EXAM Study

8/11/2019 EXAM Study

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DIABETES MELLITUS

A chronic multisystem disease related to abnormal insulin production,impaired insulin utilization, or both.

Leading cause of:

o End-stage renal diseaseo Adult blindnesso Nontraumatic lower limb amputation

Major contributing factoro Heart diseaseo Stroke

Etiology/Pathophysiologyo Theories link causes to single/combination of these factors:

Genetic, autoimmune, viral, environmentalo Two most common types: Type 1 & Type 2

Other types: gestational, prediabetes, secondary diabetes

o Regardless of its cause, diabetes is primarily a disorder of glucosemetabolism related to absent or insufficient insulin supply and/orpoor utilization of available insulin.

Normal insulin metabolism:

Produced by beta cells (Islets of Langerhans)

The insulin is continuously released into thebloodstream in small increments with larger amountsreleased after food.

Stabilizes glucose range to 70-120 mg/dL Insulin

Promotes glucose transport from the bloodstream

across cell membrane to the cytoplasm of a cell.o Decreases glucose in the bloodstream.

Insulin increases in the body after a mealo Stimulates storage of glucose as glycogen in

liver and muscle.o Inhibits gluconeogenesiso Enhances fat depositiono Increases protein synthesis

The fall in insulin level during normal overnight fastingfacilitates the release of stored glucose from the liver,protein from muscle, and fat from adipose tissue.


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o Counterregulatory Hormones Oppose effects of insulin Increases blood glucose levels Provide regulated release of glucose for energy Help maintain normal blood glucose levels

Ex. Glucagon, epinephrine, growth hormone, cortisol

Abnormal production of any or all of these hormonesmay be present in diabetes

o Skeletal muscle and adipose tissue- insulin-dependent tissues

o Other tissues (brain, liver, blood cells)- do not directly depend oninsulin for glucose transport.

Although liver cells are not considered insulin-dependenttissue, insulin receptor sites of the liver facilitate the hepaticuptake of glucose and its conversion to glycogen.

ALTEREDMECHANISMSIN TYPE I & IIDIABETES


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Formerly known as juvenile-onset or insulin-dependent diabetes.

Most often occurs inpeople younger than 40 years of age.o Occurs more frequently in younger children.

o 40% of those with Type I-onset before age of 20.

Incidence has increased by 3% to 5% over recent decades.o As a person grows older the Beta Cells take longer to respond; and

this is why the incidence has become increased, as a person getsolder.

Accounts for 5-10% of all people with diabetes.

Etiology and Pathophysiology-o End result of long-standing process

Progressive destruction of pancreatic beta cells by the

bodys own T cells. Auto antibodies cause a reduction of 80-90% in normal beta

cell functioning before manifestations occur.o Causes:

Genetic predisposition

Related to human leukocyte antigens (HLAs)

Exposure to a virus Idiopathic diabetes is a form of type 1 diabetes that is not

related to autoimmunity but is strongly inherited. This occursonly in a small number of people with type 1 diabetes, and ismost often in those of African or Asian ancestry.

RENAL FAILURE

Chronic Kidney Disease (CKD)


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o Involves progressive, irreversible loss of kidney functiono Definition: The presence of:

Kidney damage

Pathologic abnormalities

Markers of damage (blood, urine,imaging tests) Glomerular filtration rate (GFR)


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Clinical Manifestationso Result of retained substances

Urea Creatinine Phenois Hormones Electrolytes Water Other substances

o Uremia

Syndrome that incorporates all signs and symptomsseen in various systems throughout the body


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o Urinary System Polyuria

Results from inability of kidneys toconcentrate urine

Occurs most often at night

Specific gravity fixed around 1.0.10 Oliguria

Occurs as CKD worsens Anuria

Urine output


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Defective carbohydrate metabolism

Pts with diabetes who become uremic mayrequire less insulin than before the onset ofCKD.

Insulin dependent on kidneys for excretion Serum creatinine and creatinine clearancedeterminations (calculated glomerular filtration rate)are considered more accurate indicators of kidneyfunction than BUN or creatinine.

Efforts are made to initiate renal replacementtherapy before a patient becomes severelysymptomatic.

Elevated Triglycerides

Hyperinsulinemia stimulates hepatic

production of triglycerides.o Elevated glucose levels lead to

increased insulin levels, and insulinstimulates hepatic production oftriglycerides.

Altered lipid metabolismo levels of enzyme lipoprotein lipase

Important in breakdown oflipoproteins

Almost all patients with uremia developdyslipidemia, with elevated very-low-densitylipoproteins (VLDLs), normal or decreased low-density lipoproteins (LDLs), and decreased high-density lipoproteins (HDLs).

Most pts with CKD die from cardiovascular disease.o Electrolyte/Acid-Base Imbalances

Potassium

Hyperkalemiao Most serious electrolyte disorder in

kidney diseaseo Fatal dysrhythmias

Fatal dysrhythmias can occurwhen the serum potassium levelreaches 7 to 8 mEq/L (7 to 8mmol/L).


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Hyperkalemia results fromdecreased excretion of potassiumby the kidneys, breakdown ofcellular protein, bleeding, andmetabolic acidosis.

Potassium may come from thefood consumed, dietarysupplements, drugs, and IVinfusions.

Sodium

May be normal or low

Because of impaired excretion, sodiumretained

o Water is retained

Edema Hypertension CHF

Calcium and Phosphate alterations Magnesium alterations

Hypermagnesemia generally is not a problemunless the patient is ingesting magnesium

(e.g., milk of magnesia, magnesium citrate,antacids containing magnesium).

Clinical manifestations of hypermagnesemia:o can include absence of reflexes,

decreased mentalstatus, cardiacdysrhythmias, hypotension, andrespiratory failure.

Metabolic acidosis

Results from:o Inability of kidneys to excrete acid load

(primary ammonia)o Defective reabsorption/regeneration of

bicarbonateo Hematologic System

Anemia

Due to production of erythropoietino From in functioning renal tubular cells

Other factors contributing to anemia:


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o nutritional deficiencies, decreased RBClife span, increased hemolysis of RBCs,frequent blood samplings, and bleedingfrom the GI tract.

Bleeding tendencies

Defect in platelet function

Defects in platelet function are caused byimpaired platelet aggregation and impairedrelease of platelet factor III.

Infection

Changes in leukocyte function

Altered immune response and function

Diminished inflammatory responseo Cardiovascular System

Hypertension Heart failure Left ventricular hypertrophy Peripheral edema Dysrhythmias Uremic pericarditis The most common cause of death in patients with

CKD is cardiovascular disease. Even a slightreduction in GFR has been associated with a

greater risk for development of coronary arterydisease.

Traditional CV risk factors such as hypertension andelevated lipids are common in patients with CKD.However, much of the CV disease may be related tonontraditional CV risk factors such as vascularcalcification and arterial stiffness.

o Respiratory System Kussmaul respiration Dyspnea Pulmonary edema Uremic pleuritis Pleural effusion Predisposition to respiratory infection

o Gastrointestinal System Every part of the GI is affected


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Due to excessive ureao Mucosal ulcerationso Stomatitis

Found with exudates and

ulcerations A metallic taste in the moutho Uremic fetor (urinous odor of breath)o GI bleedingo Anorexia, nausea, vomiting

May develop if CKD progresses toESRD and is not treated withdialysis.

o Neurologic System

Expected as renal failure progresses. Attributed to:

nitrogenous waste products Electrolyte imbalance Metabolic acidosis Axonal atrophy Demyelination of nerve fibers

Restless leg syndrome

Muscle twitching

Irritability Decreased ability to concentrate

Peripheral neuropathy

Altered mental ability

Seizures

Coma

Dialysis encephalopathy The treatment for neurologic problems is dialysis or

transplantation. Altered mental status is often the

signal that dialysis must be initiated. Dialysis should improve general CNS symptoms

and may slow or halt the progression ofneuropathies.

o Musculoskeletal System CKD mineral and bone disorder


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Systemic disorder of mineral and bonemetabolism

Results in skeletal complicationso (osteomalacia, ostetis fibrosa) and

extraskeletal (vascular) calcificationso Integumentary System

Pruritus

Cause is multifactorial

Includes dry skin, calcium-phosphatedeposition in skin, and sensory neuropathy

The itching may be so intense that it can leadto bleeding or infection secondary toscratching

Uremic frost

Rareo Reproductive System

Infertility

Both sexes Decreased libido Low Sperm Counts Sexual dysfunction

o Psychologic Changes Personality and behavioral changes

Emotional ability Withdrawal Depression Changes in body image caused by edema,

integumentary disturbances, and access devices(e.g., fistulae, catheters) may contribute to thedevelopment of anxiety and depression.

Diagnostic Studieso History and physical examinationo Dipstick evaluationo Albumin-creatinine ratio (first morning void)o GFRo Renal ultrasoundo Renal scano CT scano Renal biopsy


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o A person with persistent proteinuria (1+ protein onstandard dipstick testing two or more times over a 3-month period) should have further assessment of riskfactors and a diagnostic workup with blood and urinetests.

o The two equations used most frequently to estimate GFRare the Cockcroft-Gault formula and the Modification ofDiet in Renal Disease (MDRD) Study equation (see Table47-8).

Collaborative Therapy Correction of extracellular fluid volume overload or

deficit Nutritional therapy Erythropoietin therapy

Calcium supplementation, phosphate binders Antihypertensive therapy Measures to lower potassium Adjustment of drug dosages to degree of renal

function.o Drug Therapy

Hyperkalemia

IV insulino IV glucose to manage hypoglycemia

IV 10% calcium gluconate Sodium polystyrene sulfonate (Kayexalate)

o Cation-exchange resino Resin in bowel exchanges potassium for

sodium. Hypertension

Weight loss

Lifestyle changes

Diet recommendations

Sodium and fluid restrictions

Antihypertensive drugso Diureticso Calcium channel blockerso ACE inhibitorso ARB agents


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It is recommended that the target BP shouldbe


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Increased hemoglobin andhematocrit in 2 to 3 weeks

Side effect: Hypertensiono Iron Supplements

If plasma ferritin


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Digitalis

Antibiotics

Pain medications (Demerol, NSAIDS)o Nutritional Therapy

Protein restriction (benefits are being studied) Water restriction (intake depends on daily urine

output) Calorie-protein malnutrition

A potential and serious problem that resultsfrom altered metabolism, anemia, proteinuria,anorexia, and nausea.

Additional factors leading to malnutritioninclude depression and complex diets thatrestrict protein, phosphorus, potassium, and

sodium. For the patient who is undergoing dialysis, protein is

not routinely restricted. Although some evidence suggests that protein

restriction has benefits, many patients find thesediets difficult to adhere to.

For CKD stages 1 through 4, many clinicians justencourage a diet with normal protein intake.

Generally, 600 mL (from insensible loss) plus an

amount equal to the previous days urine output isallowed for a patient receiving hemodialysis.

Sodium restriction

Diets vary from 2 to 4 g, depending on thedegree of edema and hypertension

Sodium and salt should not be equated.

Salt substitutes should not be used becausethey contain potassium chloride.

Instruct the patient to avoid high-sodium foods

such as cured meats, pickled foods, cannedsoups and stews, frankfurters, cold cuts, soysauce, and salad dressings.

Potassium restriction

2 to 3 g

High potassium foods should be avoided.


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o Foods with high potassium content thatshould be avoided include oranges,bananas, melons, tomatoes, prunes,raisins, deep green and yellowvegetables, beans, and legumes.

Phosphate therapy

1000 mg/day

Foods high in phosphate (dairy products)

Most foods high in phosphate are also high inprotein.

Nursing Management:o Nursing Assessment/Diagnosiso Complete hx or any existing renal disease, family historyo Long-term health problemso Dietary habitso Excess fluid volumeo Risk for injuryo Imbalanced nutrition: Less than body requirementso Grievingo Risk for infectiono Because many drugs are potentially nephrotoxic, the

nurse should ask the patient about both current and pastuse of prescription and over-the-counter drugs and herbal

preparations.o Medications of concern:

Antacids, NSAIDs, decongestants, andantihistamines.

o Planning/Implementationo Overall goals:

Demonstrate knowledge and ability to comply wththerapeutic regimen.

Participate in decision making Demonstrate effective coping strategies

Continue with ADLs within psychologic limitationso Health Promotion

ID individuals at risk for CKD

History of renal disease

Hypertension

Diabetes Mellitus


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Repeated UTI Regular checkups and changes in urinary

appearance, frequency, and volume should bereported

o

Nursing Implementationo Acute Intervention

Daily weight Daily BPs ID s/s of fluid overload ID s/s of hyperkalemia Strict dietary adherence Medication education Motivate patients in management of their diseases

o Ambulatory & Home Care

When conservative therapy is no longer effective,HD, PD, and transplantation are treatment options

Patient/family need clear expectation of dialysis andtransplantation.

o Evaluation Maintenance of ideal body weight Acceptance of chronic disease No infection No edema Hematocrit, hemoglobin, and serum albumin levelsin acceptable range

Dialysiso Half of patients with CRF eventually will require dialysiso Diffuse harmful waste out of bodyo Controls BPo Keeps safe levels of chemicals in the bodyo Two types:

Hemodialysis

3-4 times a week

Takes 2-4 hours Machine filters blood and returns it to the

body.

Types of Access:o Temporary site: Perm cath- THIS IS

THEIR LIFELINE..DO NOT ACCESS IT!


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o AV fistula

Surgeon constructs by combining

an artery and a vein 3-6 months to mature

o AV graft Man-made tube inserted by a

surgeon to connect artery and vein 2-6 weeks to mature

What this means for ME as a NURSE

Cannot take BP on the same arm as thefistula

Protect the arm from injury

Control obvious hemorrhage


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o Bleeding will be arterialo Maintain direct pressure

No IV on same arm as fistula

A thrill will be felt-this is normal

Check for bruit every shift Access Problems:

o AV graft thrombosiso AV fistula or graft bleedingo AV graft infectiono Steal phenomenon

Early post-op Ischemic distally Apply a small amount of pressure

to reverse symptoms

Peritoneal dialysis

Abdominal lining filters the blood

3 Types:o Continuous ambulatory

o Continous cyclicalo Intermittent

Considerations:o Make sure the dressing remains intacto Do not push or pull on the cathetero Do not disconnect any of the catheters


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o Always transport the patient andbags/catheters as one piece

o Never inject anything into the catheter


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LIVER FAILURE

Functions of the liver: 1. Bile Formation

2. Drug and Hormone Metabolism

3. Carb metabolism

4. Protein synthesis (includes proteins important for blood coagulation)

5. Detoxification of Noxious Substances

6. Phagocytosis by means of Kupfer Cells

Medications

Lactulose

o Acidifies intestine so ammonia can be converted into a form thatcan be eliminated via bowel movements.

Rifaximin

o Antibiotic therapy that reduces bacterial action on the protein inthe gut

Decreases ammonia production Vitamin K

o Given parenterally to lower Prothrombin time (PT)Hepato-toxic Drugs

Monitor Acetaminophen use

o Total daily dose: 4 gm/day is normalo Individuals with liver impairment-2 gm/day


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OTC drugs

o Many have Tylenol especially cold medications

Narcotic pain medicationso Percocet or Roxicet: Oxycodone with Tylenol (350-500 mg)o Vicodin or Lortab or Lorcet: Hydrocodone with Tylenol (500-750

mg)Drugs for Agitation

Oxazepam (Serax)

o Benzodiazepine/antianxietyo Not metabolized by livero Maybe used to treat acute agitation and alcohol withdrawalo Dose: 15-30 mg tid-qido Watch for hypotension

Forces Causing Ascites1. Portal HTN

a. Increases hydrostatic pressure(Forces that push fluid out of theblood vessels)

2. Congested lymph channels leak protein abdomena. Decreases colloidal osmotic pressure (Pressure that keeps fluid in

the veins)3. Damaged liver cant make albumin (60-70% COP)

a. Decreases colloidal osmotic pressureKidneys Response to Fluid Shifts

As ascites continues, decreased vascular volume causes kidneys to secretemore aldosterone

o

Retention of sodium and water Damaged liver cant inactivate aldosterone (Hyperaldosteronism)

Paracentesis

Nursing care pre-procedure

o Weight patiento Take VSo Measure abdominal girtho Have pt empty bladdero Place sitting in upright positiono Assemble needed equipment

During Procedure

o Monitor VS especially RR & efforto Reassure pt throughout procedure

Post Procedure

o Monitor VS, especially BP & Respiratory efforto Monitor for bleeding or excessive drainage from the puncture site

o Send specimens to the lab (if ordered)o Change dressing as needed


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o Monitor for infectionDiet Therapy

1. Protein restrictiona. 20-40 gm/dayb. Increase by 10 gm/day when appropriate

2. Sodium restrictiona. 2 gm/day

3. Possible fluid restrictionSkin care for Jaundice

Can cause pruritiso Comfort measures such as:

Keeping the air temp cool (68-70 degrees F) Humidity of air at 30-40 percent Avoid hot showers Use emollient lotion

Neuro Impairments Alcoholic polyneuropathy

Asterixis

Wernike-Korsakoff syndrome

o Wernike component: physical changeso Korsakoff: mental changes

Nursing Care:

o Safety measures at all timeso ABCs especially with ascities and

possible GI bleedingo

Aspiration precautions HOB up 30 degrees

o Dont give sedatives for agitated ordelirious behavior

o Monitor closely for minor changes inorientation to avoid hepatic coma

Role of Aldosterone

Spironolactoneo K+ sparing diuretico Antagonizes aldosterone-body holds onto K+ and gets rid of

Na+Portal Hypertension

Anything that interferes or obstructs portal circulation

Collateral circulation forms to go around obstruction

Other blood vessels dilateVariceal Hemorrhage

Emergent care:1. Protect airway


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a. Prevent aspirationb. Turn patient to one sidec. High Fowlers positiond. Yankauer suction catheter readily available

2. Provide hemodynamic support

a. Blood transfusions to maintain Hgb 8g/dl or Hct 24-30%

3. Treat coagulopathya. Fresh frozen plasmab. Possible parenteral vitamin K (necessary for

coagulation)4. Reduce portal pressure

a. Octreotide (Sandostatin)i. Given IV

ii. Indirecty causes vaconstriction of the viscera

iii. Decreases hepatic blood flowiv. Decreases portal vein pressure

b. Vasopressin (Pitressin)i. Given IV

ii. *Extremely potentiii. Constricts mesenteric arteriolesiv. Decreases portal flow

1. Lowers portal pressure2. Vasconstrictive effect on heart and

intestinesEndoscopic Treatment

Once hemostasis has been achieved

Endoscopic Variceal Ligation (EVL)o Preferred therapyo Use elastic band to tie off variceso Causes vessel thrombosis, necrosis, and fibrosis

Eliminates varices

Endoscopic Injection Sclerotherapy (EIS)o Inject a sclerosing agent (sodium morrhuate) directly into the

varices.TIPS Procedure

Shunts blood between the portal vein and hepatic vein


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Surgical Decompression

Sengstaken Blakemore Tube


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I. BleedingA. Due to:

1. Decreased in formation of plasma proteins-fibrinogen,prothrombin.

2. Portal hypertension can cause bleeding esophageal varices orvarices in upper part of the stomach and bleedinghemorrhoids.

3. Splenomegaly from portal hypertension can cause increase inplatelet destruction.

4. Conditions causing biliary obstruction cause lack of absorption ofVit.K.Thus the liver cannot synthesize prothrombin from Vit. K.

B. Possible Nursing Diagnosis:1. Potential for bleeding2. Altered tissue perfusion; systemic related to hemorrhagic shock.3. Activity intolerance; fatigue-weakness related to anemia from

blood loss

C. Nursing Care1. Goals: Prevent trauma and detect early bleeding.


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2. Small gauge needles used for injections; prolonged pressureneeded at injection sites and venipuncture sites.

3. Soft bristled toothbrush and gentle mouth care.4. Check stool for occult blood (guaiac)5. Observe for bleeding from nose, urine, mouth, skin, emesis, gums.

6. Move and handle extremities at joints-not muscle belly.7. Check on stool consistency. If hard, get order for stool softener.Hard stools increase chance of bleeding from hemorrhoids.

8. Dont blows nose hard or manipulate nose excessively.9. If O2 is given, be sure it is well humidified.10. Check V.S. for increased pulse, decreased BP. Do orthostatic BP

and pulse if bleeding is suspected or to monitor blood loss.11. If varices are present, no coarse foods given (mechanical soft diet),

avoid straining, vomiting, lifting, coughing, retchinganything that would increase intra-abdominal pressure.

12. Vit. K is sometimes given parenterally.a. If bleeding is due to decreased absorption of Vit. K, the

prothrombin time should return to normal.b. If liver is badly damaged, Vit. K will not help and little or

no change in pro time because liver cannot synthesizeprothrombin from Vit. K.

13. Check lab values of prothrombin tinme and INRa. Pro time: the greater in seconds from normal, the greater

the chance for bleeding.b. INR: the larger the number from 1.0, the greater the chance

for bleeding.


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II. Problem of Edema

A. Can be due to:1. Decreased plasma proteinsdecreased colloid osmotic pressure.

2. Portal hypertension

increased hydrostatic pressure in portalsystem and destruction of lymphaticsascites. Fluid high inprotein. Increased oncotic pressure of peritoneal fluid pullsfluid out from vascular compartment.

3. Decreased renal perfusion due to decreased circulating bloodvolumerenin-angiotensin-aldersterone mechanismactivatedincreased Na and water to restore blood volume.

B. Possible Nursing Diagnosis:1. Alteration in fluid volume: excess2. Alteration in body image or self-concept.3. Ineffective breathing pattern.4. Alteration in nutrition: less than body needs.5. Alteration in skin integrity: decubiti6. Alteration in tissue perfusion: peripheral & DVT7. Alteration in comfort: abdominal pain.8. Potential for injury: falls9. Potential alteration in electrolyte balance.

C. Nursing Care1. Edema usually generalized: ascities and hydrothorax often present2. Review care for patients with CHF.3. Skin care essential-total serum proteins also reduced, building and

repairing of tissue potentially decreased4. I/O, daily weights5. Know fluid goal: fluids restricted in some cases, esp. if Na+ is low.6. If ascities is present:

a. self image alteredb. may be unsteady-center of gravity is off, safety factors;

need help with foot care and parts that are difficult toreach.

c. abdomen can be very taut, tense and painful.d. may need to measure abd. girth daily. Do so at umbilicuse. increased abdominal pressure may decrease volume return

from lower extremities. Thrombo-embolic eventspossible.1) dorsiflexion exercises; avoid dependent position oflegs2) no pressure on veins; prevent injury to legs.

f. breathing difficulties-impingement on diaphragm; semi-Fowlers position most comfortable usually. Keep


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fluid in lower part of peritoneal space; decreasedactivity and need for oxygen.

g. anorexia and difficulty eating due to congestion ofabdominal viscera and liver disease per se.1) frequent small feedings

2) feed patients when they are hungry.3) calorie count kept on these patients, if necessary.4) must encourage patients to eat; diet is their medicine5) usually salt restricted diet-not too appealing.

h. administer diuretics as ordered1) watch I/O & daily weights. 1-2 lb.weight loss per day isgood2) observe for fluid and electrolyte imbalances esp.decreased K. Remember decreased K can precipitatehepatic coma.3) spironalactone is a diuretic frequently given. CausesK+ to be spared. Check K+ levels frequently and urineoutput to be sure K+ levels will not increase dangerouslydue to lack of urine output.

7. Note blood chemistry teststotal serum protein and serum albumin.8. Shunt surgery to decrease ascites.

III. Encephalopathy or Hepatic Coma

A. Mechanism involved which causes cerebral symptoms is: NH3 ties upglutamic acid needed for brain tissue activity and functioning. NH3interferes with oxidation of glucose which brain needs for energy.

B. Signs and symptomscharacterized by progressive failure of all aspects

of liver function and associated with neurological manifestations.Symptoms include:1. Mild apathy, lethargy, drowsiness, mental dullness (obtunded), loss of

memory, loss of neatness, sloppy in eating, distant stare.2. Confusion, disorientation, irritability abusiveness, slurred speech.3. Lethargy progresses to stupor and coma.4. Fetor hepaticusbad taste in mouth, sweet, musty odor of breath

characteristic of diffuse liver necrosis; may be early sign ofimpending coma.

5. Increased temperature.6. Flapping tremor or liver flap called ASTERIXIS. Check for this daily.

7. Muscular twitching and poor muscle coordination. Unable toconstruct a simple design, e.g. O or +, worsening or change inhandwriting from day to day (check this daily)

8. Unable to think clearly, e.g. subtract serial &s, translate parables.9. Increased blood NH3

C. Possible Nursing Diagnosis:1. Potential for injury (falls and other injuries)


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2. Alteration in communication: confusion, forgetfulness3. Self care deficit: ADLs4. All of the diagnoses that deal with immobility if the person is

comatose.5. Alteration in mental status and thought processes

6. Alteration in respiratory function: potential airway obstruction (ifcomatose)

D. Treatment and Nursing Care:1. Patient safety-patient is stuporous, lethargic or even comatose; does

not use good judgment and may have difficulty with muscularcoordination.

2. Good oral hygiene (fetor hepaticus)3. Dont give sedatives for delirious or agitated behavior.4. Do a mental test on patients daily-simple math, orientationtime,

place, person, who is the president of the US etc.5. Patients can be difficult to deal with due to personality changes.

Simple directions, dont argue with patients. Try to keep themoriented and safe.

6. If in a comakeep airway open, safety factors, problems ofimmobility, never leave unconscious patients on their backsunattended-may aspirate fluid into the lung. Elevate HOB 23-30degrees.

7. Observe patients frequently for even minor changes so that a coma canbe aborted by early treatment. Very important nursing function.

8. Carry out medical plan of carea. Reduction of dietary protein20 Gm/dayb. Enemas or laxatives to purge GI tract of any blood and by-

products of protein breakdown (blood is good source ofprotein on which gut bacteria can act)

c. Administration of antibiotics to sterilize the bowel may beordered

1) Neomycin may be ordered. Poorly absorbed and lesstoxic

2) Causes inhibition of bacterial action on proteinsubstances in the bowel. Destroys normal bacterialflora of gut so they are no longer present to breakdown protein with resultant production of NH3

3) With Neomycin therapy, dietary protein can often be

increasedd. Lactulose syrup (Cephulac or Duphaluc)

1) Dose 30-40 cc tid or qid po, NG or rectally.2) Mechanism: acidifies colon contents. Colon retains

NH3 as NH4; blood NH3 migrates to colon. It alsoforms NH4 and is trapped in bowel; laxative actionof lactulose expels NH4 out of colon in stool.


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3) Side effects: flatulence, belching, abd. cramps, diarrhea(watch for > 6 stools/day)

9. Avoid conditions that can precipitate coma.a. Excessive protein intake.b. Massive bleeding in GI tract

c. Certain diuretics: thiazidesd. K+ depletion (check K+ levelsif on diuretics, extremelyimportant)e. Paracentesisprobable mechanism in increased NH3

formation by kidneys or acid-base imbalance.f. Acute infections and surgical procedures; increased demands

on already failing liver due to increased metabolic needs.g. morphine (mechanism unknown)h. AZOTEMIA (increased nitrogenous products in blood)

10. Know blood ammonia level and plan care accordingly. (The higher itis, the greater the potential for coma or coma present). Patients dovary in terms of NH3 levels and presence of S&S. Some toleratehigh levels without symptoms, others may be in a coma withlower levels.

IV. Problem of Drug Toxicity1. Observe for S&S of drug toxicity or intensified action of drugs2. Dont give MSO4, barbiturates or Tylenol to these patients or only in very

small dosages.3. Patients should take no medications unless ordered by doctor. Drugs that are

metabolized or detoxified by the liver are the greatest danger.4. Further liver damage can result from effects of some drugs: Compazine

family, birth control pills, anesthetics such as Halothane and Tylenol,

certain antibiotics such as sulfa drugs.


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