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Peds Exam #3
Terms in this set (257)
CHAPTER 32 AND 37
Nursing Care of the Adolescent
Adolescent Growth and Development
-Transition between childhood and adulthood
-Rapid physical, cognitive, social, and emotional maturation
-Generally defined as beginning with onset of puberty and ending with cessation of body growth at 18-20 years.
Responses to Puberty
-Responses differ depending on stage of development
---Curiosity in early adolescence
---Concerns with "Am I normal?"
---Concerns for late-maturing teens
---Concept of "perfect body" achievement
-Dramatic increase in growth accompanies sexual maturation
---Adolescent growth spurt
---20%-25% of total height achieved during puberty
---Usually occurs within 24-36 months
---Girls 1 1/2 - 2 years ahead of boys.
---Growth spurts peaks 9 1/2 -14.
---Boys 10 ½-16.
---Seems to grow from feet up (shoes are usually the first thing they buy for their kids)
-Characteristic sequence of changes
-Size and strength of heart, blood volume, and systolic blood pressure increase
- Metabolic rate is increased esp in boys
-Pulse rate and basal heat production decrease
-Adult values for all formed elements of blood
-Respiratory volume and vital capacity increase
-Increased performance capabilities
Labs and Vitals same as adults
Erikson: Psychosocial Development
-Erikson: Identity vs. Role Confusion
---Struggle to fit in
----Group Identity vs. Alienation
-Development of personal
----Identity vs. Role Diffusion
-Sex role identity
Piaget: Cognitive Development
-Formal Operations Period
---Think beyond present (think of their future)
---Mental manipulation of multiple variables
---Concerned about others' thoughts and needs
---Can easily be swayed by emotion or peer pressure to choose unwisely
------They need to be treated like a child still rather than adult because of this
Kohlberg: Moral Development
-Internalized set of moral principles
-Questioning of existing moral values and relevance to society
-Understand duty and obligation, reciprocal rights of others
-Concepts of justice, reparation
-Some may question values and beliefs of family
-Capable of understanding abstract concepts, interpreting analogies and symbols
-May fear that others will not understand their feelings
----THIS IS A BIG PROBLEM IN THIS AGE
All about being accepted by their peers
-Goal: to define identity independently from parental authority
-Intense sociability; intense loneliness
-Acceptance by peers
Relationships with Parents
-Roles change from protection-dependency to mutual affection and equality
-Process involves turmoil and ambiguity
-Struggle of privileges and responsibility
-Emancipation from parents may begin with rejection of parents by teen
---- Early 11-14:
------Wide mood swings.
------Not battling with parents but think of them as LESS knowing (ask advice from other adults because they think parents don't know)
---- Middle 14-17:
------More introspective, sulking, dating, parents are idiots i.e. come home and slam the door and stay all day in the room
---- Late 17-20:
------Physically mature, independent from family with less conflict, peer group less important, individual friendship emotionally more stable
Relationships with Peers
-Peers assume increasingly significant role in adolescence
-Peers provide sense of belonging and feeling of strength and power
----With this strength and power comes experimenting i.e. cigarette smoking, weed, drinking, dieting
-Peers form transitional world between dependence and autonomy
-Social interaction between children of same and opposite sex is as important inside the acute care setting as it is outside.
- Teenagers enjoy playing, spending time, and hanging out together
- Emotional relationships form during adolescence
-Sexual experimentation—wide range
----They don't think about STD's or pregnancy
-Reasons for sexual experimentation
---Peer pressure to conform
Table 32-20, Slide 16
Table 32-21, Slide 17
Interests and Activities
-Leisure activities center around peers
-Adolescent work experiences may provide benefits
-Time management concerns
Development of Self-Concept and Body Image
-Feelings of confusion in early adolescence
-Acute awareness of appearance, comparison of appearance with others (internet contributes a lot to this)
-Blemishes/defects magnified out of proportion
-Mature to self-concept based on uiqueness/ individuality
----Acne, overwt, eating disorders a big concern for body image
-Interview separately from parents when possible
-Encourage participation in care and decision-making
-Encourage peer visitation
-Provide information on sexuality
The Child with Alterations in Endocrine Function
-Diabetes Mellitus is the most common metabolic disease in children
-It is a disorder of hyperglycemia resulting from defects in insulin secretion, insulin action, or both leading to abnormalities in CARBS, PROTEIN, and FAT metabolism.
-In the US 1 in every 400-600 children and adolescent have type 1 diabetes.
- Fn of insulin is to transport glucose into the cells- lack of insulin causes high levels of glucose in blood
- Renal thre 160-180 would exceed glycosuria limit and excess goes to urine and you have glucose in the urine
-Type 1 formally called insulin-dependent (IDDM) characterized by catabolism and the development of ketosis in the absence of insulin replacement therapy.
---Peak incidence 7-15 years old
---Higher incidence in Caucasian
---Boys and girls equally affected
-Type 2 formally called non-insulin dependent (NIDDM) involve resistance to insulin action and defective glucose mediated secretion (now occuring at younger age)
---Low physical level
---Intake of high-energy food
---Race (1st case found in 4y/o Pima indiana tribe in Arizona) NATIVE AMERICAN, BLACK, HISPANICS, WHITE
---Low socioeconomic status
Type 1 Diabetes: Underlying Pathophysiology
-Autoimmune response (genetic, environmental trigger)
-Beta cells of pancreas are destroyed.
-Little to no insulin is produced by the body
-Lifelong insulin replacement is needed (PO agents do not work in this type)
Type 2 Diabetes: Underlying Pathophysiology
-Pancreas may not secrete enough insulin
---Insulin secretory defect
-Cells may be resistant to insulin that is secreted
-Major risk factor: OBESITY
--- 80% of children with type 2 diabetes are obese
--- Types of foods, drinks, and activities affect this
S/S of DM by Types
-Problems with kidneys, eyes, and skin
- Type 1= 3P's, large loss of calories, thin, wt loss
- Type 2- 3P's, Not skinny, will be overwt, acanthosis nigricans
-Vaginitis due to excess sugar in urine
---Common in adolescent
Dx of DM
- Normal Sugar: 70-110
-Dx: Fasting blood sugar > or = 126 mg/dL
----(7 mmol/L). No caloric intake for 8 hours.
-Two-hour plasma glucose > or = 200 mg/dL (11.1 mmol/L) .
-Random plasma glucose concentration > or = 200 mg/dL (11.1mmol/L)
-Presentation of classic symptoms i.e. 3P's
Tx of Type 2
-PO Metformin (APPROVED FOR KIDS)
Treatment of DM Type 1
(LOOK AT PG.1542)
-1920 insulin was discovered
-Multiple approach to insulin therapy
----Once a day, three or more injection a day, or continuous infusion (pump therapy)
-Conventional insulin therapy
----A combination of a short-acting and an intermediate or long acting insulin before breakfast and the evening meal)
-HbA1c evaluation every 3 months.
-Insulin action time (PG. 1624)
(KNOW PEAK, DURATION, WHEN TO GIVE SNACK)
---Short/Regular Acting 30mins-1h and Peak 2-5h
----Give a snack with the peak time!!!
----i.e. Bfast at 0900 and snack at 1100
---- Long acting 1-2h and Peak in afternoon
---Intermediate Acting (NPH)
----Rapid Acting 10-30 mins (Lispro)
- Type of insulin: 100u/mL
-External insulin pumps
-Implantable insulin pumps
External Infusion Pump
Insulin injection sites
Best area for absorption is the abd
-Give all morning insulin in one site (e.g., arms) and all evening insulin in another (e.g., legs) because of different rates of absorption from these sites.
-Space injections about 1/2 inch (1.25 cm) apart.
-Goal to provide adequate calories for the child's normal growth and development.
-Carbohydrates 50%, protein, 10 to 20%, fats 30%.
-Conventional meal plan - three meals and three snacks a day
-Modified according to the child present food item - preserving cultural patterns and preferences.
-Learning about food groups, weighing and measuring food, reading labels for nutritional value
----Older children can do this
First teach the parents and ten gradually involve the child as they grow i.e. start with wiping with alcohol
---Able to test BG and urine
-The school-age child
---Can understand the basic concepts related to their disease and treatment.
--- Can select foods and portion sizes, test blood glucose, give injections, keep records.
-Adolescents have a difficult time adjusting
----May cause non-compliance
-Exercise is encouraged and NEVER restricted
-Physical exercise is associated with increased insulin sensitivity, reduced cardiovascular risk factors, weight loss, and improved overall well-being
-Activity decreases BG levels
----Provide extra snacks before and during prolonged activity
-Plan activity by adjusting food intake and insulin dosage.
Nursing Care: Type 2 Diabetes
-Education about disease and benefits of weight loss
-Monitoring blood glucose and blood pressure
-Assess diet and activity pattern
-Symptoms of hypoglycemia, hyperglycemia
Hypoglycemia- Insulin reaction
-Can occur within minutes in a child with DM Type 1
-Blood glucose fall below 70 mg/dL.
---Error in insulin dosage
---Inadequate calories because of missed meals
---Exercise without a corresponding increase in calorie intake.
-Severe hypoglycemia can cause seizures.
S/S of Hypo and Hyperglycemia
Treatment for Hypoglycemia
-Give glucose immediately
---Low fat carbohydrate-containing snack or drink, sugar gels, glucose tablets, glucose paste, OJ
-Unconscious give Glucagon
----Stimulates liver to release stored glucose
----Glucagon IM or SQ
-Carry a source of glucose
----Glucose tablets, life-savers, sugar cubes
- Result of extreme Hyperglycemia
-Life threatening condition.
-Occurs primarily in type 1 diabetes.
----Incorrect or missed insulin doses
----Incorrect administration of insulin
----Illness, trauma, surgery
-When insulin is absent and glucose is unavailable, the body uses fats as an alternate source of energy
-Flushed ears and cheeks
----Deep and rapid
-Acetone breath (fruity smell)
-Blood glucose >250 mg/dL.
-Acidosis pH <7.3, bicarbonate <15mEq/L
- Change in mental statis
- Distended abd
- Enlarged liver
Treatment for DKA
-Fluid and electrolyte correction
- Mannitol to treat cerebral edema
The Child with Alterations in Genitourinary Function
-Name the two major regions of the kidneys.
-What are the main functions of the kidneys?
----Two Main fns
----1) Excrete Wast Products
----2) Maintenance of Fluid and Electrolyte Balance
-What are the two hormones secreted by the kidneys?
----1) Erythropoietin (helps w/ RBC production)
----2) Calcitrol (Helps w/ Ca and Phosphorus Balance)
------When Ca too low, PO4 is secreted and increased so Calcitrol is secreted and takes Ca from bones and causes osteodystrophy
-Name an enzyme secreted by the kidney.
----Renin: Helps maintain blood pressure with the renin-angiotensin system
-What is the functional unit of the urinary system.
-What is glomerular filtration rate?
----Measures how effectively the kidneys works
----Looks at the measurement of plasma by which a substance is cleared by the body (THIS SUBSTANCE IS CREATININE)
-What is the most important estimation of glomerular filtration?
-What is the purpose of a Creatinine Clearance test?
----To find out how effective kidney's fn'ing
----Creatinine is produced from muscle tissue
----When kidneys do not fn, it excreted and causes the kidney's to overwork
Know Creatinine levels
WATCH VIDEO ON SLIDE 5
Development of the GU System
Urinary Output Norm
----0.5 to 1ml/kg/hr
----40 to 80 ml/hr
-Bladder capacity increases with age from 20-50 ml at birth to 700 ml in adulthood.
Urinary Tract Infections (UTI)
- More common in females
- Common in kids
- A UTI is an infection of bacterial, viral, or fungal origin that occurs in the urinary tract.
-Cystitis is a lower UTI that involves the urethra or bladder.
-Pyleonephritis is an upper UTI that involves the ureters, renal pelvis, renal parenchyma.
-Bacteriuria - Presence of bacteria in the urine.
Incidence of UTI
-Female 10-30 times the risk of males.
-A wide variety of organisms can be responsible for UTI.
-E-coli (MOST COMMON) 80% and other gram-negative enteric organisms.
-In neonates, the urinary tract may be infected via the blood stream; in older children bacteria ascends the urethra.
Causes - Contributing Factors
-Shorter urethra in females.
-Incomplete emptying of the bladder
-Vesicoureteral reflux (back-flow from ureters to kidney)
-Poor personal hygiene
----Wipe from front to back
----Type of underwear (cotton best)
-Indwelling catheter placement (sterile)
-Antimicrobial agents that alter the normal urinary tract flora.
-Sexually active adolescent females.
-Failure to thrive
Clinical Manifestations-Older Child >2 years
-Urgency or hesitancy
-Enuresis or new-onset incontinence
-Abdominal tenderness or lower abdominal pain
-Strong-smelling urine, cloudy urine
S/S of UTI
Dx test for GU
Urine and blood creatinine is important as well as BUN
Know BUN levels
BUN and Creatinine can be lower as the norm in younger kids
-Urinalysis C/S tells you the presence of bacteria
-Dipstick test for leukocyte esterase or nitrite
-Urethral catheterization i.e. subrapubic, straight cath
-Voiding cystourethrogram (VCUG)
-Intravenous pyleogram (IVP)
-Cystoscopy (scope placed to look at structures)
Clinical Therapy for UTI
-Assess urinary status
----Color, frequency, burning, retention, flank pain
-Administer prescribe medications
----Antibiotic begun as soon as urine sample is collected ------Sulfamethazole-trimethoprim (Bactram) preferred (EXAM: Trimethoprim part of the med is used to calculate your dose)
----Take as rx and take entire dose
-Administer antipyretics as prescribed.
-Provide comfort measures
-Adequate fluid intake
-Intake and Output
-Emotional support to family
----Medications, fluid intake, hygiene
----Pcn, aminoglycoside (gentamycin) can also be rx so teach them about measuring levels or allergies
----Wipe front to back, cotton underwear
----Encourage child to use restroom often and not holding urine
Acute Glomerulonephritis (AGN)
Acute Postinfectious Glomerulonephritis (APIGN)
-Glomerulonephritis is an inflammation of the glomeruli of the kidneys.
-AGN is an immune complex disease that results from immune injury.
- APIGN has some infection before hand i.e. URI
Etiology/Incidence AGN/ APIGN
-APIGN can occur at any age but is usually seen in school age with the peak age of 2-6 years
-More common in boys than in girls
-Once thought to be secondary to streptococcus, now other organisms are involved, including pneumococcus, staphylococcus and viruses
----In children it is most often a response to a Group A beta-hemolytic streptococcal infection of the skin and pharynx
Pathophysiology of AGN/ APIGN
Autoimmune response to the infection
-Antibody-antigen complexes becomes lodged in the glomeruli leading to inflammation and obstruction.
-Capillaries in the glomeruli are obstructed by the damaged cells, reducing glomerular filtration rate.
-Vascular permeability increases allowing RBC and cell cast to be excreted.
-Sodium and water are retained and causes edema
ACUTE POST-INFECTIOUS GLOMERULONEPHRITIS
-Infection from group A beta-hemolytic streptococcus causes an immune response that causes inflammation and damage to the glomeruli.
-Protein and red blood cells are allowed to pass through the glomeruli.
-Blood flow to the glomeruli is reduced due to obstruction with damaged cells.
-Renal insufficiency results, leading to the retention of sodium, water, and waste
Patho of Acute Postinfectious Glomerulonephritis
- Protein, leukocytes, and RBC in urine occurs
- Lose protein in the urine
Clinical Manifestations of AGN/ APIGN
-Flank or midabdominal pain
-Hypertension (this can lead to encephalopathy)
-Encephalopathy (headache, nausea, vomiting, lethargy, irritability, seizures)
-Hematuria i.e. brown or tea-colored and cloudy urine
----The urine becomes foamy/ cloudy in appearance
-Edema i.e. periorbital and generalized
----Dsynea, cough, crackle
-Oliguria (More often than not)
----May or may not be present
Dx of AGN/ APIGN
----Proteinuria 3+ to 4+
----Specific gravity ^
----EXAM: RBCs, leukocytes, no bacteria seen (because of immune complex response not bacterial response)
- Urine culture - Negative
-Serum chemistry values
----Elevated BUN and Creatinine levels
----Decreased serum protein
-Erythrocyte Sedimentation Rate (ESR) is ^
-Antistreptolysin-O (ASO) titre is elevated
----Shows generalized cardiac enlargement, pulmonary congestion
- Renal biopsy - may be performed
Nursing Management of AGN/ APIGN
----Monitor I/O to assess fluid status
-Monitor VS and BP (BP would be increased)
----Want to prevent encephalopathy from htn
----Diuretics for edema
----Antibiotics to treat existing streptococcal infection
----Digitalis to combat circulatory overload
---- "No ADDED salt" and LOW protein
-Provide support to parents
-Discharge planning teaching
----Medication regime, dietary restrictions, signs and symptoms of complication
Most cases resolve without complications, but some kids may have recurrence or end up on dialysis
A 4 y/o boy is admitted w/ glomerulonephritis. His mother asks why his eyes are so puffy. What is the best response?
A) Children cry a lot w/ glmoerulonephritis and the puffiness should subside when he feels better
B) "Has he been rubbing his eyes excessively?"
C) Periorbital edema is associated w/ htn
D) This is a common finding due to circulatory congestion in the kidneys
-EXAM: Nephrotic syndrome is a clinical state that include:
----1) MASSIVE proteinuria
-Primary disease known as Idiopathic nephrosis or Minimal-change nephrotic syndrome(MCNS)
-Secondary disorder that occur as a clinical manifestation after or in association with glomerular damage of known or presumed diseases
----SLE, DM, SCD
-A congenital form inherited as an autosomal recessive disorder
- Massive Plasma protein escapes and leads to hypoproteinemia
- Na and H2O retention leads to massive edema
Etiology/Incidence of Nephrotic Syndrome
-The onset of MCNS can occur at any age but predominantly occurs in children between 2-7 years of age.
-Immune system role
----Upper respiratory infection often precedes the edema by 2-3 days
-The pathogenesis in MCNS is not clear, but there is increased permeability to protein especially albumin
What is the fn albumin?
A) Essential structure for clotting process
B) Protects against infection
C) Prevents plasma from leaking into tissues
D) Transports formed elements and helps maintain homeostasis
What causes MCNS?
- Unclear, but immune system role suspected
Clinical Manifestations of Nephrotic Syndrome
-Puffiness of face
-Abdominal swelling (acites)
-Respiratory difficulty (pleural effusion)
-Labial or scrotal swelling
-Edema of intestinal mucosa causes Diarrhea
- Anorexia, Poor intestinal absorption
-Extreme skin pallor
-Blood pressure normal or slightly decreased
-Susceptibility to infection because losing some immunoglobulins in urine
-Urine alteration i.e. dark, frothy, decreased volume.
- Oliguria may be present
Dx of Nephrotic Syndrome
-History and Clinical Manifestations
----High specific gravity
----Decreased serum protein (protein lost in urine)
----Normal or elevated hemoglobin and hematocrit
----High platelet count
----Elevated plasma lipids
-Renal ultrasound and renal biopsy
What med is prescribed to decreased proteinuria?
Management of Nephrotic Syndrome
-Corticosteroid therapy: (#1 Tx)
----Oral dose 2mg/kg/dose
----Prednisone the safest and least expensive and is the steroid of choice.
----The drug is continued until the urine is free from protein and remains normal for 10 days to 2 weeks
----Some pt becomes steroid responsive, which = better outcomes
----Some pt are steroid resistant and this will make tx ineffective so other tx has to be considered
----Reduce the relapse rate and induce long-term remission
----Oral alkylating agent - Cyclophosphamide (Cytoxan)
----Given for 2-3 months alternating with Prednisone (Can be given for pts who aren't responding that well to steroids alone
----Loop diuretics - furosemide.
----Plasma expanders - Albumin
-Antibiotics for any infection that may be present
Type of diet for child w/ Nephrotic Syndrome ?
- Normal diet for their age
Nursing Management/ Tx of Nephrotic Syndrome
-Assess for fluid volume deficits
----Monitor increased edema
----Measure abdominal girth
-Bed rest because of edema they are lethargic and may have trouble moving
-Monitor VS and BP
-Check urine for protein and specific gravity
----Esp because they are on steroids and losing immunoglobulins
----Sick stay away from pts or wear mask
-----Visitors w/ infection not to come in
-Administer treatment as prescribed.
----"No added salt" during corticosteroid treatment
-Promote skin integrity
----Frequent change of position
----Good skin care
-Activity as tolerated
Why is it necessary to protect child from infection?
- On Prednisone and Loss of immuniglobulins in urine and both of these decrease immune system
-Renal failure is the inability of the kidneys to excrete metabolic, concentrate urine, and conserve electrolytes.
-Acute Renal Failure (ARF) occurs sudden in response to inadequate perfusion, kidney disease, or urinary tract obstruction.
-Chronic Renal Failure (CRF) develops slowly as a result of longstanding kidney disease or an anomaly.
-----Chronic renal failure results anuria.
-Both types of renal failure are characterized by:
---- Azotemia (accumulation of nitrogenous wastes in the blood)
---- Oliguria (reduced urine output for age) (EXAM: Know urine output according to age)
The best indicator for renal function is the glomerular filtration rate
Acute Renal Failure
-ARF occurs when the kidney function abruptly diminishes, and is characterized by a rapid rise in the BUN level.
-The principal feature of ARF is oliguria associated with azotemia, metabolic acidosis, and diverse electrolyte disturbances.
-Uremia occurs when there is an excess of urea and other nitrogenous waste in the blood.
-Neonates who are critically ill with asphyxia, shock, and sepsis
-In toddlers it may be caused by accidental poisoning e.g. ASA, acetaminophen, mushrooms, lead, iron, barium
-School-age child and adolescent by trauma
The most common cause of ARF in children hypovolemia secondary to DEHYDRATION
S/S of Acute vs Chronic Renal Failure
Dx Tests for Renal Failure
S/S of Electrolyte Imbalances in Acute and Chronic Renal Failure
- What types of diets and diuretics for pts with hyperkalemia?
Treatment for ARF
-Oliguria or Fluid Depletion
----Rapid fluid replacement
----Saline or Lactated Ringers Solution at 20 mL/kg given rapidly over 5 to 10 minutes (may need blous, but caution w/ overload)
------Fluid overload and pulmonary edema may occur from bolus and may require diuretic therapy
----Fluid requirement are calculated to maintain ZERO water balance at the end of 24h
----Potential sources of potassium eliminated i.e. diet
----Rapid- acting tx of hyperkalemia
------Calcium Gluconate 10%
------ Kayexelate - exchanges sodium for potassium
------Albuterol - causes potassium to move into cells
-Nephrotoxic drugs should be avoided or monitored extremely carefully
(LOOK AT PG. 1505)
---Aminoglycosides i.e. Gentamycin, Cephalosporins
----Threat of encephalopathy
----Urgent tx i.e. IV Labetalol or Sodium nitroprusside
----Less urgent situations i.e. Hydralazine, clonidine, verapamil.
----Other drugs i.e. Nifedipine, catopril, monoxidil, hydralazine, propranolol.
----Sodium Bicarbonate(Bicitrate), sodium citrate
Nutrition of Child w/ Kidney Disease
Want to reduce PO4 food, reduce high K food (orange/yellow color foods and green-leafy typically high K)
Nursing Management for ARF
-Maintain fluid balance.
----Monitor IV fluids to prevent overload
-Monitor intake and output - ZERO DAILY balance
-Monitor serum chemistry values
-Monitor VS and BP
-Administer IV medications
-Meet nutritional needs
-Provide emotional support
Chronic Renal Failure
-CRF is a progressive, irreversible reduction kidney function
-When the kidneys can no longer function, even with medical interventions, and the patient must restore to dialysis for clearing wastes, the term End Stage Renal Disease (ESRD) is applied
- 90% of nephrons are damaged
Causes of CRF
-Developmental abnormalities i.e. genital, renal and urinary tract malformations
-Glomerular and hereditary renal disease
----Chronic pyelonephritis and glomerulonephritis, congenital nephrotic syndrome, hereditary nephritis.
Clinical Manifestations of CRF
-Early in course with nephron destruction child remains asymptomatic
--Pale and complain of headache
--Nausea and fatigue with decreased mental alertness and ability to concentrate.
--Anemia leading to tachycardia, tachypnea, and dyspnea on exertion
--Loss of appetite
--Delayed sexual maturation.
--Uremic breath (smell like urine)
Dx of CRF
-Laboratory evaluation i.e. serum electrolytes, phosphate, BUN, creatinine, pH
----BUN, Creatinine elevated
----Know Electrolyte levels (K increases, Ca decreases, PO4 increases)
-Urine sample for culture and to calculate the protein-to-creatinine ratio
-Glomerular filtration rate
Management of CRF
----Maximize calorie intake
----Limit potassium, phosphorus and sodium
----Dietary supplements i.e. water soluble vitamins
----Attractive, small frequent meals.
Nutrition for child w/ Kidney Disease
Imbalance between Ca and PO4 so Ca taken from the bone
-Reduction of dietary phosphorus i.e. protein and milk intake
-Administration of a phosphorous binding agent i.e. calcium carbonate (Tums)
-Provision of supplemental calcium
-Administration of vitamin D
----Form of Ca that is given
Management Acidosis and Anemia
----Pharmacological treatment to reduce metabolic acids i.e. sodium bicarbonate (Bicitrol), combination of sodium and potassium citrate - Bictra
----Diet i.e. Sufficient sources of iron and folic acid
------Injectable iron may be required (iron can cause staining of tissue so it may be replaced in IV format rather than Z track)
----Medication i.e. recombinant human erythropoietin corrects anemia i.e. Epoetin Alfa (Epogen, Procrit)
----Initial have low sodium so tx more simple
------Fluid restriction diet and diuretics - thiazides, furosemide.
------Sodium restriction, beta-blockers and vasodilator - propanalol, hydralazine.
----Other drugsinclude nifedipine, minoxidil, capotril.
-Growth Restriction-Especially preadolescent.
----Recombinant growth hormone (rhGH).
----These pts are usually darker and shorter than they would be if they didn't have CKD
-Monitor for SIDE EFFECTS of medications
----Diuretics causes electrolyte imbalance AEB weakness, muscle cramps, dizziness, headache, nausea and vomiting
----Antihypertensives need to monitor weight
-Prevent infection -
----Signs of infection i.e. elevated temperature, strong-smelling urine, dysuria, changes in respiratory pattern, productive cough
----Good hand washing practice important
Renal Replacement Therapy
Tx for CKD
-The primary modalities are:
-The body cavity acts as a semipermeable membrane through which water and solutes of small molecular size move by osmosis and diffusion according to their respective concentrations on either side of the membranes
- Can do this at home as well
-Continuous (CAPD) and Automated peritoneal dialysis (APD).
----APD - 10-12 hours overnight
-The blood is circulated outside of the body through artificial cellophane membranes that permits a similar passage of water and solutes.
-Done in critical care settings.
-3 times a week.
-Ateriovenous (AV) fistula in children over 20 kg
- CKD have swelling or elevated areas on their skin (hands) from fluid build up
-Concern is helping kids be as normal as possible.
-Renal transplant can help with this desire to be normal kid
-Renal transplantation is now acceptable and effective means of therapy in the pediatric age-group.
-Kidney transplants are available from two sources:
----1) Living related donor (LRD)
----2) Cadaver donor (CD).
----Immunosuppresants - corticosteroids, azathioprine, cyclosporine, tacrolimus, and monoclonal antibiodies.
----Problem may be rejection
They leave diseased kidney's in the body and add the fn'ing kidney
The Child with Alterations in Hematologic Function
Components of Blood
Types of blood cells.
--1) Albumin: preventsplasma from leaking into the tissue
--2) Fibrnogen: Clotting
--3) Globulins: Protect against infections
Red Blood Cells (RBCs)
-Most abundant cells in the blood
----Process of forming new RBCs
-Formed in bone marrow
-Any condition that causes tissue hypoxia triggers new RBCs to form
-Function of RBCs
----Carry oxygen from lungs to tissues and return carbon dioxide to lungs
----Above-average increase in RBCs
----Reduction of number of RBCs
----Higher levels of RBCs at birth
----Ruddy in appearance because of this
-Formed in bone marrow and lymph tissue.
-Mobile (Move around the body)
-Part of body's protective system
-Five types of WBCs, each with a distinct function.
-CBC with diff
----Useful in identifying an illness
----Diff gives WBC
----Decrease in WBCs.
-Newborns have higher WBCs and levels decrease slowly during childhood
Neutrophil primary reactor when there is an infection
Leukocytes - Agranulocytes
-Cell fragments that form hemostatic plugs to stop bleeding.
-Formed in bone marrow and stored in spleen.
-Newborns have lower platelets at birth.
-Newborns have lower clotting factors and vitamin K to form clot
----Vitamin K injection at birth
----Decrease in platelets
Values for Hematology in Children
-Platelet range 150,000-400,000
-Avg lifespan for RBC: 120 days
---With certain conditions RBC don't last that long
- Defined as a reduction in the number of red blood cells, the quality of hemoglobin, and the volume of packed red cells to below normal levels.
- May be caused by loss or destruction of existing RBCs or by impaired or decreased rate of RBC production (blood loss or certain conditions can lead to this)
-Most common type of anemia in children
-Most common nutritional deficiency in children
-Can occur due to:
---Blood loss (acute or chronic)
---Increased demand for blood production (esp in rapidly growing adolescents)
---Poor nutritional intake
---9% to 11% of adolescent females have anemia, primarily due to menorrhagia
S/S of Iron-Deficiency Anemia
-Clinical manifestations (long-term)
----Systolic heart murmur
----Pica or consumption of nonfood items (eating a lot of junk food may be an indication)
DX of Iron-Deficiency Anemia
----RBC normal to reduced
----Low Hemoglobin and Hematocrit
----Reduced MCV & MCH
------MCH is size of RBC
------MCV is the avg volume of RBC
----RBC - Microcytic (small) and hypochromic (pale)
-Low serum iron capacity
---Need to know this level to know the response to tx
----The higher the level, the more mature RBC are present (The higher, the better)
Iron-Deficiency Anemia Hematology
-Red blood cells appear hypochromic as a result of decreased hemoglobin synthesis
TX of Iron-Deficiency Anemia
-Correction of iron deficiency with oral iron preparation for about 4 months.
-Dietary changes to increase iron in diet
-Identify cause of bleeding and treat
Nursing Management Iron-Deficiency Anemia
-Administer medication or therapy as prescribed.
----Oral iron (ferrous sulfate)
----IV or IM iron dextran.
----Parental iron and blood transfusion
-Promote adequate intake of iron rich foods
----Iron-fortified formulas and cereal, lean meat, fish, dark leafy green vegetables, beans, and whole-grain bread
----Proper administration of oral iron supplement.
-Iron supplementation and side effects
----Staining of teeth (liquid preps), constipation, GI discomfort, black stools.
------Syringe and Dropper- give in the side of mouth further back and give water after
-------Older child give in straw and then water after
----Iron is given in divided doses
----Iron ingested in excessive quantities is toxic
----Fluids, high fiber diet needed
----Color of the stool will change
Sickle Cell Disease
-Sickle cell disease (SCD) is a hereditary hemoglobinopathy characterized by the partial or complete replacement of adult hemoglobin (HbA) by abnormal sickle hemoglobin (HbS) in red blood cells.
- All babies are born with fetal Hgb (HgbF) and after 6 mos it is replaced by adult Hgb
-Sickle Cell Trait (Hb SA)
-----The child has one sickle cell hemoglobin gene and one normal hemoglobin gene.
-Sickle Cell Anemia (HbSS)
----Child has two sickle hemoglobin genes
Types of Sickle Cell
HbSS most common type
Sickle Cell Histology
- Sickle Cell anemia may have resulted from Malaria long ago-- This trait allowed people to survive malaria and allowed the gene to be passed down
- Most common people affected are African ancestry because of this
Etiology of Sickle-Cell Anemia
-Sickle cell anemia is an autosomal recessive disorder
-Therefore, there is a 25% chance of each child having sickle cell disease when both parents carry the trait.
-Sickle cell anemia occurs primarily in African American
-Although the defect is inherited, the sickling phenomenon is usually not apparent until later in infancy because of the presence of fetal hemoglobin
----Sickling process is usually what occurs that tells the pt and family that they have this problem
----Infection and other things can trigger this
When both parents have sickle cell trait, what is the chance their children will have sickle cell anemia?
-Normal hemoglobin is partly or completely replaced by abnormal hemoglobin S.
-RBC acquires shape of a crescent or sickle.
-Approximately 2 million Americans carry one SCD gene
-1 in 12 African Americans have SCT
-Mediterranean and Hispanic descent can also be affected
Sickle Cell Trait
Pathophysiology of Sickle-Cell Anemia
-In SCA abnormal HbS replaces all or part of the normal hemoglobin.
-Under conditions of decreased oxygen such as, dehydration, acidosis, hypoxia, increased temperature the relatively insoluble HbS changes it structure from round to sickle or crescent-shaped
----Dehydration is one of the primary things in kids that causes this process to occur
-The angled shaped cell are rigid and obstructs capillary blood flow causing causes clumping, thrombosis, arterial obstruction with increased blood viscosity and hemolysis
---Increased viscosity - increased risk for blood clots
-Microscopic obstruction leads to engorgement and tissue ischemia.
PATHO FROM OTHER SLIDE
-A TRIGGER causes cells to sickle
----Emotional or physical stress
----Hypoxia or low oxygen tension i.e. high altitudes, poorly pressurized airplanes, temperature extremes
-EXAM: Sickled cells occlude blood vessels causes local tissue ischemia and infarction, eventually damages tissues and organs.
-EXAM: Sickled cells can resume normal shape when rehydrated and reoxygenated
-Cell life shortened to about 10-20 days
- This people may be surviving with low Hgb levels
-Bone marrow enlarges to produce more RBC
Sickle Cell Crisis
Sickle Cell Histology
Many of these red blood cells show an elongated crescent shape characteristic of sickle cell anemia.
Hgb S an RBC Sickling
Red Blood Cells Delivery of Oxygenand Sickle Cell Anemia
-Red blood cells are like cars on the highways inside your body.
-Oxygen is a passenger.
-Lots of red blood cells are necessary to take oxygen to every part of the body.
- In sickle cell anemia, red blood cells can become curved and pointy (like a sickle) and stiff.
-Sickle red blood cell==s don't always travel smoothly through the blood vessels, so traffic jams can occur on the highways.
-If sickle cell traffic jams occur, parts of the body will not get enough blood or oxygen.
-This can cause problems in the bones, spleen, lungs, kidneys, or brain.
S/S of Sickle Cell Anemia
-Fetal hemoglobin present until 4 to 6 months
----Usually asymptomatic until fetal hemoglobin is gone
-Sickle cell crises are acute exacerbation of the disease that are markedly in severity and frequency
-Reason for hospitalization is acute painful crisis
-Pain experienced in the back, abdomen, chest, joints
-Enlarged spleen from congestion with sickled cells
-Enlarged tender liver from blood stasis
-Inability to concentrate urine
-Dactylitis (symmetric swelling of hands and feet)
-Delayed sexual maturation
-Priapism (persistent erection)
-Recurrent severe infections
Types of Sickle Cell Crises
-Vaso-occlusive crisis MOST COMMON
Sickle Cell Crises
----Acceleration of RBC destruction characterized by anemia, jaundice, reticulocytosis.
----May be associated with viral illness or glucose-6-phosphate dehydrogenase (G6PD) deficiency.
----Clinically similar to pneumonia.
----It is associated with chest pain, fever, pneumonia-like cough and anemia.
-Cerebrovascular Accident (CVA)
----Sudden and severe.
----Sickled cells block the major blood vessels in the brain, resulting in cerebral infarction.
DX of Sickle Cell Anemia
-Newborns are screened for disease at birth
----Cord blood using hemoglobin electrophoresis
-Sickle-tubidity test (Sickledex) may be used for quick screening in children OVER 6 months because the HgbF needs to be replaced by HgbA before they can determine if it is occuring
Tx of Sickle Cell Anemia
-Prevention of crises
-Supportive care during crises
----Pain control, hydration, oxygenation, bed rest, blood transfusions
-Prevention of illness
----Immunizations, prophylactic antibiotics, folic acid
Nursing Management of Sickle Cell Anemia
Pt comes to the ER, Start IV and Hydration first
----Morphine, Dilaudid via PCA. Torodol, ibuprofen
----Demerol is not commonly used in kids because it causes seizures in kids
----ALWAYS WATCH RR FOR MORPHINE PUMPS
-Oral and intravenous fluids after 2-3 days
-Oxygen to provide comfort, but wont change whats happening in the body
----Immediate attention, blood, urine and throat cultures, antibiotics.
-Comfort measures i.e. massages
-Hydroxyurea shown to reduce pain associated with the sickle crisis
-Hematopoietic stem cell transplant
-Discharge planning and home care teaching, prevention of crises.
- Warm compresses okay- NO cold compresses
Average life span 45 years
RN Dx for Sickle Cell Anemia
-Risk for Infection/Actual infection
-Impaired tissue perfusion
-Group of inherited blood disorders characterized by deficient synthesis of specific globulin chains of the hemoglobin molecule
- In the case of beta-thalassemia, the most common type the beta chains are affected.
-Hemoglobin synthesis is impaired
-Anemia can be mild or severe
-Types of B-thalassemia
----Thalassemia minor (trait): Mild anemia
----Thalassemia intermedia: Severe anemia
----Thalassemia major (Cooley's Anemia)- Requires transfusion
Etiology/Pathophysiology of β -Thalassemias
----It is an autosomal recessive disorder.
----EXAM: Seen in children of Mediterranean and Asian origins (Indians much more likely to have it)
----Defective synthesis of RBCs (beta chain)
-The defect results in compensatory increase in hemoglobin production in other hemoglobin chains that becomes unbalanced, then disintegrates and destroys RBCs.
-To compensate for the hemolysis an overabundance of erythrocytes are formed.
S/S of β -Thalassemias
-Failure to thrive
- Severe anemia. (Hgb <6) [This level would require blood transfusion]
----Folic acid deficiency
----Thick cranial bones
----Delayed sexual maturation
DX of β -Thalassemias
-Hemoglobin electrophoresis (SHOWS DEFECT IN THE HGB CHAIN)
-Decreased hemoglobin, hematocrit, reticulocytes
TX of β -Thalassemias
----GOAL is to maintain NORMAL HGB levels
----At risk for iron overload due to frequent transfusions
----Blood transfusion is the conventional therapy.
----EXAM: Transfusions are administered with Desferoxamine (Desferal), which is an iron chelator and it minimizes hemosiderosis (excess iron in tissues)
-Bone marrow transplant
Problem w/ Transfusions
-Even though transfusions are helpful, they can also cause a big problem.
-After receiving many transfusions over two years, Keisha's body will get more iron than it can use (IRON OVERLOAD)
-Extra iron is what's leftover after the red cell cars get old and worn out.
-Everybody needs iron to stay healthy but too much causes problems.
-The rusty old cars pile up in the heart, liver, and hormone-producing organs.
-The body does not have a way to get rid of iron except when there is bleeding.
-Keisha doesn't feel any different from having too much iron.
-Even though she feels fine now, if she doesn't get medicine to help remove iron, her heart will become weak and her liver will not work well.
-Iron Chelation Therapy
----Deferoxamine (or DESFERAL) is a medicine which removes iron from the body and this is called Iron Chelation Therapy
-Desferal doesn't come as a pill and it doesn't last very long in the body.
-Desferal needs to be given using a small pump
----A needle is placed under the skin
----Needle placed for 10-12 hours each night
----Done at least 5 nights each week
S/S of Blood Transfusion Reactions
-When Hgb is low, you need transfusions, and when transfusions are common, iron overload is common
Nursing Implications for β -Thalassemias
-Administer blood transfusion
----Observe for iron overload.
-Monitor iron toxicity related to blood transfusion.
-Implement iron chelation therapy
-Administer folic acid.
----Avoiding persons with infections
-Avoid activities that may increase the risk for fractures.
-Decrease dietary iron
----Educate on disease process
----EXAM: Signs and symptoms of iron overload
----Home chelation therapy
The therapeutic mgmt of children w/ B thalassemia major consists primarily of which of the following?
A) Frequent blood transfusion
B) O2 therapy
C) Adequate hydration
D) Supplemental O2
-Deficiency of the blood cells that results from failure of the bone marrow to produce adequate numbers of circulating blood cells.
---1. Congenital (Faconi Anemia) consists of multiple congenital anomalies i.e. musculoskeletal, cardiac
------S/S: Pupura, petechiae, bleeding, fatigue, pallor.
---2. Acquired- Idiopathic or Drug Reaction
----Radiation, chemotherapy, chloramphenicol or antiepileptics
S/S of Aplastic Anemia
Symptoms depend on severity of bone marrow failure
- Petechiae and purpura.
----Lack of RBC i.e. pallor, lethargy, tachycardia, SOB
----Lack of WBC i.e. recurrent infections, opportunistic infections
----Lack of platelets i.e. abnormal bleeding, petechiae, purpura, bruising
-Yellow, fatty bone marrow instead of red bone marrow
DX of Aplastic Anemia
-Bone marrow aspirate
----Yellow, fatty bone marrow instead of red bone marrow
TX of Aplastic Anemia
-Bone marrow transplant
----Infection, hemorrhage, malignancy
-Immunosuppressive drug therapy
-Transfusions of platelets and PRBCs
-Bone marrow transplant
-A group of hereditary disorders characterized by a deficiency in blood clotting factors.
-Hemophilia A or Classic Hemophilia is caused by a deficiency of factor VIII - 80%.
-Hemophilia B, is known as Christmas Disease is caused by a deficiency of factor IX - 15%.
-Hemophilia is classified as mild, moderate or severe.
Etiology/Pathophysiology of Hemophilia
-X-linked recessive trait
----Manifests almost exclusively as affected males and carrier females
----Woman carrier has 50% chance of transmitting disease to her sons
----One-third of cases have no family history and are a new mutation
-Female carriers usually do not manifest symptoms of disease, but may have prolonged bleeding during dental work or surgery
S/S of Hemophilia
-Mild to moderate to severe bleeding tendencies.
-Asymptomatic until 6 months of age
----Mobility (minor trauma occurs) makes child more subjective to injury
-Hemarthrosis (bleeding into joint spaces).
----Bleeding in the joint spaces of the knees, ankles and elbow.
----Decreased range of motion
----Bone changes i.e. deformities, contractures
-Excessive bleeding after circumcision, dental extraction, umbilical cord when it is cut
Complciations of Hemophilia
-Bone changes i.e. osteoporosis, muscle atrophy
-GI hemorrhage i.e. GI obstructions
-Hematomas in the spinal cord can lead to paralysis
-Airway obstruction due to bleeding in the neck, mouth, thorax.
-Secondary complications from transfusions i.e. Hepatitis, HIV.
Ryan White Act
- Federal funding to Hemophilia and HIV pts both medical and emotional
- This 10y/o got HIV from blood transfusion and died at 15y/o
DX of Hemophilia
----History (bruising, pain)
----Low levels of factor VIII, IX
----Prolonged activated partial prothrombin time (APPT)
----Platelet count and Prothrombin time (PT) normal
TX of Hemophilia
-Control bleeding by replacing missing clotting factors
------2- to 4-fold increase in factor VIII activity
-Gene therapy being explored for the future
-Availability of transfusion therapy
----Near normal life expectancy
Nursing Management of Hemophilia
-Prevent and control bleeding episodes
----Reduce risk for injury - close supervision
----Control any superficial bleeding by applying pressure to the affected site for at least 15 minutes
----Immobilize and elevate the affected area above the level of the heart, apply ice pack
-Limit joint involvement and manage pain:
----EXAM: During bleeding episodes, hemarthrosis is managed by elevating and immobilizing the joint and by applying ice packs (RICE- Rest, Ice, Compression, Elevation)
----Medication i.e. corticosteroid, acetaminophen (NO NSAIDS because of bleeding risk)
----No bleeding i.e. ROM exercises
----Maintain appropriate weight
----Physical activity restrictions
Nursing Implications of Hemophilia
-Avoid rectal temps or suppositories (because it is prone to injuries that can cause bleeding)
-Avoid IM, SQ injections
-Avoid aspirin, ibuprofen, other meds that affect bleeding time
-Limit joint involvement
----Elevate joints and apply ice during bleeding episodes, ROM exercises AFTER bleeding episodes
-Provide emotional support
-Home care teaching
The RN is completing discharge teaching for the parents of a child newly dx w/ hemophilia V. Which measure should be included in controlling bleeding episodes?
A) Bed rest, oral coagulants, cold compress
B) Immobilize and elevate affected area, apply constant pressure to the area for 15 mins
C) Gentian violet, ice packs,, constant pressure to the affected area for 1h
D) Elevate the affected area, alternate warm and cold compresses every 20 mins
The Child with Cancer
Incidence of Childhood Cancer
-Approximately 11,000 children under age 15 diagnosed annually.
-Leading cause of disease-related death in kids younger than 15 years
-About 1500 children die from cancer annually with cancer in 2005 in the US.
-Cancer in children is usually embryonic or oncogenic in origin.
-Mortality rates continue to improve
-Overall survival is 80%, but depend on age and cancer type
-Primary tumor site varies by age
-Leukemia is the most common, followed by brain tumors, and sympathetic nervous system tumors.
----ALL most common in kids
Percentage of primary tumors by site of origin for different age groups
Different age groups have different types of cancer
Etiology of Childhood Cancer: Three Categories
1) External stimuli that cause genetic mutations.
2) Immune system and gene abnormalities.
3) Chromosomal abnormalities.
External Stimuli that Cause Genetic Mutations (Carcinogens)
-Ultraviolet radiation from the sun (skin cancer)
Immune System and Gene Abnormalities
Babies receive some passive immunity from mom, but not fn'ing like that of adults
-Diseases that affect the immune system.
-Familial genetic abnormalities.
-Some chromosomal abnormalities linked to increase cancer risk
---Down syndrome and leukemia
---Chromosome 11 abnormalities and Wilms' tumor (aka Nephroblastoma)
Clinical Manifestations (General for Cancer)
----May the result of a neoplasm, either directly or indirectly affecting the nerve receptors through obstruction, inflammation, tissue damage, stretching of visceral tissue.
----Syndrome characterized by anorexia, weight loss, anemia, weakness, and early satiety (feeling of being full)
----Results because of an altered immature immune system.
----Occur if the bone marrow cannot produce enough platelets.
----Can be from type of cancer or medications i.e. Steroids
Common Diagnostic Tests for Childhood Cancer
-Bone marrow aspiration
-Bone marrow biopsy
EXAM: Dx Tests for Cancer
ANC <500= hospital under isolation precautions
---Complete blood count with differential
---Liver function test
---Absolute neutrophil count (ANC)
-Bone marrow aspiration/biopsy
-Lumbar puncture - blast cells
-Computed tomography (CT)
-Magnetic resonance imagine (MRI)
-Nuclear medicine scans
-Positron emission tomography (PET)
Purpose of Diagnostic Tests
-Identify source of cancer (primary site).
-Determine if cancer has metastasized.
----Refers to the process of labeling, the type of cancer cells, severity, and spread.
----Stage 1 indicates less severe cancer without spread.
----KNOW THE DIFFERENCE BETWEEN STAGES
Clinical Therapy for Cancer: Options
-Bone marrow/stem-cell transplantation
Considerations in Choice of Therapy
-Type of cancer
-Degree of metastasis
-Goal of therapy
---Supportive (transfusions, antibiotic)
---Palliative (make pt as comfortable as possible)
-Remove or debulk tumor
-May determine stage and type of cancer
-Example: Wilms' tumor (tumor of the kidney that can be removed)
- May have to shrink it (chemo/radiation) and then remove surgically
-Energy destroys DNA and cell (destroys cancer and healthy cells)
-Used for local and regional control of cancer
---May be used in combination with surgery and chemotherapy
-May be curative or palliative
-Example: Hodgkin's disease (effective in this cancer)
Potential Long-Term Effects of Radiation
-Impairs growth of bones and teeth
---Can lead to scoliosis, dental problems
-Delayed puberty, sterility
-Uses parts of the body already programmed to destroy cells to target cancer cells
-Most are new or still under investigation
---Antibodies that are specific to certain cancers
---Vaccines that help the body fight cancer
---Tumor necrosis factor (TNF)
Bone Marrow/Stem-Cell Transplant
-Goal: Kill cancer with chemotherapy or radiation, then resupply the body with stem cells
-Sources of stem cells
---Child's own bone marrow (autologous transplant)
---Compatible donor (allogenic transplant)
---Umbilical cord blood
---Embryonic (Controversial topic)
-Chemotherapy is the administration of specific drugs that kill both normal and cancerous cells
-The schedule is determined by the cell's cycle of replication.
-Combining drugs allow for optimum cell cycle destruction with minimum toxic effects.
-The DNA in a normal cell can repair itself after chemotherapy, DNA in a neoplastic cell cannot.
-A protocol is a plan of action for chemotherapy that is based on the type of cancer, its stage, and the particular cell type
-Precautions in administering and handling chemotherapeutic agents
-Many chemotherapeutic agents are vesicants (sclerosing agents) and can cause severe cellular damage if even minute amounts infiltrate surrounding tissue
----Chemo only used in central vein--peripheral vein not used
- Need to be on lots of fluids
-A protocol is a map or plan of action that directs therapy by identifying the drug and its accompanying treatment.
- Hospitals have different protocols
-Some meds work in all phases of the cell cycle and others may only work in a particular phase
CHEMOTHERAPY DRUG ACTION
-Chemotherapy drugs either act at specific parts of the cell cycle or are nonspecific for action (act throughout all cell phases)
Meds Used for Chemo
(EXAM: Side Effects)
-Methotrexate (mentioned in class)
- These meds secreted by kidneys so monitor urinary labs and I&O
The combo works best and they are selected based on where they work
Focus on Side effects of all meds for RN Implications:
- Cyclophosphamide (mentioned in class)
- Mechlorethamine (Nitrogen Mustard- used in WWI)
----Used to tx certain types of cancer i.e. Lymphoma
Side effects of hormones:
Meds used to Tx Cancer
- the chemo meds suppress RBC, platelet, or WBC so these meds can help with this
- i.e. Epogen: stimulate RBC
Clinical Manifestations - Common side effects of Chemotherapy
-Bone marrow suppression (myelosuppression)
---Can lead to infection
-Nausea and vomiting
-Anorexia and weight loss
---i.e. antiemetic, Zofran, Reglan, Benadryl
-Mouth ulceration - dental care needed
-Alopecia - hair loss
----Person after tx may have different color or texture hair after it grows back
-Cushingoid changes i.e. Moon face
Common Side Effects of Chemo
-Zofran H5___ Receptor Blocker
-Give Zofran 30mins-1h before chemotherapy
-One of the most common threats to a child's body image at any age is hair loss induced by chemotherapy. -Use of hats can improve self-concept.
- Falls off in patches/ clumps
The child with cushingoid changes frequently has a rounded face and prominent cheeks.
-The child with cancer depends on parents and family members to provide support.
-Nurses can assist families and draw upon their strengths to help the child.
Nursing Diagnoses fro Cancer
-Risk for injury related to malignant process, treatment
-Risk for deficient fluid volume related to nausea, vomiting
-Risk for imbalanced nutrition
-Impaired skin integrity
-Altered family processes
-Fear related to diagnosis, procedures, treatments
Cancer Diagnosis: Reaction of Parents
-Must gather resources, make treatment decisions
-Travel often required for treatment
-Financial strain, potential job loss
Cancer Diagnosis: Reaction of Child
-Depends upon child's age
-Infants and toddlers:
---May believe they caused illness
---Improved understanding, like to talk about it
---Like to talk with other adolescents
-Most common solid tumor in children
-Most common are:
---Cerebral cerebella astroctyoma
---Gliomas of the cerebrum and brainstem
Sites of brain tumors in children.
-Approximately 3000 children under the age of 15 years are diagnosed annually as having tumors of the brain and central nervous system.
-The four most common brain tumors in children are
---2) Gliomas of the cerebrum or brainstem
---3) Cerebral, cerebellar, and supratentorial astrocytoma
---4) Ependymoma (from ependymal cells lining the brain ventricles and spinal cord canal) and craniopharyngioma
EXAM: Brain Tumors: Clinical Manifestations
-May be rapid or slow and subtle
-Include behavioral and/or nervous system changes
--Headache (a lot of times it is in the am)
--Nausea and/or vomiting
--Change in vision or hearing
Brain Tumors DX
Diagnosed with various imaging studies :
-CT, MRI, PET
Brain Tumors TX
-Treatment depends on type of tumor
-Radiation (not used for kids younger than 3 years)
-Chemotherapy (given intrathecally due to blood-brain barrier)
Brain Tumors: Nursing Management
-Monitor neurologic status
-Monitor for complications
---Increased intracranial pressure
---Diabetes insipidus (DI)
-Discharge planning and home teaching
-Solid tumor most commonly occurring OUTSIDE the cranium.
-The average age of onset is 2 years of age.
- Find a smooth, hard, nontender mass that can occurs anywhere along the sympathetic nervous system chain
---Abdomen (MOST COMMON SITE)
Clinical Manifestations for Neuroblastoma
-Location of the mass determines the symptoms
---Weight loss, abdominal distention, enlarged liver, irritability, fatigue, fever
-Palpation is CONTRAINDICATED
---It can cause separation/ seeding of the cancer cells (move from one area to another site)
Diagnostic Tests for Neuroblastoma
---Prenatal drug exposure
---Biopsy, CT, MRI
---EXAM: Urine catecholamines: elevated Vanillmandelic acid (VMA) and Homovanaillic acid (HVA).
Diagnosis is usually made after metastasis occurred
Clinical Therapy Treatment for Neuroblastoma
-Surgical removal of mass
-Follow with chemotherapy - multiple drugs used
-Radiation used occasionally
-Child and family teaching
-Neuroblastoma is most responsive to treatment in children under 1 year of age
Wilms' Tumor (Nephroblastoma)
-Intrarenal tumor (in kidneys)
-Common abdominal tumor
-Most common age: 2 to 5 years
-A missing tumor suppressor gene has been identified that acts to promote normal kidney development
Wilms' Tumor: Clinical Manifestations
-Usually asymptomatic, but may see HTN due to renin release
-Mass may be noticed by parent
---Firm, lobulated mass
---Located to ONE side of the midline of the abdomen (usually affects one kidney)
Dx of Wilms' Tumor (Nephroblastoma)
- Abdominal ultrasound
- Renal function tests i.e. BUN, Creatinine
Tx of Wilms' Tumor (Nephroblastoma)
---Remove affected kidney
---Look for metastasis
-Chemotherapy with or without radiation therapy
-Osteosarcoma (DISTAL FEMUR commonly affected)
--Rare, malignant bone tumor
--Occurs primarily in adolescent boys (because of this we think about growth spurts and sports injuries before cx)
--Located in the metaphysis of the distal femur, proximal tibia and proximal humerus
--Small, malignant tumor
--Occurs in shaft of long bones (femur, tibia, etc.)
--May occur in any bone
Clinical Manifestations of Bone Tumors
---EXAM: Elevated serum alkaline phosphate
Diagnosis of Bone Tumors
CT, MRI, tumor biopsy, blood tests
Bone Tumors: Therapy
---Limb-salvage or amputation surgery
---Metastasis is common
---Chemotherapy to reduce tumor size
---Surgery: Limb-salvage most common
---Metastasis is common
Bone Tumors: Nursing Management
-Postoperative care and monitoring
-Body image concerns
---Support group, other adolescents with amputations (adolescent speak to another adolescent that has gone through this)
-Most common form of childhood cancer
-Abnormal proliferation of white blood cells (WBCs)
-Two main types
---1) Acute lymphoblastic leukemia (ALL)
------More common in Whites and in boys.
------Peak age 2-3 years.
---2) Acute myelogenous leukemia (AML) /ANLL
------More common in children younger than 2 years and in adolescents
Pathophysiology of Leukemia
-Stem cells in bone marrow produce large number of WBCs
-These WBCs are immature and do not function normally
-Abnormal WBC replace normal WBCs
-Risk for infection increases
-Red blood cells and platelets are replaced with corrupted RBC and Platelet as well
---RESULTS: Anemia, thrombocytopenia, immunosuppression
Lab Values in Leukemia
Clinical Manifestations in Leukemia
-Bleeding from platelet suppression
--- Tarry stool
-Immunosuppression of WBC
--- Poor wound healing
-Hepatomegaly, bone pain
- Lymphadenopathy - reticuloendothelial involvement
--- Meningeal irritation
Diagnosis in Leukemia
-Bone marrow aspiration
---EXAM: 25% lymphoblasts is definitive of the disease.
Therapy for Leukemia
-Radiation and chemotherapy
Prognosis for Leukemia
-Prognosis generally better than in the past
---Age of onset is 2 to 10 years
---Initial hemoglobin less than 10 g/dL
---Rapid response to chemotherapy
-Most important indicator is initial WBC count
---The higher it is at diagnosis, the worse the prognosis
10% relapse within 1 year after treatment
Nursing Diagnosis for Leukemia
-Imbalanced nutrition, less than body requirements
-Risk for infection
-Risk for injury
-Disturbed sleep pattern
Planning and Implementation for Leukemia
-Skin and mouth care
-Attention to renal function
-Monitor IV site for extravasation
-Red blood cell, platelet administration
-Disorder of lymphoid system
-Arises from single lymph node or group of lymph nodes
-Peak occurrence in adolescent boys
-Occurs in clusters and has been reported in families.
-This suggests a possible genetic link as well as an infectious agent or environmental hazard.
Hodgkin's Disease Clinical Manifestations
---Nontender, firm lymph node DO NOT PALPATE
---Usual location: Supraclavicular or cervical nodes
-Other symptoms seen with aggressive disease process
Dx for Hodgkin's Disease
Lymph node biopsy
Hodgkin's Disease: Therapy
---Four-drug combination used
-Radiation often used
-Bone marrow transplant
-Third most common form of cancer in kids - leukemia, brain tumor
-Malignant tumor of the lymphoreticular system (internal framework of the lymph system)
Staging for Non-Hodgkin's Lymphoma
Stage 1 is better prognosis
Non-Hodgkin's LymphomaClinical Manifestations
-Enlarged, nodular lymph nodes
Dx of Non-Hodgkin's Lymphoma
-CBC, other labs
-Bone marrow aspiration
Non-Hodgkin's Lymphoma Therapy
-Radiation not used commonly
---Treat complications caused by tumor
---Muscles around the eyes
---Muscles in the neck
-Less common sites
Rhabdomyosarcoma: Clinical Manifestations
-Depends upon tumor site
-Surgical removal of tumor
-Intraocular malignancy of the retina
-Bilateral or unilateral
-May be inherited
-Main clinical sign:
----White pupil (leukokoria)
-Surgery - eye may be removed
A 6 y/o boy w/ Ewing's Sarcoma has just finished his course of chemo. Which of the following statements by his parents indicate they understand the signs of complications from the chemo?
A) "He will be playing football next week"
B) We will keep him on a liquid diet until he feels better
C) We understand he is more suceptible to infections; we will keep him away from sick family memebers.
D) He will wear a baseball hat to bed
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