Level 3 exam 5 notes

Intussesception

ileocolon region -where small intestine meets large intestine young, infant boys 2x more likely CM sudden awake colicky abd pain -> infant cries very loud suddenly and draws knees to chest -palpable RUQ abd sausage like mass -decrease or absent bowel sounds -bilous vomiting (green) I. -bleeding, current jelly stool (bloody mucous stool) P. -peritonitis, fever, shock, pale lethargy Dx CM seems fine 1 min next screaming bring up knees, air/barium enema -> dx & TM -> introduce into lower intestine -> if present will be seen during imaging & telescope bowel foes into norm position cause force -80% successful -> if unsessful or reoccurring -> Tx monitor stool color surgical reduction, NG/NPO/IVF, 10% chance reoccurrence, monitor all stools, promote parent/child bonding Imperforate Anus: no anal opening CM newborn no passage of meconium x24 or meconium in urine due to fistula Dx abd US Tx surgery -analrectalplasy Preop NPO, NG decompress belly, IVF post prevent infection, perineal dressing drain, protect anus, positioning (on side with hips elevates, supine legs elevated 90 degrees, no laying on back cause pressure), IVF -> start feeds when return of bowel functions (sounds), colostomy care if needed, family support -> manual dilations, toliet training delayed (complete continence delayed cause not born with naturally-bowel habit training, diet modifications prevent constipation no barring down) Acute Appendicitis: average age 10yrs (as early 4yrs -> adulthood) -within 48hrs of initial complaint CM abd pain generalized -> McBurney point RLQ, low grade fever, lay on side with knees flexed, change in behavior/posture, anorexia N/V, rebound tenderness, movement aggravates pain perforation -poor outcome -sudden relief of pain then slowly comes back and increases, rigid guarding of abd increased abd distention -> increased HR RR pallor lethargy chills irritability Dx PE, CBC (WBC >10000 shift to left bands), CRP (make sure trending downward), UA, HCG, US (can see enlarged in thin or kid), CT scan adults or fatter kid if not ruptured -> surgery Tx surgery Preop NPO/IVF, bedrest, position post antibiotics, IVF until ready to feed bowel sounds passing gas -> feed when return of bowel function Ruptured -dont like to do surgery, poor prognosis don't heal as well -get kid better, rest appendix wait to healed delay surgery -surgery later, rehydrate, antibiotics high dose, pain management, NG suction, drain puss pockets (radiology), bedrest

chvostek's sign

tapping of facial nerve --> contraction of facial muscles twitching of the facial muscles in response to tapping over the area of the facial nerve. hypoparathyroidism hypocalcemia

ENDOCRINE DISORDERS

Endocrine System: -Communication and coordination of systems through chemical substances: hormones Hypopituitarism: GH Deficiency Hyperpituitarism: GH Excess Hypothyroidism Hyperthyroidism (Graves ) Hypoparathyroidism Hyperparathyroidism Cushing Syndrome Addison Disease Assessment Thorough history -past health history, meds, surgery, other treatment Physical examination -inspection -auscultation -palpation -percussion Diagnostics *Key to understanding problem lies in understanding the function of the endocrine hormones! A balancing act: A Problem of "Too Much or Too Little Hormone" Risk Factors Modifiable risk factors: medication, stress, diet, & obesity Non-modifiable risk factors: family history of endocrine illness, history of trauma, aging Assessment Factors Change in weight; hair quality & distribution; body proportions, muscle mass & fat distribution Change in LOC, mood or behavior Change in menses & libido Intolerance to heat & cold Skin color, texture & temperature changes Change in thirst; urinary patterns *Hypopituitarism: Growth Hormone Deficiency Deficient secretion of GH (somatotropin) inhibits somatic growth Most common organic etiology: tumor in pituitary or hypothalamus Usually normal at birth; growth patterns progressively decrease Chief complaint: short stature Assessment Family history/parental heights Birth size History of growth patterns Physical exam Psychosocial evaluation Drug intake Nutritional state ROS Diagnostics Endocrine studies: absent or subnormal reserves of pituitary GH Radioimmunoassay of plasma GH Radiographic surveys Radiographic exam of hand/wrist MRI of brain Clinical manifestations Short stature -Usually normal 1st year -2nd year drops below established % -Growth measurements <5th % Premature aging Height may be more retarded than weight Appear well nourished Skeletal proportions normal Relatively inactive Bone age nearly always retarded but near height age Primary teeth appear at expected age; permanent delayed Overcrowded, malpositioned teeth Sexual development delayed but normal Therapeutic Management If organic lesion: surgical removal or irradiation of tumor Replacement of GH -daily SQ injections -injections given at bedtime -treatment expensive Replacement of other hormones if deficient Prognosis: GH replacement successful in 80-90% -Attain eventual adult height at slower rate -Early diagnosis important Emotional support -Realistic expectations *Pituitary Hyperfunction: Growth Hormone Excess *Gigantism: Excess GH before closure of epiphyseal shafts results in accelerated vertical growth Overgrowth of long bones Height of 8 feet or greater Rapid & increased development of muscles *Acromegaly: Hypersecretion of GH after epiphyseal closure results in transverse growth Overgrowth of head, lips, nose, tongue, jaw, paranasal & mastoid sinuses, separation & malocclusion of teeth, disproportion of face, increased facial hair, thickened, deeply creased skin Diagnostics History of excessive growth & increased GH levels Clinical Manifestations Radiologic & endocrine studies CT, MRI, skull x-rays Management: early identification! If lesion, treat surgically with cryosurgery or hypophysectomy External irradiation & radioactive implants *hormone replacement after surgery Drug therapy to reduce GH levels in acromegaly Emotional Support *Hyperthyroidism: Hyperactivity of the thyroid gland Increase in synthesis and release of thyroid hormones T3 and T4 Most common form is Graves disease: -autoimmune disease of unknown etiology with thyroid enlargement & excessive thyroid hormone secretion Other causes include toxic nodular goiter, thyroiditis, excess iodine intake, pituitary tumors, & thyroid cancer. Clinical manifestations: r/t the effect of excess thyroid hormone. Excess circulating hormone increases metabolism & tissue sensitivity to stimulation by the SNS. Palpation: goiter. Auscultation: bruits CV: bounding, rapid pulse, palpitations, tremors GI: weight loss, increased appetite, diarrhea Integumentary: warm, moist skin; hair loss, fine silky hair Heat intolerance Exophthalmos Restlessness Amenorrhea Diagnostics History & physical exam Ophthalmologic exam ECG (a-fib) Laboratory Tests -Serum free T4 - TSH levels -Thyroid antibodies Note: Total T3 & T4 measurements not as useful since measure both free & bound to protein hormone level Thyroid scan Needle biopsy Radioactive iodine uptake (RAIU) - increased uptake with Graves' disease Malignancy (hot/cold areas) Collaborative Care GOAL: block adverse effects & stop oversecretion Radioactive Iodine Therapy (RAI) - treatment of choice* Antithyroid Drugs (PTU & Tapazole): inhibit synthesis of thyroid hormones; not curative Iodine: inhibits synthesis of T3 & T4 & blocks release Beta-adrenergic blockers (propranolol)- controls symptoms Surgical Therapy: subtotal thyroidectomy Nutritional therapy: High-calorie; high-protein; frequent meals; restrict caffeine Thyroidectomy Pre-op - teaching & preparation Post-Op: ABC's!! ***Airway obstruction is an emergency situation! - oxygen, suction, and a tracheostomy tray at bedside -assess q 2 hrs x 24 hrs Semi-Fowler's position: support head VS and assess for hypocalcemia-why?? Identify s/s; keep calcium gluconate available Control pain If total thyroidectomy: lifelong replacement. -teach s/s hypothyroidism. -reduce caloric intake to prevent weight gain -adequate iodine to promote thyroid function Nursing Management Assessment Diagnoses Planning Implementation: usually outpatient VS; CV status; diet; meds; eye care; rest. Include teaching. Note: acute intervention for thyrotoxicosis Complications Thyrotoxic crisis (thyroid storm) Acute, rare, life threatening condition All hyperthyroid manifestations are heightened Cause- stressors (infection, trauma, surgery) in patient with preexisting hyperthyroidism Manifestations: severe tachycardia, heart failure, shock, hyperthermia, HTN, restlessness, agitation, seizures, abdominal pain, N/V, diarrhea, delirium, coma, and death Treatment: hospitalization. Drug therapy; ensure adequate oxygenation; monitor for cardiac dysrhythmias; fever reduction, fluid replacement, manage stressors. *Hypothyroidism: -Insufficient circulating thyroid hormone - Most common cause: iodine deficiency Primary: destruction of thyroid tissue or defective hormone synthesis Secondary: pituitary disease with decreased TSH secretion Transient: r/t thyroiditis or d/c of thyroid hormone therapy. Also: thyroidectomy; overuse of antithyroid drugs; malfunction of pituitary gland; radioactive iodine; medication. Congenital Clinical Manifestations Manifestations vary depending on severity, duration and patients age at onset. Fatigue & lethargy Depression Weight gain Cold intolerance Personality & mental changes Mental sluggishness Myxedema -dull, puffy skin -coarse, sparse hair -periorbital edema -prominent tongue -masklike affect Menstrual disorders Constipation/Obstruction Hypothermia Decreased cardiac output *Juvenile Hypothyroidism: Congenital: born with thyroid hormone deficiency Acquired: Diagnosis: Infant Metabolic Screening (IMS); TSH level. Clinical manifestations: decelerated growth, skin changes, constipation, sleepiness, mental decline. Treatment: TH replacement. Diagnostics Clinical manifestations Serum TSH (high when defect in thyroid; but low when in pituitary or hypothalamus) Free T4 Serum T3 & T4 decreased TRH stimulation test Serum thyroid antibodies in Hashimoto's Thyroiditis Elevated cholesterol & triglycerides Anemia ECG-sinus bradycardia RAI uptake-decreased with hypothyrodism Collaborative Care Thyroid hormone replacement Levothyroxine (Synthroid) -Monitor Thyroid levels & adjust dosage prn** -Monitor pts with CV disease -Lifelong replacement Low calorie diet Complications: Myxedema coma. Medical emergency. Precipitated by infection, drugs, cold exposure, trauma. S/S: subnormal temp; hypotension; hypoventilation. Treatment: support vital functions; IV thyroid hormone replacement!! Nursing Management Assessment Diagnoses Planning Implementation -screening -acute -home care -teaching Evaluation Note: be able to identify nursing care management for the nursing process. *Hypoparathyroidism: Decreased secretion of parathyroid hormone (PTH) Most common cause is iatrogenic Labs: Decreased levels of circulating PTH cause hypocalcemia & hyperphosphatemia. Clinical manifestations due to hypocalcemia. Management: -treat acute complications (tetany) -maintain normal calcium levels -prevent long-term complications -teach drug therapy & nutrition -lifelong treatment and follow-up care *Hyperparathyroidism: Increased secretion of parathyroid hormone (PTH) PTH helps regulate calcium & phosphate levels Primary, Secondary, Tertiary Excessive levels of circulating PTH usually lead to hypercalcemia & hypophophatemia Affects multiple body systems Clinical Manifestations (may be asymptomatic or overt symptoms) Osteoporosis, fractures, generalized weakness Kidney stones Muscle weakness, loss of appetite, vague abdominal pain, constipation, fatigue, emotional disorders, & shortened attention Dysrhythmias, hypertension BONES, MOANS, & STONES" Complications: renal failure, pancreatitis, cardiac changes, & fractures Diagnostics Elevated PTH levels Increased calcium (>10mg/dL) Decreased phosphorus (<3 mg/dL) Elevated: -serum chloride, uric acid, creatinine, amylase (if pancreatitis), alkaline phosphatase (if bone disease) -urine calcium DEXA scan MRI, CT, U/S Surgical Therapy (partial or total parathyroidectomy) post-op management observe for s/s hypocalcemia -major complication: tetany Non-surgical Therapy Annual exam & diagnostics Dietary management Encourage ambulation & exercise Medications: -Biphosphonates, oral phosphate, diuretics, calcimimetic agents Teach s/s hypo & hypercalcemia *Cushing Syndrome: Caused by an excess of corticosteroids, particularly glucocorticoids Most common cause is iatrogenic administration of exogenous corticosteroids Critical thinking: which conditions predispose your client to Cushing syndrome? Endogenous causes include pituitary tumor, adrenal tumors & ectopic ACTH production by tumors. Clinical Manifestations Weight gain most common feature Truncal or generalized obesity Moon face Purplish red striae Edema of lower extremities Hirsutism in women Buffalo hump Menstrual disorders in women Hypertension Unexplained hypokalemia Bone fractures Mood disturbances Diagnostics History & physical Mental status evaluation Elevated plasma cortisol levels with loss of diurnal variations Plasma ACTH level (low, normal, or elevated depending on cause) CBC Na, K, Glucose level Dexamethasone suppression test 24 hour urine collection for free cortisol CT/MRI: adrenal & pituitary glands Collaborative Care: Intervention dependent on underlying cause Pituitary Adenoma -transsphenoidal resection -radiation Adrenocortical Adenoma, Carcinoma, or Hyperplasia -Adrenalectomy (open or lap) -Drug therapy Ectopic ACTH-secreting tumor -surgery or radiation Exogenous corticosteroid therapy Discontinue or alter dose Note: abrupt withdrawal may precipitate acute adrenal insufficiency. Gradual withdrawal is necessary! Nursing Management Assessment Diagnoses Planning Implementation: -health promotion: identify clients at risk -acute intervention: s/s hormone & drug toxicity; complicating conditions (CV, DM, infection) -preoperative care: correct HTN, hyperglycemia, hypokalemia high protein diet; teaching -postoperative care: BP, R, HR; F & E; high dose corticosteroids IV -ambulatory and home care: d/c instructions based on lack of endogenous corticosteroids & resulting inability to react to stressors. Evaluation *Adrenocortical Insufficiency: -hypofunction of the adrenal cortex Primary cause : Addison's disease Secondary cause: lack of pituitary ACTH secretion In Addison's disease all 3 classes of adrenal corticosteroids: glucocorticoids, mineralocorticoids, & androgrens are reduced. Most common cause of Addison's disease: autoimmune response. Adrenal tissue is destroyed by antibodies against patient's own adrenal cortex. Clinical Manifestations Progressive weakness Fatigue Weight loss Anorexia Skin hyperpigmentation Orthostatic hypotension Hyponatremia, salt craving Hyperkalemia Nausea & vomiting Diarrhea Irritability & depression Presidency & Addison's Exacerbating Factors -good career choice? Why/why not? Diagnostic History & Physical examination Plasma & urine cortisol levels subnormal Serum electrolytes -decreased Na & glucose, increased K ACTH-stimulation test ECG (peaked T waves) CT, MRI Collaborative Care Lifetime daily glucocorticoid (hydrocortisone) replacement -2/3 on awakening in am -1/3 late afternoon Daily mineralocorticoid (Florinef) in morning Salt additives for excess heat or humidity Increased doses of cortisol for stress situations -e.g. surgery, hospitalization Monitor for s/s infection Nursing Management: Implementation Acute intervention: frequent assessment; protect from noise, light, environmental temperature extremes IV replacement then oral corticosteroids Teach pt. importance of follow-up care Ambulatory & home care: Teaching Plan Proper administration of medication Recognizing need for extra medication & techniques for stress management S/S of corticosteroid deficiency & excess Emergency kit wit 100mg hydrocortisone, syringes, instructions at all times!! Complications: Acute Adrenal Insufficiency (Addisonian Crisis) -Life threatening emergency Triggers: stress Sudden w/d of corticosteroid replacement therapy Adrenal surgery Following pituitary gland destruction Manifestations: Hypotension, tachycardia, dehydration, hyponatremia, hyperkalemia, hypoglycemia, fever, weakness, confusion. Shock & circulatory collapse. Severe vomiting diarrhea, pain. Treatment: Shock management & high dose hydrocortisone replacement Large volumes of NS & 5% Dextrose

endocrine review

Endocrine p. 1102 Made up of glands that produce and secrete hormones. Hormones regulate the body's growth, metabolism and sexual development and function. Hypothalamus p. 1105 Located in the forebrain. Control Center of the endocrine system. It is the size of a grape with 3 regions. The hypothalamus releases substances that either stimulate or inhibit the formation and release of groups of hormones from the pituitary gland. Examples: growth hormone-releasing hormone (GHRH) - releasing hormone, corticotropin-releasing hormone, and thyrotropin -releasing hormone and Somatostatin (inhibits growth hormone). -tells PG what to do Pituitary Gland p. 1105 Master gland which is a size of an English pea. It receives messages from hypothalamus and sends messages to other glands. Anterior pituitary gland secretes several hormones. Hormones: Growth Hormone (GH) - for growth and development, Thyroid stimulating hormone (TSH) - stimulates the thyroid gland, Adrenocorticotropic hormone (ACTH) - stimulates the adrenal glands. Thyroid Gland p. 1106 The thyroid gland uses iodine from the foods we eat to make two main hormones: Triiodothyronine (T3) and Thyroxine (T4). These hormones regulate energy and metabolism and growth and development. Parathyroid Gland p. 1107 There are two pairs and they lie behind each thyroid lobe. The glands secrete Parathyroid hormone (PTH). PTH helps regulate serum calcium and phosphate levels by stimulating bone resorption of calcium, renal tubular reabsorption of calcium and activation of Vitamin D. Resorption- transfer of calcium from bone fluid to blood. Reabsorption- moves calcium from renal tubules back into blood stream and excretes phosphorus. Activation- stimulates the renal conversion of vitamin D to its most active form (Calcitriol). PTH also promotes absorption of calcium and phosphorus from the GI tract. Adrenal Gland p.1107 These glands sit above the kidneys. They secrete several hormones. We are concerned with the adrenal cortex which is the outer part of the gland. It secretes Glucocorticoid, Mineralocorticoids, and adrenal androgens. For exam five we are concerned with the two main Corticosteroid hormones: Glucocorticoid (cortisol) - Responsible for regulating glucose concentration and stress response. Mineralocorticoid (aldosterone) - Responsible for the sodium and potassium and hydrogen ion balance.

adolescent review vid

Erikson psychcosocial identity vs role confusion Key task- find identity, find out who they'd like to be if don't find identity then role confusion -don't know who they are -developing self confidence and security confusing period transition listen with nonjudgemental attitude not confident not know exactly who they are, in stage of experimentation

THREATS TO ELIMINATION IN THE CHILD

GASTROINTESTINAL SYSTEM: Hirschsprung's Disease Intussusception Imperforate anus Appendicitis Hirschsprung's Disease: Congenital Aganglionic Megacolon -Absence of ganglion cells in distal colon -Mechanical obstruction caused by inadequate motility of part of the intestine -Lack of enervation results in absence of peristalsis -Mechanical obstruction secondary to inadequate motility of part of the intestines. Occurs in 1:5000 live births - may follow a familial pattern; 4 times more common in males. Has been associated with other syndromes including Down syndrome Patho: Absence of ganglion cells in one or more segments of distal colon. 80% have aganglionosis is restricted to the internal sphincter, rectum, and a few centimeters of the sigmoid colon and is termed short-segment disease. However, the entire colon or part of the small intestiines may be involved. There may also be skipped segments. Lack of enervation results in absence of peristalsis and decreases the internal sphincters' ability to relax. Normally when a stool bolus enters the rectum, the internal sphincter relaxes and the stool is evacuated. In Hirschsprungs, the internal sphincter does not relax. Evacuation prevented and obstruction occurs. Stool accumulates proximal to the defect causing Megacolon and abdominal distention (Remember discussing megacolon in ulcerative colitis.) With no peristalsis and no evacuation of solids, liquids and gas=obstruction occurs. Intestinal distention and ischemia may occur as a result of distention of bowel wall, which contributes to the development of enterocolitis (inflammation of small bowel and colon) and the leading cause of death. Clinical Manifestations- (huge tummy) Vary according to amount of colon involved and age of child newborn-infant-child (chronic) -Abdominal distention Constipation Failure to thrive Signs of enterocolitis -Newborn: failure to pass meconium 24-48 hours, distended abdomen, feeding intolerance with bilious vomiting. Infancy: growth failure, constipation, episodes of diarrhea and vomiting. Childhood: constipation, ribbonlike, foul smelling stools, abdominal distension, visible peristalsis, papable fecal mass, undernourished, anemic appearance. Note s/s enterocolitis: fever, abdominal distention, diarrhea (explosive watery stools) and appear very ill. This can be severe and lead to life threatening dehydration or sepsis. Diagnosis- Clinical Manifestations Barium enema & abdominal x-rays Rectal Biopsy: absence of ganglion cells -Barium enema, anorectal manometric examinations. Confirmed dx: full-thickness rectal biopsy demonstrating the absence of ganglion cells. Therapeutic management- Surgical Bowel resection and colostomy Pre-Op Care Depends on age & clinical condition Newborn vs. Older Child Stabilize with fluid & electrolyte replacement Observe for s/s enterocolitis Measure abdominal circumference If malnourished: Enemas Low fiber; High calorie; High protein diet TPN prn Surgery: procedure-laprascopic or thru the rectum. Remove the section of aganglionic bowel. May have a temporary colostomy. A Soave endorectal pull-throughmay be done. This consists of pulling the end of the normal bowel to through the muscular sleeve of the rectum, from which the aganglionic mucosa has been removed. The goal is to relieve the obstruction, restore normal motility and reserve the function of the sphincters. If an infant or child is not severely ill when the diagnosis is made, this operation can often be done within a week of the diagnosis. However, some patients are extremely ill when they first present with Hirschsprung disease because of enterocolitis or a dramatically dilated colon from long-term obstruction. If significantly distended: temporary ostomy to rest bowel and allow to return to normal size; allows the colon to decompress. After several months, the definitive "pull through" operation can be performed. Relieves obstruction and restore normal bowel motility and function of the internal anal sphincter Prognosis-high rate of success Anal stricture, constipation & incontinence are potential complications after surgery p. 781 Major Conisderations.\: Help the parents adjust to a congenital defect in their child, foster infant-parent bonding, prepare them for medical-surgical intervention, assist them in colostomy care after discharge Pre op Care: Teach child at developmental level. Depends on the condition of the child when presenting. Malnourished may need to improve physical status prior to surgery. Newborn: bowel is sterile: no pre-op bowel prep Older children: saline enemas to empty bowel; systemic antibiotics & colonic irrigations with antibiotic solution to decrease bacterial flora. Before the operation, it is very important that the colon be well-irrigated and any enterocolitis be under control. This may require from several days to a week of antibiotics, rectal irrigations, and dilations. Enterocolitis is the most serious complication. Monitor for signs of shock, ibserve fir stnotins if biwek oerfiratuib sycg as fever, increasing abd. Distention (measure girth at widest part of the abdomen or at the umbilicus with a paper tape measure.) vomiting, increased tenderness, irritability, dyspnea, and cyanosis. Goal: Relieve obstruction and restore normal bowel motility and function of the internal anal sphincter Prognosis-high rate of success Anal stricture & incontinence are potential complications after surgery Post -Op Care Frequent monitoring of VS Abdominal circumference Progressive feeding Meticulous skin care If colostomy: stoma care; Foley care Observe for s/s enterocolitis Discharge teaching concerning ostomy & return for additional surgery as needed Teach s/s enterocolitis! Fever Abdominal pain Abdominal distention Bloody diarrhea Urgent medical attention Post opt: same as other abd. Surgeries. Colostomy teaching is important for parents and patient After the operation children are permitted to eat once bowel function has returned, and they may then be discharged home. This is usually within one to two days of the operation when the minimally invasive procedure has been used. Many children have difficulties with severe diaper rash after the operation due to an increased frequency of stool output. This persists until there has been accommodation to the operation. Instruct parents in the application of various cream preparations that reduce the severity of the inflammation in the skin around the anus. Regimen of occasional dilatation of the rectum can be performed at home; rectal irrigations for three months after the operation in order to decrease the incidence of colon infection. The long-term results from pull-through operations for Hirschsprung disease are good, but children are still at risk for the development of enterocolitis in the colon that remains, even though it has ganglion cells. If colostomy: Teach preschool and older child about ostomy using concrete terms and visuals-stress temporary ostomy; teach parents to be actively involved in colostomy care *Intussusception: Proximal segment of bowel telescopes into a more distal segment of bowel Intussusception p. 809 Proximal segment of bowel telescopes (invaginates) into a more distal segment; Intestinal contents cannot pass beyond defect Causes inflammation, edema, decreased blood flow; Complications include: ischemia, perforation, peritonitis, & shock Untreated: not compatible with life The most common cause of intestinal obstruction in children between the ages of 3mo. To 3 yr. During intussusception, a segment of bowel (intussusceptum) telescopes or invaginates into a more distal segment (intussuscipiens), and drags the associated mesentery, vessels, and nerves with it. This results in compression of the veins, followed by swelling of the region leading to obstruction and a subsequent decrease in blood flow to the affected part of the intestine. Almost 90% of cases affect the ileocolic region of the intestine (where the small intestine meets the large intestine). The compression of blood vessels in the involved intestine reduces the supply of blood to the affected intestine. If the blood supply is greatly reduced, the involved intestine may swell, causing an obstruction, or even die (become gangrenous) and bleed. It also may rupture and lead to abdominal infection and shock. Intussusception is an emergency and requires immediate attention. Most cases of intussusception occur in children between 5 months and 1 year of age. Boys develop the condition two times more often than girls. Intussusception can also occur in adults and older children, although it is uncommon. The causes of intussusception are not fully known. Most cases in young children are idiopathic, (meaning the cause is unknown), although some viral and bacterial infections of the intestine may possibly contribute to intussusception in infancy. Intussusception is very rare in older children and adults. In this population, the causes are believed to be due to polyps or tumors, which are often referred to as the "lead point" of the intussusception. Clinical Manifestations Sudden occurrence of acute, colicky, abdominal pain Palpable RUQ abdominal sausage-shaped mass "Currant jelly" (blood & mucus) stool Vomiting Abdominal tenderness and distention Diminished or absent bowel sounds Note: not always this "classic" presentation!! Potentially Life Threatening!! Intussusception p. 809 Manifestations Box 24-12 p. 810 History of abdominal pain and vomiting may suggest the diagnosis of intussusception; abdominal "sausage-shaped" mass (the intussusception itself) or upon auscultation with a stethoscope, may hear diminished or absent bowel sounds. Most describe the symptoms of intussusception as a triad of colicky abdominal pain, bilious vomiting, and "currant jelly" stool. The primary symptom of intussusception is described as intermittent crampy abdominal pain. This is often called "colicky pain." Intussusception in an infant usually starts with the infant suddenly crying very loudly, as if in great pain. The infant intermittently draws the knees up to the chest while crying. This reaction is caused by the abdominal pain which recurs frequently and increases in intensity and duration. These intermittent painful episodes are believed to be caused by the telescoping of the bowel and resultant compression of blood vessels and nerves. In addition to the abdominal pain, most children will also have episodes of vomiting associated with the pain. This vomiting is usually not associated with eating and may be bilious (yellow-green colored) Some affected individuals who do not seek early medical attention may pass "currant jelly stool". This is stool that is bloody and mucousy and may be a sign that the affected bowel has lost its blood supply and that the bowel may be necrotic (non-viable). As the condition progresses, the infant becomes may become weaker and develop additional symptoms, including those associated with shock, such as paleness, lethargy, and even fever, though these are not an integral part of the associated "triad." Most cases are diagnosed early, and some studies describe the development of the bloody stools as occurring in only one-third of the cases diagnosed Diagnosis Clinical Manifestations Ultrasound Air enema or Saline enema Management Hydrostatic reduction IVF NG decompression Antibiotic therapy Surgery Note: nonoperative reduction is successful in ~80% of cases Clinical manifestations. Obtain hx of s/s! Lab tests are usually not helpful, although plain abdominal X-rays can reveal signs of an intestinal obstruction, including air-fluid levels, decreased gas, and unexplained masses, usually seen in the right lower quadrant of the abdomen. An ultrasound confirms the diagnosis. A water-soluble contrast or air enema is considered both diagnostic and therapeutic in the management of intussusception. This radiologic procedure involves the introduction of the contrast into the lower intestine. If an intussusception is present, it will be seen during the imaging. Often just the introduction of the contrast will reduce the telescoped bowel to its normal position and shape. 10% risk for reoccurence. Force exerted by enema pushes portion of bowel into position Non-surgical: reduction by air enema as long as no perforation More commonly: water soluble contrast, air, or CO2 pressure instead (barium associated with increased risk of peritonitis) Early treatment-no complications Evaluation: brown formed stool is passed If unsuccessful, surgical reduction Careful parental history of S/S Explain procedures and need for possible surgery Maintain NPO status and assess for electrolyte imbalance MONITOR ALL STOOLS! passage of normal brown stool usually indicates it has reduced itself!! Post-op: Bowel sounds, passage of barium or water soluble contrast media, formed brown stools Preserve parent-child bonding-may be first hospitalization Child may be treated on an outpatient basis. Nursing Care Management Careful history of S/S NPO Assess F & E balance Monitor bowel sounds, passage of contrast Parent-child bonding Evaluation Report to practitioner if passage of a normal brown stool! *Imperforate Anus: Malformation of anorectal region without an obvious anal opening Diagnosis Newborn assessment -No passage of meconium x 24 hrs -Absence of normal anal opening -Meconium in urine or other orifice (fistula may be present) Abdominal ultrasound (assess for other malformations) Management Anal stenosis: manual dilations. Surgery: anorectoplasty Prognosis Wong p. 810 1 in 5000 births May be associated with other defects. Imperforate anus is a malformation of the anorectal region that may occur in several forms without an obvious anal opening. The rectum may end in a blind pouch that does not connect with the colon, or it may have openings to the urethra, bladder, or vagina (fistula from the distal rectum to the perineum or genitourinary system.) A condition of stenosis, or narrowing of the anus, or absence of the anus may be present. May be isolated or as part of other syndromes Manual dilations-begun by MD, continued by RN and by parents at home Larger malformations corrected by surgery Prognosis-depends on type of defect, anatomy of the sacrum, quality of anal sphincter Nursing Care Management Pre-op: Diagnostic evaluation; GI decompression; IVF Post op: prevent infection & complications. -strictures, recurrent fistula, prolapse, constipation Meticulous perineal care Temporary dressing/drain Protective ointments Positioning IVFs then initiate feedings Colostomy care (if needed) Family support Note: Toilet training delayed Keep anal area clean Decrease skin irritation Position to prevent pressure on perineal sutures: Position on side with hips elevated or supine with legs suspended 90 degrees May have NG tube for abdominal decompression IV feedings Formula when evidence of peristalsis Toilet training delayed-complete continence is not achieved until late childhood or adolescence Bowel habit training, diet modification and administration of stool softeners or fiber (avoid constipation!) *Acute Appendicitis: Obstruction & inflammation of the vermiform appendix Acute condition that progresses to perforation and peritonitis if undiagnosed. Why do you think younger children have a greater risk of perforation? -Inflammatory disorder of the vermiform appendix (blind sac at the end of the cecum) Acute condition that progresses to perforation and peritonitis if undiagnosed Pediatric-early diagnosis frequently delayed, unable to verbalize, clinical signs mistaken for other illnesses (increased mortality under 2 years of age) Cause not understood; Average age 10 years with boys & girls equally affected. 60-80,000 cases per year. Mortality high (5% perforated); On diagnosis: 1/3 already perforated Abdominal pain common complaint Obstruction of lumen of appendix by hardened fecal material (fecalith); swollen lymphoid tissue (after virus); or parasite. Pressure builds with lumen, resulting in compression of blood vessels, ischemia, & ulceration. Perforation within 48 hours of initial complaint Early recognition important!!! Necrosis occurs causing perforation or rupture with fecal and bacterial contamination of the peritoneal cavity Spreads into abdomen -> peritonitis. Perforation within 48 hours of initial complaint Early recognition important!!! Diagnosis based on history & physical low fever, rigid abdomen, RLQ pain, mcburney point, assess severity, side lying with knees flexed, change in behavior, anorexia, N/V -numerous infections & inflammatory processes have similar features- avoid misdiagnosis! PAIN cardinal feature: initially generalized; however usually descends to lower right quadrant; most intense at McBurney point. Rebound tenderness not reliable- referred pain indicates peritoneal irritation. Movement (riding over bumps in car) aggravates the pain. NOTE: nonverbal younger child will assume a rigid, motionless, sidelying posture with knees flexed on abdomen. Fever, change in behavior, anorexia, vomiting. LAB: cbc (WBC >10,000 with shift to left ^bands); U/A (r/o UTI); Females HCG to r/o ectopic pregnancy CT scan (positive with enlarged appendiceal diameter; wall thicening; inflammatory changes U/S Often confused with: UTIs, PID, GE, RLL pneumonia, constipation, intussusception PainRebound tenderness-not reliable and painful to child; ask child to cough instead Riding over bumps in auto aggravates pain Bands -indicating an inflammatory process Vomiting Constipation/diarrhea Anorexia NeutroSpec,, scintigraphic imaging is an imaging agent that provides non-invasive, fast, and accurate for patients five years of age or older with equivocal signs and symptoms of appendicitis. It allows physicians to see clearly the "function" of the appendix rather than just the anatomy Attaches to the white blood cells (and myeloid precursors) at the site of the infected appendix, "lighting up" the infection at its source Labs & Diagnostic Tests CBC -WBC >10,000 with "shift to the left" CRP U/A HCG U/S CT scan Signs of Peritonitis sudden relief from pain after perforation subsequent increase in pain rigid guarding of abdomen progressive abdominal distention tachycardia rapid shallow breathing pallor chills Irritability Identify s/s of appendicitis before perforation!! -Tachycardia Rapid shallow breathing Pallor Lethargy Irritability\Stooped posture LAB: cbc (WBC >10,000 with shift to left ^bands); U/A (r/o UTI); Females HCG to r/o ectopic pregnancy Nursing Care Management DO NOT: administer laxatives or enemas or apply DO: maintain bed rest, place in a position of comfort, assess hydration, assess distention, bowel sounds, passage of stool or flatus, pain Pre-op: Rehydration Antibiotics Pain Management Appendectomy -lap to treat non-perforated -open (RLQ incision) What are the benefits? If ruptured- NG suction Wound care -Lap surgery: rapid recovery; if no complications hospital stay is short. Ruptured: preop IV fluid and electolytes, systemic antibiotics (triple), NG suction. Post-op: IVF, antibiotics, NG suction for abdominal decompression until intestinal activity. GENITOURINARY SYSTEM: Urinary Tract Infection (UTI) Nephrosis (Nephrotic Sndrome) -Minimal Change Nephrotic Sydrome (MCNS) Acute Poststreptococcal Glomerulonephritis (APSGN) Wilm's Tumor *URINARY TRACT INFECTIONS (UTIs): Classification by location Etiology: anatomic & physical factors -STASIS: single most important host factor -reflux altered urine & bladder chemistry Risk Factors Renal stasis: children should void 5-6 x/day Incomplete emptying & over distention Sexual abuse and sexual activity Bubble baths Surgical instrumentation Wiping anus to urethra Abnormality in structure High heels A child who exhibits : Incontinence Strong-smelling urine Frequency or urgency Should be evaluated for a UTI!! Clinical Manifestations Lower UTI's: frequency, dysuria, urgency, enuresis, strong smelling urine Upper UTI's: systemic symptoms- high fever, chills, abdominal pain, flank pain, persistent vomiting, moderate to severe dehydration Note: Older adults have abdominal distention rather than dysuria and pain. Cognitive impairment with no fever is characteristic! Diagnostics Clinical manifestations Urinalysis Urine culture & sensitivity Elevated WBC in urine KUB Renal ultrasound: detect masses, differentiate cysts VCUG IVP Therapeutic Management Antibiotics Common Anti-infectives include: Penicillins, Sulfonamides, Cephalosporins & Nitrofurantoin Rehydration and Increased fluid intake Vitamin C Encourage frequent voiding Antipyretics and or antispasmodics Surgical intervention to correct anatomic defects Teaching & Follow-Up -recognition -prevention strategies *Vesicoureteral Reflux (VUR): Retrograde flow of bladder urine into the ureters Causes recurring kidney infections-pyelonephritis High fever, vomiting & chills; renal scarring Primary reflux: due to anatomical defects Secondary reflux: result of an acquired condition Conservative treatment: Low dose daily antibiotics Urine culture q 2-3 months May outgrow reflux Surgical intervention *Nephrotic Syndrome: Disorder characterized by increased glomerular permeability to plasma protein resulting in massive urinary protein loss especially albumin. Includes: massive proteinuria, hypoalbuminemia, hyperlipidemia, and edema. Primary disease: Minimal-change nephrotic syndrme (MCNS) Secondary disease Minimal-change Nephrotic Syndrome Pathogenesis unknown Fluid accumulates in the interstitial spaces causing edema and hypovolemia Predominantly occurs in children between 2 & 7 years More common in males Pathogenesis not understood Clinical Manifestations Weight gain Generalized edema Facial edema Ascites Anorexia/Malnourished Less active & irritable Pallor and fatigue Blood pressure normal to slightly decreased Decreased urine output Clinical manifestations Edema NO hypertension Urinalysis HALLMARK: massive proteinuria (>3+) Frothy urine Sometimes few RBCs but no hematuria GFR normal or high Labs Hypoproteinemia Hypoalbuminemia Hyperlipidemia H/H normal-high (hemoconcentration) Low platelets Hyponatremia Renal biopsy if no response to tx Therapeutic Management Dietary Corticosteroids: first line of therapy!! -Note side effects Diuretics (if complications from edema develop) Antibiotics PRN 2/3 children relapse: Treat with repeated course of high dose steroid therapy -Note: relapses often in conjunction with bacterial, viral infection or allergy, immunizations May continue over many years Complications Overall prognosis favorable Nursing Considerations VS Strict I & O U/A Daily Weight Abdominal Girth Assess Edema Meticulous Skin Care Monitor for complications including infection Nutrition: Dietary considerations Recreational & diversional activities Family support & Teaching!! -identify teaching strategies -s/s nephrotic syndrome *Acute Glomerulonephritis (AGN): post-infectious renal disease of childhood APSGN: Acute poststreptococcal glomerulonephritis occurs after a streptococcal infection with group A beta hemolytic strep. Immune-complex disease Disease commonly secondary to strep throat or impetigo Most commonly early school-aged children 6-7 years Clinical Manifestations Edema Anorexia Urine -cloudy, smoky brown -severely reduced volume Pallor Irritability Lethargy Appears ill Non-Specific complaints Older children c/o: headaches, abdominal pain, dysuria, vomiting, vomiting Mild to moderately increased Bp Diagnostics Clinical s/s appear 10 days after strep infection U/A during acute phase gross hematuria and 3-4 + proteinuria -Note: proteinuria <MCNS -No bacteria Azotemia from impaired glomerular filtration Increased BUN & Creatinine + Serum antibodies to streptococcus (ASO) CXR Renal biopsy rarely needed Therapeutic Management Early recognition & treatment of complications Home care if: BP WNL & urine output qs Hospitalize if: Substantial edema, HTN, gross hematuria, significant oliguria Dietary restrictions depend on severity of edema: Regular diet but no added salt! Moderate sodium restriction & fluid restriction Potassium restriction with oliguria VS with BP Daily weight Intake & Output Antihypertensives & diuretics to control HTN PRN Antibiotics only if persistent strep infection Bedrest & frequent rest periods Prognosis: most recover completely *Wilms Tumor (Nephroblastoma): Most common malignant renal & intra-abdominal tumor of childhood Peak age at diagnosis ~ 3 years, most < 5 years Arises from a malignant cluster of cells more often in left kidney Most present with abdominal swelling or mass Clinical Manifestations Abdominal swelling or mass -Firm, non-tender, confined to one side Weight loss HTN (occasionally) secondary to excess renin production Hematuria (<1/4 of cases) Fatigue/Malaise Anemia Lymphadenopathy Fever HSM If mets then symptoms of lung involvement DIAGNOSTIC EVALUATION- History & Physical examination Radiographic studies Abdominal U/S CT abdomen & chest MRI Hematologic & biochemical studies U/A HISTORY & PHYSICAL EXAMINATION DO NOT PALPATE ABDOMEN!!!!!!!! Staging Therapeutic Management- Surgery & chemotherapy with or without radiation Surgery within 24-48 hours Tumor, affected kidney & adrenal removed Keep encapsulated tumor intact Post-op radiation for large tumors, mets, residual postoperative disease, unfavorable histology, or recurrence Chemotherapy for all stages 6-15 months Prognosis: 90% with stage I & II Pre-op: Swift diagnosis-keep explanations simple, repetitive, focused Monitor bp Explanation of chemotherapy: benefits & side effects DO NOT PALPATE TUMOR Post-op: Observe for intestinal obstruction Monitor bp; urine output Signs of infection Pulmonary hygiene Family support & Teaching Note: Because one kidney certain precautions needed Avoid contact sports, detection and treatment of GU s/s

endocrine vid pt 2

Hypoparathyroidsim: -sits on top of thyroid E iatrogenic (accidentale) removed during thyroidectomy or neck surgery or radiation ruining glands stops break down of bone, decreased Ca in blood, Ca excreted, increased phosphate, increased binding ca -> phosphate -> decreased serum Ca levels CM decreased Ca -muscular system- tetany positive chovestek and trasseau, dysphagia laryngeal spasms (compromised airway), tingling (lips, fingers, toes) -nervous system- lethargy, anxiety, personality changes -vitamin D deficiency (tx. vitamin D supplements) Dx labs, decreased PTH, decreased Ca, increased phospate Tx calcium + vitamin D supplements Hyperparathyroidism: E -tumor in gland -decreased Ca level from medical condition (ex. vit d deficiency /malabsorption syndrome) -increased PTH with normal Ca levels CM -bones weak osteoporosis -> fractures -increased Ca (serum) overwhelms renal tubules -> increased Ca in urine -> kidney stones -> -increased phosphate -> kidney stones --renal failure and pancreatitis -increased vitamin D -> increase Ca absorption in small intestine -> increased Ca in blood -> cardiac changes CM muscle weakness/fatigue, decreased appetite, constipation, emotion d/o, shortened attention, dysrhythmias, HTN Dx CM, labs (increased amylase if pancreatitis, increased PTH, increased Ca >10, decreased phosphate <3, increased cl uric acid creatine, dexa scan (show bone loss), MRI CT US (tumors) Tx surgery if tumor, supplements calcimetric agents (helps get rid of Ca -monitor for hypocalemia. tx calcium gluconate) -biphosphonate (foams inhibit bone breakdown), ambulate/exercise build muscle mass ex. swimming, moderate Ca intake, increase fluids, diuretics help excrete Ca, oral phosphate (inhibit absorption of vit d) Cushing Syndrome: -caused by excess of corticosteroids -ACTH imbalance -at risk- asthma, ulcerative colitis, arthritis E -overuse of steroids (most common ex. asthma lupus RA) --most common cortizole. med -ectopic tumor (in pancreas lung etc increased in secretes ACTH) everything increased -adrenal tumor (increased corticosteroids) everything increased ACTH low increased sex hormones, mineral corticosteroids, gluccorticosteroids Adrenal gland -stimulation of adrenal gland from hyper secretion of ATCH by pituitary -women hitruism hair on face mood swings, amenorrhea -HTN LE edema high Na low K -increased glucose levels > glucose intolerance - type 2 DM -muscle wasting -> muscle weakness, high gastric secretion, lipidosis -> fat distribution (buffalo hump, moon face, skinny legs, truncal obestiy, purplish.red striae, delayed wound healing, HTN heart disease, osteoporosis -> bone fractures Dx H&P, increased plasma cortisol levels with diurnal variations, plasma ACTH levels, dexa scan, 24 urine collection for free cortizole 80-120 norm, CT MRI show if tumor, CBC Na hypo k hyper glucose Tx taper off steroids, nizoral/cytaden- drug therapy inhibit corticosteroid synthesis, surgery to remove radiate -minimize stress (triggers cortizole), limit water intake, monitor blood glucose (glucose intolerance), increase protein diet, treat infection, protect from falls (dont heal as well), anti HTN meds, if heart disease assess for edema check daily wts preop correct HTN hyperglycemia lower K high protein post get high doses IV corticosteroids don't react to stressors treat infection balance hormones electrolytes BP hemorrhage fluid balance Adrenalcortical Insufficiency: -decreased ACTH hypo function of adrenal cortex E -Addisons disease (autoimmune- adrenal gland is destroyed by disease etc) -hypofunction of adrenal cortex (everything down) CM dumping water -hyponatremia, hyperkalemic, irritable depression, hypoglycemia, progressive weakness, fatigue, wt loss/anorexia, lower BMR, N/V/D, hypotension, skin hyper pigmented in exposed areas of body (pressure points), bronzed skin pigmentation, decreased development of secondary sex characteristics Dx H&P, plasma/serum cortizole low, low NA/glucose, anemia, BUN high, ECG peaked T waves, ACTH stimulation test cortizole fails to rise, CT/MRI Tx cause, daily mineral corticoid in AM (Florinet), daily glucocorticoids (hydrocortisone) 2/3 AM 1/3 PM, encourage fluid intake (esp in hot weather) aldosterone low + spilling water, salt additives fix hypo NA, very irritable = quite environment, relieve anxiety, increase doses cortizole for stressful situations, monitor blood glucose, assist ADLs, avoid stressors exercise, monitor S/S infection, antacids -CM not dx usually till 90% destroyed Addisons Crisis triggers- stress, sudden withdraw corticosteroids, after adrenal surgery, life threatening / emergency, decrease BP increased HR dehydration low Na high K decreased glucose fever shock confusion -Tx shock management hydration 5% dextrose NS (in circulatory collapse) -teach S/S stress management avoid over the counter medicine carry hydrocortisone

Threats to Child Elimination Part 1 GI

Hirschsprungs disease: megacolon,high fiber diet, fliiuds, surgery (colostomy) Newborn -cant pass meconium 24-48 hr Older child -constipation -FTT Megacolon S&S fever bloody diarrhea dehydration sepsis/shock bowel perforation -pain 4x more common in males, inherited Dx cm (new born not passing meconium), barium enema, abd X-ray, rectal bx Tx pull through procedure (remove bad part of bowel, has to wait to stablize 1st, sometimes to get better stable need temp bosomy if distended, then reattach) Sx open or laparoscopic Pre systemic antibiotics, enema to clean bowel (new born sterile) Complications anal sutures, incontinence (delayed toilet training), nutrition Post VS (infection), abdominal circumference (distention , should have norm BM), feed and return of bowel sounds (day or 2 after surgery), stoma care, teach s&s entercholitis, regimen occasional dilation of rectum (bullet into rectum to help open stricture decrease constriction), rectal irrigation x3 month at home -nutrition low fiber high calorie high protein

endocrine vid pt 1

Overview of Endocrine: secrete hormones into blood stream -pituitay brain, thymus neck area Hx past medical hx, meds, surgery (brain), tx (ex. chemo) PE VS, wt/ht, emotional status Dx blood, urine, US, cry, CT, MRI Tx too little or too much (correct imbalance) (modifiable vs non modifiable Access findings auscultation, palpation, perfusion, effects of aging (decrease) Hypopituitarism: (anterior, base of brain) Anti pituitary (hypo) norm at birth, secondary due to tumor Assessment kids height correlates with parents ht? nutrition Dx GH levels, MRI, Xray (hands and wrists bone growth) CM short statue, sexual development delayed, decreased body mass, decreased energy (feel tired al the time), permanent teeth delayed (over crowded or crooked) Tx remove tumor, growth hormone somatatroph SQ q hr expensive -89% with tx will maintain norm adult ht, increase lean body mass, increase energy, emotional support, releastic expectations Hyperpituitarism: anti pituitary (hyper) increase GH growth hormone Gigantism -increased too much GH before closure of epithetial plates -> overgrowth of long bones -> ht over 8ft Acromegaly (swelling) increase GH after closure of epithelial plates -> soft tissue swelling (ex. head lips, ear, nose, tongue, feet, organs) CM overgrowth of bones and soft tissue of hands/feet/face, increase fatty acid (increased risk for atherosclerosis) carb high blood glucose (increased diabetes hyperglycemia) life expectancy decreased 5-10 yrs, joint pain, soft tissue swelling -> swelling of organs -> organ failure (kidney, heart), enlargement of tongue -> malocclusion of teeth -> speech difficulties, hypertrophy of vocal cords -> deep voice, increased pharyngeal tissue -> narrows upper airway -> sleep apnea, skin is thick, leathery oily (deep creases) Dx increased GH, CM, X-ray, CT/MRI, endocrine (from tumor Tx hormone therapy, temp somatostatin until surgery/radiation, radiate or remove tumor, supplement all hormones after surgery -if hyper need to remove tumor + everything else = after needing supplement hormones Hypothalamus: pituitary TRF TSH -> thyroid regulate T3 T4 Hyper Thyroid enlarged -autoimmune graves (75% cases women more than men 20-40 children 12-14 peak incidence) disease, toxic nodule goiter (lack or too much iodine), pit tumor, cancer, thyroiditis thyroid continuing to make T3 T4 T3 regulates metabolic rate CM increased metabolic rate, wt loss/muscle wasting, increased appetite very skin hungry, diarrhea, bounding increased HR palpations increased BP tremors, heat intolerance, warm moist skin (facial flushing), amenorrhea, exothalmus (protrusion of eye balls cause impaired drainage), nervousness/restlessness/can't concentrate T4 controls cell growth CM hair loss, goiter bruit, increase Dx labs (decreased TSH, increased free T4, ECG (afib, palpations), thyroid scan, eye exam, needle biopsy, CM radioactive iodine uptake RAIU Tx radioactive iodine - kills thyroid 6-8 wks, then tx for hypothyroidism after -antithyroid drugs (PTU SE sore throat fever, tepazole) doesn't cure -thyroidectomy (ABCs, hypothyroid, calorie decrease (or will gain wt) -have low Ca (S&S cramping muscle twitch tx calcium gluconate) -high calorie high protein high carbs 6 meals a day (no high fiber foods), proponalol limit caffeine to decrease HR BP, artificial tears for budging eyes exophthalmus Thyroid Storm TS antibody attach to thyroid- fast and life threatening -acute rare, all CM heightened, secondary to stress, CM increased HR heart failure HTN EKG, Tx decrease stressors fluids drug therapy O2 fever, dysrythmias Hypothyroidism: E -not enough iodine/destruction of tissue -decreased T3 T4 -not enough thyroid tissue -pituitary disease so TSH low TRF high -hashomotos autoimmune disease that destroys the thyroid -more in women low T3 T4 CM T3 decreased metabolic rate, constipation, mentally sluggish, wt gain, tired/fatigue/lethargy, depressed, decreased RBC production/anemia, cold intolerance, personality changes, menstrual d/o a lot bleeding, decreased CO, high cholesterol/triglycerides T4 decreased rate body cell growth, myxedema (doughy), coarse sparse skin/dull, periorbital edema, mask like face, dry coarse hair, thick swollen lips/tongue Congenital (infants) -severe developmental delay, sleepy, delayed growth, constipation Dx labs (decrease free T4), ECK (bradycardia), IMS (infant metabolic screen pretinisim), thyroid antibodies, RAI low Tx replace T4 (levothyroxine) timing (not with food) monitor SE too much hyperthyroidism S&S, give iodine, stool softener, encourage mental stimulation, avoid sedation, decreased calorie, high fiber high protein, warm environment, encourage express feelings, encourage activity to increase IMB activity as tolerated (sleep a lot cause metabolic activity slow) Complication Myxedema coma -triggered by stress infection, trauma, cold, drugs CM heightened S&S severe hypotension hypoventilation hypothermic low temp -Tx. IV T4 ex. tiger hyperthyroidism, eor hypothyroidism

Health Promotion of the Adolescent and Family

Promoting Optimum Growth and Development: -Transition between childhood and adulthood -Rapid physical, cognitive, social, and emotional maturation -Generally defined as beginning with the onset of puberty and ending with the cessation of body growth at 18 to 20 years -rapid growth Prepubescence: About 2 years before puberty, heralding physical changes Puberty: Sexual maturity is achieved Postpubescence: 1 to 2 years after puberty; skeletal growth is complete and reproductive functions become established Adolescence: Time of growing into psychological, social, and physical maturation -Early 11-14 Middle 15-17 Late 18-20 Post puberty - grow taller Biologic Development: -Primary sex characteristics External and internal organs necessary for reproduction -Secondary sex characteristics Result of hormonal changes: Voice change, hair growth, fat deposits Play no direct role in reproduction (2ndary- nothing to do with making baby) Hormonal Changes of Puberty: Role of anterior pituitary and hypothalamus Hormones stimulate gonads Gonads produce and release gametes Gonads secrete sex-appropriate hormones -Hypothalmus - controler 'master' - tells pituitary to stimulate LH estrogen FSH testrogen Sex Hormones: Secreted by ovaries, testes, and adrenal glands Produced in varying amounts by both sexes throughout the life span Adrenal cortex causes small amount of secretion before puberty Maturation of gonads produces biologic changes of puberty -Males + females have both estrogen and testrogene Estrogen: "Feminizing hormone" Low production during childhood In males, there is gradual production throughout maturation In females, levels increase until about 3 years after menarche; estrogen then remains at this maximum level throughout reproductive life -'female hormone' stay high during reproductive yrs Androgens: "Masculinizing hormones" Secreted in small and gradually increasing amounts up to 7 to 9 years; then rapid increase in both sexes until 15 years Responsible for rapid growth of the early teenager Testes secrete testosterone; levels increase to a maximum level at maturity -'males' Growth hormone Sexual Maturation: Tanner stages of sexual maturity Stages of development of secondary sex characteristics and genital development Defined as a guide for estimating sexual maturity tanner staging males and females -breasts (females) and hair -stage 1 nothing, stage 5 thigh -males testes grow 1st Sexual Maturation for Females: Thelarche (8 to 13 years): Breast buds Adrenarche (8 to 13 years): Pubic hair growth Menarche: About 2 years after thelarche, menstruation begins Puberty "delay": No thelarche by age 13 years -Genetic makeup Sexual Maturation for Males: Stage 1 (91/2 to 14 years): Testicular enlargement and sparse pubic hair Stage 3: Penile enlargement, voice changes, early facial hair; gynecomastia (temporary breast enlargement) occurs in 1/3 of males in midpuberty Stage 5: Penile growth, first ejaculation, axillary, groin, and facial hair, final voice change -Puberty delay no scrotum elargement by 14 Gynocomastia -breast tissue developed in males -elevated estrogen Physical Growth: Dramatic increase in growth accompanies sexual maturation Adolescent growth spurt 20% to 25% of total height is achieved during puberty Usually occurs within a 24- to 36-month period Characteristic sequence of changes -Grow out -> in In ~6 yrs ¼ of growth ht Sex Differences in General Growth Patterns: Appear to be the result of hormonal effects during puberty Skeletal growth Voice changes Lean body mass Non-lean body mass Skin, glands, and hair -18-20 epithelial bones growth plates close Boys- high to low tones hypertrophic leringic muscle Boys tend to be leaner Girls tend to have high fatter % Body made to reproduce Physiologic Changes: Size and strength of heart, blood volume, and systolic blood pressure increase Pulse rate and basal heat production decrease Adult values for all formed elements of blood Respiratory volume and vital capacity increase Increased performance capabilities -VS more like adults Psychosocial Development: Erikson: Sense of identity Early adolescent: Group identity versus alienation Development of personal identity versus role diffusion Sex role identity Emotionality -Separate from parents Sexual orientation-who attracted to Piaget: Cognitive Development: Formal operations period Abstract thinking Think beyond present Mental manipulation of multiple variables Concerned about others' thoughts and needs -Use logic think about future May have incorrect logic / abstract think -still need parents to help guide them 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 -Figure out norms of society Spiritual Development: Some may question the values and beliefs of the family Capable of understanding abstract concepts and interpreting analogies and symbols May fear that others will not understand their feelings Tendency for introspection and emotional intensity -More so taking ideas from peers, trying to figure out who they want to be -parents still guide- but teens don't want as much Social Development: Goal is to define one's identity independently from parental authority Much ambivalence Intense sociability; intense loneliness Acceptance by peers -Goal- independence from parents Doesn't like being alone- not being included with friends - afraid being alone outcast -peer group 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 the rejection of parents by the teenager -16 17 18 start letting child make choices -parents guide Relationships with Peers: Peers assume an increasingly significant role in adolescence ("best friend") Peers provide a sense of belonging and a feeling of strength and power Peers form a transitional world between dependence and autonomy Role of social media and advanced technology Adolescent Sexuality: Dating Sexual orientation Sexual experimentation (wide range) Reasons for sexual experimentation Curiosity Pleasure Conquest Peer pressure to conform -Decrease sexual activity + preg Increase STDs Dangers- tinder, snapchat, nudes (have full access to phones) How many sexual partners (not bf/gf) Development of Self-Concept and Body Image: Feelings of confusion in early adolescence Acute awareness of appearance, comparison of appearance with others Blemishes and defects are magnified out of proportion Matures to self-concept based on uniqueness and individuality Responses to Puberty: Responses differ depending on the stage of development Curiosity in early adolescence Concerns with "Am I normal?" Concerns for late-maturing teens Concept of "perfect body" achievement Promoting Optimum Health during Adolescence: Assumption of responsibility for health Assess for risk factors (GAPS) Immunizations Nutrition Eating habits and behaviors Healthy lifestyle habits -Need to assume all responsibility for health (ex. meds, etc.) - need to take control (parents cant remind everyday- step back and see how they do- give child some control) -TDAP Before 7th grade 11-12 yrs age -Manigilcoccul 11-12 follow up at 18 (bacterial menningitus spread resp) -HPV - very comon, can lead to cancer (has vaccine) girls after 9 (plus boys too) given in 3 doses Promoting Optimum Health during Adolescence (cont'd): Sleep and rest Exercise and activity Dental health Personal care Vision, hearing Posture Body art (piercing and tattooing) Suntanning, ultraviolet damage -Bad diet -More calories- less nutritous -Fast metabolism- not gaining wait -Teach- healthy behaviors, lifestyles -A lot of energy, want to do things; logical thinking sucks (may make bad decisions) -9 hours of sleep -More kids participate in sports But more obese kids -School- screen posture allans test for scoliosis screen vision hearing -Piercing tattos, educate being safe (not doing it in friends bathroom- risk for infections can get septic) -Tanning- make sure using sunscreen (c) Stress reduction Sexuality education and guidance Media influences Knowledge from peers, TV, movies, magazines Need factual information, presentation based on developmental maturity and ability to ask questions Role modeling -Encourgae share feelings -get knowledge peers, tv, media -give factual info Injury Prevention: Motor vehicle crashes are the single greatest cause of serious and fatal injuries in teens Other vehicles Firearms and other weapons Sports injuries Water safety Poisoning, tobacco, alcohol, and other drugs -Cell phones -motor vechile accidents -Water safety- no diving shallow, tubing, flips etc dangerous Anticipatory Guidance: Care of Families: Parents need support and guidance Information needs regarding developmental changes and process of gaining independence Help "letting go" and promoting independence -Mood swings norm, will out grow Help let parents let go, still be there and guide

Threats to child elimination pt 2 urinary

UTIs E 80% ecoli or gram - bacteria, anatomic or physical factors, stasis, VU reflex retrograde flow of urine, altered urine chemistry (keep on acidic side) RF stasis, females (urethra shorter), incomplete emptying, sex, bubble bath, whipping, anatomic abnormalities CM Lower -frequency, dysuria, urgency, enuresis, strong smelling urine, incontinent, decreased appetite, abd/back pain Upper -systemic, high fever, chills, abd pain, flank pain, vomiting, dehydration Infants- poor feeding, FTT, V/D, irritable older- abd distention, confusion Dx CM, UA (WBC (norm 0-5000) > 10000), urine culture & sensitivity (Cath or supra pubic Cath, clean catch whip front to back urinate little in toilet then stop then into cup best results morning), KUB (kidneys uriner bladder X-ray), renal US (could be mass), VCUG (fill bladder with contrast, are able to empty bladder? any stasis?), IVP (kidney function) Tx -wait till get culture 1st antibiotics (penicillins, cephlamids cephlasporins sulfamides mitroforine -rehydrate, vitamin C (more acidic urine), dried cranberries, cranberry juice prevent bacteria on wall, encourage frequent voiding, antipyretics if fever, antispasmodics (tx pain) -if anatomical defect -> surgery (reflux, may outgrow, low dose antibiotics, urine cultures q 2-3mnths) -teach cotton underwear, no bubble baths, no tight clothing, abstinence void after sex prevent constipation Nephrotic Syndrome: protein leaks out into urine (decreased serum albumin) primary minimal change nephrotic syndrome NCMS, idiopathic (E unknown) 2/3 relapse, have for year, 2-7 yrs, males more common, favorable outcome secondary due to disease (something damaged kidneys ex. drugs) CM protienurina (>3 should be none), hypoprotienemia + hypoalbumineama -> anorexia malnourished decreased activity/irritable pallor fatigue hyperlipidemia, edema wt gain facial edema ascites, BP norm to slightly decreased, markers edema, decrease urine output Dx UA massive proteinuria, frothy urine no blood, H/H norm -high (very concentrated loss volume), decrease platelets, low Na, renal biopsy Tx goal- stop urine protien loss, corticosteroids 7-12 days (SE wt gain increases appetite growth probs bone deminilerzation increase insulin, infection), diuretics (for edema if complications ex airway), antibiotics, decrease salt diet fluid restriction, VS, I&O/daily wts, measure abd girth, assess edema, nutrition, infection, rec/diversional activities, family support - teach S&S of relapse Complications infection - paritinitus cellulitus pnemonia, circulatory insufficiency decrease CO cause hypovolemic, thromboembolism blood thicker more likely to be blocked Acute poststreptoccual Glomerulonephritis APSGN: 6-7 2x more common males (usually not under 2 don't get strep throat), 10-21 days after strep infection CM (or impetigo) -good prognosis CM anorexia, pallor/appears ill, irritable/lethargic, nonspecific complaints in older children (headache, abd pain, dysuria, vomiting) -decreased urine output (cloudy smokey frothy ea color, increased BP, period, perioritable edema (start in face then spread extremities abd) Dx UA hematuria (grossed discoloration) proteinuria no bacteria, ASO titer (if have strep), increased nitrogen (if lack protein then builds up), CXR (heart pulmonary overload etc, increased BUN/creat, increased K if not urinating Tx home tx if normal BP, host if edema HTN gross hematuria oliguric, mod Na (fluid restriction, K restriction if oliguric, daily wt/ I&O, antihypertensive/diuretics, bedrest, antibiotics if have strep throat Complication cerebral complication, if edema/HTN/gross hematuria -> seizure precautions anticonvulsants Wilms Tumor ~3 most less than 5 malignant renal/intra abd tumor ( CM abd mass/swelling (usually left), wt loss, anemia, lymphaseopathy, fever, metastasis rare, fatigue/malaise Dx H&P (dont palpate! don't want to burst and spread) abd US, MRI, hematological/biochemical studies, UA, staging (90% stage 1-2 very good prognosis) Tx dont palpate! don't want to rupture encapsulated tumor -surgery (with 24-48hrs of diagnosis), chemo 6-15 months, possibly radiation (if large, metasiss, if unfavorable hx) Preop explain procedure/chemo post observe intestinal obstruction, monitor BP, urine output I&O, S/S infection, pulm hygiene, family support, careful because only 1 kidney (can't live on 0 must protect 1 have no contact sports be careful GU infection must be treated right away

adolescents vid -entire time of growing

early 11-14 middle 15-17 late 18-20 prepubescence 2 yrs before puberty puberty when sexual maturation achieved post puberty 1-2 yrs after puberty after skeletal growth ends

Trousseau's Sign

carpal spasm after occlusion of blood in forearm with BP cuff hypoparathyroidism hypocalcemia

HYPERTHYROIDISM "TIGGER"

• Bulging eyes exopthalmus • (Grave's Disease) • ↑energy • ↑T3 & T4 • ↑hunger • ↓weight • ↓TSH • A-Fib • Heat Intolerance • Tachycardia • Bruit over Thyroid Thick neck & skins

HYPOTHYROIDISM "EEYORE"

• Puffy eyelids • Hashimoto (↓iodine) • ↓energy • ↓T3 & T4 • ↓CO • ↑weight • ↑cholest. & Trigly. • ↑TSH • Fatigue • Lethargic • Dry flaky skin • Edema • Cold intolerance • Coarse hair • Thick tongue • Swollen lips • Menstrual disorders • Constipation • Hypothermia • Anemic Sinus bradycardia

ADDISON'S DISEASE "ADD STERIODS"

• ↑K+ • ↓Na+ • ↓Cortisol • ↓weight • Slow onset • Weakness • Fatigue • Anorexia • Hyperpigmentation • Orthostatic hypotension • Nausea & vomiting Diarrhea

CUSHING'S DISEASE "TOO MUCH CUSHING"

• ↓K+ • ↑Cortisol • ↑weight (obesity) • ↑hypertension • ↑hyperglycemia • Moonface • Buffalo hump • Orbital edema • Excess body hair (Hirsutism) • Purple striate abd. Diet • ↓carbs. • ↓Na+ • ↓Ca+ • Fluid restriction • Diuretics