Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

goiter

A

Hypertorphy of the thyroid gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

acquired goiter

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

graves disease

A

Tachycardia
Sweating
Weight loss/failure to gain weight
Increased CO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

graves disease treatment

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

diabetes diagnosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

diabetes management

A

Insulin replacement
Lifestyle changes
Monitoring blood sugar
Insulin pumps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
how is severity defined by pediatric glasgow coma scale
Mild score 13-15 Moderate score 9-12 Severe score <8
26
what is the pathophysiology of head injury
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
27
what are types of head trauma
- concussions - contusions and lacerations - skull fractures - complications
28
describe the different skull fractures
Linear Depressed- part of skull is sunken Comminuted- multiple fractures Basilar- at the base of the head Open- open skin Diastatic- along suture line
29
what is an epidural hemorrhage
between dura and skull
30
Subdural hemorrhage
between dura and arachnoid mater
31
Cerebral edema
swelling
32
Herniation
sign of very high intracranial pressure
33
head injury diagnostic evaluation
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
why do we avoid opioid use in care of comatose child
want to avoid opioids as dont want to give something that may affect their neurological status
35
s/s of nervous sys tumors
Headaches Vomiting Increased headsize Vision loss Memory changes Physical changes
36
diagnostic eval nervous sys tumors
Presenting clinical signs Lumbar puncture (meningitis, increased CSF, ICP) MRI, CT, EEG, LP (depends on presentation) Histologic diagnosis via surgery
37
nervous sys tumour management
Surgery depending on where it is Radiotherapy (for comfort if palliative) Chemotherapy
38
nervous sys tumour prognosis
Will vary greatly and depends on Type of tumor Size of tumor Extent of disease Child’s age Surgical resectability
39
intracranial infections
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
bacterial meningitis
Acute inflammation of the meninges and CSF, there has been a decreased incidence following the use of the Hib vaccine
41
causative agents of bacterial meningitis
Streptococcus pneumoniae Group B streptococci Escherichia coli
42
bacterial meningitis lab testing
Lumbar puncture for culture Leukocytes in CSF Glucose low protein high? CBC, diff Viral
43
bacterial meningitis clinical manifestations
Fever Stiff neck Flu-like symptoms Headache Vomiting No appetite Vital sign changes Changes in LOC
44
transmission of bacterial meningitis
Droplet infection from nasopharyngeal secretions (contact droplet). Appears as extensions of other bacterial infection through vascular dissemination. Organisms then spread through CSF
45
bacterial meningitis management
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
nonbacterial meningitis causative agents + s/s
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
treatment of nonbacterial meningitis
Treatment is primarily symptomatic
48
encephalitis
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
causative organisms of encephalitis
Variety of causative organisms, they are most frequently viral. May take longer to treat as viral management is simply supportive.
50
Clinical manifestations of encephalitis: sudden or gradual onset
Malaise Fever Headache/dizziness Stiff neck Ataxia Speech difficulties Poor feeding
51
Clinical manifestations of severe encephalitis
High fever Stupor/seizures Disorientation/spasticity Coma Ocular palsies Paralysis
52
therapeutic management of encephalitis
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
Reye’s syndrome
Disorder defined as toxic encephalopathy associated with other characteristics of organ involvement. Do not give aspirin to children due to this.
54
reye's syndrome s/s
fever, profuse vomiting, decreased LOC profoundly impaired consciousness, and disordered hepatic function. usually post virus
55
Seizure disorders
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
etiology of acute symptomatic seizure disorders
Occur with head trauma or meningitis
57
etiology of remote symptomatic seizure disorders
prior brain injury such as encephalitis or stroke
58
etiology of cryptogenic seizure disorders
no clear cause
59
etiology of idiopathic seizure disorders
genetic in origin
60
focal seizure classification
Local onset and involves a relatively small location of the. Classified based on awareness during the seizure.
61
Generalized Seizure classification
Involves both hemispheres without local onset. Awareness is impaired. Motor involvement is bilateral and they may be convulsive or nonconvulsive.
62
Epileptic spasms-(include infantile spasms) Seizure classification
Spasms of the muscles of neck, trunk, & extremities.
63
epilepsy
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
generalized absence seizures
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
Focal, generalized, unknown onset epileptic spasms
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
febrile seizures
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
how do we manage seizures
- treat the cause - pharma (hepra) - diet: ketogenic diet - vagus nerve stim - surgery - avoid triggers (dehydration, sleep deprivation)
68
what is hydrocephalus
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
what does hydrocephalus cause
Impaired absorption of CSF within the subarachnoid space Obstruction through the ventricular system Communicating and noncommunicating hydrocephalus
70
what is the etiology behind hydrocephalus
Developmental abnormalities usually apparent in early infancy. Often associated with myelomeningocele. Other causes include neoplasm, infection and trauma
71
therapeutic management hydrocephalus
Relief of hydrocephalus, treatment of complications, most often surgical, placing a ventriculoperitoneal shunt. Problems are related to the effects of motor development.
72
s/s of shunt infection
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions