340 Final Study

8/11/2019 340 Final 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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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 clearance

determinations (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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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 limitations

o 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

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340 Final Study