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Pediatrics > Haluk > Flashcards

Haluk Flashcards

1
Q

First convulsion causes

A

Hypo calcemia/natremia/glycemia
Hypernatremia
Diabetic ketoacidosis

Acute encephalopathy
Hepatic encephalopathy
Htn
İntoxications
Burns
Acute nephritis, hemolytic uremic syndrome

Inborn errors of metabolism
Galactosea
Aminoacidopathies
Respiratory chain
Urea cycle defects
Glycogen storage
Pyrodixine deficiency

Head trauma
Cerebral hypoxia
Cerebrovascular
Tumour
Cortical dysplasia

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2
Q

Paroxysmal conditions mimicking convulsions

A

Anoxic convulsions:syncope, breath holding
Toxic seizures: drugs
Bening paroxysmal vertigo of infancy/ torticollis
Paroxysmal dystonia, dyskinesia,athetosis

Hypereplexia
Hyperventilation syndrome
Pseudoseizures
Migraine
Psychosis
Night terros
Alternating hemiplegia of chilhood

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3
Q

Physical examination for convulsions

A

Vitals
Skin: pigmentation,petechia,hemangioma, open sinus, burn/ injection scars, hair
Vit D deficiency in infant
CVS

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4
Q

Neurological examination for convulsions

A

Awareness
Pupils,fundi: hemorhage,retinit,degen.
Menimgeal signs
Tonus,reflexes
!asymetrical!

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5
Q

Laboratory for convulsions

A

Cbc,urine,sugar,electrolytes,BUN, liver fnx,blood gases, Ca, Mg!
Anti epileptic drug levels
Toxic screening
Cranial imaging
Lumbar puncture
EEG

İmaging: cranial CT, MRI, MR angiogram

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6
Q

Treatment for convulsions
General

A

İNİTİALLY: 1.airway 2.iv 3.BP 4.biochemistry
1.airway: benzodiazepines or barbiturates
2.glucose: ıf cant be measured: start glucose %25 2 ml/kg in children
3. BP: hypertensive first 30-45 mins, later hypotensive
4.temperature: hyperthermia, anti pyretics

Careful:
Dont open mouth at tonic phase
Aspirate and position
Vital signs
Determine the cause immediatly
İv
%5 glucose to begin with

Prevent brain edema, acidosis,hypotension:
Reduce iv fluid, bicarbonate, dopamine

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7
Q

Status epilepticus

A

Epilepsy: spontanous convulsions more than one

  1. First 5 minutes:
    İv Diazepam 0.2-0.3, midazolam 0.1-0.2
    (No iv diazepam rectal mida. İm buccal or nasal)

2.Early(5-20)
Same as first

  1. Established(20-60)
    Fenitoin: %0,9 SF, 15-20 mg/kg, 1 mg/kg/min iv
    If not within 20 min:
    20 mg FENOBARBİTAL TABLET, under 3y: 100 mg iv PRİDOKSİN
    Or: LEVETİRACETAM 30 mg
    Or: > 2y: VALPROATE 30 mg

Diazepam, midazolam, fenitoin
Fenobarbital tablet, pridoksin, valproate. Levetiracetam

  1. Refractory(>60):
    Midazolam 0,2 followed by 0.05 infusion, increase every 15 min, clinical and eeg monitoring
    Continues: Thiopental 3-5 mg, 3-5 minutes until burst suppression at EEG
    Propofol 1-2 mg if cardiac is okay

Midazolam, thiopental,propofol

5.still continues: ketamine, mg, methylprednisolone, iv ig, plasma exchange, hypothermia. Csf drainage

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8
Q

Treatment for convulsions
Drugs

A

Active seizure: benzodiazepines
Serial: long acting anti convulsants

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9
Q

History for convulsions

A

Previous seizures
Stopping of medications
Drugs, toxins
Chronic ilness
Febrile conditions
Trauma
General appearance

Birth history
Family history

Infections, electrolyte status

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10
Q

General aproach to convulsions

A

1.history
2. PE
3.neurologic examination
4.laboratory, eeg,imaging
5.treatment

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11
Q

Encephalopathy triad

A

Variation in awareness
Reception and personal lack
Seizures

Encephalitis: encephalopathy + CSF pleocytosis

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12
Q

Neuromuscular disorders depending on site on nerve

A
  1. Anterior horn cell: poliomyelitis, SMA
    2.nerve fiber: Neuropathies:
    -demyelinating: muscular atrophy, polyneuritis, leukodystrophies
    • axonal: lead,diabetes,porphyria
  2. Neuromuscular junction: myasthenia gravis
  3. Muscles:
    -Hereditary: muscular dystrophy, congenital/metabolic myopathies
    -Acquired: dermatomyositis/ polymyositis, endocrine myopathy, iateogenic myopathy(steroid)
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13
Q

Clues from history for neuromuscular disorders

A

Age of onset
Family history
Rate of progression
Muscle involvement pattern
Myalgia and cramps: metabolic
Wasting and enlargement
Muscle stifness: myotonia
Myoglobinuria: metabolic
Respiratory and cardiac
General anesthesia: malignant hyperthermia

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14
Q

Some causes of toe gait

A

Muscular dystrophies
Motor neuropathies
Spastic syndromes
Early stages of walking

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15
Q

Investigations for neuromuscular disorders

A

CK
Metabolic test
Genetic analiz
ENMG
Muscle biopsy
MRI/ muscle USG

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16
Q

Creatine kinase levels and what they mean

A

Very high in muscular dystrophies, mildly elevated at myopathies, normal in motor neuron disorders and neuropathies

Normal: congenital myopathy, motor neuron disorders, mitochondrial disorders

Low: Neuromuscular(end stage or prolonged steroid use) , hyperthyroidism

High:
Hereditary: muscular dystrophy(duchenne/becker, limb girdle, acid maltase deficiency(pompe disease)
Acquired: JDM/ Pm, hypothyroidism
Acute muscle breakdown: (CK VERY HİGH) rhabdomyolysis,trauma, injection to site

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17
Q

Check CK if the ptx has these symptoms:

A

Delayed walking
Hypotonia
Myalgias
Muscle hypertrophy
Family history
Mental retardation
Autistic features
Persistent liver enzymes elevation

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18
Q

Causes of episodic weakness(muscular)
Autoimmun düşün

A

Chronic guillain-barre syndrome
Dermatomyosit/polymyosit
Myasthenia gravis
Rhabdomyolysis
Periodic paralysis

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19
Q

Specific treatments for muscular disorders

A

Duchenne MD: corticosteroids, gen tedavisi
Myotonic dystrophy:carbamazepine
Poly/dermatomyosit: ımmunosupressant
Myotonia:mexitil
Periodic paralysis:acetozolamide
M hyperthermia: dantrolene
Mitochondrial: CoQ10
Acid maltase def: enzyme replacement therapy

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20
Q

Aproach to ptx with muscular disorder suspicion?

A

Biologic, medical, social, personal

CK
Biochemistry
Muscle USG
EMG
Muscle biopsy( abcense of dystrophin
Genetic test

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21
Q

MRC scale for muscle power

A

5 normal
4 gravity+resistance
3 gravity
2 no gravity
1 flicker/trace of contraction
0 no contraction

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22
Q

Muscle cramps and what they mean

A

Occuring at rest: not muscle disorder
Occurs at exertion, relieved by rest+ myoglobinuria= muscle disorder

1.genetic:
Benign/low grade muscular dystrophy: limb girdle or becker type
Metabolic disorders: glycogen depo,lipid metabolism, mitochondrial
2.Acquired:
Idiopathic ınflammatory myopathies: dermatomyosit( b cell),polymyosit,i(t cell),inclusion body myosit
Drug induced myopathies: statins,corticosteroids, alcohol cocaine

23
Q

Motor milestones for children

A

3m: definite head control
6m: takes weight on legs
9m: sit, pivot, pulls to stand
1y: cruises, walk w help
15m: walks, creeps up stairs
18m: runs, climbs stairs
2y: kicks ball
3y: stands on one leg, jumps off step
4y:hops on one foot
5: hops on either foot

24
Q

Clinical cues and signs for muscular disorder examination

A

Gowers sign: proximal muscle weakness
Amyoplasia
Juvenile dermatomyosit
Mitochondrial(myopathic face)
Myotonia
Ptosis
Myotonic dystrophy: labial fold silikse fascial tutulum, myotonic yüz
SMA 1: flask posture, abdominal solunum
Sma 2: myopathic yüz yok
Distal involvement in CMT: tenar tutulum
Arthrogyroposis
Multiple contractures
Psudohupertrophy

25
Q

Acute flaccid paralysis

A

Rapid onset weakness involving respiratory and bulbar weakness
Reaches maximum in days or weeks
Flaccid indicates abscense of spasticity and CNS damage(hyperreflexia,clonus,extensor plantar response)
May result in respiratory failure and death
! Polio surveillance. Within 14 days of paralysis, 2 stool samples 24 hours apart

26
Q

Differential dgx of acute flaccid paralysis

A

Guillain barre syndrome
Acute anterior/ vaccine associated poliomyelitis, other viruses
Cord compression
Acute axonal/toxic/infectious/ critiical ilness neuropathy
Acute myopathy
MS
Poliomyosit/dermatomyosit
Mitochondrial diseases
Vascular malformation
Botulism
İnsecticide,tick paralysis, snakebite

27
Q

Acıte management of acute flaccid paralysis

A
  1. Respiratory muscle weakness evaluation
  2. Bulbar weakness assesment
    3.CV assesment
  3. Electrolyte imbalance/ toxemia assesment
  4. Exclusion of spinal cord compression
28
Q

Laboratory for acute flaccid paralysis

A

CK
Spinal MRI: cord compression, acute transverse myelitis
CSF examination: cell count, protein level
EMG

29
Q

Diagnosis of acute flaccid paralysis by location 1.peripheric neuropathy

A

Guillan barre syndrome
axonal neuropathy
Infectious disease neuropathy(diptheria,neuroborreliosis)
Toxic neuropathy (heavy metals,snake venom)
Arthropod bites

30
Q

Diagnosis of acute flaccid paralysis by location 2. Anterior horn disease

A

Anterior poliomyelitis
Vaccine assoc poliomyelitis
Other neurotropic viruses(enterovirus, echovirus,coxsackie)

31
Q

Diagnosis of acute flaccid paralysis by location 3. Acute myelopathy

A

Cord compression
Vascular malformation(bleeding, thrombos)

32
Q

Diagnosis of acute flaccid paralysis by location 4. Demyelinating diseases
(Not by location?)

A

MS( multiple sclerosis)
ADEM( acute disseminated encephalomyelit)
NMO( neuromyelitis optica)
acute transverse myelitis( ATM)
MOGAD ( antibody disease)

33
Q

Diagnosis of acute flaccid paralysis by location 5.neuromuscular junction disorders

A

Myastenia gravis
Botulism
Insecticide poisoning
Tick paralysis
Snake bite

34
Q

Diagnosis of acute flaccid paralysis by location 5.muscle diseases

A

Polymyositis, dermatomyosit, trichinosis
Periodic paralysis
Mitochondrial diseases
Steroids and blocking agents

35
Q

Demyelinating disease of acute flaccid paralysis case

A

Weakness in left arm for 5 days
Strength in left decreased
Sensory loss between right side of body
Cervical mri: hyperintense lesion in spinal cord c2-c5, more visible after contrast(myelitis)

ACUTE TRANSVERSE MYELİTİS

36
Q

Demyelinating disease of acute flaccid paralysis case

A

Difficulty walking for 4 days
Diplegia
Sensory loss, deep tendon reflexes increased, extensor plantar response, clonus
Hyperintense lesion T1-T7 , CSF protein increased,
ANTİ AQP4 antibody positive

NEUROMYELİTİS OPTİCA

37
Q

Neuromuscular junction disease of acute flaccid paralysis case

A

3 month baby after vacation
Decreased sucking, constipation, high pitched crying
Hypotonia, ptosis, respiratory distress
Unresponsive to painful stimule, loss of light reflexes, mydriasis, nystagmus
EMG: motor endplate dysfunction of presynaptic type
Stool sample positive for clostridium botulinum toxin A, B
Botulinum heptavalent antitoxin healed baby

INFANTILE BOTULİSM

38
Q

Acute myelopathy disease of acute flaccid paralysis case

A

Kid with progressive weakness and sensory loss at lower extremities for 15 days
Strength loss at lower extremities
Deep tendon reflexes increased, extensor plantar response
Absence of sensation below T10
Spinal MRI: mass compressing cord at thoracic region

CORD COMPRESSİON( thoracic tumor)

39
Q

Anterior horn disease: Acute flaccid myelitis case

A

Weakness, inability to sit, starting at left upper extremity and face, 7 days after upper respiratory tract infection
Left side upper lower strength decrease
Couldnt walk, facial paralysis at left
Deep tendon reflexes absent
Meningeal irritation signs positive
Brain MRI: hyperintensity at dorsal pons
Spinal MRI: hyperintensity predominantly in anterior horn cells at cervical region
CSF: 10 lymphocytes
ACUTE FLACCİD MYELİTİS
İvig, pulse steroid, plasmapheresis given.

40
Q

Poliomyelitis and other enteroviruses

A

RNA viruses
Transmission through fecal-oral route, respiratory route
Can lead to: self limiting aseptic meningitis to poliomyelitis and brainstem encephalitis

41
Q

Acute poliomyelitis case

A

Affects anterior horn cells, cranial nuclei of medulla, reticular formation, cerebrllar vermis
İncubation 3-35 days, then initially:
Headache, vomiting, fever
2-5 days later:
meningeal irritation,pain in lumbar region and extremities
Asymetric flaccid paralysis
Loss of deep tendon reflexes
Urinaey retention
NO SENSORY LOSS
Encephalitis signs respiratory failure by brainstem involvement or diağhragmatic/intercostaş muscle paralysis

CSF : cell count increased(PMN,lymphocytes)
Protein virus isolation from stool and nasopharynx
MRI: anterior horn substantia nigra involvement
Antibody titers
Muscles paralyzed after a month remain paralyzed
Seen in adults after attack, 20 years: progressive motor neuron disease like amyotrophic lateral sclerosis(post-polio syndrome)

Anterior horn cells, no sensory loss, deep tendon reflex loss,asymmetric flaccid paralysis, csf cell count increased by pmn and lymphocytes, meningeal irritation, pain in lumbar and extremities, protein virus isolation from stool, antibody titers,urinary retention
Headache vomiting fever

42
Q

Neonatal encephalopathy

A

After 35th, born with impaired conciousness, convulsions, respiratory compromise, hypotonia

43
Q

Dgx of neonatal encephalopathy

A

Hypoxemia
Multiorgan dysfunction from ischemia
Acidemia
Bradycardia
Hypotonia
Seizures
Stupor/coma
Decreased scalp ph
Decreased apgar score

44
Q

Pathophysiology of neonatal encephalopathy

A

Gas exchange fault in placenta or postnatal pulmanory insufficiency
Dilated cerebral vessels as compensation, to prevent neuronal damage(autoregulation)
Hypoxemia, hypercarbia,acidosis
Hypoxia and hemorhage go together; increased co2 causes increased blood flow

Hypoxic insult at premature: periventricular leukomalacia( beyaz cevher)
Term asphyxia: basal ganglia lesions (gri cevher)

45
Q

Clinic of the baby with neonatal encephalopathy( hypoxic ischemic encephalopathy)

A

Resp/ feeding difficulty, diminished reflexes, hyperalert or lethargic, low APGAR score

Mild: irritable, hyperexcitable, increased reflexes,sympathetic overreactivity, muscle tone change
Moderate: lethargy,hypotonia,decreased reflex, seizures
Severe: suck/ swallow abnormal, Apnea, refractory seizures, increased ICT, coma, flaccid,brainstem dysf.

Cranial USG: ischemic white matter injury

Therapeutic hypothermia: for babies born >35 weeks, APGAR <5 or intubated right after birth
Initiation first 6 HOURS of life
Lowering temperature lowers brain metabolism, head cooling or whole body

46
Q

Cerebral palsy:

A

NON PROGRESSİVE
Caused by non progressive defects of immature brain, a persistent movement and posture disorder

Caused by hypoperfusion or failure to match demand

Before 20 weeks: CNS malformation: cortical and basal ganglia damge at first trimester in term babies
After 20 weeks: white matter abnormality

47
Q

Cerebral palsy risk factors and types

A

Prenatal(%80) or postnatal
Prematurity, low birth weight
Newborn jaundice
Hypoxic encephalopathy
Stroke<1 y
CNS/ intrauterine infections
Genetic

!Premature: diplegia (legs)
!Full term: athethosis
Athethosis: mixed form, scissored legs, spastic,babinski+
Hemiplegia: one side
Quadriparesis: all limbs

48
Q

Causes of Cerebral palsy

A

PREGNANCY: congenital/intrauterine infections, maternal ilness, cerebral dysgenesis, placental anomaly, multiple pregnancy,toxemia of pregnancy,drugs cervix torsion,bleeding

BİRTH: prematurity, low birth weight,HIE, abnormal presentation, placental anomaly, bleedimg, early membrane rupture,chorionitis, umbilical cord

NEWBORN: CNS infections, IC bleeding, polycytemia, coagulopathy,hypoglycemia, hyperbilirubinemia

49
Q

Comorbidities for Cerebral palsy

A

Epilepsy, mental retardation, eye/hearing/swallowing/speech, language/pulmanory/orthopedic problems
Behavioral and sleep problems

50
Q

Dgx of Cerebral palsy

A

History : if loss of gained fnx: another disease!!!(neurodegenarative)
Family history( if more than 1 family member another disease)
PE
Investigations

No loss of gained fnx and not much in family

51
Q

Prognosis of Cerebral palsy

A

Sits alone by 2 years, primitive reflexes lost by 18 months
Neck control by 9 m,crawls by 30 m
:
Expected to walk

52
Q

Prevention and trx of Cerebral palsy

A

Prematurity history in family, genetic disorders in family, pregnancy follow ups, delivery room yanı ameliyathane, NICU

Treatment: lifelong
Fizyoterapi, occuptional therapy, fine motor coordination, orthopedic surgery, drugs for spasticity, comorbidites, nutrition

53
Q

CNS Malformations (cerebral palsy)

A

Genetic,toxic or intreuterin infections, associated defects
1/4 of spontaneous fetal deaths, %40 of deaths of first year
Many chromosomal abnormalties aborted early

Hemimegalencephaly,pachygria
Lissencephaly
Silent brain

Pediatrics (10 decks)

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