nursing 4 week 6 (hepatic)

prevention and manage of Hep A

*good handwashing*, safe water, proper sewage disposal. *vaccine* If not vaccinated get IGG for contacts to get passive immunity, lasts 6 - 8 weeks Bed rest during acute stage *Nutritional support: fluids, protein, calories* proper home sanitation, individual hygiene, safe food prep, mandatory reporting of the disease, recommend vaccines esp- travling out of country, male having sex with male, illegal drug users, recipients of pooled plasma products. vaccine for community outbreak Adults, 2 part vaccine before travel Kids get 3 part vaccinations

assessment ascites

* Record abdominal girth and weight daily * Patient may have striae, distended veins, and umbilical hernia from increased pressure * Assess for fluid in abdominal cavity by percussion for shifting dullness or by fluid wave * Monitor for potential fluid and electrolyte imbalances. hypovolemia and low potassium contribute to encephalopathy Give Potassium if low. HOB 90 deg to promote breathing, SOB from enlarged abd.

Hep A

*Fecal-oral transmission Travel to developing country* Spread primarily by poor hygiene; fecal-oral route, close contact, or through *food and fluids *(shellfish from sewage contaminated water) Incubation: 2-6 weeks Illness may last 4-8 weeks Mortality is 0.5% for younger than age 40 and 1-2% for those over age 40 *Manifestations: mild flu-like symptoms, low-grade fever, anorexia, later jaundice and dark urine, indigestion and epigastric distress, enlargement of liver and spleen* Anti-HAV antibody in serum after symptoms appear. not as likely to spread after jaundice occurs.

Cirrhosis

Asterixis reversal sleep-wake ascites fetor hepaticus esophageal varices gi bleeds hepatomegaly increased circulating estrogens (men bald, shrinking testes) right sided HF small nodular kidney impaired coag splenomegaly palmer erethema caput medusa (enlarged veins around unbilicus) priritus spiderangioma

signs of cholecystitis

40, fat, female, ITIS: *fever* amalase^, and leukocytosis, increased serume bilirubin abd pain in right upper quad or epigastric, pain increase with deep breath, jaundice, *N/V*, fat ingestion intolerance, feeling of fullness, abd distension. empyema: pus in gallbladder h/o: DM, cystic fibrosis,hyperlipedemia, obesity biliary coli: comes and goes, may have change in odor/color of dark urine, may have fatty, floaty, oily, smelly poop

the liver lab values

AST and ALT= are enzymes released from damage liver cells so elevated is bad(AST-10-40, ALT-8-40). GGT and GGTP= 0-30 value high in *alcohol abuse* and marker for biliary cholestasis. LDH= 100-200 u. PTT- 12-16 s may be prolonged in liver disease

Balloon tamponade

Blakemore temporary control hemorrhage to stablize pt w/ massive bleeding, no longer than 12 h pt in ICU continuous monitoring>blood mouth/obstruction mouth and nasal care oral suction make sure don't pull it out sedate, but not too much

Complications and collaborative probs, cirrhosis

Bleeding and hemorrhage: put on bleeding precautions, get FFP or platelets to prevent DIC, trnsfusion if platelets low <70. if <50 padding bed bec anything can cause bleeding. soft toothbrush, electric razor, PPI/H2 agonist to prevent gastric distress/blood loss Hepatic encephalopathy: Look at ammonia levels, anything that breaks down protein (e.g. bleeding), adds to that encephalopathy

causes of acute and chronic pancreatitis

Causes of acute- alcohol abuse, pancreatic duct obstruction with gallstones, bacterial or viral infections, peptic ulcer, abdominal trauma, ischemia, hyperlipidemia- triglycerides, hypercalcemia, corticosteroids, thiazides, oral contraceptives, surgery. Causes of chronic- acute, alcoholism with malnutrition

what you may see in a obstructive jaundice

Dark orange-brown urine and light clay-colored stools, because bile not getting into GI diverted to blood. Also staining skin, sclerae, mucous membranes. Dyspepsia and intolerance of fats, impaired digestion Pruritus Increased Bilirubin & Posphatase

cancer of the liver

Few cancers originate in the liver Usually associated with hepatitis B and C Hepatocellular carcinoma (HCC)rapid grow, in hepatocytes Liver metastasis from GI, lungs, breast by portal system or lymphatic Liver is a frequent site of metastatic cancer Manifestations: Pain, *a dull continuous ache in RUQ*, epigastrium, or back (unique) Weight loss, loss of strength, anorexia, anemia may occur (all cancer) Jaundice if bile ducts occluded, ascites if obstructed portal veins Increased: serume bilirubin, alk phos, AST, ALT, GTTWBC, RBC, hypercalcemic HyPOglycemic HYPOcholesterol because liver isn't metabolizing it

factors which increase hepatoencephalopathy in liver disease

GI bleed High protein Infection uremia Hypokalemia (watch electrolytes, use K+ sparring duiretics) Hypovolemia (dehydration, excessive diuresis) fever surgery Meds: sedatives, tranquilizers, analgesics Mercaptans (toxic metabolics normally excreted by liver)

Managment of Hep C

Prevention (no vaccine yet), standard precaustions, prevent needlesticks screening of blood measures to prevent spread of infection as with Hep B STOP ALCOHOL: alcohol encourages progression of disease, so alcohol and tylenol (meds that effect liver) should be avoided Antiviral agents: interferon and ribavirin (have to use protease inhibitors *Gamma globulin is NOT effective in Hep C*

hep D and E

Hepatitis D Only persons with hepatitis B are at risk for hepatitis D. replicates surface antigen. Transmission is through blood and body fluids sexual contact. Symptoms lots abd pain, jaundice sclera, arthralgia, joint pain, muscle pain. and treatment are similar to hepatitis B but more likely to develop fulminant liver failure and chronic active hepatitis and cirrhosis. Hepatitis E Transmitted by fecal-oral route, Incubation period 15-65 days, Resembles hepatitis A and is self-limited with an *abrupt onset*. No chronic form.

post opp care for gul stones

Low Fowler's position May have NG NPO until bowel sounds return, then a soft, low-fat, high-carbohydrate diet postoperatively Care of biliary drainage system Administer analgesics as ordered and medicate to promote/permit ambulation and activities, including deep breathing Turn, and encourage coughing and deep breathing, splinting to reduce pain Early ambulation

nursing care for bleeding esophogeal varices

Monitor condition frequently, including emotional responses and cognitive status. LOC Monitor for associated complications such as hepatic encephalopathy resulting from blood breakdown in the GI tract (^nitrogen, ^ ammonia) and delirium related to alcohol withdrawal. Also pneumonia. Monitor treatments including tube care and GI suction. NG tube patentcy, vomiting around tube, if clogged occluded. If stuff coming up NG tube, then irrigate, people should not vomit around NG tube Oral care ALL THE TIME Quiet calm environment and reassuring manner Implement measures to reduce anxiety and agitation, explain pt going to be on IV fluids Teaching and support of patient and family If splenectomy monitor hemorrhage Restrict protein, sodium and fat. Increase carbs, give small frequent meals, supplemental vitamins & minerals, esp B vitamins. Monitor H&H, BUN, creat, ammonia, electrolytes Record daily abd widths and wts Seizure precaustions/neuro Bleeding

what you may see in a hepatocellular jaundice

Often alcohol related May appear mildly or severely ill Lack of appetite, nausea, weight loss Malaise, fatigue, weakness Headache chills and fever if infectious in origin

managment of Hep B

Prevention Vaccine: for persons at high risk, routine vaccination of infants (birth, 1 mo, 6 mo) Passive immunization IGG gamma glubulin for those exposed Standard precautions/infection control measures: hand wash, gloves, treat everyone like possibly infected. Screening of blood and blood products Bed rest Nutritional support -protein restricted Medications for chronic hepatitis type B include alpha interferon and antiviral agents: lamividine (Epivir), adefovir (Hepsera)$$$ 5 mo daily IM injection Antacids and antiemetics As carrier you can infect others even if no S/S

Nursing hepatic encephalopathy

RISK FOR INJURY, r/t nuero disorder maintain safe environment A&O, *mood* changes (irritable) assess mental status, LOC, frequent vitals, seizure precautions pad rails, secure airway fetor hepaticus- sweet fecal breath, blowing off ammonia Monitor fluid, electrolyte and ammonia levels. With lactu, watch dehydration and hypoK Reflexia: hyper, then as worsens, flaccid, absent DTRs EEGs- watch for slowing risk aspiration impaired gas exchange Prevent atelectisis/pneumonia Protect airway wts, I&O, girth worse/better, protein intake

medical treatment for pt with hepatic encephalopathy

Reduce ammonia levels (collaborative) -Administer lactulose by NG or *enema* (goal 2-3 soft stools/day) Lactulose will cause loose stools, cramping, watery diarrhea indx overdose. Hypokalemia and dehydration risk. -Neomycin or Flagyl (knocks out gut bacteria) -Gastric suction and enemas -Serum Ammonia levels Monitor LOC, O x3, mental status, vitals 4h, handwriting assess Discontinue sedatives, analgesics, and tranquilizers. NO BENZOS!!!! Restrict protein to 1.2 - 1.5g/kg/day. Small freq meals. Give IV glucose to minimize protein catabolism, minimize protein breakdown Monitor for and promptly treat complications and infections *Reduce Risk for injury: seizure precautions, monitor mental status, mood changes, LOC, protect airway.*

manifestations of cholelithiasis

STONES Epigastric distress: fullness, abdominal distention, vague upper right quadrant pain- after eating a fatty meal. Acute symptoms occur with obstruction and inflammation or infection: fever, palpable abdominal mass, severe right abdominal pain that radiates to the back or right shoulder, nausea and vomiting. Biliary colic is episodes of severe pain usually associated with nausea and vomiting, which usually occur several hours after a heavy meal. Jaundice may develop due to blockage of the common bile duct. Vitamin deficiency, fat soluble (A,D, E, K)

hep C

Transmitted by blood and sexual contact, including needle sticks and sharing of needles *The most common blood-borne infection. Hep C is more common than Hep B* thanks boomers. A cause of *1/3 of cases of liver cancer* and the most common reason for liver transplant Risk factors (see Chart 49-10) : share needles, blood, body fluids Incubation period is variable Symptoms are usually mild Chronic carrier state frequently occurs Working on a vaccine. HCV rising rates for women in 40s with tattoos, baby boomers (aymp but treating?)

treatment for bleeding varices

Treatment of shock Oxygen IV fluids electrolytes and volume expanders Blood and blood products Vasopressin (in urgent situations, NO if CAD,HTN=MI), somatostatin, *octreotide* to decrease bleeding *ocreotide decreases blood flow to GI, 1st line drug* Nitroglycerin may be used in combination with vasopressin to reduce coronary vasoconstriction Propranolol (Inderal)and nadolol (Corgard)- beta-blocking agents - to decrease portal pressure; used in combination with other treatment and as prophylaxis Also use endoscopy to identify area of bleeding, then sclerosing or banding TIPS and shunting decrease portal pressure

pancreatitis pain and discomfort

Use of analgesics/opioids Nasogastric suction to relieve nausea and distention Frequent oral care Bed rest Promote comfort and relieve anxiety Maintain NPO Milky drainage - may signify pancreatic leak Patient teaching: may have hyperglycemia or malabsorption due to loss of pancreatic enzymes. Need lowfat diet, possible enzyme and insulin replacement

functions of the liver: protein metabolism

amino acids are used by the liver to metabolize almost all proteins like albumin and other proteins that help in clotting. vit k is required to make prothrombin. (role in coagulopathy)

jaundice

Yellow- or green-tinged body tissues; sclera and skin due to increased serum bilirubin levels. can happen when the flow of bile is blocked(obstructive), if there is a lot of RBC destruction (hemolytic), or when hepatic cells are damaged and cant clear bili (hepatocellular) is evident when bili is above 2.5.

chronic pancreatitis

a progressive inflammatory disorder with destruction of the pancreas. Cells are replaced by fibrous tissue, and pressure within the pancreas increases. Mechanical obstruction of the pancreatic and common bile ducts and destruction of the secreting cells of the pancreas occur. Recurrent attacks of severe upper abdominal and back pain accompanied by vomiting Weight loss Steatorrhea

viral hepatitis

a systemic viral infection that causes necrosis and inflammation of the liver cells with characteristic changes and cellular biochemical changes. of the liver causing a cluster of clinical signs. Types A B C D E G GB virus-C A&E are oral fecal. 60% of cases go un diagnosed.

nursing diagnosis and treatments for pancreatitis

acute pain of pancreas- give anticholinergic meds to reduce gastric and pancreatic secretions. NPO. maintain bed rest. NG suction. ineffective breathing pattern related splinting and severe pain- maintain semi fowers, cough and deep breathing.

asterixis

aka Liver Flap, a flapping tremor of the hands. When the client extends the arms & hands in front of the body, the hands rapidly flex & extend. Stage 2 hepatic encephalopathy

functions of the liver: ammonia conversion

ammonia is a by product of gluconeogenesis. the liver converts the ammonia into urea. ammonia produced by gut bacteria removed from portal blood and made into urea. so the toxic ammonia (now urea) is able to be excreted in the urine.

functions of the liver: bile formation

bile is continuously formed in the hepatocytes and collected in the canaliculi. bile function is excretory of bilirubin, and helps emulsify fats. bile salts are made by the hepatocytes from cholesterol. bile salts are secreted into bile to help it do its job--picked back up in ileum, sent to liver, excreted again. the process of bile salt reabsorption is called enterohepatic circulation

functions of the liver: bilirubin excretion

bilirubin is a pigment derived from the break down of hemoglobin. hepatocytes remove bilirubin from the blood. it is then secreted out with the bile into the duodenum.

signs of hepatic encephalopathy

brain blood ammonia high, causing= decreased LOC, confusion, stuporous(not responding to low stimuli), asterixis(flaping hands), hyperreflexia, impaired thinking. these can all be increased by= high protein, infection, hypovolemia, hypokalemia, GI bleeding

cirrhosis

chronic liver disorder characterized by fibrotic changes , formation of dense connective tissues w/in the liver, then degenerative changes and loss of functional liver tissue.

prevention teaching for hep b

vaccine for ppl at risk(health care workers, drug users, hemodialysis, homosexuals, bisexual men, multiple sex partners, tattooing, getting blood), advise against high risk behavior, use standard precautions, using needleless IV sites, barrier precautions for blood, avoid multidose vials.

Age related changes to liver

decreased drug metabolism clearance capabilities. size and weight decreases (esp in women), typically proportionate to decrease in stature. decrease intestinal and portal vein flow. decrease rate replication/repair liver cells after injury. metabolism of medications by liver decreased. *careful medication admin, if approp. reduced dosage to prevent medication toxicity. watch polypharmacy*

portal hypertension

dialated abdominal veins, and hemorrhoids, a large spleen, ascites, portal pressure can be measured with insertion of a cath with balloon.

edema and bleeding

edema results from low levels of albumin. the reduction in production of clotting factor also occurs making bleeding and bruising common. blood can pool in spleen causing hypersplenism.

ERCP

endoscopic retrograde cholangiopancreatography. allows direct visualization, examines the hepatobiliary system with a side viewing scope. nurse looks for resp depression, over sedation, hypotension.

functions of the liver: fat metabolism

fatty acids are broken down for production of energy and ketone bodies. these ketones can be used in the blood stream for more energy (usually when there is no available glucose). Fatty acids and their metabolic products also used to make cholesterol, lipid components.

the stages of hepatic encephalopathy and symptoms seen

stage 1- conscious with periods of lethargy and reversal of day and night. impaired writing. normal EEG. stage 2- drowsiness, inappropriate behavior, mood swings. *asterixis*, fetor hepaticus (ammonia breath/sweet fecal), *slowing EEG*. stage 3- stuporous, sleeps a lot. asterixis, *INCREASED deep tendon reflexes, rigid extremities*. EEG abnormal. stage 4- comatose. no asterixis, FLACCID *no deep tendon reflexes*, EEG abnormal

clinical manifestation of esophageal varices

hematemesis, melena, low LOC and history of alcohol abuse, signs of shock. Pt with cirrhosis (HepB) screening endoscopy needed every 2- 3years to check portal HTN & large varices. If there are small varices every 1-2 years.

esophageal varices

high risk of death from first occurrence and even higher after. dilated tortuous veins lower esophagus caused by portal hypertension from obstruction of portal venous circulation w/in damaged liver. venous blood from the intestine and spleen seek a new path. *prone to rupture>Massive hemorrhage & shock can occur suddenly.* don't lift heavy, or strain during stool, sneezing coughing vomiting. don't give salicylates>erodes esophagus. Liver is responsible for for coag, so if not working= increased risk bleeding out/hemorrhage, shock.

constructional apraxia

inability to draw figures in two or three dimensions. sign of hepatic encephalopathy

care for pt with cirohsis and the different possible nursing diagnosis

ineffective breathing pattern r/t ascites and reduced thoracic expansion fluid volume excess: ascites, edema: restrict Na, abb girth activity intolerance related to weakness/fatigue/malaise- reduce demand of liver and increases liver blood supply assist with activities, encourage rest periods, position for respiratory efficeincy HOB 30d. O2, give high cal/carb diet and protein consistent with liver function, give vits A,B,C,K. measure to prevent hazards of immobility: decibitis, muscle wasting, atrphy, contracture, pnuemonia, imbalance nutrition less than needed-I&O, daily wt, abd girth, assess edema, encourage pt to eat, *high carb diet, give low Na*, protein modified to patient need, restricted if at risk for encephalopathhy, give small frequent meals, consider pt prefernces, supple vits and minerals, B complex, water soluable forms fat sol vits if steatorrhaeno alcohol, increase fluid and exercise if the pt has constipation. (Reduce trauma, fluid restric, oral hygeine, assess nocturia/oliguria) impaired skin integrity related to edema, spider angiomas pruritus and jaundice caput medusus- assess discomfort, keep fingernails short/mittens for confused prevent in fection leukopenia, avoid soap and alcohol based lotion, turn Q2H, perform ROM Q4H. risk for injury and bleeding related to altered clotting, decreased LOC- assess LOC, electric razor use, look at stool for blood, look for bruising, cold liquids PO when done bleeding. measures to prevent falls, prevent trauma, careful eval of any injury r/t risk bleed. Confusion r/t elevated serum ammonia Pain enlarged liver, tender abdomen Abstain alcohol, no Benzos, tylenol, careful Nsaids, give K-sparring diuretics.. maintain sodium/fluid/prot restrict REPORT: weight gain, increased abd girth, bleeding, change mentation.

hepatitis

inflammatory disease. may be acute or chronic. may start with flu-like symptoms; fever, chills, malaise, muscle aches, anorexia, muscle aches. Later progresses to jaundice and dark urine

hepatic cirrhosis types

is a disease characterized by the replacement of normal liver tissue with fibrous scar tissue that impairs liver function. Types: -alcoholic: most common, scar tissue surroundsportal area -postnecrotic: broad bands of scarring -biliary: scarring in liver around liver ducts usually following bile duct obstruction or infection Liver enlargement, portal obstruction and ascites, gastrointestinal varices, edema, vitamin deficiency and anemia, mental deterioration

hepatic encephalopathy

is a life threatening complication of liver failure. liver can't metabolize bi=products, so there is an accumulation of ammonia in blood. this enters the brain this increases GABA. *Increased then decreased, then absent reflexes*, Impaired judgement, confusion, disorientation, coma, dysrhythmia. Avoid commercial salt substitutes, may contain ammonia. May be precipitated by dehydration and hypovolemia.

signs and symptoms of cirrhosis

jaundice, esophageal varices, ascites, hepatomegaly, splenomegaly, hemorrhoids, edema, change in mental stat, spider angiomas(face, neck, shoulders), anemia thrombocytopenia, coagulation disorders, palmar erythema, sexual characteristic changes, peripheral neuropathy. asterixis, abb pain, anorexia, increased aldosterone, ADH, estrogen, glucocorticoids, hypocalemia, sparse body hair, white nails, weakness, weight loss, clubing fingers, easy bruising. 30 degrees. pro is restricted with encephalopathy.

treatment for ascites

low Na diet, may need vit supplement, and high in powdered milk and milk products. usually *spironolactone* is the diuretic used bec. binds to aldosterone and slows action. lasix may cause hyponatremia. fluid restriction is not used unless Na is low. weight loss should not be more than 1-2 kg per day. WAtch for dehydration and hypovolemia because lead to encephlopathy. upright standing position may activate renin-angio-aldosterone system making fluid retention more severe. bed rest is good but keep HOB 90 degrees so pt can breath. If paracentisis (sterile), sample of aspirate *sent to lab for cell count*, albumin & total protein levels, culture and other tests. give IV salt-poor albumin to decrease vasodilation, prevent ascites cycle continuing Transjugular intrahepatic portosystemic shunt (TIPS)-surgical procedure for refractive ascites

functions of the liver: drug metabolism

metabolism usually inactivates meds but some times activates them. conjugation is the binding of the med with another thing so that it can be excreted. this is where the first pass affect can lower the bio availability of the med.

risk factors for choleDOUBLECHECK

obesity, women with multiple pregnancies, frequent changes in weight, rapid weight loss, treatment with estrogen, cystic fibrosis, diabetes, fair, forty

nursing assess: cirrhosis

onset of symptoms and precipitating factors: alcohol, meds, sex, job exposure to heavy metals/chemicals, travel abroad, possibleexposure to oral fecal or bloodborne. drug use, alcohol use, OTC meds/herbs, diet, nutrition, exposure to toxic agents or drugs/meds *ASSESS MENTAL STATUS:IRRITABILITY is a symptom: AMMONIA in brain, hepatoencephalitis* Ability to carry on ADLs hygeine, dressing, toileting, cooking, walking,; maintain job and social relationships. Monitor s/s r/t disease: bleeding, fluid volume changes, lab values

functions of the liver: glucose metabolism

plays a big role, converts glucose to glycogen, then with glycogenisis back to glucose. this is then released to the blood stream when needed. can also do gluconeogenesis (liver uses amino acids from protein break down.

ascites

portal hypertension is a common cause, this increases capilary pressure. liver fails to metabolize aldosterone causing water retention. this elevates Na and water. albumin moves into the peritoneal space and is then followed by the fluid. increase weight abd girth and F+E imbalances

pt teaching after a laparoscopic cholecystectomy

pt may have pain in right shoulder from inflation gas, walking, sitting up and heat pads may help. dont shower/ bath for 2 days, no driving for 4 days, no lifting heavy objects for a week, resume sex when desired. gradually add fat back into diet.

diet managment of hepatitis

small frequent meals, normal amount of protein, careful with fluids, no alcohol during and 6 months after, st johns wart can affect liver function bed rest

fulminant hepatic failure

sudden impaired and severely impaired liver fxn in previously healthy person, develops within 8 weeks after first symptoms of jaundice commonly caused by viral hep. A, B, C, D, E Lecture Treat: physical and psych rest, diet, antiemetics, antivirals, mabs (immune modulators) none of this in book.

Transjugular intrahepatic portosystemic shunt (TIPS)

surgical procedure to refractive ascites to decrease portal HTN decrease Na retention increase response to diuretics help with fluid retention

fetor hepaticus

sweet, slightly fecal odor to the breath, presumed to be intestinal origin, prevalent with the extensive collateral portal circulation in chronic liver disease*blowing off ammonia* sign hepatic encephalopathy

pancreatoduodenestomy whipples procedure

the gullbladder is removed, the duodenum is removed from the stomach and connected to the remaining pancreas and the bile duct, then the stomach is connected at a lowwer spot on the doudenum.

acute pancreatitis

the pancreatic duct becomes obstructed and enzymes (trypsin) back up through the pancreatic duct, causing auto digestion and inflammation of the pancreas. Severe abdominal pain Patient appears acutely ill Abdominal guarding Nausea and vomiting Fever, jaundice, confusion, and agitation may occur Ecchymosis in the flank or umbilical area may occur May develop respiratory distress, hypoxia, renal failure, hypovolemia, and shock

nonviral hepatitis

toxic: chemicals, chloroform, heavy metals, gold. meds: isoniazid, methyl-dopa, haldol and drug induced Tylenol (MAX DOSE 2g daily) , anorexia, nausea or arthalgia. fever rash pruritis: stop taking asap according to text outcome depends on level of toxicity, idetifying causative agent. may need a transplant.

Hep B

transmission is through blood&body fluids, sex, mother to baby. #1 occupational hazard to healthcare workers major worldwide cause cirrhosis and liver cancer sex, needlesticks, tattoes, transfusion, dialysis, glucometer incubation 28-160 d. (1-6 mo) Signs are limited, arthralgias rash common. high risk for chronic hepatitis, cirrhosis, and hepatic cancer. Manifestations: insidious and variable, similar to hepatitis A Virus has antigenic particles that eleicit specific antibody markers during different stages of disease: antigen BGsAg is a surface carrier antigen which can activate and replicate; antibody HBs you've been exposed, but immune If someone has had hepatitis they will do tests to see how active and contiagious based on DNA. Notify contacts**

what are some of the possible vitamin deficiencies.

vit a- can result in night blindness. thiamine- beriberi(a disease causing inflammation of the nerves and heart failure, caused by a deficiency of vitamin B1), polyneuritis, wernicke-korsakoff psychosis. riboflavin- skin and membrane lessions. pyridoxine- skin and membrane lessions. vit C- hemorrhagic lesions of scurvy. vit K- hypoprothombinemia, bleeding and bruising. folic acid- macrocytic anemia

functions of the liver: vitamin and iron storage

vits A B and D are stored in the liver(the fat soluble ones). iron and copper (mag>important for blood)) are stored in the liver. this is why people eat animal liver for health (?E&K)