Types Acute Pancreatitis

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Edematous Pancreatitis=fluid accumulation & swelling; mild & self limiting; goes away on its own Necrotizing Pancreatitis=more severe; causes cell death & tissue damage, serious systemic complications; starts attacking itself; severe pain that causes patient to seek medical care -Both are inflammatory and causes other systems to fail; *severity measured by RANSON scale and gives an idea of mortality rate*

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Causes In the US Pancreatitis (6)

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Obstruction (ampule of vater) Alcoholism(70%) Trauma (abdominal trauma; rare but sometimes ERCP & injection used can worsen pancreatitis) Certain medications (immunosuppressant) Viral infections Travel (parasites may cause it)

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Causes Pancreatitis contd

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Autoimmune Genetic predisposition (1st degree relative/gene) Hypertriglyceridemia (if triglycerides over 1k) Idiopathic

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Other causes especially for Acute (5)

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Cystitic fibrosis Hemolytic uremic syndrome Hyperparathyroid disease Kawasaki disease (acute febrile disease in children) Reye syndrome (acute encephalopathy with fatty infiltrates)

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Epidemiology

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Majority are 55-65 yo Obstructive common cause in females Alcoholism common cause males (<55 yo male) Acute Pancreatitis: mild to severe, most cases last about A WEEK; overall mortality 10% determined by ranson scale;

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Pathophysiology Pancreatitis: what causes coagulopathy?

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Increased vascular permeability, vasodilation, stickiness of leukocytes (fluid shift, wbcs clump together=form emboli throughout body) Increased coagulapathy=DIC (little clots throughout body) may be caused by a lot of blood transfusions

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PATHO contd: systems that are affected by fluid shift?

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Massive fluid shift=circulatory insufficiency (d/t change in permeability): Altered cardiac function Impaired renal function (d/t alteration of renin-angiotensin causes fluid retention=edematous)

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Diagnostic Tests Pancreatitis: what is the gold standard?

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Increase Serum Amylase (0-130), Lipase (0-140) & BUN, *(amylase=4x norm, stay elevated 24-72h; Lipase rise 3x norm levels w in 24 hours, stay elevated for 7-14 days)* Increase Bilirubin, & Alk phos, WBC's (Leukocytosis) & LFT's, Hyperglycemia Decrease Albumin, Magnesium, Platelets & Fibrinogen, Hematocrit (bleeding) *CT IS GOLD STANDARD*

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Diagnostics Contd Pancreatitis: significant physical sign*

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Paracentesis: Peritoneal fluid evaluated for increase pancreatic enzymes ECCT, ERCP (inflamm seen) EUS (lower risk of irritating pancreas), XRAY Genetic test Board like abdomen=guarding reigidity; (indicates infection spread to peritoneum); will find them in a side laying with knees bent d/t swelling bc it relieves pressure)

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Ransom's Criteria for Estimating Severity of Pancreatitis: determining factor acute?

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Signs on admission & Signs during first 48 hours **If serum amylase level 4x elevated is def ACUTE pancreatitis, will also see elevated lipase, amylase in the URINE ***

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Acute Pancreatitis Symptoms

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Pain 5+, after eating or drinking; *Radiates to back/below left shoulder* N&V, sweating VS: Low BP, Increase pulse, temp (102), resp, Rigid abdomen, guarding, Worse when lying down; supine with knees bent *BOWL SOUNDS HYPOACTIVE (Paralytic ileus) (require NG, TPN (no fats)*; may have double/triple lumen for more fluids

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Classic Acute Symptoms Pancreatitis: classic look?

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Clay colored stool, Mild Jaundice, Skin rash or sore(bile salts)=ALL bili probs Gaseous abdominal fullness, Hiccups, Indigestion *Swollen abdomen (bluish discoloration)* SHOCK SXS: hypovolemic shock, tachycardia, (no urine output) *Sudden severe abdominal pain with N&V is a CLASSIC look*

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Chronic Pancreatitis Symptoms: how to manage

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Pain continuous, Worse with eating or drinking but do not have the N&V, Abdominal pain greatest in upper abdomen & Felt in the back Chronic weight loss cannot maintain wt; continues even when eating a lot (do not have digestive ability to utilize food) GI probs: Pale/clay colored stools, Diarrhea, Fatty/oily stools, ***Manage chronic by giving them pancreatic enzymes! (Viokas, Creon) with meals do help digest***

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Clinical Manifestations Chronic Pancreatitis : additional signs (2)

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Mental confusion, Agitation Severe Pain, Hypotension, Respiratory distress (hypoxia), Fever Vomiting, Jaundice Stools (bulky, pale, & foul smelling) Additional signs with fulminating disease -Grey Turner's sign (intraperitoneal hemorrhage blueish discoloration in flank) -Cullen's sign (hemorrhage; discoloration in the periumbilical area)

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Management Chronic Pancreatitis Medications (5) All meds are ____?

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*ALL IV MEDS* Antibiotics (if developing an abscess: will be worsening in condition, elevated WBCs, may need to operate to drain), Pancreatic enzymes if eating (not for acute) Histamine-2 (H2)receptor antagonists (PPIs) Antiemetics (Zofran) Pain meds = parental opiods NPO + TPN with INSULIN, no fats + NG Suctioning (this is used to relieve N/V, decrease abdominal distention and parialytic ileus, remove hydrocholic acid)

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Management Chronic Pancreatitis Contd: how to time coverage? when to feed?

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*Do not feed until pain resolves & decrease in lipase!!!* Creon (pancrelipase)/Viokase with food *TPN: Insulin Q6 does not need to be timed with meals* Respiratory therapy (abdomen swelling may impair breathing), Foley (there is severely decreased output so helps MONITOR Bed rest, Peritoneal Lavage, Endoscopy: remove pancreatic duct stones, Surgery (diagnosis, drainage,resection, debridement)

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Nursing Assessment & Care Chronic Pancreatitis: what kind of diet

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Monitoring of: Pain, labs, NPO status, NG tube (good oral care) hydration status, I&O, consistency of stools, Bowel sounds esp when they start eating, TPN, bleeding, respiratory status Assist patient to assume position of comfort which is on their side legs drawn up to chest Surgery=assist with diagnosis & place drains (for abscess) Teach: Relaxation, prevention, high carbohydrate diet

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Complications Acute Pancreatitis (6) try to avoid giving ___ for pain?

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Pancreatic Pseudo cysts & Abscess Cardiovascular: shock , DIC, Pericardial effusion, Hypotension Respiratory (diffuse pulmonary infiltrates=pneumonia) GI Hemorrhage, Ulcers, Varices, (Ileus) Tubular necrosis of renal sys (oliguria) Blood: Hypocalcemia, hyperglycemia=r/t TPN so MUST WEAN off TPN ***TRY to avoid morphine for pain bc may cause spasm of sphincter of pancreas so more likely to give Demerol***

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Nursing Diagnosis Pancreatitis

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Acute Pain Risk for Fluid Volume Deficit (d/t NPO/vomitting/etc) Alteration in Nutrition (less than) Risk for Ineffective Management Ineffective breathing pattern

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Overview PPN/TPN

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PPN - Peripheral parenteral nutrition (isotonic solutions; short term) more likely to infiltrate TPN- Total parenteral nutrition; meets all nutritional needs (HYPERTONIC SOLUTION, central line only, nutritional support for at least 10 days) cal, dextrose, ami acids, essential nutrients (ex. Wound healing, burn patients)

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TPN: contains? Used for people who ___

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Complete nutrition: can supply all calories, dextrose, amino acids, trace elements, & other essential nutrients needed for growth, weight gain, wound healing, convalescence, and other health sustaining functions. For a NOT intact GI tract

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Signs of Wasting Away Malnourishment (check during assessment) apendime

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Adventitious Breath sounds Poor skin turgor, Pigmentation (Darkening of the lining of the mouth) Exophthalmos Neck swelling Dental carries, Poor fitting dentures (lost weight) Infections (massive) Muscle/Abdominal wasting, masses/tenderness Enlarged liver

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Before TPN: why use Enteral?

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less expensive, less chance of infection; if you can use GI must use bc cilia of mucosa may waste away if not used enough

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TPN Indications (5)

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GI problems *Anorexia OR Cannot eat (5-7 days without food + extra 7 days will start TPN: Rule of 5)* *Altered LOC* Increased metabolic demands (*burn pts* w/ negative nitrogen balance) Hyperemesis of Pregnancy

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Effectiveness TPN

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Assess baselines Weight gain Healing Electrolytes Glucose Output (poor in malnourished pt)

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Evaluate the effectiveness of drug therapy by confirming that:

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■ The client demonstrates improved nutritional status. ■ The client is free of infection or injury related to the TPN. ■ The client's lab results shows electrolyte levels and glucose levels are within normal range. ■ The client's intake and output indicates patient is free of signs of fluid overload.

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TPN Composition

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40%fat,, 40% protein, 20% Carbohydrate, Dextrose, Fats (lipids), Potassium phosphate Yellow color bag: VITAMINS Individualized, ***CAN HAVE MEDS IN IT* *Never add anything bc high glucose content = hi risk infection bacteria growth* Electrolytes , Vitamins (A,D,E), Trace elements, Amino acids, Medications

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TPN - Vascular Access Devices

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Catheter inserted through a needle over a guide wire (Risk of catheter puncture) Multilumen available PICCs included: MUST BE AT SVC/RA: *before giving med must check BLOOD RETURN; will ensure that catheter is in the right place; XRAY report to confirm position*

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TPN Nursing Implications & Care: what is important to monitor?

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Baseline Docs Order /check against label Consent/Explain procedure *Weight (daily, then weekly)* Initial start (warm to room temp, & inspect solution) Sterile technique

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Nursing Implications Assess TPN:

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Pump Dressing changes (q7 days/when soiled) Site Assessment (measure circumference of the arm and how much of the catheter is out of the skin***tell if it is in the right place) Discontinuation: TAPER

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Nursing Implications Patient Assessment before start: what to report?

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insertion site PICC (cephalic/brachial/basilic) *measure the mid-arm circumference & external length of catheter every shift*, and *changes greater than 3 cms to PICC Team/MD*

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Infusion Rates

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Rapid=hyper glycemia Slow=hypoglycemia

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Nursing Diagnosis

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High Risk for Infection Fluid Volume (excess/deficit) Alteration in Nutrition Self care Deficit Impaired Skin Integrity Risk for Altered Glucose Metabolism Ineffective breathing pattern

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Catheter Types: Single or Multi Lumen PICC

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(in the Arm; surgically inserted under fluoroscopy/at bedside)

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Catheter Types: Portacath

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=usually stays in after chemo; no care to site unless something attached; ensure correct access

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Female Malignant Conditions: keys to prevention (3)

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Statistics: (excluding breast cancer) 274,000 women diagnosed per/year 27,100 women die per/year Key to prevention: Papanicolaou test (HPV typing & cervical) Pelvic exams (OVARIAN & uterine) Vaccinations (HPV)

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Cancer of the Cervix

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Squamos cell (90%), Adenocarcinoma (10%) Age 30-45 3rd most common reproductive cancer

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Risk Factors KNOW THIS***(6)

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-Multiple partners, Early age less than 20 at first coitus, Early childbearing -HPV types 16 &18 (trying to prevent cervical cells from turning cancerous), HIV (suppresses immune system cells more prone to turning cancerous) -Smoking, DES (used to prevent HG) exposure in utero: more likely to hve cervical cancer -Low socioeconomic status: reduced screening -Nutritional deficiencies (folate, beta-carotene, & vitamin C) -Chronic cervical infections (cells irritated)

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Prevention Exams and Education

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Exams: general rule is do not get papsmear until 3 yrs after intercourse or at age 21; If have 3 consecutive normal papsmears can go to q3 years; liquid based pap smear will be more likely to see abnormalities Education: condom use, New HPV Vaccination (9-26 yo) 3 shots RISKS: 35+ at risk, Smoking

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Screening Recommendations Cervical Ca**Low risk group? Symptoms?

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After Hysterectomy: depending on the type (cervix present/not), may still need paps, must know & label which cells are taken Low Risk: normal paps for 3-5 yrs; over age 70 no abnormal paps Symptoms: *usually none*; if penis hits cervix hard enough there may be spotting bc malignant cervical cells are friable; Leg pain, rectal bleed, dysuria (advanced)

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Assessment & Diagnosis Cervical Ca

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Most cervical malignancy can catch early -PAP annual screen (if find abnormal PAP, tell them to come back after 3 periods); If still abnormal PAP do a Culposcopy: cervix painted with vinegar abnormal cells show up white (margin normal=no action; abnormal margin=do a LEEP procedure) -Biopsy (Clinical staging) -Possible: (dependent on stage) D&C, MRI, Cystogram, CT Scan, IVU, Barium X-rays

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Cervical Cancer Stages (3)

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Stage I = early dysplasia Stage 2 = early carcinoma Stage 3= Late carcinoma

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Medical Management for Preinvasive Lesions (4) What is given if bleeding occurs with LEEP? rare procedure?

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Office procedures (conservative TX) : Colposcopy with biopsy Conization Cryotherapy Electrocautery (LEEP; for unclear margins) may cause cramping; try to do procedure as close to the end of the period to give the tissue time to heal (monocells used to clot if bleeding occurs) Hospital procedure = Hysterectomy **rarely leads to this

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Medical Management (make a med card) just read

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Invasive cancer: (less than 3mm) Depends on: Stage Age General health Surgery Radiation (intracavity) Hysterectomy (must talk if they have chidren/not? plan?)

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Medical Management (make a med card) just read

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Extreme Cases: ( > than 3mm ) Chemotherapy + radiation Cisplantin Carboplatin Paclitaxel (taxol) Radical hysterectomy=lymph node dissection & aortic node assessment

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Surgical Management (5)

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-Total hysterectomy TAH BSO: total abdominal hysterectomy B/L salpingo oophrectomy=abd. incision/laparoscope (uterus, cervix, tubes, ovaries) -Radical hysterectomy=remove uterus + cervix -Radical vaginal hysterectomy: top of vagina + uterus, cervix -B/L pelvic lymphadenectomy: remove as many lymph nodes possible -Pelvic exenteration: take out some other organs in area

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Cancer of Uterus & Endometrium

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Statistics: 37,400 cases per year 6,400 deaths per year Adenocarcenoma Endometrial 4th most common

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Risk Factors: age group? pimpon

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*OLDER* compare to cervical ca (younger) Increased weight (fatty tissue makes estrogen which promote cancer growth female repro) Post menopausal bleeding (menopause=12 full mo. w/out period) Nulliparity Menopause after age 52 (uterus exposed to estrogen longer; ex. start period early and end it later) Possibly use of tamoxifen (increases endometrial/uterine ca)

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Medical & Surgical Management Endometrial Uterine Ca

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Treatment: TAHBSO (if uterine Ca is incapsulated will treat with this; assess lymph node to see if there is Mets) Depending on stage: intracavity or external radiation Metastasis: treated with progestin

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Ovarian Cancer

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Silent onset =advanced by discovery (due to position of ovaries in abdomen not caught early) Statistics: 25,200 new cases per / year 14,500 deaths per / year Usually 50-59 Ovarian cancer patient: 3-4X risk for breast cancer

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Causes Ovarian Cancer: what is considered protective?

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Heredity (1st degree relative with breast/ovarian; BRAC1/2 gene) Birth control pills (protective; prevents ovulation which reduces ovarian irritation, PREVENTS ovarian cancer)

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Theories about Causes

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Inflammatory theory/Incessant-ovulation theory= irregular/dificult ovulation may cause inflammatory process to ovary=irritation Pituitary/Gonadotropin hypothesis (didn't say much)

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Detection Ovarian Cancer: there is no ___?

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No early screening BI-ANUAL pelvic exam if over 50 CA 125 (if over 50; if positive not specific to ovarian but indicates a problem) will do: Pelvis & Transvaginal US Genetic testing: BRCA - 1 BRCA - 2

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Risk Ovarian Cancer

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Age (older) First birth over age 35 Anovulation->Nulliparity Infertility (high doses infertility drugs)

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Screening Recommendations

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With increased risk: Bimanual Pevlic/transvaginal US Doppler

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Clinical Manifestations Ovarian Cancer: they are usually ___?

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Most common: VAGUE Enlargement of abdomen, Pants may not fit, Abdomen/back pain, Pelvic pressure Breast tenderness, Irregular/HEAVY menses, early menopause, Ascites/Accumulation of fluid Change in bowel habits, GI reflux, Bladder changes

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Significant Manifestations Ovarian Cancer (3) clues that it is Cancer? (pay attention to)***

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Flatulence Fullness (dim appetite) Increased abdomen girth 2 clues that it is ovarian Ca: Long history of ovarian dysfunction, Vague GI symptoms (next action: Do a CA 125 and go from there)

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Diagnosis Ovarian Ca (4): when to do a laparotomy ?

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Transvaginal US (full bladder needed) CT of abdomen & pelvis CA 125 Laparotomy (if ovarian cancer detected; used to STAGE)

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Assessment & Diagnostics Ovarian Cancer

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Metastases screening (full body scan, etc) BIOPSY: Cell types (didn't say much) Epithelial cancers, Germ cell cancersm Stromal cell cancers

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Work Up Ovarian Cancer Includes: standard tx?

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Barium Enema (Upper GI) Proctosigmoidoscopy Chest X-RAY *Standard Tx = TAHBSO

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Survival Rates and Staging of Ovarian Cancer (4 stages)

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Stage dependent/where it has spread Stage 1 = tumor growth limited to ovaries Stage 2 = one or both ovaries with pelvic extension Stage 3 = lymph nodes positive Stage 4 = distant metastases

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Pharmacologic Treatment***: Chemo

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-Cytoxin, adriamycin, cisplatin *(Cisplatin is used in intraperitioneal applications)* -Other treatments: Bone marrow transplant, Peripheral stem cells

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Side Effect from Chemo

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Myelosuppression: Leukopenia Fever, Hypotension, Dyspnea Neurotoxicity Hair loss Angioedema Urticaria

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Lipsomal Therapy

answer

Encapsulated chemo Given IV(is specific/targeted; does not irritate other tissue)=Increased action, Better targeting

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Management with Advancing Disease Ovarian

answer

If comes back and is not operable Lymphedema, DVT Pleural Effusion, Ascites=Abdminal distention* may need to do paracentesis to drain fluid and may find abnormal cells Intestinal obstruction (in colon/etc) Malnutrition,

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Nursing Management

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Emotional support Comfort (pain relief) After surgery Age dependent TPN Fluid & electrolytes Pain Relief

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Radiation Therapy Types Internal/Intracavity: patient care?

answer

(radium & cesium) =delivers radiation from a cylinder inside;*pt on bedrest for day/couple of days; foley is inserted with this procedure so they don't get up, packing the vagina to prevent it from coming out; Urine/stool/patient is radioactive, decrease time, exposure, distance* Will feel weak once completed, gradually get them up

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Radiation Therapy Benefits: main benefit?

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Decreasing tumor size & bulk (easier to operate) Control infection, Pain, Bleeding

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Radiation Therapy: Biggest S/E (3) how to treat s/e?

answer

*GastroEnteritis* *Cramping*->Low residue diet (GI sxs) *Cystitis*->Antispasmodics (cystitis) Treatment of Side Effects: May stop Treatment

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Nursing Considerations with Internal RT

answer

Less time Increased distance Shielding No pregnant nurses

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Nursing Priorities with Internal Irradiation

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Patient on bedrest-->Skin care, Teds Low residue diet Check patients for Temp, N&V, infection/perforation, report any profuse vaginal discharge Provide: Mild sedatives (sleep), Muscle relaxants, Mild narcotics

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Nursing Considerations With Radiation: 3 things patient can't do

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Wear film badges(time & distance), Rubber gloves, Specific laundry & housekeeping instructions *Not leaving room (Patient restricted to room) No visitors under 18 No pregnant visitors*

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Applicator Removal Post Removal Care

answer

Ambulation Diet No douching

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Nursing Diagnosis: Reproductive Cancers

answer

Anxiety Body Image Pain Elimination Knowledge Deficit Anticipatory grieving Self care deficit

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Nursing Diagnosis: Reproductive Cancers

answer

Anxiety Body Image Pain Elimination Knowledge Deficit Anticipatory grieving Self care deficit

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Hysterectomy: 2 reasons for performing?

answer

Definition: Removal of Uterus & Cervix For MALIGNANT: TAHBSO=Removal of uterus, cervix, fallopian tubes & ovaries FOR NON MALIGNANT (non cancer) CASES: done d/t *dysfunctional bleeding (anemic/tired of bleeing) OR fibroid (benign growth)*: causes pressure on bladder/pain

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To Shrink The Fibroid (3) Lupron****

answer

-Laser TX (Hysteroscopic Resection) -Leuprolide (Lupron) monthly injections=induces surgical Menopause=causes fibroid to shrink by removing estrogen; will have sxs of menopause (will prevent use of major abdominal surgery if it reduces the size to operate better/remove vaginally) -Uterine artery embolization (UAE): blocks bf to fibroid=shrink and do less invasive procedure

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Reasons for Surgery (Non malignant reasons) (4)

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-Dysfunctional uterine bleeding, Endometriosis -Injury to Uterus -Fibroids (Leiomyomas, Myomas) -Prolapse (may have diaphragm/surgery to manage)

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Laporscopic Assisted Hysterectomy Benefits:

answer

Fast recovery Small incisions Shorted hospital stays Decrease post op complication

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Pre Op Preparations for Hysterectomy

answer

Abdomen shaved (doctor preference) GI tract cleaned out w/ enema, Vaginal douche (betadine based on MD order) Pre Op meds; Pre Op teaching: What to report, Kegals (after procedure), Emotional/cultural issues

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Nursing Management Hysterectomy: major compss of TAHBSO? frequent short term complication?

answer

Post Op comps with abdominal surgery: Paralytic ileus, DVT (throw clot) Major complications after TAHBSO are *hemorrhage & infection* *Watch for: Most frequent short term complication is VOIDING ISSUES* d/t swelling of urethra after the procedure (may need to straight cath)

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Complications of Hysterectomy (4)

answer

Clots: P.E./MI/CVA Pulmonary Edema, Leg Edema Sepsis Fistulas (stool coming out of vagina/urine from rectum)

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Conditions of the Prostate: Benign Prostatic Hyperplasia (BPH)

answer

NON malignant =Enlarged prostate, Obstructs urine flow (pinch urethra) Usually men above 50; Most common condition in older men

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Diagnostics BPH (3): what brings them in?

answer

Physical (DRE/digital rectal exam) Testicular exam US & Urodynamic studie (see how bladder is contracting) Renal function: IVP, BUN/Cr *Come in when there is major disruption* (walking up at night, frequency, stream is less strong, blood tinged urine)

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Blood Work BPH: PSA?

answer

-Blood studies (PSA) prostate specific antigen: show elevation (may show false elevation in PSA if DRE; must wait 72 hrs before getting blood work) -Clotting studies: if surgery planned, biggest complication:hemorrhage

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Clinical Manifestations BPH

answer

Hydroureter, Hydronephrosis (back up into ureter/kidneys), Blood in urine Nocturia, Frequency, Urgency, Hesitancy, Less volume & force->Feeling bladder not empty, Dribbling UTI Abdomen straining

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Management BPH: (methods can either affect/not affect prostate)

answer

Non pharmacologic: Watchful waiting (WATCHING PSA if over 70) & Increase fluids to decrease risk for UTI Pharmacologic/surgical: Saw palmetto (interferes with testosterone) -TUIP (slit in prostate to release the pressure on urethra) -Balloon Dilation (catheter + balloon to dilate urethra; short term) -Microwave therapy, Transurethral laser resection & Transurethral needle ablation (BREAKDOWN PROSTATE), US guidance resection

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Drugs for BPH: Alpha-andrenergic receptor blockers***does not do what? do not take with

answer

Cardura (doxazosin) Flomax (tamsulosin) Uroxatral (alfuzosin) Hytin (terazosin) Relax smooth muscle in prostate=allow flow of urine; relaxes opening to bladder=allow filling; full effect in 2-3 wks; *does not prevent growth of prostate* Side effects: ***low BP***, weakness or tiredness, HA & stuffy nose due to vessel dilation, constipation (do not take with Viagra bc dilates vessels may drop BP more)

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Drugs for BPH***5-alpha reductase Inhibitor

answer

Avodart (dutasteride), Proscar (finasteride) Prevent increase of size of prostate, interferes testosterone production S/E: Difficulty erection, decreased libido & semen released during ejaculation, gynecomastia

question

Prostate Cancer: 2x more prevalent in?

answer

Most common cancer in OLDER males, *2X more prevalent in African Americans* 2nd leading cause of death in American men over 55 I in 6 men in US develop it 2.3 million men diagnosed in 2007

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Risk Factors Prostate Ca

answer

Increasing age Familial predisposition Diet high in fat & red meat

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Manifestations Prostate Ca; most common (3)

answer

No early S/S (Increased prostate growth causes symptoms) Most common complaints: *Blood in urine; more common in prostate Ca than BPH, Dysuria (pain/cant stop/start)* Low back pain (if tumor is large enough) Weight loss & anemia (common in Ca)

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Diagnosis Prostate Cancer

answer

DRE & PSA (< 4 is normal; 4-10 =25% chance it is prostate Ca, 10+= 50%) Increasing, if elevated but stable may not do surgery Transrectal US; Transrectal biopsy- a biopsy gun is used to obtain small sample with thin needle, also used for staging Bone scan/CT (see if it is anywhere else) IVP (kidney fx)

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Factors Determining Treatment Prostate Ca (3)

answer

-STAGE: (NCI 0-4) range encapsulated->metastasis; Gleason scale(staging 2-10) staging based on biopsy -Patients age, Health status -Personal preference (surgery may result in erectile/sexual function)

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Treatment Options Prostate Cancer (4)

answer

-Watchful waiting (active surveillance) -Chemo therapy, Radiation Therapy: External beam, Brachy therapy, *Proton beam (extreme precision) less erectile/sexual dysfunction* -Hormone therapy (decrease/block testosterone production=reduce prostate growth) -Orchiectomy (removal testicles in order to remove one of the testosterone sources)

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Radiation Therapy for Prostate Cancer Brachytherapy: for stages?

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*for stages 1-2* Interstitial seed implantation=Radioactive seeds are placed PERMENANTLY in prostate; amount of radiation decrease over time Side effects: Urinary frequency, retention, Incontinence, Rectal burning/pain, Diarrhea **first 3 mo. Should not be around children/pregnant ladies; have radioactive fluids, condom for couple of weeks after d/t radioactive ejaculate**

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Radiation Therapy for Prostate Cancer: External Beam Radition

answer

Used in stages 1-3; Localized & Metastasized Treatments consist of: 8 weeks, 5 day weeks, Few minutes day Side effects: *Red & dry skin*, Fatigue, colitis, burning with urination

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Hormonal Therapy Prostate Cancer: not used for?

answer

Theory: decrease/block production testosterone supply in order to slow growth of tumor *used for control to slow growth NOT cure* Orchiectomy Estrogen therapy; Des, LH-RH, Lupron & Zoladex, Cyprotertone , Bicalutamide, Flutamide

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Side Effects of Hormonal Therapy: will need what type of monitoring? CFGS

answer

Sex: Impotence, Decreased libido, Gynecomastia Female Hormonal: Fatigue, Hot flashes GI: N & V, Diarrhea Chemical hepatitis Any patient on hormone therapy need CARDIVASCULAR MONITORING*

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Cryosurgery: candidate?

answer

freezing/Ablation of cancer tissue in prostate Done with US guidance on patients who can't tolerate surgery OR *in recurrence cases*

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Preoperative Concerns

answer

Anxiety about the procedure & outcome Acute pain from bladder distention Knowledge deficit Sperm donation

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Minimally Invasive Surgical Procedures Prostate Ca (2)

answer

TUMT (transurethral microwave treatment) cook the tumor and slough TUNA (trans urethral needle ablation): radiofrequency energy; needly placed IN prostate and wave destroys tumor

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Surgical Resection Prostate Cancer (2)

answer

TURP: trans urethral resection prostate (endoscopic/guided US, up through penis and "scraping" inner portion of prostate gland; ) TUIP: Transurethral incision into prostate (1 or 2 cuts into prostate to relieve pressure; done with individuals who are not candidates for other options)

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Surgical Procedures for Prostate Cancer: Radical Prostatectomy (3)

answer

Suprapubic=abdominal incision through the bladder to feel prostate Perineal=incision and tissue removed through space between scrotum and perineum; use a drain Retropubic=direct entrance to prostate through abdominal incision

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Laparoscopic Radical Prostatectomy + Mgmt: when to do continuous bladder irrigation?

answer

no open incision; prostate is removed through laparoscope often with assist from a robot Management: *biggest comp is BLEEDING; avoid anything into rectum* 3 way foley; Continuous Bladder Irrigation w. 3000 mL bags (after all these procedures esp. TURP): decrease clots; irrigate depending on color in bag (run to Tidal); mark/know how much went in (if decrease amount of drainage & leakage around tip of penis, may have clot, flush 50 mLs)

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Surgical Complications

answer

Hemorrhage Clot formation->Catheter obstruction Sexual dysfunction->Infertility *Transurethal Resection Syndrome: confusion, LOC change, hypotension/bradycardia (d/t absorbtion of fluid from continuous irrigation )*

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Nursing Management Post Op Prostectomy: how to manage bleeding?

answer

Pain control Wound management->Preventing immobility complications *Manage complications->Hemorrhage ->Amicar/aminocaproic acid* I & O, Manage bladder irrigations (CBI) (Irrigate as needed & maintain tension on catheter) Manage drains and dressings

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Nursing Management Post Op watch

answer

DVT, Pulmonary and wound infection Rectal complications=stool softeners (avoid anything in rectum) Keep in mind positioning (will not want to sit on incision sites)

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Options for Sexual Activity: AUS?

answer

Prosthetic penile implants (water/air) Nerve pressure vacuum devices Pharmacologic interventions:Viagra, Penile suppository: Injection of meds into penis *AUS= artificial urethra sphincter (helps control dribbling)*

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Teaching for Discharge Patient & family

answer

Drainage system, Patients go home with catheters in place for 2-3 weeks allowing for healing ; dribbling is normal for 6-8 weeks, May need pads for lack of control for up to 6 months Wound care What to report to doctor (infection, catheter blockage) Patient: Kegals, Urinate with 1st urge, Avoid valsalva, strenuous exercise, long car rides

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Testicular Cancer

answer

Leading cause of death from cancer in males age 15-35. If untreated death in 2-3years. If detected early 90-100% chance of cure; chemo very effective with this cancer even w/ mets

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Testicular Cancer: higher risk in ___?

answer

Statistics: Most common cancer in men 15-35 2nd peak after age 60 2nd most common cancer in men 35-39 8,590 (estimated) Dx in 2012 35x higher in men with undescended testicles (cryptorchidism) heat from abdominal cavity may cause abnormal cell formation Model for curable solid tumors

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Cell Types

answer

95% are Germinal divided into 2 types Seminomas which are sensitive to radition Nonseminomas which are more aggressive and likely to spread throughout the body

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Causes Testicular Cancer (4)

answer

Cryptorchidism Infection DES exposure Genetic/Endocrine

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Clinical Manifestations Testicular Ca: main one ?

answer

*Enlarged/Painless lump in testicle feels Heaviness in scrotum & inguinal areas** Low back pain, Pain in abdomen Anorexia, Weight loss /N&V Cough, SOB mets to lung Confusion= met brain

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Assessment & Diagnosis Testicular Cancer

answer

Tumor Markers: AFP, (HCG), LDH elevated Imaging -US (usually first) visualize mass -Chest x-ray, CT of abdomen & pelvis to determine spread

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Medical & Surgical Management (3)

answer

Very curable solid tumor; Treatment based on cell type, anatomic spread/staging -Orchiectomy = removal testes (common); usually only U/L with Prosthesis for -RPLND = retroperitoneal lymph node dissection -Sperm Bank

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Medical and Surgical Management: chemo (2)/rad; most important to know

answer

Chemo very effective: Results in high complete remission rates (Cisplatin, neomyacin); Radiation used if no response to chemo *Must be aware that they have an increased chance for cancer later in life; must have regular screening/follow up*

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Follow Up for Testicular cancer: what is important to have?

answer

Subsequent Tumors @ Increased Rate (interval for follow up varies) *MUST HAVE REGULAR SCREENING* Chest X-ray, Excretory Urography, AFP & HCG, Exam of lymph nodes, Sexual dysfunction & infertility

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Nursing Care with Testicular Cancer

answer

Postop care= wound management, pain control may be localized to an area: ice pack 15 minutes q1hour, athletic support (extra support to area) *FOLLOW UP ENCOURAGED STRONGLY* monthly/bimonthly/annual AFP, chest xray

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Nursing Management

answer

Instruct patient on importance of follow up Help with body image Deal with sexuality issues Reassure about fertility issues

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ETIOLOGY & RISK FACTORS BLADDER CANCER (sofpic)

answer

*Smoking—most significant risk factor a DIRECT CAUSE* Chemical & Carcinogens—textile, rubber, paint & printing Occupations—truck & bus drivers, miners, drycleaners INFECTIONS=any chronic irritation/infection, Schistosoma haematobium (parasite) infection Fried meats & fats Pelvic radiation—causes secondary bladder cancer

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PREVENTION & SCREENING

answer

1. Smoking cessation 2. Identification of people high risk because of occupational hazards

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CLINICAL MANIFESTATIONS Bladder Ca: most common presenting sign?

answer

Painless, gross hematuria—most common presenting sign *MAY ONLY HAVE MICROSCOPIC HEMATURIA; may need to test for blood* Urgency, dysuria, frequency OR Obstructive symptoms: hesitancy, decrease in stream force (d/t large tumors/metastases pushing on urethra) Flank pain—d/t hydronephrosis=ureteral obstruction & back up, colicky pain/back pain, rectal pain or suprapubic pain

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DIAGNOSTIC Bladder Ca: reason for delayed dx? Gold standard?

answer

*Can be delayed because look like UTI* C&S (R/O infection) CT, CBC & chemistries, UA (microscopic blood) *Gold Standard: CYSTOSCOPY & biopsy* of tumor/wall allows direct visualization (done in OR with anesthesia)

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TREATMENT Non-invasive tumors Bladder

answer

=has not penetrated into wall of bladder (if penetrated is more severe) Immunologic/chemotherapy agents administered by intravesicalular instillation into bladder; Used for 6 weeks qweek; may be used as primary treatment/prevention; S/E=(NOT systemic chemo, only in BLADDER; s/e NOT systemic)

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Intravesicular Instillation

answer

Before procedure decrease amount of fluid to allow chemo to flow, clamp off foley, *instilled into bladder, leave in for 2 hours. Patient turn side to side q15; increase fluid intake after to flush out, foley bag discareded & handled with chemo spill kit*

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More Non Surgical Bladder Cancer (4)

answer

-Bacille Calmette-Guerin (BCG): Live mycobacterium bovis—patient must *void after instillation to ensure proper disposal of contaminated urine* (May also use—doxorubicin, mitomycin C or interfero; S/E: burn, frequency, urgency (NAIDs, antispasmodics) -TUR-Transurethral resection excision=Stage 1(non penetrating) excise tumor, may do intravesicular instillation after -Fulguration=destruction of tissue using electric sparks -Laser surgery=(not for large tumors) lasers to kill tumor; decrease risk of bleeding

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Invasive Procedures Bladder Cancer (3)

answer

Invasive tumors=invaded wall/into peritoneal cavity/other organs -Radical cystectomy=removal of bladder -Urinary Diversions (after removal of bladder) may need chemo/raditation prior -Ureterostomies a. Ileal Conduit: stoma brought out into bag; make a stoma using the ileum and attach ureters b. Continent Internal Ileal Reservoir (Kock's pouch)=valve, catheterize to drain

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ENDOCRINE SYSTEMDEFINITION: depends on the coordinated function of

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Homeostatic mechanism to maintain metabolism, growth, repro, energy productionWorks with nervous & immune systemsl Composed of glands or glandular tissue that synthesize, store & secrete hormones that travel to specific tissues—target tissues *Depends on the coordinated function of the hypothalmic-pituitary axis (negative feedback system for major organs and endocrine organs)*

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ENDOCRINE SYSTEMHYPOTHALMIC-PITUITARY AXIS

answer

Negative feedback system that regulates the secretion of most classic hormones needed by the body (maintain the amount hormone and stops it when the wanted amount is reached) When a body condition starts to move away from the normal range and a specific action is needed to correct this change secretion of the hormone capable of cuasing the correcting action or response is stimulated until the need (demand) is met As the correction occurs, hormone secretion decreases and may even halt

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ENDOCRINE SYSTEMHYPOTHALMIC-PITUITARY AXIS

answer

Example of the "negative feedback" system (simple): Control of insulin secretion—When blood glucose levels rise above normal, insulin is secreted. Insulin increases glucose uptake by the cells causing a decrease in blood glucose. The body responds by turning off the secretion of insulin

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ENDOCRINE SYSTEMMAJOR COMPONENTS

answer

HYPOTHALMUS=stimulates pituitary *Link between CNS & endocrine system* -"Neuroendocrine transmitter"=converts stimuli to hormone release=travel to the anterior pituitary where they either stimulate/inhibit the release of anterior pit hormones -Produces TRH (thyrotropin releasing hormone), CRH (corticotropin releasing hormone), GHRH (growth hormone- releasing hormone), PIH (prolactin-inhibiting hormone)

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ENDOCRINE SYSTEMMAJOR COMPONENTS

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PITUITARY GLAND= "Master gland" ant pit: releases tropic hormones which bind to receptors on endocrine target organs stimulating growth/metabolism, etc; LH, GH (growth hormone), TSH (thyroid-stimulating hormone), ACTH (adrenocorticotropic hormone), (luteinizing hormone), FSH (follicle-stimulating hormone) Posterior pituitary: ADH & oxytocin

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ENDOCRINE SYSTEMCLASSIFICATION OF DISORDERS

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1. Primary disorders—target endocrine gland 2. Secondary disorders—anterior pituitary (EX. Tumor bc pituitary controls everything else) 3. Tertiary disorders—defect lies within hypothalamus (brain injury)

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FUNCTIONS OF THYROID GLAND

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BMR Growth & development Carbohydrate metabolism (norm: increase insulin secretion, increases uptake of glu by cell & GI tract, utilize proteins for energy), Lipid metabolism (norm decreases serum cholesterol & triglycerides) Appetite (norm stimulates) Cardiovascular (norm increase CO and perfusion, HR, contractility), Respiratory (norm increases rate and depth) CNS (norm regulates reaction to stimuli) Sleep (regulates) Sexual (regulates libido/menstruation)

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ENDOCRINE SYSTEMTHYROID DIAGNOSTICS

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TSH Serum-free T4 T3 and T4 T4 resin uptake Thyroid antibodies Radioactive iodine uptake Fine-needle biopsy (tumor) Thyroid scan, radio scan, or scintiscan Serum thyroglobulin If hyper=decrease TSH and increase T3 and T4; hypo=increased TSH and decreased T3 and T4

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ENDOCRINE SYSTEMTHYROID DISORDERS

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Cretinism Hypothyroidism Hyperthyroidism Thyroiditis Goiter Thyroid cancer

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ENDOCRINE SYSTEM HYPOTHYROIDISM

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Insufficient amount of circulating hormones in peripheral tissues when thyroid cells are no longer functioning normally/they are functioning, but decreased ingestion of substances that produce thyroid hormones—iodide and tyrosine Decreased BMR: stimulates the hypothalamus & anterior pituitary to make TSH in an attempt to trigger production of T3 & T4 (thyroid unable to produce enough T3 or T4)

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GOITER & Hyperglycemia: what does not increase

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Excess TSH binds to thyroid cells and causes the thyroid gland to enlarge (Goiter) **CAN HAVE in both HYOPO (binding of TSH to cells) /HYPER (d/t hyperactivity) *HYPERGLYCEMIA: in both; HYPO (glands not utilizing glu and not enough insulin) HYPER=producing more glucose to meet increased BMR* Thyroid hormone production DOES NOT increase (hypo)

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ENDOCRINE SYSTEM HYPOTHYROIDISM ETIOLOGY (4)

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PRIMARY—95% (d/o of the gland itself) Decreased thyroid tissue Autoimmune thyroid destruction—Hashimoto's thyroiditis Surgical removal of thyroid Cancer->Radiation-induced thyroid destruction (for hyperthyroidism to destroy the tissue) Congenital condition

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PRIMARY & Drugs that cause HYPOthyroidism**(4)

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Decreased synthesis of T3 and T4 d/t: -Endemic iodine deficiency OR Excessive exposure to iodine -Drugs 1. Lithium 2. Propylthiuracil (PTU)=for hyper, given to much lowers too much 3. Phenylbutazone (Butazolidine) (NSAID) 4. (Cytadren)—inhibitor of adrenocortical synthesis

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SECONDARY Hypothyroidism

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—anything pituitary Inadequate production TSH Tumors, trauma, infections or infarcts Congenital

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ENDOCRINE SYSTEMHYPOTHYROIDISMCLINICAL MANIFESTATIONS memo

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SKIN—Yellowish, dry, coarse, scaly skin, thick, brittle nails and dry, coarse, brittle hair, hair thinning and loss CARDIAC—Bradycardia, dysrhythmias, decreased activity tolerance, hypotension, decreased CO and contractility METABOLIC—Decreased body temperature, cold intolerance MUSCULOSKELETAL—Muscle aches and pain, delayed contraction & relaxation of muscles NEUROLOGICAL—Slowing of intellectual functions, slurring of speech, impaired memory, inattentiveness, lethargy or somnolence, confusion, poor short term memory, decreased reflexes, paresthesia and fatigue GI—Weight gain, anorexia, constipation, abdominal distention

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ENDOCRINE SYSTEMHYPOTHYROIDISMCLINICAL MANIFESTATIONS

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PSYCHOLOGICAL—Depression, apathy, paranoia, withdrawal REPRODUCTIVE—FEMALE—Changes in menses, decreased libido, anovulation MALE—Impotence, decreased libido OTHERS—Periorbital edema, facial puffiness, nonpitting edema of hands and feet, hoarseness, goiter, weakness, fatigue, decreased urine output, anemia, easy bruising, and iron, folate and vitamin B12 deficiencies

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ENDOCRINE SYSTEMHYPOTHYROI DISMDIAGNOSTICS

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History & Physical Serum thyroid tests: Increased TSH levels, Decreased T3 & T4 levels, Decreased T3 resin uptake test, Decreased BMR, Decreased radioactive iodine uptake Thyroid Scan (cold areas), US of thyroid gland EKG (heart problems decrease CO/contractility/perfusion)

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ENDOCRINE SYSTEMHYPOTHYROIDISM TREATMENT HORMONE REPLACEMENT THERAPY****med card

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1. Levothyroxine—Synthroid, Levoxyl, Levothyroid (must take the same one eacho time); Most frequently used because of its predictability and reliability; Synthetic salt of T4 2. Liothyronine—Cytomel, Triostat 3. Liotrix—Thyrolar 4. Thyroid dessicated/Armour thyroid —increase metabolic rate

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HORMONE REPLACEMENT THERAPY Patient teaching

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Lifelong therapy *No adverse effects (may notice slight skin rash/hair loss in first few months)* WITH FOOD, same time every day (before breakfast with a full glass of water) DON'T STOP without consulting your physician DO NOT change brands (might cause myxedema coma) REPORT—chest pain, difficulty breathing, fever, chills, unusual sweating, weight gain, agitation, (may be on a too low/too high dose) if sxs of hyper, too much; if not sxs not relieved, too little; BLOOD WORK will tell you what is needed*

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HORMONE REPLACEMENT THERAPY *DO NOT DO WHAT*

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Avoid OTC medications without checking with physician Avoid excessive amounts of foods that inhibit thyroid hormone Wear medic-alert bracelet Watch drug interactions—ex: hormone potentiates the effects of Digoxin DO NOT CHANGE THE BRAND YOU TAKE

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ENDOCRINE SYSTEM HYPOTHYROIDISM TREATMENT

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Report S/S of hypo/hyper, increases in pulse/temp Weekly weights, Stress lab appointments to monitor hormone levels Increase fluids and fiber to prevent constipation (hypo) diarrhea in hyper Avoid chilling: wear additional clothing, increase room temp (hypo) Provide rest periods for fatigue and activity intolerance (d/t slowed metabolism hypo)

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ENDOCRINE SYSTE MYXEDEMA COMA

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EXTREMELY low throid; emergency situation; no energy source = accumulation of metabolites (proteins and sugars) increases the mucous+water edema; APPEARANCE: Nonpitting edema—esp around eyes, in the hands, feet, between the shoulder blades. Tongue thickens, edema forms in the larynx, making the voice husky; Physiologic function is decreased.

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ENDOCRINE SYSTEMMYX EDEMA COMA: affect on heart?

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Rare, life threatening: D/C/under/inadequate treatment of hypothyroidism, acute illness, surgery, OD use of sedatives/opioids, Decreased metabolism causes heart to be flabby & increase chamber size.

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MYXEDEMA RESULT

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decrease CO & perfusion to the brain and vital organs:lead to unresponsiveness, organ failure, CV collapse Hypotension->bradycardia, hypoventilation, hypothermia, cerebral hypoxia, hyponatremia, hypoglycemia

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TREATMENT OF MYXEDEMA COMA (5) airway, hemodynamic, medicine, monitor, positioning?

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Maintain patent airway—intubation, Aspiration precautions Replace fluids NS/hypertonic saline (d/t decrease CO/BP) *Administer glucose IV, treat precipitating cause, Give levothyroxine (Synthroid) IV, Give Hydrocortisone 100 mg IV—rapid administration of IV Synthroid may cause adrenal insufficiency* Monitor for changes in mental status, Monitor BP & temp hourly (HYPOthermia so Avoid chilling—cover patient with warm blankets) Turn patient every 2 hours to prevent skin breakdown from edema

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ENDOCRINE SYSTEM HYPERTHYROIDISM GRAVES DISEASE

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Excessive thyroid hormone secretion; Manifestations=thyrotoxicosis=hypermetabolism and increased sympathetic nervous system activity: increases HR and stoke volume=cardiac output and BP****MONITOR THESE*

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ENDOCRINE SYSTEM HYPERTHYROIDISM ETIOLOGY (3)

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A. Graves' disease—toxic diffuse goiter; Autoimmune Ab attach to the thyroid stimulating hormone (TSH) receptor sites on thyroid tissue; bind to the thyroid gland and causes an increase in size+overproduces thyroid hormones B. Toxic multinodular goiter: Multiple nodules in gland secreting excessive thyroid hormone C. Exogenous hyperthyroidis: Excessive use of thyroid hormones

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ENDOCRINE SYSTEMHYPERTHYROIDISMCLINICAL MANIFESTATIONS

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SKIN—Excessive sweating, smooth, warm, moist skin, thinning of scalp hair RESPIRATORY—SOB with or without exertion, rapid, shallow respirations CARDIAC—Palpitations, chest pain, tachycardia, dysrhythmias, increased BP GI—Weight loss, increased appetite, diarrhea, fat metabolism increased, negative nitrogen balance MUSCULOSKELETAL—Muscle weakness and wasting NEUROLOGIC—Blurred or double vision, corneal ulcers or infections, increased tears, photophobia, exophthalmos, tremors, insomnia, hyperactive deep tendon reflexes, red conjunctiva Goiter and hyperglycemia present in both***

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ENDOCRINE SYSTEMHYPERTHYROIDISMCLINICAL MANIFESTATIONS

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METABOLIC—Increased metabolic rate, heat intolerance, low-grade fever, fatigue PSYCHOLOGICAL—Decreased attention span, restlessness, irritability, emotional lability, manic behavior REPRODUCTIVE—Amenorrhea, decreased menstrual flow, increased libido OTHERS—Goiter, wide-eyed appearance, decreased total WBC, enlarged spleen

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ENDOCRINE SYSTEMHYPERTHYROI DISMDIAGNOSTICS

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History & physical Serum thyroid tests: Decreased TSH, Increased T3 & T4, BMR increased, Radioactive iodine & T3 resin uptake Thyroid scan (hot areas=autoimmune issue), US, EKG—Sinus tachycardia, a-fib Plasma cortisol increase=Blood sugar increased

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ENDOCRINE SYSTEMHYPERTHYROIDISM TREATMENT: med card Thiomides****

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ANTITHYROID MEDICATIONS *(therapy for hyper not as life long)* 1. Thioamides -Propylthiouracil (PTU, Propyl-Thyracil): Prevents new formation of thyroid hormones by inhibiting thyroid binding of iodide & preventing T4 from converting to T3 in the tissues -Methimazole (Tapazole, Northyx) Prevents the formation of thyroid hormones

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ANTITHYROID MEDICATION Thioamides Patient Teaching (4)

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*Drug must be taken every 8 hours to maintain action* (compare with hypo meds taken 1/day) Avoid food with high iodine content, Avoid crowds/people who are ill (causes immunosuppression) Monitor HR, weekly weight & cold intolerance Report darkening of urine, jaundice skin & sclera and bruises—may be indicative of liver toxicity

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ANTITHYROID MEDICATIONS***med card

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-Iodine and iodine-containing agents (Lugol's solution) : not used as maintenance; used for surgery to shrink vascular system of tumor on gland -Saturated solution of potassium iodide (SSKI) Sudden excess of iodine rapidly inhibits thyroid hormone release & resolves cardiac & other manifestations

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Patient Teaching for Iodine and iodine-containing agents: s/s of iodine toxicity?

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Thioamide agent may be given first to prevent that initial increase in thyroid hormone production; use: adjunct med/pre-op to decrease vascularity of gland -Mix with milk or juice (tastes bad) & Drink with a straw (stains teeth) *Monitor IODISM TOXICITY*: fever, rash, metallic taste, mouth sores, sore throat, GI distress (may require D/C)

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ANTITHYROID MEDICATIONS Radioactive Iodine—I131

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permanently destroy thyroid tissue so it will not secrete hormones—renders patient euthyroid/hypothyroid *Must be on thyroid replacement lifelong bc this suppresses thyroid production* Teach patient signs of hypothyroidism & REPORT Depending on size & sensitivity to rad. and it may take 6 - 8 weeks to have complete symptom relief—may still need to take other meds; May/may not need radiation precautions for 24 hours (very low dose of radiation) Oral administration—may need more than one dose

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Medications and Nursing Care for HYPER***med card

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1. Beta-blockers: Controls sympathetic hyperactivity (cardiac effects) 2. Glucocorticoids=Prevents conversion of T4 to T3 & Helps with infiltrative opthamology 3. Monitor heart rate, BP & temp (increased in hyper) every 4 hours 4. Reduce stimulation, rest, Promote comfort—reduce room temp, cool showers or baths, keep sheets dry from diaphoresis

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TOTAL OR SUB-TOTAL THYROIDECTOMY

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Used when goiter is compressing trachea/esophagus/patient does not have a good response to antithyroid meds PRE-OPERATIVELY: Want patient to be euthyroid (close to normal thyroid functioning) & decrease vascularity of gland through use of meds (will prevent release of hormones and prevent thyrpid storm), CARDIAC problems stabilized before operating Coughing & deep breathing exercises supporting neck while coughing—reduces strain on suture line; DO NOT HYPER EXTEND NECK; May experience hoarseness after surgery DIET: High protein, high carbohydrate diet days before surgery

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TOTAL OR SUB-TOTAL THYROIDECTOMY POST-OPERATIVE****most important monitoring?

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Monitor for complications—most important *Monitor for bleeding-monitor drainage in JP drain can be d/t hemorrhage (hit carotid)* *Monitor respiratory status—distress may be caused by swelling, damage to laryngeal nerve/tetany* VS q15mins until stable, then q30 mins Humidify air, suction if needed, coughing & deep breathing q30-1 hour, 2. Sandbags or pillows to support head & neck & semi-fowlers position 3. Pain control as needed

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COMPLICATIONS OF THYROIDECTOMY (Respiratory) medication for calcium gluconate

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Respiratory distress—may be due to hemorrhage (hematoma pushes against larynx); Monitor for *laryngeal stridor—harsh, high-pitched sounds*; Keep tracheostomy equipment at bedside along with oxygen & suction equipment; *Laryngeal nerve damage*: Assess voice q2 hours for hoarseness & weakness; Hypocalcemia & tetany: Occurs if hypoparathyroid glands are damaged; require calcium replacement if hypoparathyroid is removed; Monitor hourly for tingling around mouth, toes & fingers, muscle twitching—Treated with calcium gluconate

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ENDOCRINE SYSTEMHYPERTHYROIDISMTHYROID "STORM" OR "CRISIS"

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Life-threatening emergency when hyperthyroidism is uncontrolled or Triggered by stressors—trauma, infection, DKA, pregnancy; surgery d/t manipulation of thyroid *MAIN Symptoms—fever (102-106), tachycardia(>130), systolic HTN* Other: PANIC anxiety/confusion, GI distress, psychomotor agitation, dyspnea, extreme diaphoresis=dehydration, seizures, death *Treatment: Maintain patent airway and adequate ventilation*

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Treatment & Care Thyroid Storm****what medication do you not give?

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-antithyroid drugs—PTU, Tapazole *(IN MUCH HIGHER DOSES) ONLY A PO med * *Every other med is IV* -Sodium iodide solution IV -Propanolol (Inderal) IV to decrease cardiac complications & BP decrease HR -Glucocorticoids IV (solumedrol)—suppresses the release of thyroid hormone. Monitor vital signs q 30 mins Provide comfort measures—Tylenol or cooling blanket for increased temp—*NO ASA—thought to increase thyroid hormone*, Correct dehydration & electrolyte imbalances (diaphoresis)

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Thyroid cancer

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Removal 5/6th of thyroid + surrounding lymph nodes Pre/Post Op care the same for subtotal/total thyroidectomy Radioactive iodine (if lymph node involvement) may be given (isolation for 3 days) No other treatment available

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ENDOCRINE SYSTEMPARATHYROID GLANDS

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Parathyroid hormone (Parathormone) regulates calcium & phosphorus (IF Ca up, P down and vice versa); *Secretion of PTH decreases if serum calcium is high and increases if serum calcium is low*; PTH increases bone resorption (fr kidneys)=increase serum calcium and activates Vitamin D to increase absorption of calcium & phosphorus in the intestines (helps hold onto it so they don't pee it out; take from GI) Serum phosphorus may also affect PTH levels due to its relation with calcium (Ca has more of an effect; Ca and P work together)

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ENDOCRINE SYSTEM HYPO PARATHYROIDISM (3 causes)

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=lack of PTH=decreased serum calcium & increased serum phosphorus Idiopathic=spontaneous/autoimmune Iatrogenic=most common; caused by removal of tissue during thyroid surgery/radiation/ablation Hypomagnesemia=impairs PTH secretion

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ENDOCRINE SYSTEM HYPOPARATHYROIDISMCLINICAL MANIFESTATIONS (2 signs)

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-Decrease Ca increase P -Tetany: PARESTHESIAS, stiffness of hands and fingers, (severe hypocalcemia) Muscle cramps, Spasms of hands and feet, Laryngospasms, EKG changes (cardiac muscle spasm) *Chvostek's sign—tap face just below & in front of the ear to trigger facial twitching (twitche moves towards the tapping)* *Trousseau's sign—hands and fingers go into spasm in plantar flexion w/ inflation of BP (1-4min)*

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ENDOCRINE SYSTEMHYPOPARATHYROIDISMTREATMENT

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IV Calcium gluconate or chloride—10% solution over 10-15 minutes Long term oral Calcium—0.5-2 grams daily in divided doses Vitamin D deficiency treated with calcitriol (Rocaltrol) 0.5-2g daily (help utilize Ca) Long term Vitamin D deficiency—50,000-400,000 units of ergocalciferol daily Acute hypomagnesemia—Mag sulfate in 2 mL doses IM or IV Eat foods high in calcium, low in phosphorus—vegetables; can take phosphate binder (combines with phosphate in intestine in order to excrete) Respiratory support as needed Reduction of stimuli—low lights, decrease noise, no sudden movements Lifelong therapy of Calcium, Medic-Alert bracelet

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ENDOCRINE SYSTEM HYPERPARATHYROIDISM + Primary

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Excessive secretion of parathormone (PTH) with increased serum calcium levels and decreased serum phosphorus levels and reduces bone density Primary hyperparathyroidism (direct on parathyroid) a. Parathyroid adenoma/carcinoma b. Congenital hyperplasia c. Neck trauma/radiation d. Vitamin D deficiency

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Secondary hyperparathyroidism

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-Chronic renal failure: d/t deficiency Vit D=decrease Ca and increase P. parathyroid hormone secretes more PTH to increase Ca, *but cannot regulate d/t renal failure; so MUST BE ON vitamin D and Ca therapy* -Parathyroid hormone-secreting tumors of lung, kidney , GI tract

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ENDOCRINE SYSTEM HYPERPARATHYROIDISMCLINICAL MANIFESTATIONS

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Bone fractures, osteoporosis, "painful" bones Anorexia, weight loss, N/V, epigastric pain, constipation, *peptic ulcer disease due to elevated serum gastrin levels* Psychological distress, *psychosis with mental confusion with calcium levels above 12 mg/dl* Renal calculi Cardiac arrhythmias, Coma, death

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ENDOCRINE SYSTEM HYPERPARATHYROIDISM TREATMENT****med card

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Diuretic and hydration therapies *Saline diuresis—rapid infusion NS 1 liter over 3-4 hours Furosemide (Lasix) given with fluids (rapid excretion of Ca)*-->Strict intake & output!!! ▪ Monitor cardiac function (Continuous cardiac monitoring)

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ENDOCRINE SYSTEM HYPERPARATHYROIDISMTREATMENT Drug therapy

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Phosphates IV-rapid removal of calcium or oral (increase P decrease Ca) Inhibits bone resorption (break down & release Ca) & interferes with calcium absorption Calcitonin=reduce breakdown & release Ca & increases kidney excretion; Give with glucocorticoids to enhance Calcium chelators=bind to calcium & reduces free Ca Penicillamine (Cuprimine, Pendramine),*Mithramycin IV—cytotoxic agent—most effective*

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ENDOCRINE SYSTEMADRENAL GLANDS

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ADRENAL CORTEX HAS: Glucocorticoids—principle one is CORTISOL: Affects CHO, protein and fat metabolism Increases rate of gluconeogenesis occurs in liver (increases sugar for use) Decreases use of amino acids for protein synthesis so that amino acids are available for gluconeogenesis Mobilizes fatty acids from fatty tissues (UTILIZE fat for energy)

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ADRENAL CORTEX (2 corticoids)

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Glucocorticoids -Decreases inflammatory response, Maintains blood glucose, Stimulates gastric acid secretion, Maintain behavior and cognitive functions Mineralocorticoids -Produces and secretes aldosterone, Sex hormones

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ENDOCRINE SYSTEMADRENAL INSUFFICIENCY: ADDISON'S DISEASE

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Impaired secretion of cortisol and aldosterone Primary causes Adrenalectomy Idiopathic (autoimmune) TB, AIDS, Fungal lesions, gram negative sepsis *Metastatic cancer->Abdominal radiation therapy* Drugs and toxins

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ENDOCRINE SYSTEM ADDISON'S DISEASE SECONDARY CAUSES

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*Pituitary tumors* Postpartum pituitary necrosis Hypophysectomy (removal pituitary) High-dose pituitary/whole-brain radiation

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ENDOCRINE SYSTEM ADDISON'S DISEASE treat with?

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*DECREASED CORTISOL production*=ant. pituitary tries to increase it by secreting adrenocorticotropic hormone (ACTH) to increase production of cortisol by the adrenals (decreased circulating cortisol = increased ACTH; vice versa) Hypoglycemia (Decrease gluconeogenesis) leading to Hyperkalemia (Decreased aldosterone: decrease ability to hold onto Na+water/increase K) Treat adrenal insufficiency with Cortisone

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ENDOCRINE SYSTEM ADDISON'S DISEASE CLINICAL MANIFESTATIONS

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Neuromuscular: Fatigue, Muscle weakness, joint/muscle pain, mood changes Cardiovascular: Hypotension, tachycardia (no vol.) Hyponatremia, hyperkalemia, hypercalcemia, dehydration GI: Anorexia,Weight loss, N/V. abdominal pain, Bowel changes—constipation/diarrhea, salt craving Integumentary: Hyperpigmentation

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ENDOCRINE SYSTEMADDISON'S DISEASETREATMENT CORTISOL REPLACEMENT THERAPY med card (don't memo dosage)

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*Given once daily in AM to follow body's natural secretion of cortisol. If it must be divided, give 2/3 in AM and 1/3 in PM* a. Cortisone (Cortistan)—25-300 mg daily b. Hydrocortisone (Cortef)—2-80 mg TID or QID c. Prednisone (Deltasone)—5-60 mg 1-4 times/day *Fludrocortisone (Florinef)—0.05-0.2 mg daily =Mineralocorticoid: Increases sodium reabsorption; excretes potassium; Maintains BP*

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PATIENT TEACHING FOR CORTISOL THERAPY

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STEROIDS MUST BE TAPERED Limit salt intake and increase proteins in your diet Increased appetite->wt gain PSYCH disturbance: restlessness and sleeplessness IMMUNOSUPRESSION (avoid crowds/infections) *Report: (indicates too much; opposite s/s if there is not enough) sudden weight gain, flu sxs, bleeding/bruising (GI Bleed fr cortisone), swelling of hands and feet*

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PATIENT TEACHING Steroid therapy: 2 situations that will require dose adjustments?

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Avoid use of OTC drugs without consulting physician; Notify all health care personnel that you are taking this drug Medic-Alert bracelet Take medication with food *Dose may need to be increased/decreased with periods of physical or emotional stress—surgery, fever, pregnancy; may need to be adjusted when taking insulin or anti- coagulants (these drugs decrease effectiveness of steroids)*

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ENDOCRINE SYSTEM ADDISONIAN CRISIS

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Complication of Addison's disease that is a life threatening emergency Occurs in response to a stressful event—surgery, trauma, severe infection, dehydration Problems are the same as Addison's disease, but much more severe—decreased BP, decreased sodium and water (no aldosterone; no fluid retained), increased potassium, increased hypoglycemia (no cortisol; cortisol increases BS) *Can lead to circulatory collapse* Cortisone given (to increase cortisol and increase all other steroids); too much cortisol will cause increase Na decrease K, weight gain, GI bleed (ALL s/e of too much prednisone)

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ENDOCRINE SYSTEMADDISONIAN CRISIS TREATMENT HORMONE REPLACEMENT med card(3)

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-Rapid infusion of NS/D5W in NS (volume and energy) -Initial dose of hydrocortisone sodium succinate (Solu-Cortef) is 100-300 mg or dexamethasone (Decadron) 4-12 mg as an IV bolus; additional 100 mg hydrocortisone sodium succinate by continuous IV drip over the next 8 hours ; Give hydrocortisone 50 mg IM q12 hours along with drip -*Histamine blocker IV: ulcer prevention (must be on acid blocker if on steroids always because it causes GI bleed; prednisone with meals)*

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HYPERKALEMIA MANAGEMENT Drug Therapy and Care

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1. Insulin and dextrose in normal saline to shift potassium into the cells (increase uptake of Glucose and will pull K with it into the cell to reduce K concentration) 2. Administer Kayexalate, loop or thiazide diuretics Avoid potassium-sparing diuretics, Potassium restricted diet Monitor intake and output; *Monitor heart rate, rhythm, EKG for signs of hyperkalemia—bradycardia, cardiac instability*

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HYPOGLYCEMIA MANAGEMENT* 5 S's****

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Administer IV glucose & glucagon as needed Monitor blood glucose hourly OTHERS 1. Keep patient flat with legs elevated *Five s's—salt (hold onto water), sugar (energy), steroids (replacement), source for precipitating event (cause), support*

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ENDOCRINE DISEASE HYPERCORTISOLISM CUSHING'S DISEASE

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Excessive secretion of cortisol from adrenal cortex=Exaggerated actions of glucocorticoids; due to problem in adrenal cortex/anterior pituitary/hypothalamus OR Long term glucocorticoid therapy=—asthma, COPD, chronic fibrosis, autoimmune disorders, transplants, allergic responses, chemo, (anything that will increase cortisol)

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ENDOCRINE SYSTEMCUSHING'S DISEASECLINICAL MANIFESTATIONS

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Same sxs of long term steroid therapy GENERAL APPEARANCE: Fat redistribution—moon face, buffalo hump, truncal obesity, Weight gain, hyperglycemia ▪ CARDIOVASCULAR 1. Hypertension, increased sodium, decreased potassium 2. Increased risk for thromboembolic events (increases coagulation) 3. Frequent dependent edema 4. Capillary fragility—bruising, petechiae ▪ MUSCULOSKELETAL 1. Muscle atrophy or wasting, Osteoporosis, fractures, decreased height

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ENDOCRINE SYSTEM CUSHING'S DISEASECLINICAL MANIFESTATIONS

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SKIN 1. Thinning skin—"paper-like" appearance 2. Striae, acne 3. Increased pigmentation 4. Poor wound healing ▪ IMMUNE SYSTEM 1. Increased risk for infection 2. Decreased immune function 3. Decreased inflammatory response 4. Manifestations of infection/inflammation may be masked ▪ Emotional lability, mood swings, confusion, psychosis

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ENDOCRINE SYSTEM CUSHING'S DISEASE DIAGNOSTICS

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-Increased plasma cortisol levels -ACTH levels—increased if problem is with pituitary and decreased if problem is with adrenal -24-hour urines for 17-Ketosteroids or 17-Hydroxycorticosteroids= measures the amount of cortisol and androgens in urine which will be increased along with calcium, potassium and glucose -Dexamethasone suppression testing—administer set doses of dexamethasone and testing 24-hour urine collections= *If urinary cortisol levels and hydroxycorticosteroids are suppressed, Cushing's is ruled out* ▪ CT, MRI, US to r/o tumors

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ENDOCRINE SYSTEM CUSHING'S Drug Therapy***

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1. Drug therapy—drugs that interfere with ACTH production or adrenal hormone synthesis (want to decrease) a. Aminoglutethimide (Elipten,Cytradren) and metyrapone (Metopirone)—decreases cortisol production b. Cyproheptane (Periactin)—interferes with ACTH production c. Mitotane (Lysodren)—adrenal cytotoxic agent used for inoperable adrenal tumors d. Monitor for response to drugs—especially weight loss and increased urine output

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NONSURGICAL MANAGEMENT Patient safety: prophylactic medication?

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*Monitor for fluid overload (bounding pulse, edema, rales, wheeping); Monitor intake & output, Daily weights* b. *Risk for skin breakdown due to edema (also d/t paper thin skin***) d. Monitor blood sugars g. Prophylactic H2 antagonists or PPI—No ASA or NSAIDs (bleeding) h. Monitor for infection (immunosupression) i. safe from falls and fractures

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ENDOCRINE SYSTEMCUSHING'S DISEASETREATMENT Hypophysectomy

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Removal of tumor of adrenals or tumor of pituitary— hypophysectomy Pre-op—Correct any electrolyte imbalances, blood glucose levels, glucocorticoids given before surgery and during surgery to prevent adrenal crisis Post-op—Assess patient q15 mins for shock due to, insufficient glucocorticoids, monitor vital signs, intake and output, daily weights and serum electrolyte levels *Lifelong corticosteroid replacement therapy will be needed if adrenal glands are removed*

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PHEOCHROMOCYTOMA

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Catecholamine-producing tumor that arises in adrenal medulla; Single lesion, B/L, abdomen, Usually benign, but 10% are malignant *Tumors produce, store and release epinephrine and norepinephrine (catecholamines) which stimulate adrenergic receptors and SNS* Cause is unknown, but may occur in neurofibromatosis and multiple endocrine neoplasia

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PHEOCHROMOCYTOMA CLINICAL MANIFESTATIONS: CARDINAL SIGN?

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***Cardinal sign is HTN that does not respond to usual drug therapy; Intermittent attacks of HTN lasts min-hours (high as 200-300/150-175)* OTHER: severe headache & dizziness, N/V, palpitations, fever, profuse diaphoresis, sense of impending doom, chest/abd pain; may also report heat intolerance, weight loss, tremors *Hypertension must be present for a pheochromocytoma to be diagnosed***

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ENDOCRINE SYSTEM PHEOCHROMOCYTOMA DIAGNOSTICS (3) medications witheld prior to a VMA + 24 hour urine?

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-24-hour urine for vanillymandelic acid (VMA)=byproduct of catecholamine metabolism (elevated) 1. *3 days before test must stop having coffee, tea, cola, cocoa, chocolate, bananas, avocados, beer—any foods containing caffeine; Medications withheld prior to test—ASA, amoxicillin, sinemet* -Clonidine suppression test; Normally suppresses the release of catecholamines,(POTENT vasodilator and if does not work on them then something is wrong); when taken will not affect BP - CT scan, MRI to locate tumors on adrenal glands

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PHEOCHROMOCYTOMA TREATMENT: main comp?

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Surgical removal of one or both adrenal glands Stabilize BP, Hydrate patient before surgery HTN may occur after surgery because of manipulation of adrenals and a sudden release of catecholamines Same nursing care post adrenalectomy as in Cushing's disease, Cortisol replacement therapy if both adrenals removed

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INCIDENCE OF COLON/RECTAL CANCER: most occur where?

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3rd most common cancer in United States 11% of all cancers; 2nd only to lung cancer in incidence and mortality 141,210 new cases/year; 49,380 annual mortality Affects both male and female Increased incidence in people over 50 years of age Varies among race and ethnicity Occurs most frequently in industrialized nations 98% of colon/rectal cancers are adenocarcinomas—tumors that arise from glandular epithelium tissue in colon *35% of lesions occur in the sigmoid colon (rectum may need to be removed; will have to have colostomy) further down the cancer is the more formed stool ***

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ETIOLOGY OF COLON/RECTAL CANCER Risk Factors: what is the biggest presenting sign?

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Cause is unknown Familial history—first degree relative Diet, Smoking, Alcohol, Obesity Colitis, Crohn's, Polyps Personal history of colorectal, ovarian, endometrial or breast cancer ;Exposure to radiation Age over 50 ***most have mets to LIVER; most that come in with OBSTRUCTION HAVE COLON CA *BIGGEST PRESENTING SX IS OBSTRUCTION*

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ETIOLOGY OF COLON/RECTAL CANCER: FAP

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Familial Adenomatous Polyposis (FAP) 100% chance of becoming malignant 1. Accounts for 1% of colon/rectal cases 2. Thousands of adenomatous polyps develop over the course of 10-15 years 3. By age 20—individuals require surgical intervention—colectomy with a colostomy to prevent colon/rectal cancer

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Hereditary Nonpolyposis Colon/Rectal Cancer (HNPCC)

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1. 10% of all colon/rectal cancers 2. Caused by genetic mutations *VERY HIGH IF IN THE FAMILY* 3. 80% chance of getting colon/rectal cancer at 45 years old *HAVE colonoscopy much earlier @ 35-40!!!!!* 4. Increased incidence of endometrial, ovarian, stomach, ureteral cancers

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PREVENTION OF COLON/RECTAL CANCER

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Genetic testing for individuals with family history of colon/rectal cancer for FAP & HNPCC Regular exercise, multivitamins, Modify diet—decrease fat, refined carbs & increase fiber *Use of NSAIDs and ASA decrease incidence of colon/rectal cancer* Screenings: a. Yearly—DRE, fecal occult blood b. Sigmoidoscopy & colonoscopy every 5 years *(if polyps/cancer found, DO q3 years)*

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PREVENTION OF COLON/RECTAL CANCER screen

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a. Yearly—Fecal occult blood (FOBT), Fecal immunochemical test (FIT) **Stool for DNA—frequency undetermined** b. Sigmoidoscopy or Double contrast barium enema or CT colonoscopy every 5 years c. Colonoscopy every 10 years

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PATHOPHYSIOLOGY OF COLON/RECTAL CANCER

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Occurs in different areas of the colon—2/3 in rectosigmoidal region By the time symptoms occur, the disease may have spread into deeper layers of bowel and adjacent organs Metastasis (indicated by OBSTRUCTION) is by means of direct extension or through blood and lymph—may spread into 4 layers of bowel wall and neighboring organs (when tumor spread through the wall) Must have clean margin if removing Liver most frequent site of metastasis

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CLINICAL MANIFESTATIONS OF COLON/RECTAL CANCER

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*Change in bowel habits or size, shape, color of stool*Alterations in bowel function—constipation alternating with diarrhea; Feeling of incomplete evacuation (stools may be thinner) *Blood in stool (must know what is causing it) *Anemia* IF LOW H/H will go for endoscopy/colposcopy Anorexia & indigestion Flatulence

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Late signs & symptoms

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Late signs & symptoms 1. Weight loss 2. Abdominal pain 3. Fatigue 4. Decline in general health 5. Jaundice (elevated LFTs, ascites) *BC METS TO THE LIVER* 6. By the time signs and symptoms appear, could be late with mets to liver

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COLON/RECTAL CANCERDIAGNOSTICS: what is used for staging?

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CBC, AST, LDH, Alkaline Phosphate, Electrolytes, BUN, Creatinine CEA—carcinoembryonic antigen elevated colon cancer Stool for occult blood Barium enema Colonoscopy Chest x-ray CT scan, MRI, PET scan Rectal ultrasound used for *Staging (can see if penetration to the wall/not)*

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COLON/RECTAL CANCER TREATMENT use packet***

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SURGICAL-REQUIRE CLEAN MARGINS 1. Removal of tumor with margins free of disease is the treatment of choice; may want to shrink with chemo before surgery or may do chemo after if severe may only need mass removed + chemo 2. Anal sphincter preserved whenever possible to avoid colostomy 3. Types of surgery: (THE LOWER IT IS = more you need to remove) a. Colon resection—removal of tumor and regional lymph nodes with reanastamosis b. Colectomy—removal of entire colon (total) or a portion of the colon (partial) with a possible colostomy or ileostomy which could be temporary or permanent *(if down towards rectal/sigmoid MUST close up the rectum; if further up can just take it out/build j pouch)*

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COLON/RECTAL CANCER TREATMENT Surgical: which surgery do they try to avoid? why?

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c. Hemicolectomy—removal of (R) or (L) portion of colon d. Minimally invasive resection—laproscopic e. Abdominoperineal (AP) resection—used for low rectal cancers. Permanent colostomy created. Distal colon, rectum and anal sphincter removed using anterior abdominal incision and perineal incision * VERY INVASIVE VERY LONG RECOVERY TRY TO AVOID THIS* f. Ileoanal pouch—"J" pouch—last part of small intestine or ileum is connected to anus when large intestine is removed. Rectal muscle left intact. Patient has a temporary ileostomy.

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J pouch

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Ileoanal pouch—"J" Pouch: * MUST discuss with wound/stoma nurse* 1. Pouch created to act as a receptacle for stool 2. Takes 4-6 weeks to heal 3. Ileostomy reversed in 2-3 months 4. Stools are first liquid and could experience urgency and leakage of stool 5. Improves over time as sphincter muscles strengthen. 6. Stools become thicker as small intestine absorbs more fluid 7. After 6 months, 5-6 semi-formed stools daily 8. Takes about one year for pouch to adapt

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COLON/RECTAL CANCERPRE-OP PATIENT PREP

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Refer patient to ET (Enterostomal therapist—ostomy nurse) to discuss general principles of colostomy care (note: Low rectal surgery—AP resection—possible sexual & urinary dysfunction d/t nerve damage during surgery) Bowel prep=minimize bacterial growth a. Mechanical cleaning—laxatives, enemas Oral/IV antibiotics prior to surgery NGT will be in place after surgery—not needed if procedure done laprascopically Coughing and deep breathing

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COLON/RECTAL CANCERPOST -OP PATIENT CARE

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1. Without a colostomy, post-op care is the same as any other abdominal surgery Monitor bowel sounds, abdominal distention passing of flatus NGT connected to low suction for decompression, Maintenance of IV fluids to replace fluids lost with NGT suction; Diet progression from liquids to solids after NGT removal PCA pump for pain for first 24-36 hours; SEVERE PAIN, OOB right away If patient had AP resection—no rectal temps or suppositories (no rectum)

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COLON/RECTAL CANCERCOLOSTOMY/ILEOSTOMY MGMT***READ PACKET****know stools/surgeris

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Return from surgery with appliance in place Assess stoma—color, integrity, should be reddish pink,(never grey/dusky) moist and protrude about ¾ of an inch; Cut the bag as close to the stoma as possible check for leakage around pouch; Report signs of ischemia of stoma, unusual bleeding or breakdown of the suture line securing the stoma Ileostomy start functioning 24-48 hrs; Colostomy should start functioning in 2-4 days or longer post-op. May begin with gas. Initial stool will be liquid and will become more formed depending on location of stoma which would indicate section of bowel removed ***DEPENDING ON SURGERY AND LOCATION OF REMOVAL WILL DETERMINE WHAT TYPE OF STOOL (higher up is liquid lower down is formed)*

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COLON/RECTAL CANCERTREATMENT Non surgical

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Chemotherapy—considered adjuvant therapy after surgery Monoclonal Antibodies—use in combination with chemo Radiation—has not demonstrated any increased survival. Used more frequently with rectal cancer Clinical trials—vaccine, other monoclonal antibodies

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COMPARISON OF ULCERATIVE COLITIS & CROHN'S DISEASE REC****

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Etiology of both disease processes are unknown Both diseases have a genetic and geographic component a. Genetic 1. American Jewish people of European descent are 4-5 times more likely to develop either disease 2. Increase in IBD in African Americans 3. Lower prevalence rates of IBD in Asians & Hispanics b. Geographic 1. Occurs more frequently in US & northern European nation

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COMPARISON OF ULCERATIVE COLITIS & CROHN'S DISEASE do not memo

answer

One million Americans have IBD Peak incidences of IBD are between 15-35 years of age Chronic recurrent disease processes Physiological & psychological stresses play a role in the exacerbation of the disease Factors that play a role of development of IBD a. Infectious agents & altered immune responses b. Autoimmune process c. Lifestyle factors-Smoking d. Family history

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ULCERATIVE COLITIS: what is the most vital issue?

answer

1. Definition: Chronic, inflammatory bowel disorder that affects mucosa & sub-mucosa of colon & rectum Results in loose stools containing blood & mucus Poor absorption of vital nutrients & thickening of colon wall can result : NUTRITION VITAL ISSUE Tenesmus—unpleasant & urgent sensation to defecate (are afraid to leave the house or know wher br are) Associated with periodic remissions & exacerbations Increased risk for colorectal cancer d/t chronic inflammation/irritation

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ULCERATIVE COLITIS

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(portion of colon is affected; more systemic affects with chrons)

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ULCERATIVE COLITIS PATHO

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Diffuse inflammation of intestinal mucosa with resultant loss of surface epithelium & possible abscess formation with tissue damage; may be confined to large intestine (entire or portion) Usually begins in rectal area & progresses proximally towards cecum Usually confined to rectum & sigmoid colon in most patients. May progress to entire colon

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UC Stages

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Pathophysiology (cont) d. Acute stage: epithelial cell damage & loss which leave areas of ulceration, redness & bleeding e. Chronic stage: fibrosis, retraction & hypertrophy of bowel, colon is narrower & shorter with deposits of fat & fibrous tissues. -Dysplastic*** changes to surface epithelium & these changes are associated with an increased risk of colon cancer

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UC Clinical Manifestations

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a. Predominant signs & symptoms** 1. Diarrhea 2. Abdominal pain 3. Nocturnal diarrhea 4. Tenesmus=urgency b. Mild colitis 1. Characterized by < 4 stools/day with or without blood and/or with or without mucus 2. Could be asymptomatic. Lab values WNL (ex. No bleeding no affect on HCT)

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Clinical Manifestations Moderate Colitis

answer

Characterized by > 4 stools/day with or without blood 2. Minimal sxs—mild abdominal pain, intermittent nausea 3. Possible increased CRP/ESR (inflammation)

question

Clinical Manifestations Severe Colitis

answer

Characterized by > 6 bloody stools/day Rectal inflammation, tenesmus, LLQ cramping relieved by defecation Fatigue, fever, anorexia, weakness, anemia, hypovolemia, & tachycardia DEFINITE Elevated CRP and/or ESR

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Clinical Manifestations Fulminant Colitis

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Characterized by > 10 BLOODY stools/day Anemia may require transfusion, Colonic distention on x-ray, *systemic manifestations***—arthritis, skin & mm lesions, uveitis (inflamm vascular layer eye), thromboemboli & gallstones

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Clinical Manifestations (cont) Psychological Manifestations

answer

Apprehension a. Frequency of stools, inability to control diarrhea, presence of blood b. Eating may be associated with pain, cramping & frequency of stools 2. Anxiety a. Limitation of patient's activities outside the home, fear of fecal incontinence resulting in feeling "tied to the br

question

CROHN'S DISEASE

answer

Definition: *CAN AFFECT BOTH LARGE/SMALL INTRESINES OR ANY WHERE ALONG ENTIRE GI TRACT* Inflammatory disease of the small intestine @ terminal ileum (most often)—chronic & relapsing Slow, progressive, unpredictable & recurrent disease with involvement of multiple regions of the intestine with normal sections inbetween—*called "skip lesions" cobblestone appearance; do not have white ulcerations on x-ray*

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CROHN'S DISEASE PATHO

answer

Begins with small inflammatory aphthoid lesion (shallow ulcer with a white base similar to a canker sore) of the mucosa and submucosaof the bowel These beginning lesions may regress or the inflammatory process will progress to all layers of intestinal wall (transmural) which creates a thickened bowel wall=fibrosis

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PATHO CHRONS CONTD

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Bowel wall has a cobblestone appearance due to strictures & deep ulcerations which predispose patient to developing bowel fistulas, abscesses & local obstructions (deep ulceration/fistula will predispose to INFECTION) =severe diarrhea, *malabsorption of vital nutrients & anemia is common usually from iron deficiency or malabsorption of nutrients (more severe malabsorption with more involvement of GI tract; esp if Chrons is in SMALL int. bc it absorbs most nutrients) =Patients with Crohn's can become very malnourished & debilitated*

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CROHNS Clinical Manifestations

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GI : Diarrhea—if disease in ileum—5-6 times/day, liquid/semi-formed, Abdominal pain NOT with defecation, *Steatorrhea, typically does not contain blood (more common in colitis)* Low grade fever—common with fistulas, abscesses & severe inflammation Weight loss, bowel sounds may be decreased/absent with obstruction or severe inflammation Anorectal lesions—fissures, ulcers, fistulas,abscesses

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Other Manifestations Crohns

answer

2. Tenderness, guarding, palpable mass in RLQ, N/V, epigastric pain if stomach & duodenum involved 4. Fluid & electrolyte imbalances from malabsorption c. Psychological symptoms: Assess coping skills—chronicity of disease & troublesome complications become a problem

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DIAGNOSTICSCOLITIS & CROHN'S

answer

Laboratory a. CBC b. *Serum levels of folic acid & vitamin B12 (because not absorbing it; worse in chrons)* c. Albumin levels d. C-reactive protein & ESR e. Serum chemistry f. Urinalysis g. *Stool examination for mucus & blood & cultures to rule out infection (C-diff, CMV)*

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DIAGNOSTICS COLITIS & CROHN'S: what gives the definitive diagnosis?

answer

1. Abdominal X-rays—shows narrowing, ulcerations, strictures & fistulas 2. Abdominal ultrasound 3. CT Scan 4. Sigmoidoscopy *Colonoscopy—biopsy of tissue verifies the diagnosis—most definitive****+ BIOPSY* *Barium enema—may show differences between colitis & crohn's, identify complications, mucosal patterns & the distribution & depth of disease involvement*

question

Common in Colitis Comps (3)

answer

Hemorrhage Toxic Megacolon= Motor paralysis of colon (fever, tachycardia, hypotension, dehydration, abdominal pain) Perforation=bowel contents spill into peritoneum, Bleeding erodes abdominal wall; Leads to peritonitis; Increased risk if toxic megacolon is present

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Common in CROHNS Comps Contd

answer

Abscess formation *MAIN CONCERN IS INFECTION*=Localized pockets of infection develop in ulcerations—can occur from fistulas (chills, fever, abdominal mass) Bowel obstruction=from toxic megacolon or cancer, repeated inflammations—scarring of bowel (abdominal distention, N/V, cramping)

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Common in Colitis Comps Contd

answer

Fistulas=May be asymptomatic if between loops of bowel; Occurs between bowel & bladder—pyuria & fecaluria Malabsorption (more in chrons due to small intestine involvement) Cancer=Risk greater in colitis esp when there is a 10 year history; Colorectal cancer seen with colitis & colon cancer with crohn's

question

Extraintestinal/systemic complications: more common in?

answer

*more common in chrons* Arthritis, Osteoporosis, Hepatic & biliary disease, Oral & skin lesions, Ocular disorders—iritis

question

TREATMENTCOLITIS & CROHN'S

answer

1. Goals of Treatment a. Achievement of remission—induction b. Prevention of disease flare-ups—maintenance 2. Nonsurgical Management a. Drug therapy—Step Wise Therapy

question

Step One Treatment of Colitis and Crohns: more effective in?

answer

Aminosalicylates 5-aminosalicylic acid (5-ASA) 1. Treat flares and/or maintain remission—effective in 2-4 wk 2. *Appears to be more effective in colitis*; Mechanism of action unknown, but thought to have an anti-inflammatory effect by inhibiting prostaglandins

question

Aminosalicylates: what is NOT effective in Crohn's?***

answer

Drugs in this category: sulfasalazine (Azulidine, Azulidine EN) mesalamine (Asacol, Asacol HD, Pentasa) balsalazide (Colazol) olsalazine (Dipentum) **Mesalamine is not effective in Crohn's**

question

Treatment Colitis and Crohns Step 2: more effective in?

answer

Corticosteroids (do not want long term d/t side effects) = Anti-inflammatory agents, Used during exacerbations; taper during remissions *More effective in Crohn's Most commonly used is Prednisone & Budesonide*— delayed release of high concentrations of corticosteroids to terminal ileum and (R) side of colon

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Treatment of Colitis and Chrons Step 2 Part 2: more effective in?

answer

Immunomodulators—alter the immune response (may use earlier prevent complications, maintain remission, improve outcomes) Used when patients not responding to other treatments and/or if patient is on steroids too long; May have a synergistic effect with steroids to shorten healing time, Slower onset of action Maybe more effective in colitis

question

Treatment of Colitis and Chrons Step 3

answer

Infliximab (Remicade)—monoclonal antibody; Decreases bowel inflammation, promotes mucosal healing & heals fistulas *Most effective in Crohn's, but may be used for refractory colitis/toxic megacolon* Three (3) separate infusions for induction of remission at weeks 0, 2 & 6 followed by infusions q8 weeks for maintenance; *Pre-treat patient with Tylenol & Benadryl* SE (uncommon) hypersensitivity & flulike symptoms

question

Step 3 Additional monoclonal antibodies-

answer

b. natalizumab (Tysabri)—IV—Prevent accumulation of lymphocytes in diseased bowel c. adalimumab (Humira)—SQ injection q2 weeks after loading dose of 6 injections over 4 weeks d. certolizumab (Cimzia)—SQ q4 weeks

question

Treatment Colitis and Crohns Step 4 (4)

answer

Clinical trial agents—Thalidomide & Interleukin Anti-diarrheals—diphenoxylate & atropine (Lomotil) & loperamide (Imodium) PPIs—Protonix, Prilosec, Nexium, Aciphex; H2 Antagonists—Pepcid, Tagamet, Zantac Antibiotics—*metronidazole (Flagyl)—has anti- inflammatory effects. ciprofloxacin (Cipro) is the alternative (abscess /other infection)*

question

Nonsurgical Management Nutrition therapy IBD: Nutrition therapy

answer

Severe disease—patient *NPO with flare up to give rest & started on TPN, reduce lactose* Less severe symptoms—elemental formulas such as *Vivonex (proteins/nutrients)* Significant, but less severe symptoms—*Low residue diet/low fiber (Although fiber can help thicken stool, may not help with diarrhea)* Reduce /eliminate Caffeine, pepper, alcohol, smoking, common GI stimulants

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Nonsurgical Management Rest

answer

to reduce intestinal activity, provide comfort & promote healing d. Complementary & Alternative Therapies (not used for acute exacerbation) 1. Herbs—flaxseed, selenium, vitamin C 2. Biofeedback 3. Hypnosis 4. Yoga 5. Breathing exercises

question

Surgical Management Crohns (4 types)

answer

-Portion=colectomy + anastamose -Permanent colostomy= make sure stoma is pink, shrinks in size in 6-8 weeks, use of bag -Hartman's procedure= form stoma, remove diseased part, temporary colostomy, reattach back after rested -J pouch=create rectum, temporary colostomy, attach intestine that is left->anus (more liquidy, no stoma)

question

Surgery Goals IBD

answer

Depends on primary disease process & portion of bowel affected b. Surgery only performed when necessary for complications of disease or failure of conservative treatment measures c. Bowel obstruction is leading indication for surgery in Crohn's d. Goal—preserve as much bowel as possible

question

Total Colectomy With Ileostomy

answer

for extensive ulcerative colitis—removal of colon, rectum & anus with permanant stoma 1. Indications—bowel perforation, toxic megacolon, hemorrhage, cancer, failure of conventional treatment & colon cancer

question

Total Colectomy With Ileostomy: progression of stool, what does the small intestine start doing?

answer

Initially after surgery output is loose, dark green liquid that may contain some blood. Over time, stool volume decreases, becomes thicker & turns yellow-green or yellow-brown because the small intestine begins to perform some of the functions of the colon including absorption of increased amount of sodium & water

question

J Pouch

answer

(same as J pouch) Entire colon and rectum is removed, a pouch is formed from the terminal ileum and the pouch is brought into the pelvis and anastomosed to the anal canal A temporary or loop ileostomy may be formed to eliminate feces and allow tissue healing for 2-3 months—may then be reversed & restores elimination through anus; Patient will have 6-8 daily bowel movements through the anus

question

Total Colectomy With Continent Ileostomy-Kock's Ileostomy/Pouch

answer

(same as colostomy but theres a valve with catheter to drain instead of a bag) 1. Intra-abdominal reservoir constructed from the terminal ileum where stool is stored via a nipple-like valve in the pouch until the patient drains it by using a catheter *Immediately after surgery, an indwelling urinary catheter is placed in pouch & is connected to low intermittent suction & irrigated as prescribed* *Initially pouch holds 50-75 ml. Over time it stretches and can hold 500-700 ml. When pouch needs to be emptied, patient has a sense of fullness; Pouch is drained several times a day* 4. Monitor quality of drainage and teach patient to drain stoma

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Ileoanal Reservoir/J Pouch again...

answer

"J" pouch—spares rectal sphincter & eliminates need for ostomy Colon removed & ileum is sutured into rectal; stump to form a reservoir More liquid stool, j pouch enlarges over time, no stoma

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TREATMENTCOLITIS & CROHN'S: post op

answer

NPO with nasogastric tube with suction for 1-2 days Teaching ostomy care; Drainage begins to slow down after about a week & becomes thicker Ileostomy should begin to drain within 24 hours after surgery *MAIN PROB: Fluid & electrolyte replacement should be 500 ml+ each day to prevent dehydration (more water than stool & unable to absorb enough nutrients)*

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