Nursing 212

Health Differences Across the Lifespan 2 Study Guide Interventions: monitor I&O, BG, urine ketones, vital signs, oxygenation, and breathing patterns; maintain skin integrity; promote healing of impaired skin and prevent infection by repositioning the patient every 2 hours; provide pressure relief as indicated; manage incontinence and perspiration with skin protective barriers and cleansing; provide appropriate nutritional and oxygen support; promote safety; assist the patient in verbalizing concerns and help with coping effectively with illness and fears; reinforce patient teaching about the nature and causes of DKA (excessive glucose intake, insufficient medications, physiological and/or psychological stressors, and any new medications) Hyperglycemic Hyperosmolar Nonketotic Syndrome Hyperglycemic hyperosmolar nonketotic syndrome (HHNK) is a life threatening metabolic disorder of hyperglycemia. It usually occurs with type 2 DM and is triggered by stressors such as medications, infection, acute illness, invasive procedures, or chronic illness. Increased insulin resistance (caused by one or more triggers), along with increased CHO intake, leads to hyperglycemia. Polyuria and decreased plasma volume also occur. There is a subsequent decreased glomerular filtration rate (GFR), which leads to glucose retention and sodium and water excretion. Hyperosmolarity causes dehydration and reduced intracellular water (cell shrinkage). Assessment: symptoms gradually occur over 24 hours to 2 weeks; decreased LOC, dry mucous membranes, polydipsia, hyperthermia, impaired sensory, and motor function; positive Babinski sign and seizures; elevated serum sodium with a serum osmolality greater than 340 mOsm/L and serum glucose greater than 600 mg/dL; abnormal serum potassium and chloride; no serum ketones and normal serum pH Treatment: determine and treat triggering situation; treat coexisting health deviations; provide IV infusion of NS to replace fluids and sodium, use a regular insulin IV to manage hyperglycemia and potassium to replace losses and shifts; monitor I&O, weight, vital signs, lab values, sensory function and cognitive function; maintain intact skin by repositioning every two hours, using pressure relief aids, nutritional support, skin moisturizers, barriers, and managing incontinence; prevent aspiration by using appropriate feeding precautions, elevate head of bead (HOB) 15-30 degrees during and after feeding for one hour; if BP is too unstable to elevate HOB with feeding, then withhold oral feedings; reinforce client teaching of HHNK symptoms to report and new medications Phenylketonuria Phenylketonuria (PKU) is an inherited autosomal recessive disorder affecting protein utilization. It is caused by abnormal metabolism of the essential amino acid phenylalanine, which is found in many natural protein foods. It affects mostly white children; PKU is rare in African Americans, Japanese, and Jewish populations. A deficiency in the liver enzyme phenylalanine hydroxylase (which breaks down phenylalanine into tyrosine) causes serum phenylalanine metabolite levels to rise, leading to musty body and urine odor (excretion of phenol acids), seizures, hyperactivity, irritability, vomiting, and an eczema type rash. Decreased tyrosine levels cause a deficiency of pigment melanin, causing most children with PKU to have blond hair, blue eyes and fair skin that is prone to eczema. Continued accumulation of phenylalanine affects protein synthesis and myelinization and results in seizure disorder and untreatable mental retardation if phenylalanine level is not decreased.

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