AMS Exam 3 11.18.08

-comfort
-nutrition
-fluid & electrolyte imbalances
-elimination
-activity tolerance
-neurological changes
-exposure to possible causative agents

-pain
-pruritis: discomfort usually r/t ascites. Fluid around intestines puts pressure on other organs. Itching is common.

-Anorexia: may lose appetite
-N/V
-pain w/ eating fatty foods: esp w/ gallbladder probs
-weight loss, malnutrition
-true weight loss may be hidden w/ ascites: look normal in other parts of body but may have large abdomen
-alcohol use/abuse: may be very malnourished by the time they come in bc don't want to come in bc of alcohol abuse

-vomiting, bleeding
-renal retention bc of sodium & water (has the pt noticed any edema?)

-stool color: may look clay-colored bc don't have bile coming 4m gallbladder
-urine color: may be dark bc bilirubin being excreted in urine, almost brownish color
-blood in stool: black, tarry stools or frank blood
-steatorrhea

W/ significant liver dz usually have neurological probs, not coherent. Ask fam if any changes in mental status, memory changes, etc. Usually caused by a build-up of ammonia.

-toxins
-infectious diseases (hepatitis)
-substance abuse, drugs, ETOH
-industrial chemicals
-viruses
-Tylenol (how much using, taking per day? max is 4 gm/day)
-blood transfusion history or other bld products (or have they ever been rejected as a blood donor)

-appearance, skin
-neurological
-abdomen

-color (jaundice),edema,ascites,
bruising,spider angiomas: often seen in pts w/ liver dysfunction, czed by high estrogen content in body, will see in trunk

-VS
-weight
-skin turgor
-edema

-fluid wave: have so much ascites when tap abdomen,can see a wave of fluid go to the other side. usually done by doc
-tender or enlarged liver
-abdominal girth: mark skin so everyone is measuring skin in same place
-ask pt have you noticed changes in way clothes fit?

-albumin: manufactured in the liver, must have normal intake of protein in diet so liver can make albumin. Low albumin could be nutrition/liver prob or strictly liver prob.

-increase in direct bilirubin sign of liver dz: usually late sign, damage is usually non-reversible by this point

will show up earlier than bilirubin as an indicator of dz. Simply a marker of liver infl.
-AST: (SGOT) - liver heart, skeleton
-ALT: (SGPT) - most specific for liver (pt def has liver damage is this is elevated)
-GGT - liver, kidneys (elevated)
-alkaline phosphatase - obstruction in biliary tree, bone disease

expect these to be high bc have lost ability to clot blood

elevated late in disease

see if are a hepatitis carrier

to dx esophageal varices
-CT/MRI/ultrasound

diagnostic & as a txment. Can draw fluid off from abdomen if have ascites to help w/ comfort, can also analyze to check for tumor cells. Is mostly a palliative measure bc once liver is destroyed, fluid will just re-accumulate
-lose protein & K (when removing fluid from abdomen), danger of infection, bleeding

will be done on ppl w/ Hep B/C when contemplating to see how advanced dz is.
-risk of bleeding
-VS frequently
-lie on affected side w/ pressure dressing
-Bed rest for 24 hrs

-most recover normal liver function: regardless of the cz. Usually Hep A.
-chronic persistent hepatitis: Hep B or Hep C,person who doesn't clear the virus but it doesn't cz ongoing destruction of liver. Are contagious to others but will not have liver cancer, failure, etc.
-chronic active hepatitis: hep B or hep C, virus over time czs destruction of cells & damage that is not reversible.
- may develop cirrhosis,liver failure or liver cancer.

-may be subclinical inf. Infectious to other chronically but they don't remember being sick,jaundiced,feeling bad.
-fever,chills,malaise,anorexia,N,V (most common)
-R upper quadrant pain: when liver is inflamed/tender
-elevated liver enzymes, elevated bilirubin (may see in acute hep)
-jaundice, dark urine, clay colored stool
-pruritis
-antigen antibody tests for hepatitis (only way to know for sure is to do lab tests)

-depends on the type of hepatitis
-pruritis: give antihistamines
-N/V: give antiemetics
-bleeding: most commonly give vitamin K
-alcohol avoidance
-rest, adequate nutrition: to help heal liver
-watch drugs metabolized by the liver: watch closely for SE, overdose,esp in sedation type meds bc metabolized in liver.

-activity intolerance
-fluid deficit
-nutrition: may be nutritionally depleted bc of substance abuser
-skin integrity: skin may not heal bc of substance abuse
-bleeding
-potential for drug toxicity
-transmission to others: educate! sex partners need to be tested/vaccinated
-education regarding transmission,meds (bc of all the SE)

95% of adults who get Hep B resolve inf
-produces lasting immunity, can never get Hep B again
-1% fulminate and die of acute liver failure
-rest to become chronic carriers: never produce antibody to virus
*70-80% chronic persistent
*20-30% chronic active, 5 yr mortality 50%, over time cirrhosis, cancer, liver failure

kids more likely to become chronic carriers if exposed to virus. Prob bc aren't healthy enough at birth to clear the virus.
*90-95% become chronic carriers
*only 5-10% resolve the inf

-children
-steroid dependent (bc depresses immune system)
-male
-high viral load

+anti-HBC (core): first to appear in both those that clear & those that become chronic carriers
+anti-HBSAG (surface antibody): indicates person has resolved or will resolve infection. Will have this if vaccinated against Hep. B.
+HBSAG (surface antigen): 2 tests 6 months apart indicates chronic carrier

-Same as HIV
-Post-exposure HBIG (w/in 2 wks)
-Hep B vaccine (Engerix-B, Recombivax HB)
*must get those vaccinated that will be missed due to age when universal vaccination was started
*Twinrix is Hep A & B vaccine together
-check all pregnant women for Hep B surface antigen so infant can be treated
-vaccinate sex partners of chronic carriers

-45% of blood
-originate 4m single stem cell
-formation stimulated by erythropoietin from the kidneys

-bone marrow
other sites: lymph nodes, thymus, spleen

-transport oxygen
-live 120 days
*liver,spleen break them down
*iron is recycled,bilirubin is waste

-stem cells (origin of RBC)
-bone marrow
-adequate amts of iron
-B12,FA,protein,B6, copper (from nutrition)

-usually production & destruction equal each other.
*if loss exceeds prod, decr O2 stimulates the kidney to release EPO & bone marrow is stimulated

-immature RBC
-normal amt is 1%

-anemia
-jaundice
-bleeding

-prior illnesses,chronic illnesses
-surgeries
-transfusions
-liver disease
-renal disease
-Meds (GI irritants, anticoagulants, chemo)

-employment, exposure to toxins
-ETOH
-nutrition: esp. vegan vegetarians bc don't get enough B12 bc it's from meat
-effects of sx on ADL

SOB,fatigue,palpitations,pruritis,fever,
bleeding,pain,confusion,neuropathy,
sore tongue (only thing that could cz
this is pernicious anemia)

-skin color: pallor,jaundice,integrity,bruising,
petechiae
-BP,pulse,resp (incr), murmur
-enlarged liver, spleen
-smooth,sore tongue
-pain
-neurological symptoms
*depression,syncope,confusion,
H/A

-RBC 4-6 million, Hgb 13-16, Hct 40%
*increased by: dehydration, high altitude, chronic hypoxia, polycythemia
*decreased in anemia,fluid overload,recent blood loss

-Ferritin measures free iron in plasma (assesses iron stores)
-Transferrin: protein that transports iron
-TIBC: incr in iron deficiency
-serum iron,B12,folate (folic acid) levels
-pernicious anemia studies

-AA normal adult hemoglobin
-all have a small amt of A2
-all have a small amt of fetal hemoglobin

-consent
-sedation
-note clotting studies
-equipment
-lab

-site
-prep
-procedure
-post-procedure

-pressure, observe for bleeding
-LOC, respiratory status

-anemia is more often a symptom rather than a disease unto itself
-think cancer, especially along the gut/colon & esp if pt > 50

-usually trauma,surgery,GI bleed
-symptomatic of loss > 500 mL
-SOB,fatigue,weakness,pallor,restless-
ness,hypotension,tachycardia,murmur
-severity of symptoms will correlate w/ degree of blood loss

-men:GI women: menses
-hypochromic,microcytic, low Se iron, high TIBC, low reticulocyte count

-decreased intake
-impaired absorption
-persistent loss

often absent until severe

-cause
-Fe supplement (how to take)

-macrocytic anemia
-FA, B12 levels (if take B12, pt will feel better w/in days. Sometimes to save $ will just administer B12 instead of performing expensive tests)
-Schillings test: B12 absorption (test that is specific to pernicious anemia)

-Replacement po (can just take B12 if PA is from being vegan/diet?
-Pt w/ PA must take B12
*by inj until levels are normalized
*can then use nasal spray (Nascobal) for maintenance.

-Usually associated w/ chronic inflammatory dzs, infections, ca, AIDS, Crohn's
-normochromic, normocytic anemai
-tx underlying cz

-phlebotomy
-anticoagulants
-hydration
-oral chemo agents
-bone marrow transplant

-aka ATP or ITP
-antibody directed toward the person's platelets
-prod of platelets is normal

-ecchymoses,petechia,bleeding,anemia
-IC bleed can cause neuro symptoms

-immunosuppressive drugs
-platelet transfusions
-splenectomy

-TTP
-disorder of platelet aggregation leading to a low platelet count
-autoimmune

-renal failure
-MI
-stroke
*fatal in 3 mo if not treated

-immunosuppression
-antiplatelet medications
-FFP

-usually develops after 5 days on heparin or sooner w/ past exposure to heparin
-about 5% of exposed pts develop HIT & up to 50% in selected pts (cardiac surgery)
-20% of HIT pts w/ thrombotic complications lose a limb
-about 30% die w/o alternative therapy for anti-coagulation
-occurs w/ LMWH also & heparin flushes for lines

-antibodies formed to heparin bind to platelets, the platelets form clots (also called white clots), & then are destroyed czing a drop in the platelet cnt (bleeding not usually a prob)
-a thrombotic state develops as a result of activation of procoagulant particles & and incr in thrombin generation

DVT,PE,MI,CVA,occlusion of limb arteries, end organ damage, skin necrosis & death can result

-If platelet count drops during or after heparin therapy (<150,000 or <50% of baseline) notify doc!
*IV heparin should have platelets done at least every other day, SQ form of heparin not as frequently
-no other cz for thrombocytopenia is IDed
-lab tests done

-functional assays detect platelet activation
-antigenic assays detect antibody binding to the heparin complex

-heparin is stopped
-alternative anti-coagulation therapy started
-nurse must monitor
-Epoetin alfa

Argatroban
-only for IV administration (used when want to stop heparin as alternative anti-coagulant therapy)

must monitor labs & observe for signs of thrombus formation in any organ system in patients on heparin products (renal dysfunction common as well as small vessels in legs)
-watch BUN/creatinine

(Procrit, Epogen)
-indicated for the tx of anemia r/t chronic renal failure (very common), drug side effect (AZT), chemotherapy, & to reduce the need for transfusions. Used commonly in anemic pts or in pts who are on meds that cz anemia (chemo)

-stimulates erythropoisis in the bone marrow

-administered SQ or IV
-usually 3x a week, onset 10 days, peak 2-6 weeks

-allergy to albumin
-uncontrolled hypertension (if stimulating RBC prod are actually stimulating blood vol increase so would make hypertension worse)
-Drug interactions: may increase the requirement for heparin

-monitor BP before & throughout tx
-monitor for signs of improving anemia
-notify MD if BP elevated or HCT has reached normal levels

(fewer, larger cells) cells normal in color but large in size.
-folic acid deficiency
-B12 deficiency

(extra folic acid isn't much of a prob like extra iron is)
- ETOH abuse, meds, (anticonvulsants) things that antagonize folic acid, pregnancy (NTD)
S/S: anemia

will have more nervous system symptoms bc B12 is necessary for nervous system.
- Diet (vegetarian), pernicious anemia (autoimmune disorder where person makes antibodies against intrinsic factor which is necessary to make B12. Can't absorb B12 4m food w/ this), stomach surgery, malabsorption

peripheral neuropathy, mental status changes, dementia, depression, sore tongue

-overgrowth of lymphocytes after release 4m bone marrow
-lymph nodes & spleen most common sites - solid tumors not cellular suspensions

-HL very curable in early stages, radiation, chemo

NHL 6th cz of cancer related deaths in US, also treated radiation & chemo

-any age: most common 20s & >50
-possible causes: viral, chemical agents
-1 node or node chain becomes cancerous (Reed-Sternberg cells) malignant cell that undergoes the changes. This cell is what they look for when doing biopsy.
-spreads to nearby lymph tissue then non-lymph tissue

-all lymphomas w/o Reed-Sternberg
-12 sub-types w/ great range of progression & survival rates
-most start in lymph nodes but can start in other tissues

-swollen, painless nodes most common presentation (anywhere in body)
-Dx by biopsy
-nursing intervention as in HL

-Supportive: if pt has persistent liver dz will not tx bc SE of meds are significant & would not help.
-chronic carrier w/ active dz
-Interferon: what body produces when exposed to virus. Prob is it has horrible SE.
-lamivudine (3TC,Epivir) HIV drug w/ activity against Hep B
-Entecavir (Baraclude) new: HIV drug w/ activity against Hep B
-only 50% respond, 25-40% sustained
-33% lose the E antigen: still consider this successful
-cost $2150 for 6-mo course
-liver transplant

mood swings, depression, flu-like symptoms (SE)

-most common blood-borne infection in the US
-most common cause of chronic hepatitis, liver cancer
-most common reason for liver transplant

-spread like HIV
-can be transmitted sexually & from mother to child but not as easily as HIV
-high risk behaviors

*IVDU, nasal cocaine, tattoos, hemodialysis, sexual, *blood transfusion before 1992
60% IVDU, 20% high risk sexual behavior, 4% HCW, 10% no risk factor id'ed

-complex virus w/ many genotypes
*genotype 1 most common in US & most resistant to tx
*will be difficult to make a vaccine: has a lot of different strains & it mutates
-rarely fulminant in nature
-2/3 have no symptoms
-1/3 have common hep symptoms (mild symptoms)
-#1 cz of cirrhosis, liver cancer, liver transplantation

-safe sex, needle exchange programs
-need for monitoring
-SE of drugs
-protect your liver, ETOH is poison!!!

etiology: hepatitis, alcoholism, malnutrition

-stop drinking
-hep prevention & tx when indicated

-eliminate or tx the cz
-anti-histamines for pruritis
-diuretics
-vitamins esp folic acid & thiamin
-low Na, high protein,high CHO, fluid restriction
-serum albumin
-paracentesis
-lactulose
-transplantation
-vaccinate against flu,pneumonia,hep A & B
-

-help get rid of some of fluids
-lasix
-spironolactone: diuretic used bc it antagonizes aldosterone bc retention of aldosterone is 1 of the underlying etiologies of the fluid retention.

high protein helps w/ ascites & repair of tissue. Once have significant damage will put on low protein diet bc of ammonia levels will contribute to neurological probs.
-protein restriction late in the dz when serum ammonia is elevated

common to tx ascites. Is blood prod.
Helps to pull fluid back into the blood vessels 4m abdominal cavity, extremities. The a few hrs afterwards will give diuretics to get rid of fluid in 3rd spaces.

(most common) type of laxative that accelerates the propulsion of feces by preventing ammonia 4m being absorbed into GI tract. Will have 3-4 soft stools/day & mental symptoms will usually begin to clear
-antibiotic that works on bacteria in gut. Works on ammonia absorption to lower serum ammonia levels.

-complication of cirrhosis of the liver
-incr pressure w/in liver czed by changes in liver not allowing normal bld flow. Bld backs up, spleen enlarges, bld vessels burst, esp around esophagus.

-splenomegaly
-ascites
-development of collateral circulation (esophageal varices)

diuretics, serum albumin, paracentesis, peritoneal-venous shunt
*allows for continuous reinfusion of ascitic fluid into the venous system

-mortality is 50% once have
-control bleeding (Sengstaken-Blakemore tube)
-drugs to decr portal pressure (inderal,vasopressin),
-sclerotherapy: burn or compress w/ heat to seal off the bleeding to cut it off
-surgical (TIPS procedure, surgical shunt, transplant)
*measures taken to decr bld flow thru the portal vascular system & decr portal hypertension

-Lactulose
-Antibiotics: neomycin metronidazole

-stores glucose as glycogen
-site of gluconeogenesis: making glucose out of fats & proteins
-makes plasma proteins such as albumin & clotting factors
-uses nitrogen to form nonessential amino acids from cholesterol, aids in fat metabolism which is an alternate form of energy

-Incubation averages 6-7 wks
-Immunity: there is no protective antibody response (like HIV) can have antibodies to Hep C but will not receive any immunity 4m these antibodies. Just mean that you are/have been infected.
-mutates like HIV
-75-85% will become chronic carriers
-slow progression to dz states
*10 yrs cirrhosis
*20 yrs liver failure
*30 yrs liver cancer

-1/3 will not progress to liver dz & LFTs will be normal: so will be chronic/persistent carriers of Hep C
-2/3 will have abnormal LFTs & will have chronic active hep
*20-40% will develop cirrhosis
*1-5% will develop liver cancer
-transmission 4m mother to infant occurs in about 5% of chronic carriers
-sexual transmission < HIV

-if LFT's normal, monitor (tx may be offered)
-LFT's tend to rise & fall as a natural history of the inf
-if LFT's elevated referred for liver biopsy & tx is considered
-vaccinate against A & B

-tx w/ multiple drugs like HIV, 30-40% respond: usually 2 drug combo
-12 mo of txment
-goal is undetectable viral load
-Interferon, new pegylated interferon

(Intron A): usually used
-SC injection 3 times/wk for 12 mo
-contraindications to txment are significant depression, autoimmune dz, & estab cirrhosis
-czs flu-like syndrome
-monitor for pancytopenia, depression (anti-depressants used to tx)

(Peg-Intron, Pegasys)
-given once a week

(Rebetol, Copegus)
-used commonly in combo w/ interferon
-po med
-czs a hemolytic anemia in all pts: 2-3 g drop in hemoglobin. Monitor for tachycardia, pallor, activity intolerance, Signs of anemia.
-average 2-3 gm drop in hemoglobin
-teratogenic (extremely)
-recommended that both women & men use 2 forms of contraception during & for 6 mo after D/C

-diffuse infl & fibrosis of the liver resulting in decr liver function. Over time liver changes result in obstruction of hepatic bld flow results in hypertension. Indicates incr in pressure.
-liver has a remarkable ability to regenerate itself w/ similar tissue; however when the damage is repeated or continued normal liver cells are replaced w/ connective tissue: cirrhosis

-fatty infiltration is first alteration seen & is reversible if causative factor is removed
-repeated insults cz fibrotic changes
-obstruction of hepatic blood flow: edema, ascites, splenomegaly,esophageal varices,hemorrhoids
-3/4 of liver function gone before physiological function is altered

-altered serum proteins:albumin decr,low blood glucose
-altered clotting
-altered metabolism of drugs, hormones: estrogens, aldosterone
-hypoglycemia
-altered protein, fat metabolism
-buildup of waste products (bilirubin, ammonia)

-Elective procedure so patient should be in prime condition-stop smoking, improve nutrition, control other conditions (diabetes, hypertension, cardiac)
-Improve oral hygiene to decrease post operative infection-good oral care, visit the dentist, remove any dental cavities, will receive antibiotics pre operatively
-Patient teaching-what to expect post operatively
-Emotional support

-Nutritional support-care of patient with TPN or tube feedings, weight patient daily, calorie counts, keep HOB elevated after meals, thicken liquids, assess for aspiration
-Swallowing support-lollipop will improve tongue strength, offer food with head in chin tuck position, place food in back of mouth, check to be sure patient is not pocketing food in cheeks, monitor for aspiration, elevate HOB when eating
-Chemotherapy-nursing care as we discussed in the cancer lecture related to a patient receiving chemo
-Radiation-nursing care as we discussed in the cancer lecture related to a patient undergoing radiation treatment

-Patient will need nutrition support
-Speech therapy for swallowing therapy
-Chemotherapy-has only been moderately effective
-Radiation-has only been moderately effective
-Photodynamic therapy-used as palliative therapy only
-Esophageal dilation
-Esophagectomy
-Esophagogastrostomy
-Minimally invasive esophagectomy (MIE)

-diet will be what patient can tolerate at the time, may need supplements, may need feeding tube or TPN

dilates the esophagus to provide temporary relief to dysphagia, stents may be inserted to keep the esophagus open

surgical procedure to remove all of the esophagus

-surgical procedure to remove all of the esophagus and part of the stomach

removal of esophagus via laparoscopy-not done often

-respiratory care
-cardiovascular care
-Monitor for atrial fibrillation which may develop due to irritation of the vagus nerve during surgery.
-If in ICU would need to monitor hemodynamics-cardiac output, cardiac index, etc.
-Wound care
-NG tube mgmt
-nutritional care

highest priority, may be on ventilator, T, C and DB, q 2 hours, assess breath sounds, semi fowler’s to high fowler’s position, oxygen therapy, oxygen saturation levels, Chest tube care if applicable

assess for hypotension which occurs due to pressure that may have been placed on the heart during surgery, administer IV fluids to combat hypotension but monitor for signs of fluid overload (you know what they would be)

support incision lines to prevent dehiscence (do you remember what that is?), assess for infection at incision line, assess for leaking at the surgical site (inside the body), assess for signs of shock

DO NOT REPOSITION THIS NG TUBE, monitor for patency, keep taped in place, assess drainage color and amount, drainage should be greenish yellow in color, provide oral hygiene

initially feedings are usually via a jejunostomy tube and are started slowly, if giving feedings by mouth eventually need to continue to monitor for signs of aspiration, feed patient with head of bed elevated, give 2 small meals instead of 3 large meals daily, drink fluids inbetween meals and not with meals, may need to control post eating diarrhea with loperamide (Imodium)

-Assessment of patients at risk: increased ingestion of pickled foods, salted fish/meat, nitrates; H. pyloric infections, pernicious anemia, gastritis, achlorhydria; family history; previous gastric surgery or polyps
-Labs-decreased hemoglobin and hematocrit, decreased iron levels, stool positive for occult blood, hypoalbuminemia, abnormal live function tests, elevated CEA
-Upper GI series/CT scan
-EGD-definitive (see information under esophageal cancer)

-Depends on how advanced the disease is
-Chemo-unlikely
-Radiation-unlikely
-Surgery-preferred treatment option-usually will have a total gastrectomy (removal of the entire stomach) or partial gastrectomy (removal of part of the stomach). Will be done either as a Billroth I or Billroth II (discussed last year with peptic ulcer disease.

-Preoperative teaching-same as for any abdominal surgery
-Post operative-same as for any abdominal surgery
Monitor for dumping syndrome-(remember we discussed that last year under peptic ulcer disease)- signs and symptoms-vertigo, tachycardia, syncope, sweating, pallor, palpitations, desire to lie down. -Symptoms usually occur 30 minutes after eating. Dumping syndrome occurs due to the rapid emptying of food into the small intestines. Can be minimized by eating small meals more frequently and by not drinking liquids and eating solid foods at the same time.
-NG tube-DO NOT REPOSITION THIS NG TUBE
-Provide emotional support-patient may be terminal-quality of life important

-CEA lab monitors this disease (should initially be elevated and then will be decreased as treatment is initiate, CEA is monitored after treatment to determine if cancer comes back because the CEA would go up again)
-Patient education is important especially related to dumping syndrome

This is cancer of the colon or rectum which may develop anywhere along the bowel usually from the epithelial lining. These tumors often develop from precancerous polyps (screening for this is important). Metastasis occurs because the cells/tumor spreads into neighboring organs or via the blood stream or lymphatic system.

-Symptoms will depend on location of tumor
-Rectal bleeding-common
-Hematochezia
-Anemia-common. Due to blood loss
-Change in bowel habits/stool
-Abdominal cramping/feeling bloated
-May have a palpable or visible abdominal mass
-May have signs of bowel obstruction

Bleeding may or may not be visible to the naked eye.
-common

passage of red blood through the rectum

common. May become constipated, may strain to have BM, stools may narrow (pencil like)

If tumor on right side of colon-symptoms may not be as noticeable (remember the waste products are very liquid on the right side of the colon)

initially high pitched hyperactive bowel sounds as peristalsis tries to push the obstruction out-but then progressing to absent bowel sounds as the peristalsis gives up

-Patient history
-Labs
Positive test for occult blood in the stool (fecal occult blood test or FOBT
-Barium enema/CT scan
-Colonscopy-definitive

decreased hemoglobin and hematocrit, elevated liver function tests with liver metastasis

May be false positive, should have more than one positive result with other diagnostic tests confirming the diagnosis of cancer

-Depends on the extent of the disease but surgery is the primary treatment which may be done alone, with radiation or with chemo
-radiation
-chemo
-Surgical procedure will depend on location and extent of tumor
-Colon resection
-Colectomy
-Abdominoperineal (AP) resection
-May have surgeries done laparoscopically in some cases

-tumor is removed (with some extra to ensure that all cancer was removed) and the colon is sewed back together. NG can be moved in colon resection bc tube is not in contact w/ suture line. NG tube can be removed when bowel sounds heard.

-colon is removed and a colostomy is created which maybe temporary or permanent

removal of sigmoid colon, rectum, and anus through abdominal and perineal incisions

-Make sure patient understands the procedure he is having (will he have a colostomy, will it be permanent or temporary, will it depend on what the surgeon finds)
-Get the ET nurse involved-stoma location
-Will need a bowel prep to decrease chance of post operative infection
-Explain post operative routine-same as for other abdominal surgeries-T, C, DB, ambulate, SCD hose, NG tube (this NG could be reposition), NPO until bowel sounds return, IV fluids

-prevent respiratory probs
-NPO
-NG tube
-stoma care
-drain/tube care

-supplemental oxygen, o2 sats, T, C, DB, get up and moving

listen for bowel sounds, get up and moving, progressive diet (clear liquids, to soft to regular)

ensure patency, monitor bowel sounds, measure output, assess drainage

(if colostomy done) Assess the color of the stoma (should be shiny, pink, healthy looking, if not call the doctor). Assess the drainage from the ostomy (drainage from the right side of the colon will be liquid and will require a bag over the stoma all the time. Drainage as you move across and down the colon becomes more solid and patients can sometimes control the evacuation of stool). Be careful not to let the drainage from the ostomy come in contact with the patient’s skin (very irritiating). Empty the ostomy bag as needed and observe the contents

may have a hemovac or Jackson pratt drain in (remember we talked about them last year). Make sure that suction is maintained and that the drainage is measured and assessed

An inability to absorb nutrients due to flattening of the mucosa of the small intestines. May involve deficiencies of bile salts, enzyme, presence of bacteria, changes in the lining of the small intestines, or changes in lymph or circulatory system

Symptoms depend on the nutrient that is involved.
Diarrhea-common
Steatorrhea ( fat in stools)-common
Weight loss
Bloating and flatus
Easy bruising
Anemia
Bone pain
edema

-Lab tests which show anemia, decreased Hemoglobin and hematocrit, decreased iron levels, decreased levels of selected vitamins, decreased albumin/protein (again depends on the nutrient that is involved)
-Biopsy via endoscopy (again depends on what they are looking for)

-Depends on the nutrient involved
-Avoid dietary products that cause the problem or supplement the nutrient lost
-May have surgery (depends on the what is causing the problem)
-May be on antibiotic therapy-depends on what is causing the problem
-May be on antidiearrheal meds or anticholineergics agents-depends on what is causing the problem

-Leukoplakia
-Erythroplakia
-Unusual thickening or lumps on the buccal mucosa
-Sore that does not heal
-Soreness, pain or burning sensation
-Pain that radiates into the ear-advanced
-Enlarged lymph nodes-spread

-premalignant lesion, thickened, white firmly attached patches on the oral membranes (can be differentiated from Candidiasis because these lesions will not scrape off while Candidiasis lesions can be scraped off)

red, velvety mucosal lesions on the oral mucosa (often are difficult to tell the difference between this and inflammation if lasts for a long time, should get looked at) Both erythroplakia & leukoplakia are pre-cancerous lesions. Must get checked out.

-Patients risk factors-tobacco use, alcohol consumption, sun exposure, certain occupations
-Patient assessment
-CT scan-tells about spread
-Biopsy-definitive

-Airway management-highest priority. May need trach
-radiation therapy
-chemo
-surgery

Oral cancers are one of those cancers that can be treated with internal radiation. Remember time, distance and shielding

small lesions can be removed in out patient surgical units. Larger lesions require more extensive surgery and admission to the hospital. Surgery may involve the removal of all or part of the tongue, mandible, and palate. May be done with a radical neck dissection

-Airway management-highest priority. Both preop and post operatively
-Assess for aspiration
-Provide good oral hygiene
-Pt education preoperatively
-Pain control-postoperatively
-Nutritional support

Airway management-highest priority. Both preop and post operatively
Assess breath sounds, respiratory rate, oxygen saturation level
Provide trach care if patient has one
Manage secretions-have suction available
Position in semi fowlers or high fowlers position
Increase fluids to loosen up secretions
T, C, DB

Eat in sitting position
Thicken liquids
Feed in small amounts
Have suction ready

soft toothbrush, no commercial mouthwashes, no lemon and glycerin swabs

make sure patient understands what their surgery is going to involve

post-operatively-NPO initially, may need tube feedings, TPN, assess for aspiration, monitor weight/calorie count, nutrition supplements,

Make sure the patient knows that with the trach they may not be able to talk, have an alternate form a communication available for them
Discharge instructions
Ongoing dental care
Suction machine at home
Explain to patient that their tastes may change
May need to thicken liquids
Assess ability to swallow/assess for aspiration
Inspect oral cavity/good oral hygiene