📚 Reading: Thyroid, type 1 DM, DKA, growth hormone, PKU
💡 The one idea
Type 1 diabetes is the pediatric one, and it presents as the three polys plus weight loss.A child who is drinking and weeing constantly and losing weight has type 1 until proven otherwise.
🖼️ Insulin: onset, peak and duration.Swipe it sideways if it is cut off, or tap to open it full size.
💧 The classic presentation
Polyuria · Polydipsia · Polyphagia — with weight loss. Often the first
clue is new bedwetting in a previously dry child.
Many present in DKA: Kussmaul breathing, fruity breath, vomiting, abdominal pain that
can mimic appendicitis.
🚨 Hypoglycemia in a child — act first, ask later
Shaky, sweaty, pale, irritable, confused, hungry. In a young child it often looks like a
sudden behavior change.
Conscious: 15 g fast carbohydrate, wait 15 minutes, recheck.
Unconscious: nothing by mouth — IM glucagon or IV dextrose.
When you cannot tell high from low, treat as LOW. Low kills in minutes.
⭐ Sick day rules — the teaching that prevents admissions
Never stop insulin, even when not eating — illness raises glucose
Check glucose every 2–4 hours, and check ketones when above 250
Push sugar-free fluids to stay hydrated
Call for persistent vomiting, moderate/large ketones, or glucose that will not come down
Exercise lowers glucose — eat a snack before sport and carry fast sugar.
🖼️ Type 1 diabetes in children.Swipe it sideways if it is cut off, or tap to open it full size.
🧠 Two more you should recognize
Congenital hypothyroidism — screened at birth. Untreated it causes irreversible
intellectual disability, so lifelong levothyroxine started early is everything.
Signs: prolonged jaundice, poor feeding, constipation, large tongue, hoarse cry, sluggishness.
Growth hormone deficiency — short stature with normal proportions.
Injections given at bedtime to mimic natural release.
⭐ High-yield — what the exam actually asks
Show 5 moreHide these 5
Thyroid panels invert: congenital hypothyroidism is low T3/T4 with HIGH TSH; hyperthyroid/Graves is high T3/T4 with LOW TSH.
Congenital hypothyroidism is caught on the newborn metabolic screen. Levothyroxine is lifelong, and early treatment prevents irreversible cognitive delay. Too high a dose looks like hyperthyroidism (tachycardia, tremor, weight loss).
Antithyroid drugs (propylthiouracil, methimazole) need WBC and platelet monitoring. Propranolol controls cardiac symptoms. Partial thyroidectomy risks thyroid storm.
Hypocalcemia: Chvostek (cheek tap → facial twitch) and Trousseau (cuff → carpal spasm). Normal calcium 8.8–10.4 mg/dL. Calcium and phosphorus move inversely.
Type 1 DM diagnostics: fasting glucose >126, random >200, GTT >200, A1c >6. Classic three Ps plus new-onset bedwetting and weight loss.
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Regular insulin is the only IV-compatible insulin. When mixing, draw clear before cloudy (regular before NPH). Rapid-acting lispro goes in right before eating.
Hypoglycemia is cold and clammy: 10–15 g simple carbohydrate, recheck in 15 min, then a complex carb. Glucagon SC/IM if unconscious.
Hyperglycemia is hot and dry. Sick-day rules: check glucose and ketones every 3 hours and never skip insulin.
DKA: glucose >330, positive ketones, Kussmaul respirations, fruity breath, and hyperkalemia because without insulin potassium stays extracellular. Treat with isotonic fluids, then a continuous IV regular insulin drip, adding dextrose once glucose falls to about 200–250.
Growth hormone is injected at night, and treatment stops when the growth plates close.
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PKU needs a lifelong low-phenylalanine diet and special formula. Galactosemia needs soy or lactose-free formula and no breast milk.
Diagnostic thresholds: fasting glucose ≥126 mg/dL after an 8-hour fast, random ≥200 with symptoms, 2-hour OGTT ≥200, or A1C over 6.5%.
Hypoglycemia is under 70 mg/dL; hyperglycemia is generally over 180.
Type 1 is beta-cell destruction — genetics, toxins and viruses. Type 2 is insulin resistance driven by obesity, inactivity, high triglycerides and hypertension.
Recurrent vaginal yeast infections are an early clue to type 2 in an adolescent girl — easy to miss.
Before an OGTT: a balanced diet for 3 days, then fasting 8–12 hours with water only, and antidiabetic medication held until after the draw.
📚 From your Maternal & Child textbook
Pillitteri, Maternal and Child Health Nursing — ch. 48 (endocrine and metabolic).
Hypoglycemia is under 70 mg/dL and needs fast-acting carbohydrate, then protein. Insulin is not simply skipped on a sick day — illness usually raises the requirement.
⚠️ Exam traps
Potassium in DKA looks high on the draw but total body potassium is depleted and falls once insulin starts.
Hypo (cold and clammy) vs hyper (hot and dry) is the fastest sorting rule.
Growth hormone therapy is time-limited; levothyroxine and insulin are lifelong.
🧠 Mind maps 2
One per disorder, built from the structure of your ATI chapter.
Diabetes Mellitus
🎯 Who gets it
Genetic predisposition to both type 1 and type 2
Toxins and viruses can destroy beta cells and lead to type 1
Obesity, physical inactivity, high triglycerides, and hypertension cause insulin resistance and type 2
👀 What you see
Hypoglycemia is blood glucose under 70 mg/dL
Hypoglycemia: hunger, lightheadedness, shakiness, anxiety and irritability, pallor with cool skin, diaphoresis, dizziness
Hypoglycemia: normal or shallow respirations, tachycardia and palpitations, strange feelings, falling level of consciousness, trouble thinking and concentrating, emotional change, slurred speech, headache, blurred vision, seizures progressing to coma
Hyperglycemia is blood glucose usually above 180 mg/dL
🧪 What confirms it
Diagnosis: 8-hr fasting blood glucose 126 mg/dL or higher
Diagnosis: random blood glucose 200 mg/dL or higher with diabetes symptoms
Diagnosis: oral glucose tolerance test 200 mg/dL or higher on the 2-hr sample
Diagnosis: HbA1c above 6.5%
🩺 What you do
Monitor vital signs, blood glucose and the factors affecting it (medications, diet, activity), intake and output, and weight
Assess skin integrity and wound healing, especially the feet and skin folds
Watch for signs of poor control such as paresthesias, visual changes, and recurrent infections
Assess dietary practices, exercise patterns, and the child's proficiency at self-monitoring and self-administering medication
💊 Drugs
Insulin manages type 1 diabetes, with onset, peak, and duration varying by type
Check test strip accuracy against the control solution
Keep a log with time, date, glucose level, insulin dose, food intake, and anything else affecting glucose such as activity or illness
Sick day rules: check blood glucose every 3 hr, test urine for ketones, never stop insulin, and call the provider for glucose above 240 mg/dL
⚠️ What goes wrong
Diabetic ketoacidosis — acute and life-threatening, with glucose above 200 mg/dL, ketones in blood or urine, and acidosis with pH under 7.30 and bicarbonate under 15 mmol/L
DKA care: admit to intensive care, place on a cardiac monitor, obtain venous access for fluids, electrolytes, and insulin
Read left to right: who gets it → what you see → what confirms it → what you do → what goes wrong. Cover a column and rebuild it out loud.
Growth Hormone Deficiency
🎯 Who gets it
Structural causes: tumors, trauma, structural defects, surgery
Hereditary disorders
Other pituitary hormone deficiencies such as TSH or ACTH deficiency
Most GH deficiency is idiopathic
👀 What you see
Short stature with proportional height and weight — height is affected more than weight and bone age usually matches height age
Delayed epiphyseal closure and delayed bone age
Increased insulin sensitivity
Delayed or altered dentition with an underdeveloped jaw
🧪 What confirms it
Plasma insulin-like growth factor-1 and IGF binding protein-3 — values below the mean for age prompt further evaluation
GH stimulation testing for children with low IGF-1 and IGFBP-3 plus short stature
Skeletal radiographs assess maturity by comparing epiphyseal centers to published age standards — a general skeletal survey under 3 years and hand and wrist films in older children
Series of skull films can reveal structural abnormality such as a small sella turcica
🩺 What you do
Measure and plot height and weight on an appropriate growth chart at every visit
Assess height velocity over time, the height-to-weight relationship, and projected target height against genetic potential
GH stimulation test: explain the procedure, draw a baseline sample, give the agent that triggers GH release (arginine or GH-releasing hormone), then draw samples every 15-30 min for 3-4 hr
Keep the child NPO and limit activity for 10-12 hr before the stimulation test
💊 Drugs
Somatropin replaces human growth hormone and stimulates growth of bone and skeletal muscle
Give subcutaneously into the abdomen, thigh, buttock, or back of the upper arm
Use cautiously in children receiving insulin
💬 What you teach
Nothing to eat or drink and limited activity for 10-12 hr before the stimulation test
Provide emotional support through imaging studies and help position the child
⚠️ What goes wrong
Untreated GH deficiency disrupts vertical growth and causes short stature, delayed epiphyseal closure, delayed bone age, and delayed sexual development
Read left to right: who gets it → what you see → what confirms it → what you do → what goes wrong. Cover a column and rebuild it out loud.
🎥 Lecture recordings 2
Tap a card to open that recording in Google Drive. The same list lives in the lecture library.
ATI Active Learning Template — System DisorderDiabetes Mellitus
Filled from ATI chapter 32, row by row from that chapter’s own sections — 12 of 12 rows have content.
🧭 What it isAlterations in Health (Diagnosis) · Health Promotion & Disease Prevention
Alterations in Health (Diagnosis)
Diabetes mellitus means insulin is metabolically deficient, either partly or entirely. In type 1 the pancreatic beta cells are destroyed; in type 2 the body cannot use insulin properly. Over time diabetes contributes to cardiovascular disease, hypertension, renal failure, blindness, and stroke.
Health Promotion & Disease Prevention
From this module — built from the notes above on this page, not a section of the ATI chapter.
Type 1 cannot be prevented; teach recognition instead — polyuria, polydipsia, weight loss and new bedwetting in a previously dry child.
Type 2 prevention: activity, nutrition and weight in at-risk children.
Sick-day rules taught before the first illness, not during it.
Annual influenza vaccination; foot, eye and kidney screening from the recommended age.
School plan in writing, with staff trained to recognize and treat hypoglycemia.
👀 How it shows upAssessment — Risk Factors · Assessment — Expected Findings
Assessment — Risk Factors
Genetic predisposition to both type 1 and type 2
Toxins and viruses can destroy beta cells and lead to type 1
Obesity, physical inactivity, high triglycerides, and hypertension cause insulin resistance and type 2
Assessment — Expected Findings
Hypoglycemia is blood glucose under 70 mg/dL
Hypoglycemia: hunger, lightheadedness, shakiness, anxiety and irritability, pallor with cool skin, diaphoresis, dizziness
Hypoglycemia: normal or shallow respirations, tachycardia and palpitations, strange feelings, falling level of consciousness, trouble thinking and concentrating, emotional change, slurred speech, headache, blurred vision, seizures progressing to coma
Hyperglycemia is blood glucose usually above 180 mg/dL
Hyperglycemia: thirst, polyuria early and oliguria late, polyphagia, weight loss, nausea, vomiting, abdominal pain
Insulin pumps deliver a steady programmed basal dose with boluses before meals; injections are self-given two or more times daily
When mixing, draw up rapid-acting before intermediate-acting; never mix glargine with another insulin because they are incompatible
Therapeutic Procedures
From this module — built from the notes above on this page, not a section of the ATI chapter.
Insulin by injection or pump; carbohydrate counting matched to the regimen.
Rotate injection sites within one region to prevent lipohypertrophy, which makes absorption erratic.
Continuous glucose monitoring where available; teach what to do with an alarm.
Rule of 15 for hypoglycemia, and glucagon taught to the family and the school.
Adolescents: expect deteriorating control and address it as developmental, not as failure.
💬 Around the patientClient Education · Interprofessional Care
Client Education
Check test strip accuracy against the control solution
Keep a log with time, date, glucose level, insulin dose, food intake, and anything else affecting glucose such as activity or illness
Sick day rules: check blood glucose every 3 hr, test urine for ketones, never stop insulin, and call the provider for glucose above 240 mg/dL
Goals: keep glucose and HbA1c in target range, administer insulin correctly, recognize and treat complications, and maintain intake adequate for growth and development
Interprofessional Care
Refer to a diabetes nurse educator for comprehensive management education
Pediatric endocrinologist, nutritionist, and exercise physiologist
Involve teachers, school nurses, guidance counselors, and coaches
⚠️ What goes wrongComplications
Complications
Diabetic ketoacidosis — acute and life-threatening, with glucose above 200 mg/dL, ketones in blood or urine, and acidosis with pH under 7.30 and bicarbonate under 15 mmol/L
DKA care: admit to intensive care, place on a cardiac monitor, obtain venous access for fluids, electrolytes, and insulin
DKA monitoring: blood and urine ketones, blood glucose, and labs for glucose, electrolytes, BUN, ABG, and CBC
📋 Growth Hormone Deficiency6 parts
ATI Active Learning Template — System DisorderGrowth Hormone Deficiency
Filled from ATI chapter 33, row by row from that chapter’s own sections — 12 of 12 rows have content.
🧭 What it isAlterations in Health (Diagnosis) · Health Promotion & Disease Prevention
Alterations in Health (Diagnosis)
Growth hormone (somatotropin) is secreted by the pituitary and drives normal growth, development, and cellular metabolism. Deficiency prevents normal somatic growth. GH works alongside ACTH, TSH, and the gonadotropins FSH and LH to regulate metabolic processes. Hypopituitarism is diminished or absent pituitary hormone secretion, chiefly GH, and its consequences depend on the degree of deficiency. Note: this chapter's file also repeats the full text of chapter 32 (diabetes mellitus); that duplicated material is captured under chapter 32.
Health Promotion & Disease Prevention
From this module — built from the notes above on this page, not a section of the ATI chapter.
Plot height and weight at every visit. A child crossing downward through centile lines is the finding, not short stature itself.
Mid-parental height gives the expected range; a child well below it needs assessment.
Screen for the treatable mimics first: hypothyroidism, celiac disease, chronic illness, malnutrition.
Address the psychosocial effect — short children are routinely treated as younger than they are.
👀 How it shows upAssessment — Risk Factors · Assessment — Expected Findings
Assessment — Risk Factors
Structural causes: tumors, trauma, structural defects, surgery
Hereditary disorders
Other pituitary hormone deficiencies such as TSH or ACTH deficiency
Most GH deficiency is idiopathic
Assessment — Expected Findings
Short stature with proportional height and weight — height is affected more than weight and bone age usually matches height age
Delayed epiphyseal closure and delayed bone age
Increased insulin sensitivity
Delayed or altered dentition with an underdeveloped jaw
Delayed sexual development
Linear growth velocity 2 standard deviations or more below the mean, under the 2.3 percentile
Growth failure thresholds: height velocity under 2.2 in/year at ages 2-4, under 2 in/year at ages 4-6, under 1.6 in/year for boys over 6, under 1.8 in/year for girls over 6
🧪 How it is confirmedLaboratory Tests · Diagnostic Procedures
Laboratory Tests
Plasma insulin-like growth factor-1 and IGF binding protein-3 — values below the mean for age prompt further evaluation
Diagnostic Procedures
GH stimulation testing for children with low IGF-1 and IGFBP-3 plus short stature
Skeletal radiographs assess maturity by comparing epiphyseal centers to published age standards — a general skeletal survey under 3 years and hand and wrist films in older children
Series of skull films can reveal structural abnormality such as a small sella turcica
CT and MRI identify tumors or other brain lesions
🩺 What you doNursing Care · Medications · Therapeutic Procedures
Nursing Care
Measure and plot height and weight on an appropriate growth chart at every visit
Assess height velocity over time, the height-to-weight relationship, and projected target height against genetic potential
GH stimulation test: explain the procedure, draw a baseline sample, give the agent that triggers GH release (arginine or GH-releasing hormone), then draw samples every 15-30 min for 3-4 hr
Keep the child NPO and limit activity for 10-12 hr before the stimulation test
Assess the effectiveness of GH replacement, which is produced by recombinant DNA technology
Give other hormone replacements such as thyroid hormone if prescribed
Support the child and family with psychosocial concerns including altered body image and depression, and stress realistic expectations for the child's age and abilities
Medications
Somatropin replaces human growth hormone and stimulates growth of bone and skeletal muscle
Give subcutaneously into the abdomen, thigh, buttock, or back of the upper arm
Use cautiously in children receiving insulin
Therapeutic Procedures
From this module — built from the notes above on this page, not a section of the ATI chapter.
Daily subcutaneous growth hormone, usually at bedtime to mirror natural secretion.
Teach injection technique and site rotation; involve the child as they get older.
Regular height measurement on the same stadiometer to judge response.
Monitor for slipped capital femoral epiphysis and raised intracranial pressure during therapy.
Treat associated hormone deficiencies; therapy continues until growth plates close.
💬 Around the patientClient Education · Interprofessional Care
Client Education
Nothing to eat or drink and limited activity for 10-12 hr before the stimulation test
Provide emotional support through imaging studies and help position the child
Interprofessional Care
Endocrinology consultation
Psychological counseling for child and family coping
⚠️ What goes wrongComplications
Complications
Untreated GH deficiency disrupts vertical growth and causes short stature, delayed epiphyseal closure, delayed bone age, and delayed sexual development
📝 Notes & key concepts
The lines from this module that carry a number, a dose or an absolute rule — the ones that decide questions. Everything else is on the cards above.
Thyroid panels invert: congenital hypothyroidism is low T3/T4 with HIGH TSH; hyperthyroid/Graves is high T3/T4 with LOW TSH.
Hypocalcemia: Chvostek (cheek tap → facial twitch) and Trousseau (cuff → carpal spasm). Normal calcium 8.8–10.4 mg/dL. Calcium and phosphorus move inversely.
Type 1 DM diagnostics: fasting glucose >126, random >200, GTT >200, A1c >6. Classic three Ps plus new-onset bedwetting and weight loss.
Hypoglycemia is cold and clammy: 10–15 g simple carbohydrate, recheck in 15 min, then a complex carb. Glucagon SC/IM if unconscious.
Hyperglycemia is hot and dry. Sick-day rules: check glucose and ketones every 3 hours and never skip insulin.
DKA: glucose >330, positive ketones, Kussmaul respirations, fruity breath, and hyperkalemia because without insulin potassium stays extracellular. Treat with isotonic fluids, then a continuous IV regular insulin drip, adding dextrose once glucose falls to about 200–250.
🎯 Module quiz
Questions for this module. They also feed the Mega Quiz.
