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peds - growth and development > Week 6 - Chronic illness, Disability, and Home Care > Flashcards

Week 6 - Chronic illness, Disability, and Home Care Flashcards

1
Q

Define chronic illness

A

A condition that has the potentital to:
- interfere w/ daily FN for > 3 months/yr
- causes hospitalization of > 1 month/yr

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2
Q

What is the most common endocrine disorder in childhood? When is this disorder most prevalent?

A

Diabetes Mellitus
- peak incidence in early adolescence

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3
Q

What are the major groups of DM? Explain.

A

Type 1 - pancreas does NOT make insulin d/t destruction of Beta cells
Type 2 - body cells cannot USE insulin properly
Maturity-onset diabetes of the young (MODY) - rare autosomal dominant disorder w/ abnormally formed insulin and decreased biologic activity

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4
Q

Which type of diabetes affects children?

A

Type 1

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5
Q

How do you diagnose diabetes?

A
  • 8 hr fasting blood glucose level of 126 mg/dl (7 mmol/L)
  • random blood glucose value of 200 mg/dl (11.1 mmol/L)
  • oral glucose tolerance test finding of > 200 mg/dl in the 2 hour sample, or
  • hemoglobin A1C of 6.55 or more = type 2 DM
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6
Q

Can cystic fibrosis cause diabetes?

A

Yes, CF affects the pancreas
- loses ability to make insulin over time

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7
Q

What type of medications can increase the risk of developing diabetes?

A

Steroid medications
Dexamethasone and prednisone - long term use

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8
Q

At what age is MODY diagnosed?

A

Usually before the age of 25, onset occurs before 25 generally

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9
Q

What is the therapeutic management of type 1 DM?

A

nutrition
exercise
patient teaching
illness management
management of DKA

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10
Q

What do you include in your teaching about blood sugar checks?

A
  • monitor BG levels before meals, before bed, and at specific additional times as indicated
  • monitor before and after exercise
  • monitor for symptoms of hypoglycemia
  • monitor more frequently when sick
  • optimal BG target: 4-8 mmol/L
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11
Q

What is the plasma BG goal for a toddler with Type 1 DM?
- before meals?
- before bed?
- hemoglobin A1C

A

before meals: 100-180 mg/dl
before bed: 110-200 mg/dl
hemoglobic A1C: < 8.5% (but > 7.5%)

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12
Q

What is the plasma BG goal for a preschooler with Type 1 DM?
- before meals?
- before bed?
- hemoglobin A1C

A

before meals: 100-180 mg/dl
before bed: 110-200 mg/dl
hemoglobic A1C: < 8.5% (but > 7.5%)

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13
Q

What is the plasma BG goal for a school-aged child with Type 1 DM?
- before meals?
- before bed?
- hemoglobin A1C

A

before meals: 90-180 mg/dl
before bed: 100-180 mg/dl
hemoglobic A1C: < 8 %

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14
Q

What is the plasma BG goal for an adolescent with Type 1 DM?
- before meals?
- before bed?
- hemoglobin A1C

A

before meals: 90-130 mg/dl
before bed: 90-150 mg/dl
hemoglobic A1C: < 7.5%

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15
Q

What are the signs of hyperglycemia?

A
  • feeling tired
  • irritability
  • polyuria
  • polydipsia
  • blurry vision
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16
Q

What are signs of hypoglycemia

A
  • feeling tired
  • irritability
  • blurry vision
  • dizziness
  • shakiness
  • paleness
  • increased hunger
  • sweatiness
  • headache
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17
Q

What are the signs and symptoms of DKA?

A
  • high blood sugar levels and ketones in urine
  • excessive thirst
  • polyuria - in large amounts
  • sudden weight loss
  • stomach pain or nausea
  • vomiting
  • dehydration - dry mucus membranes, mouth
  • deep heavy breathing
  • fruity smelling breath
  • drowsiness leading in time to unconsciousness
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18
Q

Explain ketoacidosis

A
  • when the body breaks down fat for energy, in the absence of glucose
  • ketones released
  • excess ketones eliminated in urine (ketonuria) or by the lungs (acetone breath)
  • ketones make the blood more acidic (lowers pH ==> ketoacidosis)
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19
Q

What lab values indicate metabolic acidosis?

A

glucose > 11 mmol/L
pH < 7.3
HCO3 < 15 mmol/L
Ketones in blood and/or urine

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20
Q

Which type of DM is DKA more common in?

A

Type 1
10-20% of kids w/ new-onset type 1 DM present w/ DKA

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21
Q

How do we manage DKA?

A

1) Fluid rehydration w/ 0.9% NaCl (deficits replaced at a rate of 50% over the first 8-12 hrs, and the remaining 50% over the next 16-24 hrs)
2) IV insulin infusion starting with 0.1 unit/kg/hr
3) IV fluids w/ K+ replacement –> but check electrolytes and renal FN first
4) blood glucose levels should decrease by 50 to 100 mg/dl/hr (2.8-5.6 mmol/L)

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22
Q

What are some tips to minimize pain during glucose monitoring?

A
  • use a warm compress to enhance blood flow to the finger before pricking
  • use the ring finger or thumb, and puncture the finger just to the side of the finger pads
  • use lancet device w/ adjustable dept tips; use a shallow one
  • use glucose monitors that require small blood samples
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23
Q

What is asthma?

A

Chronic inflammatory disorder of the airways
- bronchial hyperresponsiveness
- episodic
- limited airflow or obstruction that reverses spontaneously or w/ tx

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24
Q

What are common clinical manifestations of asthma?

A

Dyspnea, wheezing, and cough

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25
Q

List therapeutic management for asthma

A

allergen control and avoidance
drug therapy to prevent or relieve bronchospasm
maintain health and prevent complications
promote self-care
support child and family

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26
Q

What are long term control meds for asthma?

A
  • inhaled corticosteroids
  • cromolyn sodium and nedocromil
  • long-acting B2-agonist
  • Flovent, Alvesco
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27
Q

What are quick-relief (rescue) medications for asthma?

A

Bronchodilators
- short-acting B2-agonists (salbutamol)
- anticholinergics (Ipratropium)
- systemic steroid (prednisolone)

28
Q

What are 2 IV meds given for asthma?

A

IV Magnesium sulphate
IV salbutamol

29
Q

What have inhaled medications for asthma?

A

MDI w/ spacer
Nebulizer

30
Q

What is the significance of using a spacer when administering MDI?

A

A spacer/chamber holds the puff from the MDI in a tube or “chamber” for a few seconds, so that you don’t have to both breathe in AND spray the MDI exactly at the same time. This helps get more medicine into your lungs

31
Q

What are the signs of mild asthma exacerbation?

A
  • Breathlessness while walking
  • talking in sentences
  • may be agitated
  • increased RR
  • moderate expiratory wheezes
  • pulse < 100
  • pulsus paradoxus: absent or < 10 mmHg
32
Q

What are the signs of moderate asthma exacerbation?

A
  • breathlessness at rest, prefers sitting
  • softer and shorter cries in infants
  • talking in phrases
  • agitated
  • increased RR
  • accessory muscle use
  • loud expiratory wheezes
  • pulse: 100-120
  • pulsus paradoxus: may be present, 10-25 mmHg
33
Q

Signs of severe asthma exacerbation?

A
  • breathlessness at rest
  • infant stops feeding
  • talking in words
  • agitated
  • RR > 30
  • accessory muscle use present
  • loud wheezes on inspiration and exhalation
  • pulse >120
  • pulses paradoxus: present, 20-40 mmHg
34
Q

What are some visible late warning signs of asthma exacerbation?

A
  • flared nostrils
  • blue or grey skin around the mouth
  • tracheal tug
  • skin under ribs pulled inward
35
Q

Signs of severe respiratory distress in children w/ asthma

A
  • sitting upright, refusing to lie down
  • younger one stops feeding
  • talk with few words only
  • agitated
  • diaphoresis
  • pale
  • fast RR
36
Q

What PRAM score do you assign to a child presenting with suprasternal indrawing, wheezing on exhalation, widespread decreased air entry, and a SpO2 reading of 92%

A

suprasternal indrawing - 2
expiratory wheezes - 1
widespread diminished air entry - 2
92% O2 - 1

total: 6 (Moderate)

37
Q

What PRAM score do you assign to a child coming in with suprasternal indrawing, scalene retractions, audible wheezing, widespread decrease in air entry, and O2 sat of 88%

A

2 + 2 + 3 +2 + 2 = 11 (Severe)

38
Q

What are the PRAM scores for mild, moderate, and severe asthma?

A

mild: 0-4
moderate: 5-8
severe: 9-12

39
Q

How do you manage someone w/ a PRAM score of 2

A

2 = mild
- give salbutamol every 20 mins, 1-2 doses in the first hour delivered via an MDI and spacer
- reassess 20 mins after each dose of salbutamol
- observe for at least 1 hr after the last dose of salbutamol; if the PRAM score remains mild, provide asthma teaching and discharge instructions

40
Q

How do you manage someone with a PRAM score of 5

A

5 - Moderate
- Salbutamol every 20 minutes, X 3 doses delivered via MDI and spacer
- Ipratropium every 20 minutes, X 3 doses delivered in
the first hour only, 3 delivered via MDI and spacer
- Give oral corticosteroid before or immediately after
the first dose of salbutamol
- reassess 20 mins after each dose
- if PRAM score is still greater than or equal to 4, give salbutamol every 30-60 minutes

41
Q

How do you manage someone w/ a PRAM score of 9

A

9 = severe
1. Call MRP Immediately
2. Salbutamol continuous nebulization with oxygen
* Bronchodilators delivered continuously for 60-180 minutes via aerosol result in more rapid improvement compared to intermittent delivery
3. Ipratropium nebulized every 20 minutes for 3 doses if not already given
4. Establish IV access, run maintenance fluids
5. Methylprednisolone IV 1 mg/kg/dose every 6 hours even if a previous steroid has been given
6. Continuous cardio/respiratory/SaO2 monitoring
7. Consider chest X-ray

If PRAM score is still severe after reassessment:
- Magnesium Sulfate IV
* In addition to continuous bronchodilator therapy
* Consider 0.9% sodium chloride bolus IV of 20mL/kg over 20 minutes to vent hypotension
- consult pediatrician and RT

42
Q

What is cystic fibrosis?

A
  • Exocrine gland dysFN
  • an autosomal recessive genetic disease (abnormal gene on chromosome 7)
  • affects the respiratory and GI systems d/t pancreatic enzyme deficiency
43
Q

How is CF diagnosed?

A

Thorough PMHx + testing
- newborn screening
- genetic testing
- sweat chloride test
- chest radiography
- History + physical exam

44
Q

Explain the pathophysiology of CF

A

Pancreatic enzyme deficiency that results in increased viscosity of mucous gland secretion
- thick secretions = mechanical obstruction
- mostly affecting the respiratory tract and pancreas

45
Q

How does CF affect the respiratory tract?

A

Thick stagnant mucus in the respiratory tract
- increased risk of bacterial colonization (Pseudomonas aeruginosa) –> destruct the lung tissues
- secretions difficult to expectorate –> obstructs the bronchi/bronchioles
- causes impaired gas exchange –> hypoxia, hypercapnia, acidosis
- compression of pulmonary blood vessels and progressive lung dysFN leading to pulmonary HTN, cor pulmonale, resp. failure, and death

46
Q

what are interventions for CF on the respiratory system?

A

bronchodilators - open the airway
mucus thinners - hypotonic saline (inhalation form), or adding extra salt into the airways (to pull water into the airways)

47
Q

What is the effect of CF on the GI tract?

A

thick secretions block the pancreatic ducts –> cystic dilation –> degeneration –> diffuse fibrosis
- scarring (fibrosis) prevents pancreatic enzymes from reaching the duodenum
- impaired digestion/absorption of fat + protein
- pancreatic fibrosis/scarring ==> diabetes
- focal biliary obstruction results in multilobular biliary cirrhosis
- impaired salivation

48
Q

What are the clinical manifestations of CF?

A

Trouble gaining weight, stunted growth, failure to thrive
meconium ileus in the early postnatal period
pancreatic enzyme deficiency
progressive COPD associated w/ infection
sweat gland dysFN
- gradual respiratory deterioration

49
Q

CF respiratory management

A

remove excessive mucous secretions
- chest PT
- bronchodilator medication
- forced expiration (breathing exercise)

aggressive treatment of pulmonary infections
- home IV antibiotic therapy
- aerosolized antibiotics

steroid use/NSAIDs
Transplant

50
Q

What are goals for CF patients?

A
  • prevent and minimize pulmonary complications
  • adequate nutrition for growth
  • assist in adapting to chronic illness
51
Q

CF gastrointestinal management

A
  • replace pancreatic enzymes
  • high protein, high calorie diet (150% of RDA)
  • prevent/manage intestinal obstruction
  • salt supplementation
  • oral glucose-lowering agents or insulin injections
  • diet and exercise management
52
Q

What is sickle cell anemia

A
  • hereditary hemoglobinopathy
  • autosomal recessivee
  • RBCs are sickle cell –> carry less O2
53
Q

What is the most serious type of sickle cell anemia?

A

SS

54
Q

In which ethnicity is sickle cell anemia most prevalent?

A

African ancestry
- also seen in children of the middle east, Mediterranean, and South Asia

55
Q

Explain the pathophysiology of sickle cell

A
  • partial or complete replacement of normal Hgb w/ abnormal
  • RBCs are elongated (sickle) shape
  • sickled cells are rigid and can block capillary blood flow –> micro obstructions can lead to tissue ischemia
  • hypoxia occurs and causes sickling
  • large tissue infarctions occur –> organ damage
  • spleen sequestration: RBCs are trapped; may require splenectomy
56
Q

How is Sickle Cell treated?

A

NO CURE (except bone marrow transplant)
supportive care - prevent episodes
immunocompromised - treat infections

57
Q

What is hydroxyurea? What is it used for?

A

A chemotherapy drug
- also used for sickle cell anemia; prevents:
- pain crisis, episodes of acute chest syndrome, blood transfusions, hospital stays

58
Q

What causes a sickle cell crisis?

A
  • anything that increases the body’s need for O2 or alters the transport of O2
  • trauma
  • infection, fever
  • physical and emotional stress
  • increased blood viscosity d/t dehydration
  • hypoxia (from high altitude, poorly pressurized planes, hypoventilation, hypothermia)
59
Q

What are the types of sickle cell crisis?

A

Vasoocclusive thrombotic (VOC)
- painful episodes caused by the stasis of blood
- blood clumps –> ischemia –> infarction
- signs: fever, pain, tissue engorgement

Splenic sequestration
- when blood pools in the spleen –> spleen enlarged
- hb levels drop significantly –> can result in death within hours
- signs: profound anemia, hypovolemia, shock

Aplastic crises
- Diminished production and increased destruction of RBCs
- triggered by viral infection (Parvovirus B19) or depletion of folic acid
- signs: anemia, pallor

60
Q

What is Acute chest syndrome?

A

similar to pneumonia
VOC or infection results in sickling in the lungs
causes chest pain, fever, cough, tachypnea, wheezing and hypoxia

61
Q

How is ACS managed?

A

A medical emergency
- aggressive tx of infection: give IV broad-spectrum antibiotics, prophylactic w/ oral penicillin
- pain management
- Monitor CBC and reticulocyte count to evaluate bone marrow function
- blood transfusion
- exchange transfusion

62
Q

What part of the GI tract is impacted by Crohn’s disease vs Ulcerative colitis?

A

Crohn’s: any part of GI tract
UC: colon + rectum

63
Q

What are the s/s of Crohn’s disease?

A

stomach pain
vomiting
loss of appetite
fever
diarrhea
weight loss
poor growth
mouth ulcers
swollen lips

64
Q

What are major differences between crohn’s disease and UC?

A

fistulas, strictures, and anal lesions
- rare in UC
- common in Crohn’s

Rectal bleeding
- common in UC
- uncommon in Crohns

65
Q

How is Crohn’s disease and UC managed?

A

Medications:
- 5-ASAs
- corticosteroids
- immunomodulators
- antibiotics
- biologic therapy

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