Renal and Endocrine (WEDNESDAY) Flashcards
Most common pathogen of UTI?
Symptoms of UTI in a child? 5
Escherichia coli most common pathogen (80% of cases)
Dysuria (e.g., crying on urination or vocalized pain)
Frequent urination (>q 2 h)
Urgency
Suprapubic discomfort or pressure “Tummy/belly aches”
New onset bedwetting or incontinence
UTI Diagnostic Studies
preferred method?
What method is not used?
Whats used for older child?
Catherization is the preferred sample in child not potty-trained
U-bag- not used to diagnose UTIs-easily contaminated
Clean-catch outpatient older child
UTI TREATMENT—Antibiotics
Tx guided by ?
Treatment?
SNAP
Tx guided by clinical features, age, local resistance patterns and C&S
TREATMENT
-3rd generation Cephalosporin
Septra-Trimethoprim-sulfamethoxazole (Bactrim)
-Sulfa allergy contraindication
-Steven’s- Johnson Syndrome
-Nitrofurantoin (Macrobid)
-Amoxicillin
-Pyridium (OTC and prescribed)
-Relieves symptoms of UTI
-Stains urine reddish-orange (mistaken for blood)
Calculate normal urine output for a child.
Normal urine output: 1-2cc/kg/hour
Minimum urine output = 1 cc/kg/hour
Acute Poststreptococcal Glomerulonephritis
Caused by?
Onset?
Sudden onset of?
(PHOGE)
Caused by group A β-hemolytic streptococci (strep throat)
Onset 14 days after infection
antibody complexes collect in the glomeruli causing inflammation
Leukocytes occlude capillary
Proteinuria
HYPERTENSION
Oliguria (decreased urinary output)
Gross hematuria
EDEMA
Acute Poststeptococcal Glomerulonephritis lab tests
Four
Most important blood test?
Urinalysis: Proteinuria and Hematuria
Renal function: Elevated BUN and creatinine (renal insufficiency)
C-Reactive Protein (CRP) increased indicating inflammation
Erythrocyte Sedimentation Rate (ESR)
**Antistreptolysin O (ASO) blood test: circulating antibodies in the body in response to streptococcal infection. (4-6 weeks)
Acute Poststeptococcal Glomerulonephritis Management
Diuretics (Furosemide-Lasix)
Daily weights
Strict I&O
**Sodium restriction if hypertension or edema
Monitor vital signs
NEPHROTIC SYNDROME
What is lost in the urine?
Fluid shifts where and causes what?
Nephrotic syndrome is the most common chronic glomerular injury in children
Etiology is not completely understood: 70-80% cases from “minimal change disease”
Glomerular membrane becomes permeable to large proteins, especially albumin.
Albumin (Protein) is lost in the urine (Hyperalbuminuria)
Albumin in the blood decreases (Hypoalbuminemia) due to loss of albumin in the urine.
Due to the low albumin in the blood, fluid shifts to interstitial spaces resulting in edema.
Nephrotic Syndrome continued
three things happen?
Most common presentation?
BP is what?
at risk for what?
Massive proteinuria
Hypoalbuminemia
Hyperlipidemia
Edema: most common presentation
BP IS USUALLY NORMAL OR SLIGHTLY DECREASED!!!!!!!
At risk of chronic kidney disease and end stage renal disease
Nursing Alert nephrotic syndrome
Edema where?
3 other things
Periorbital, abdominal, gonadal, or lower extremity edema
Weight gain greater than expected based on previous pattern
Decreased urinary output (Fluid goes to interstitial space)
Pallor, fatigue
Nephrotic Syndrome Management
Whats restricted?
whats the therapy?
-Protein restricted if azotemia or renal failure
Sodium restrictions
Steroids (Prednisone)
-2 mg/kg divided into BID doses
-4-6 weeks of therapy then weaned (steroid duration of 3 months)
Immunosuppressant therapy (Cytoxan)
-more susceptible to infection
Diuretics (Lasix-Furosemide)
Nephrotic Syndrome (chart)
Damage to the glomerular increases permeability of the membrane to *protein (albumin)
*Massive proteinuria (3+-4+)
Hypovolemia (shift of fluid to interstitial space)
*Decreased urine output
Hyperlipidemia
Hypoalbuminemia
Normal or low B/P
*Edema r/t hypoalbuminemia
*Hematuria
Steroids, diuretics, immunosuppressants (Cytoxan)
acute glomerulonephritis chart
Immune complex disease following Group A β-hemolytic streptococci infection
*Mild proteinuria
Total body volume overload
*Decreased urine output
Normal(lipids)
Normal(albumin)
Hypertension
*Edema r/t decreased glomerular filtration rate (sodium and water retention)
Antistreptolysin O (ASO) titer: positive
*Hematuria
Antihypertensives, diuretics
What do nephrotic syndrome and APGN have in common?
Proteinuria
Decreased urine output
Edema
Hematuria
Acute Kidney Injury (AKI)
Principal feature?
Most common cause of AKI?
Usually what?
what may be needed?
-Definition—kidneys suddenly unable to regulate the volume and composition of urine
-Principal feature is oliguria: URINE OUTPUT< 1ml/kg/hr
severe dehydration
USUALLY REVERSIBLE
-Dialysis may be needed temporarily
Chronic Renal Failure (CRF)
Begins when?
progressive what?
Reversible?
Treatement?
Begins when diseased kidneys cannot maintain normal chemical structure of body fluids
Progressive deterioration over months to years
Final stage (End Stage Renal Disease) is irreversible
Treatment with dialysis and medication
Transplant if a candidate
Potential Causes of Chronic Renal Failure
Congenital renal and urinary tract malformations
VUR (Vesicoureteral Reflux) associated with recurrent UTIs
Chronic pyelonephritis
Chronic glomerulonephritis
Chronic Renal Failure: Signs and Symptoms
Uremia- vague ill-health, lassitude, anorexia and vomiting.
-Urea increases with renal failure.
Growth Failure
Osteodystrophy
Anemia
Convulsions (Seizure)
-Hypertension, hypocalcemia or uremia
Nursing consideration CRF
monitor what?
Administer what?
Diet?
Monitor BP, labs (BUN/creatinine), growth
Administer Diuretics
Regulation of diet most effective means 2nd to dialysis
-Low sodium, fluid restrictions initially
-Recommended Dietary Allowance (RDA) protein
-Potassium limitations if increased creatinine
Hemodialysis
Requires creation of?
Preferred for who?
Best suited for children who?
Achieves what?
Requires creation of a vascular access and special dialysis equipment
Preferred dialysis method for children over 20 kg
Best suited for children who live close to dialysis center (requires 3 visits per week for 3-5hrs
Achieves rapid correction of fluid and electrolyte abnormalities
Child Receiving Hemodialysis?
no what?
NO BPs in the arm AV fistula
PERITONEAL DIALYSIS
primary osmotic agent to remove water
-Fluid instilled into the peritoneal cavity and left for prescribed time
-Glucose is primary osmotic agent to remove water
-Fluid is allowed to drain thus removing waste products and excess water
-Tidal continuous cycling PD
-Dialysate absorbs or pulls waste and fluids from blood vessels in the abdominal lining.
-Can be managed at home-child can receive treatment while sleeping.
-Slower and gentle compared to hemodialysis
-Indicated for neonates, children.
Nursing Management Peritoneal Dialysis
-Assess peritoneal insertion site for redness, edema, discharge
-Assess peritoneal fluid (if cloudy contact provider)- R/O peritonitis
-Daily weight
-Measure abdominal girth
Type 1 diabetes
What is it?
Onset?
Symptoms? 3 ps and what?
Labs?
Autoimmune destruction of pancreatic beta cells
Absolute insulin deficiency
Onset: Abrupt
Polyuria (new onset bedwetting)
polydipsia
polyphagia
Rapid weight loss
Insulin (injections or pump)
Balance diet and activity
Labs: Monitor glucose level multiple times a day (goal 80-120 mg/dl)
Hemoglobin A1C- average blood sugar over the past 3 months.
Urine testing for ketones done during illness and Diabetic Ketoacidosis
Type I diabetes Management
What should be monitered?
Postive ketones indicate?
encourage what?
Insulin should never be?
Children require what?
Parents should monitor blood glucose levels and urinary ketones every 3 hours. Positive ketones indicate acidosis and DKA.
Encourage fluids to prevent dehydration
Dont stop insulin during illness
Children require more insulin when they are sick r/t hyperglycemia
Hypoglycemia
(definition and causes)
Blood sugar < 70 mg/dl
Causes
-Too much medications (i.e., insulin)
-Medication mistakes (i.e., accidental too much insulin administered)
-Missed meals
-Too little food eaten after insulin
-Excessive exercise - sports
hypoglycemia management
3
-Hold insulin
-Have child eat or drink something that has sugar in it (ie.g., Orange juice, cake icing, hard candy, milk)
-Administer Glucagon IM or SQ
Diabetic Ketoacidosis (DKA)
DKA results in? 3
Life-threatening situation
Newly diagnosed diabetic, insulin omission in known diabetics, acute gastroenteritis with persistent vomiting
DKA results in:
**Metabolic acidosis (ph < 7.30 or Bicarb (HCO3) < 15 mmol/L)
**Hyperglycemia (Serum glucose > 250 mg/dL)
**Fluid and electrolyte shifts
Hypokalemia
Hyponatremia
DKA-Clinical Manifestations
what is a complication of DKA treatment?
Monitor what?
5 other signs?
**Cerebral edema is a complication of DKA treatment.
**Monitor neurological status (Glasgow Coma Scale)
Vomiting
Signs of dehydration-Hypotension, tachycardia
Kussmaul respirations- deep rapid breathing (metabolic acidosis)
Acetone odor on breath
Decreased level of consciousness
Management of DKA
Avoid what?
Do not push what?
Iv fluid therapy
insulin therapy
potassium
**Avoid rapid bolus of fluids or insulin
**DO NOT PUSH K+
IV Fluid Therapy
Corrects what?
Correct dehydration
0.9 Normal Saline
Then D10NS (balances insulin to avoid hypoglycemia and decreases cerebral edema due to fluid shift)
insulin therapy
Corrects what?
Corrects Ketoacidosis
Continuous infusion
Regular Insulin 0.1 units/kg
per hour
Begin IV insulin after Initial IV hydration and urine
potassium
Electrolyte Shifts
IV Potassium after IV fluid and urinating (Never give Potassium absence of urine).
Potassium is mixed in IV fluids - not given in a syringe IV push.
