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NURS 373: Pediatrics > week 11: caring for child & family with endocrine and cerebral dysfunction > Flashcards

week 11: caring for child & family with endocrine and cerebral dysfunction Flashcards

1
Q

the thyroid hormone (TH) regulates the body’s basal metabolic rate and secretes 2 hormones

A
  1. TH
    - made up thyroxine (T4) that regulates energy, wt, temp, triiodothyronine (T3) which plays vital roles in metabolisms, muscle function, heart development, skin hair and nail growth
  2. calcitonin
    - helps to maintain blood calcium levels
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2
Q

what is congenital juvenile hypothyroidism

A
  • congenital hypoplastic thyroid gland. wants to identity as early as possible to prevent development delay, and therefore is part of the newborn screen
  • if mom took antithyroid drugs may cause this
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3
Q

what is acquired juvenile hypothyroidism

A
  • partial or complete thyroidectomy for CA or thyrotoxicosis
  • following radiation for hodgkin or other malignancy
  • infectious processes
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4
Q

clinical manifestations of juvenile hypothyroidism

A

Cognitive decline such as developmental delay and not meeting milestones, decline is reversible with treatment if started early
Constipation
Growth decline
Sleepiness
Myxedematous skin changes (dry skin, sparse hair, puffiness around eyes)

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5
Q

therapeutic management of juvenile hypothyroidism

A

Oral TH replacement as a lifelong treatment
May need to supplement with vitamin D if there is rapid bone growth
Prompt treatment needed for brain growth in infant
May administer in increasing amounts over 4 to 8 weeks to avoid symptoms of hyperthydroidism. If dose is too high may see tachycardia or hypertension, if treatment is too low may see lethargy. Compliance with medication regimen is crucial.

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6
Q

goiter

A

Hypertorphy of the thyroid gland

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7
Q

congenital goiter

A

Usually results from maternal ingestion of antithyroid drugs during pregnancy. If the infant is born one may need to prepare for airway management as it may be large enough to cause airway issues.

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8
Q

acquired goiter

A

Result of neoplasm, inflammatory disease, dietary deficiency (but rarely in children), or increased secretion of pituitary thyrotropic hormone.

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9
Q

graves disease

A

Most common cause of hyperthydroidism in childhood, believed to be caused by an autoimmune response to TSH receptors but there is no specific etiology. There is a familial association and the peak incidence is at 12-14 years of age but may also be present at birth.

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10
Q

graves disease

A

Tachycardia
Sweating
Weight loss/failure to gain weight
Increased CO

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11
Q

graves disease management

A

Monitor for symptoms as they may be hidden
Want to slow down the rate of hormone secretion
Therapy is not firmly established
Emotional management and increased dietary needs

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12
Q

graves disease treatment

A

Antithyroid drugs
Subtotal thyroidectomy if other treatment is not successful
Ablation with radioiodine

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13
Q

diabetes

A

Is a disorder of pancreatic hormone secretion, that is characterized by a total or partial deficiency of the hormone insulin. Is the most common endocrine disorder of childhood, with its peak incidence being between 10 and 15 years of age.

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14
Q

type 1 diabetes

A

Characterized by destruction of beta cells which leads to absolute insulin deficiency. Typical onset in childhood and adolescence but can occur at any age.
This is most seen in childhood
Most prominent in causasians

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15
Q

type 2 diabetes

A

Arises because of insulin resistance with onset usually being after 40.
Native american, hispanic, and african american children are at an increased risk of type II DM.
Affected people may require insulin injections.
Type II is now more common in children due to the lack of physical activity, SES and rise of obesity.

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16
Q

diabetes symptoms

A

Polyuria
Polydipsia
Polyfagia
Weight loss
Mood changes
Decreased energy
Vision changes
Frequent infection
Bedwetting in child who has been toilet trained

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17
Q

diabetes diagnosis

A

A1C to check average blood sugar over the past while
DKA
symptoms

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18
Q

diabetes management

A

Insulin replacement
Lifestyle changes
Monitoring blood sugar
Insulin pumps

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19
Q

diabetes education priorities

A

Community supports
Signs of hyperglycemia (ketones, frequent peeing, blurry vision, vomiting, pain, fruity breath)
Signs of hypoglycemia (decreased LOC, weakness, tremors, sweating)
How to administer insulin

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20
Q

sympt of cerebral dysfunction

A

*LOC is the most important indicator of neurological health

Decreased LOC
Altered reflexes (absent that should be there, or present that shouldnt be there)
Not meeting developmental milestones or regressing milestones
Changing behaviour
Decreased physical activity
Lack of coordination
Problems with breathing
Abnormal sized pupils
Headaches/migranes
Sensory problems
Sunken or bulging fontanelles
Head size

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21
Q

how do we assess cerebral functioning

A

*Complete neurological examination includes LOC, posture, sensory, cranial nerve, reflex testing, vital signs.

Infants and young children: observe spontaneous and elicited reflex responses, how they react and what their responses are to behaviour
Family history - genetic conditions, growth patterns
Health history - birth history, resuscitation at birth, exposures during pregnancy, substance abuse, meningitis, illness during infancy
Physical examination - measure head, coordination of suck & swallow
Developmental - what milestones have they hit and when, were they premature

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22
Q

early signs of increased intracranial pressure

A

Buldging fontanelles, high pitched crying, irritability, sunset eyes (sunken), decreased LOC, headaches, vomiting w/o nausea, dizziness, vision changes.
As pressure increases signs and symptoms become more pronounced, and level of consciousness deteriorates.
Infants will compensate by skull expansion and widened sutures, however still have limitations for spatial compensation.

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23
Q

personality and behaviour signs of increased ICP

A

Irritability
Restlessness
Drowsiness, indifference, decrease in physical activity and motor skills
Inability to follow commands, memory loss
Lethargy and drowsiness

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24
Q

late signs of increasing ICP

A

Decreased LOC
Bradycardia
Decreased motor response to command
Decreased sensory response to painful stimuli
Alterations in pupil size and reactivity
Papilledema
Decebrate or decorticate posturing
Cheyne-stokes respirations (periods of apnea, going between shallow and deep breathing)
*Obtunded, stupor, coma, vegetative state.

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25
Q

how is severity defined by pediatric glasgow coma scale

A

Mild score 13-15
Moderate score 9-12
Severe score <8

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26
Q

what is the pathophysiology of head injury

A

Force of intracranial contents cannot be absorbed by the skull and musculoligamentous support of the head
Especially vulnerable to acceleration-deceleration injuries
A child’s response is different because of their larger head size and insufficient musculoskeletal support

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27
Q

what are types of head trauma

A
  • concussions
  • contusions and lacerations
  • skull fractures
  • complications
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28
Q

describe the different skull fractures

A

Linear
Depressed- part of skull is sunken
Comminuted- multiple fractures
Basilar- at the base of the head
Open- open skin
Diastatic- along suture line

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29
Q

what is an epidural hemorrhage

A

between dura and skull

30
Q

Subdural hemorrhage

A

between dura and arachnoid mater

31
Q

Cerebral edema

A

swelling

32
Q

Herniation

A

sign of very high intracranial pressure

33
Q

head injury diagnostic evaluation

A

Detailed history
Assessment of ABCs (may need to be intubated if GCS is <8)
Evaluation for shock
Vital signs
Neurologic examination LOC
Special tests: CT scans, MRI, behavioural assessment

34
Q

why do we avoid opioid use in care of comatose child

A

want to avoid opioids as dont want to give something that may affect their neurological status

35
Q

s/s of nervous sys tumors

A

Headaches
Vomiting
Increased headsize
Vision loss
Memory changes
Physical changes

36
Q

diagnostic eval nervous sys tumors

A

Presenting clinical signs
Lumbar puncture (meningitis, increased CSF, ICP)
MRI, CT, EEG, LP (depends on presentation)
Histologic diagnosis via surgery

37
Q

nervous sys tumour management

A

Surgery depending on where it is
Radiotherapy (for comfort if palliative)
Chemotherapy

38
Q

nervous sys tumour prognosis

A

Will vary greatly and depends on
Type of tumor
Size of tumor
Extent of disease
Child’s age
Surgical resectability

39
Q

intracranial infections

A

The CNS has a limited response to injury, and it is difficult to distinguish etiology by looking at clinical manifestations. Lab studies are required to identify the causative agent.
Inflammation can affect the meninges, brain, or spinal cord.

40
Q

bacterial meningitis

A

Acute inflammation of the meninges and CSF, there has been a decreased incidence following the use of the Hib vaccine

41
Q

causative agents of bacterial meningitis

A

Streptococcus pneumoniae
Group B streptococci
Escherichia coli

42
Q

bacterial meningitis lab testing

A

Lumbar puncture for culture
Leukocytes in CSF
Glucose low protein high?
CBC, diff
Viral

43
Q

bacterial meningitis clinical manifestations

A

Fever
Stiff neck
Flu-like symptoms
Headache
Vomiting
No appetite
Vital sign changes
Changes in LOC

44
Q

transmission of bacterial meningitis

A

Droplet infection from nasopharyngeal secretions (contact droplet).
Appears as extensions of other bacterial infection through vascular dissemination.
Organisms then spread through CSF

45
Q

bacterial meningitis management

A

LP definitive diagnostic test.
Isolation precautions.
Initiation of antimicrobial therapy, giving broad spectrum antibiotics and once the pathogen is known then more specific.
Restrict hydration
Assessment & stabilization of ventilation and perfusion
Initiation of hemodynamic monitoring
Management of system shock
Control of seizures and tempurature
Treatment of complications
Response to therapy monitored clinically

46
Q

nonbacterial meningitis causative agents + s/s

A

Causative agents are primarily viruses, and manifestations are like bacterial meningitis but less severe. Onset can be abrupt or gradual.
Meningeal irritation
Headache
Fever
Malaise

47
Q

treatment of nonbacterial meningitis

A

Treatment is primarily symptomatic

48
Q

encephalitis

A

Inflammatory process of CNS with altered function of brain and spinal cord, inflammation of direct brain tissue is the result. Can occur as a result of direct invasion of the CNS by a virus, or post-infectious involvement of the CNS after a viral disease

49
Q

causative organisms of encephalitis

A

Variety of causative organisms, they are most frequently viral. May take longer to treat as viral management is simply supportive.

50
Q

Clinical manifestations of encephalitis: sudden or gradual onset

A

Malaise
Fever
Headache/dizziness
Stiff neck
Ataxia
Speech difficulties
Poor feeding

51
Q

Clinical manifestations of severe encephalitis

A

High fever
Stupor/seizures
Disorientation/spasticity
Coma
Ocular palsies
Paralysis

52
Q

therapeutic management of encephalitis

A

Hospitalized for observation
Treatment is antimicrobial therapy (IV acyclovir & vancomycin) and supportive care - early intro of nutrition
Management of complications
Cerebral edema
Fluid and electrolyte disturbance
Status epilepticus
Abrupt cardiac & respiratory arrest
Long term effects
Follow up care with reevaluation and rehabilitation (often need rehab as their motor control is really affected, there are often long term consequences)
Very young children may exhibit increased neurological disability

53
Q

Reye’s syndrome

A

Disorder defined as toxic encephalopathy associated with other characteristics of organ involvement. Do not give aspirin to children due to this.

54
Q

reye’s syndrome s/s

A

fever, profuse vomiting, decreased LOC profoundly impaired consciousness, and disordered hepatic function.

usually post virus

55
Q

Seizure disorders

A

Seizures are a symptom of an underlying pathologic condition
Caused by malfunctions of the electrical system of the brain, and are the most common neurological dysfunction in children. Determined by the site of origin, and occur with a wide variety of CNS conditions.

56
Q

etiology of acute symptomatic seizure disorders

A

Occur with head trauma or meningitis

57
Q

etiology of remote symptomatic seizure disorders

A

prior brain injury such as encephalitis or stroke

58
Q

etiology of cryptogenic seizure disorders

A

no clear cause

59
Q

etiology of idiopathic seizure disorders

A

genetic in origin

60
Q

focal seizure classification

A

Local onset and involves a relatively small location of the. Classified based on awareness during the seizure.

61
Q

Generalized Seizure classification

A

Involves both hemispheres without local onset. Awareness is impaired. Motor involvement is bilateral and they may be convulsive or nonconvulsive.

62
Q

Epileptic spasms-(include infantile spasms) Seizure classification

A

Spasms of the muscles of neck, trunk, & extremities.

63
Q

epilepsy

A

Individual is considered to have epilepsy when there are at least two unprovoked seizures occuring more than 24 hours apart
Caused by a variety of pathologic processes in the brain
Optimal treatment and prognosis requires an accurate diagnosis (done with ECG) and determination of the cause
In approximately 50% of cases in childhood epilepsy seizures disappear completely
Cause of epilepsy is unknown in 50-60% of cases

64
Q

generalized absence seizures

A

There is a brief loss of consciousness with a blank stare, could even keep on mobilixing during the seizure.
Minimal or no change in muscle tone
Can be mistaken for daydreaming
4-12 years of age is the normal onset, and then they stop at puberty

65
Q

Focal, generalized, unknown onset epileptic spasms

A

Onset in the first 6 to 8 months of life
Usually associated with some degree of cognitive impairment
Cause: possibly caused by disturbance of central neurotransmitter regulator at specific phase of brain development
Emergency but is hard to diagnose

66
Q

febrile seizures

A

Most common in childhood
Transient disorder of childhood where a seizure occurs with a fever, not a CNS illness, and resolves within 15 minsutes with a return to mental status. Do not have typical post-seizure symptoms.
Affects approximately 3% to 8% of children and usually occurs between ages 6 months and 3 years

67
Q

how do we manage seizures

A
  • treat the cause
  • pharma (hepra)
  • diet: ketogenic diet
  • vagus nerve stim
  • surgery
  • avoid triggers (dehydration, sleep deprivation)
68
Q

what is hydrocephalus

A

Caused by an imbalance in the production and absorption of cerebrospinal fluid, a symptom of an underlying brain pathologic condition that is demonstrated by impaired absorption of CSF.

69
Q

what does hydrocephalus cause

A

Impaired absorption of CSF within the subarachnoid space
Obstruction through the ventricular system
Communicating and noncommunicating hydrocephalus

70
Q

what is the etiology behind hydrocephalus

A

Developmental abnormalities usually apparent in early infancy. Often associated with myelomeningocele. Other causes include neoplasm, infection and trauma

71
Q

therapeutic management hydrocephalus

A

Relief of hydrocephalus, treatment of complications, most often surgical, placing a ventriculoperitoneal shunt. Problems are related to the effects of motor development.

72
Q

s/s of shunt infection

A

Period of greatest risk if 1 to 2 months after placement, requires massive dose antibiotics or shunt removal
Septicemia
Bacterial endocarditis
Wound infection
Shunt nephritis
Meningitis

NURS 373: Pediatrics (16 decks)

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