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Pediatrics 5th year > Topic list > Flashcards

Topic list Flashcards

1
Q

Classification of pneumonia

A

Typical bacteria, atypical bacteria, viral

Based on inflitrate: lobar, bronchopulmonary, interstitial

Based on place of acquisition: community-acquired or hospital acquired.

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2
Q

Symptoms of pneumonia

A

– fever, weakness, lethargy.
– cough, tachypnea, wheezing, dyspnea, cyanosis
– vomiting, diarrhea, abd. pain
– convulsions, apathy, restlessness
– tachycardia, cardiac decompensation

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3
Q

Specific symptoms of pneumonia based on pathogens

A

Unproductive cough: viruses, M. pneumonia, C. pneumonia
Herpes labialis: S. pneumonia
Erythema multiforme: M. pneumonia

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4
Q

Characteristics and differences in typical-, atypical-, and viral pneumonia

A

Atypical bact. > 5y, all seasons, mild fever, gradual, unproductive cough, dyspneavery rare.

Typical bact all ages, winter, sudden, high fever, dyspnea frequent, productive cough, creptiation at ascul., alveolar inf. on x-ray, common w. pleural effusion

Atypical viral: all ages, winter, sudden, high fever, unproductive cough, dyspnea frequent, interstital inf. on x-ray, not typical w. pleural effusion

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5
Q

Age related pathogens

A

Newborn: GBS, staph. aureus
1-3 mo: RSV, chlam. trachomatis, S. pneumonia
3mo - 5y: RSV, S. pneumonia
>5y: M. pneumonia, Chl. pneumonia

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6
Q

Diagnosis of pneumonia

A

– Lab: incr. WBC, decr. neutrophils, increased ESR and CRP.
– Imaging: CXR (empyema, pulm. abscess and PTX suggests bacterial origin) and US
– Specific testing: hemoculture (in suspected bacterial pneumonia), mycoplasma and chlam. testing (in suspected atypical bact.), Rapid antigen test (in suspected viral, e.g. RSV)

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7
Q

Treatment of pneumonia

A

Mild lower RTI in young children and infants do not require ab treatment.
Bacterial pneumonia emperical treatment:
– Mild: < 5y = amoxicillin, >5y = macrlide
– Severe: 0-6mo = cefotaxime + ampicillin, > 6mo = II and III gen. cephalosporins (cefuroxime, cefotaxime + macrolide.

Prevention: vaccination

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8
Q

What is cystic fibrosis?

A

Genetic autosomal recessive disorder, CFTR gene mutation. Chloride channel disorder leading to dysfunction of exocrine glands. It’s a multiorgan disease affecting reproductive tract, sinus, lungs, sweat gl., liver, pancreas and GI tract

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9
Q

Most common symptoms of cystic fibrosis

A

Respiratory (90% of CF patients)

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10
Q

Respiratory symptoms of CF

A

– Irreversible lung injury
– Cough, bronchitis, PTX, fibrosis, cor pulmunola, respiratory failure

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11
Q

What happens with chloride in CF

A

Decreased uptake of Cl in sweat glands, increased uptake in mucous membranes.

(increased NaCl in sweat of babies, but thick sticky secretions in mucous membranes)

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12
Q

Diagnosis of CF

A

Sweat test (high Nacl), Guthrie screening test, genetic testing

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13
Q

Define obstructive bronchitis

A

Swelling or inflammation of the main airways (bronchi) of the lungs

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14
Q

Etiology of obstructive bronchitis

A

– Common cold
– Acute asthma exacerbation
– Viral bronchiolitis
– Foreign body aspiration
– Acute bronchitis
– Croup
– Tracheomalacia
– CF

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15
Q

Pathophysiology of asthma bronchiale

A

Respiratory hyperactivity –> Incr. cap. permeability and histamine release –> incr. gland secr. and proliferation –> decreased airflow due to airway narrowing and hyperinflated + collapsed alveoli –> insufficient ventilation

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16
Q

Symptoms of asthma

A

Cough, wheezing in expiratory, dyspnea, chest tightness

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17
Q

Treatment of asthma

A

Acute:
– SABA: salbutamol, terbutaline
– SAMA: ipratropium

Chronic:
– 1st line: Inhaled corticosteroids (budesonide, fluticasone)
– 2nd line: bronchodilation: LABA (formoterol, salmeterol)

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18
Q

Define acute subglottic laryngitis

A

Pseudocroup. Inflammation of tissues in subglottic space +/- tracheobronchial tree.

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19
Q

Pathogens of pseudocroup (acute subglottic laryngitis)

A

Parainfluenza virus, RSV

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20
Q

Common symptoms of pseuodocroup

A

Commenly starts at night and resolves suddenly.
– Inspiratory stridor, hoarsness, barking cough.

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21
Q

Treatment of pseudocroup

A

Mild – cold humidified air, fluid intake, rectal steroids
Moderate – hospital admission, epinephrine inhalation, systemic glucocorticoids
Severe – same as moderate + ICU admission

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22
Q

What is the croup score?

A

Score based on inspiration, stridor, cough, retraction + nasal flaring and cyanosis.

mild = 1-2 p
moderate = 3-5 p
severe = 6-10 p

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23
Q

Alarming signs of CNS diseases

A

– Acute encephalopathy
– Signs and symptoms on increased intracranial pressure
– Meningeal signs and symptoms

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24
Q

Signs and symptoms of increased intracranial pressure

A

Cushing’s triad:
1. bradycardia
2. irregular respiration
3. increased blood pressure

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25
Q

Signs of increased intracranial pressure in infants

A

Bulging of the fontanelle, setting-sun eyes, irritability

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26
Q

Meningeal signs and symptoms

A

Nuchal rigidity, Brudzinski sign and Kernig sign

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27
Q

Define acute encephalopathy

A

Acute onset of mental changes +/- hypnoid disturbance of conciousness (bw. wake state/confusion/deep coma)

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28
Q

Etiology of encephalopathy

A

Trauma, neurology infection, vascular/hemotological disorders, ischemic lesions, tumor, intoxications, fluid electrolyte imbalance, acid-base disturbance, endocrine disorders, renal- and hepatic insufficiency, Reye disease, cong. metabolic disorder, chronic neurological diseases with sudden onset.

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29
Q

What is lumbar puncture used for?

A

Used to obtain sample of CSF for microbiological, biochemical or metabolic analysis.

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30
Q

Contraindications of lumbar puncture

A

Thrombocytopenia or coagulation defect
Raised ICP
Significant cardiorespiratory compromise

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31
Q

Where is the lumbar puncture done?

A

L3-L4 intervertebral space

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32
Q

Name some inflammatory diseases of the nervous system

A

Meningitis, encephalitis

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33
Q

Etiology of meningitis

A

Septic (bacterial)
Aseptic (non-bacterial)
Granulomatous

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34
Q

Laboratory characteristics of septic, aseptic and granulomatous meningitis

A

Septic: CSF > 1000, very high proteins, low glc
Aseptic: CSF < 1000, high proteins, norm glc
Granulomatous: CSF < 1000, very high proteins, low glc

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35
Q

Pathogens causing bacterial meningitis

A

< 3 mo - 10 y: GBS, S. pneumonia, N. meningitis,
In > 10y: mainly N. meningitis only

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36
Q

Define meningitis

A

Inflammation of the meningitis. Inflammation is in the subarachnoid space, causing swollen tissue and CSF changes.

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37
Q

Symptoms of meningitis based on age

A

Infants: fever/hypothermia, vomit, irritable, bulging fontanelle
Older children: fever, loss of appetite, joint and muscles pain, altered mental state, increased ICP, positive meningeal signs
All ages: petechiae, seizures, photophobia, fever

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38
Q

Assessment/treatment of meningitis

A
  1. ABCDE assessment
  2. OMV (IV or OM access)
  3. Fluid resuscitation
  4. Vasopressors
  5. Take lab tests: WBC, CRP, PCT, liver, kidney, glc, coagulation, b.gas, microbiology
  6. Antibiotics: <3mo: cefotaxime + ampicillin, >3mo: cefriaxone
  7. Steroids: dexamethasone or hydrocortisone
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39
Q

Prophylaxis against meningitis

A

Meningococcus A/C/W/Y + B. vaccination
HiB vaccination
Pneumococcus vaccination

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40
Q

Define encephalitis

A

Inflammation of brain tissue. Usually involves meninges as well. Caused by direct injury or viral infection.

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41
Q

Prophylaxis given to people close contact with meningitis patients

A

Ciprofloxacin

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42
Q

Types of encephalitis

A

Viral
Immune-mediated
Autoimmune

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43
Q

Etiology of viral encephalitis

A

Enterovirus, arbovirus, herpes, adenovirus, TBE

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44
Q

Mechanism of immune mediated encephalitis

A

ADEM: acute dissaminated encephalomyelitis (demyelination disease in kids)

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45
Q

Mechanism of autoimmune encephalitis

A

NMDAe: antibodies against NMDA receptors cause the inflammation

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46
Q

Signs and symptoms of encephalitis

A

Fever, headache, light sensitivity, vomiting, change in consciousness, hallucination, delirium, seizures

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47
Q

Diagnosis of encephalitis

A

CSF: detect virus, autoantibodies
MRI
EEG

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48
Q

Treatment of encephalitis

A

– HSV: acyclovir
– ADEM, NMDAe: high dose methylprednisolone, IVIG, plasmapheresis
– Supportive treatment: pain management, electrolytes

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49
Q

Complications of encephalitis

A

Cognitive impairment, epilepsy

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50
Q

Difference in lesions of central- and peripheral facial nerve palsy

A

Central facial palsy: supranuclear and nuclear lesion
Peripheral facial palsy: infranuclear lesion

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51
Q

Etiology of central nerve palsy

A

MS, poliomyelitis, cerebral tumors, lacunar infarction, stroke, TIA

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52
Q

Etiology of peripheral nerve palsy

A

Infections: herpes zoster oticus, HSV, EBV, Lyme
Trauma
Bells palsy (idiopathic)
Inflammation
Tumor

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53
Q

Clinical signs of central nerve palsy

A

– Paralysis of inferior 1/4 of the face contralat. to the lesion
– Loss of nasolabial folds and drooping of lower lip
– Preservation of forehead and brow movements

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54
Q

Clinical signs of peripheral nerve palsy

A

– Paralysis of lateral half of the face ipsilateral to the lesion
– Loss of forehead and brow movements
– Inability to close eyes and drooping of eyelids
– Loss of nasolabial folds and drooping of lower lip

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55
Q

Diagnosis of facial nerve palsy

A

– History
– Lab tests
– Imaging
– Inspection

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56
Q

Diagnosis of facial nerve palsy

A

– History
– Lab tests
– Imaging
– Inspection

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57
Q

Testing motor function of facial nerve

A

Frontal branch: Wrinkling of forehead
Ophthalmic branch: Rapid blinking, lip closure
Oral branch: Baring of teeth, whistling, inflating cheeks

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58
Q

Testing of parasympathetic function of facial nerve

A

Schirmer’s test:
Gaustometry: evaluation of taste anterior 2/3

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59
Q

Testing of sensory function of facial nerve

A

Skin around the ear de

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60
Q

Phenotypes of seizures in childhood

A

Generalized, focal, myovlonic, non-compulsive

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61
Q

Etiology of seizures

A
  • Febrile convulsions (2/3 causes under 3y)
  • Epilepsy
  • CNS pathology
  • Metabolic problems, electrolyte disorders, toxins
  • Idiopathic (10-20% in all ages)
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62
Q

Define seizures

A

A seizure is a clinical event in which there is a sudden
disturbance of neurological function caused by an
abnormal or excessive neuronal discharge. Seizures
may be epileptic or non-epileptic.

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63
Q

Causes of seizures

A

Epilepsy
* Idiopathic (70–80%) – cause unknown but
presumed genetic
* Secondary
– Cerebral dysgenesis/malformation
– Cerebral vascular occlusion
– Cerebral damage, e.g. congenital infection,
hypoxic-ischaemic encephalopathy,
intraventricular haemorrhage/ischaemia
* Cerebral tumour
* Neurodegenerative disorders
* Neurocutaneous syndromes

Non-epileptic
* Febrile seizures
* Metabolic
– Hypoglycaemia
– Hypocalcaemia/hypomagnesaemia
– Hypo/hypernatraemia
* Head trauma
* Meningitis/encephalitis
* Poisons/toxins.

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64
Q

Define febrile seizures

A

seizure accompanied by a fever in
the absence of intracranial infection due to bacterial
meningitis or viral encephalitis

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65
Q

Management of seizure first 5 min

A

Provide safe environment and assess pt. with ABCDE. Keep airway open, start O2 and exclude hypoglycemia. Most of the seizure resolve within 5 min

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66
Q

Management of seizures 5-10 min

A

Now it’s status epilepticus (>5min). Give benzodiazepines. Give 2 doses with 2-3 min in bw.

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67
Q

Management of seizures 10-20 min

A

If benzo was ineffective, run ABG (to exclude electrolyte imbalance), regularly assess ABCDE.
drugs: levetirecetam, valproic acid

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68
Q

Managament of seizure after 15 min

A

Admit to ICU/emergency dep., intubate and sedate.
Drugs: potent antiepileptics (propofol, ketamine) and muscle paralytics. Consider rare etiologies (NORSE).

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69
Q

Complications of seizures

A

Hypoventilation –> hypoxia, hypercapnia
Rhabdomyolysis –> kidney failure
Incr. lactic acid –> met. acidosis
If >24h –> brain edema, CNS injury, high mortality

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70
Q

Pathomechanism of febrile seizures

A

Increased body temperature leads to cytokine release and neuronal hyperexcitability

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71
Q

Complication of febrile seizure

A

High risk of developing epilepsy with recurrent episodes of febrile seizures

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72
Q

Define DM1

A

Chronic hyperglycemia due to destruction of B-cells in the pancreas, so they are unable to produce insulin. This is an autoimmune process.

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73
Q

Symptoms of hyperglycemia in infants and children

A

Infants: vomiting, dehydration, coma
Children: Polyuria, enuresis, polydypsia, weight loss, blurred vision

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74
Q

Diagnosis of DM1 in children

A

– Investigate b.glc and ketones and/or urinary glc and ketones
– Fasting glc > 7mmol/L + random b.glc > 11 mmol/L twice
– Clinical signs

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75
Q

Frequent differential diagnosis/misdiagnosis of DM1 in children

A

Misdiagnosis done bc. of the symptoms:
– Kussmaul breathing –> lung/heart disease
– Polyuria –> UTI
– Unconsciousness –> meningitis, encephalitis

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76
Q

Causes of DKA

A

Infections (50%)
Not taking insulin
Puberty

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77
Q

Clinical signs of DKA

A

Metabaolic acidosis
Hyperglycemia
Ketones in blood/urine

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78
Q

Symptoms of DKA

A

– Fq. urination
– Incr. thirs
– Dry mouth
– Blurry vision
– Sweet breath (bc. of ketones)
– Nausea, vomiting
– Abd. pain

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79
Q

Treatment of DKA

A
  1. ABCDE assessment
  2. Fluids (balanced crystalloids)
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80
Q

Treatment of DKA

A
  1. ABCDE assessment
  2. Fluids (balanced crystalloids)
  3. Insulin
  4. Insulin + glc
  5. Electrolyte resuscitation (K+)
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81
Q

Fluid therapy in children

A
  1. fluid bolus = 10ml/kg
    1st. 10kg = 150ml/kg
    2nd. 10kg = 50ml/kg
    3rd. 10kg = 20ml/kg
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82
Q

Define congenital adrenal hyperplasia

A

group of autosomal recessive defects in the enzymes that are responsible for cortisol/aldosterone/androgen synthesi

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83
Q

Characteristic of all CAH (cong. adrenal hyperplasia) subtypes

A
  • Low levels of cortisol
    – High levels of ACTH
    – Adrenal hyperplasia
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84
Q

Subtypes of CAH (cong. adrenal hyperplasia)

A

21b-hydroxylase defect (95%)
11b-hydroxylase defect (5%)
17a-hydroxylase defect (rare)

85
Q

Pathophysiology of CAH

A

Low levels of cortisol leads to lack of negative feedback to the pituitary. Increased ACTH –> adrenal hyperplasia + increased synthesis of adrenal precursor steroids

86
Q

Clinical features of CAH

A

– Low levels of cortisol leads to hypoglycemia
– Adrenal crisis

21b-hydroxylase defect: hypotension
11b-hydroxylase defect: hypertension
17a-hydroxylase defect: hypertension

21b-hydroxylase defect and 11b-hydroxylase defect
– female clitoromegaly or male genitalia, virilization, infertility, precocious puberty
– male normal external genitalia, precocious puberty

17a-hydroxylase defect
– female normal ext. genitialia at birth, delayed puberty, sexual infantilism
– male: female ext. genitalia, delayed puberty, sexual infantilism

87
Q

Treatment of CAH

A

Replace the deficient hormones and reduce excess androgen production. Glucocorticoid replacement therapy is indicated in all subtypes (hydrocortisone in pediatrics).

21b – fludrocortisone
11b – spironolactone
17a – spironolactone, estrogen replacement ther.

88
Q

Etiology of primary congenital hypothyroidism

A

Ectopic thyroid gland (50%)
Thyroid aplasia/hypoplasia (30%)
Thyroxin synthesis defects

89
Q

Most common etiology of hypothyroidism in children

A

The most common cause is an autoimmune reaction that destroys the thyroid gland. (autoimmune thyroiditis, Hashimoto)

90
Q

Etiology of secondary congenital hypothyroidism

A

Pituitary aplasia/hypoplasia, perinatal stress

91
Q

What is congenital hypothyroidism?

A

Congenital hypothyroidism (CHT) is a condition resulting from an absent or under-developed thyroid gland (dysgenesis) or one that has developed but cannot make thyroid hormone because of a ‘production line’ problem (dyshormonogenesis). Babies with CHT cannot produce enough thyroid hormone for the body’s needs.11. sep. 2019

92
Q

Symptoms of congenital hypothyroidism

A

Usually asymptomatic and picked up on screening. Otherwise:
Failure to thrive
Feeding problems
Prolonged jaundice
Constipation
Pale, cold, mottled dry
skin
Coarse facies
Large tongue
Hoarse cry
Goitre (occasionally)
Umbilical hernia
Delayed development

93
Q

Complication of untreated hypothyroidism

A

Cretinism: impaired dev. of brain and skeleton.
Low stature (in autoimmune thyroiditis, which can go on for a very long time undiagnosed bc. of no screening for it)

94
Q

Screening of congenital hypothyroidism

A

Measure TSH from dried b. sample in postnatal 48-72h. Increased levels are indicative of cong. hypothyroidism

95
Q

Symptoms and clinical signs of Hashimoto’s thyroiditis

A

Dry skin, thin hair
Bradycardia
Goitre
Short stature/growth restriction
Delayed puberty
Obesity
Vold intolerance
Cold peripheries

96
Q

Treatment of Hashimoto’s thyroiditis

A

Thyroxine

97
Q

Most common cause of hyperthyroidism in pediatrics

A

Grave’s disease

98
Q

Define Grave’s disease

A

Immune (autoimmune) disorder leading to increased production of thyroid hormones

99
Q

Symptoms of Graves’ disease

A

Heat intolerance, excessive sweating (incr. met. rate)
Weight loss (incr met. rate)
Glucose intolerance
Exapthalmos
Tachycardia
Increased BP
Anxiety, insomnia

100
Q

Treatment of Graves’ disease

A

Antithyroid medications: methamizole
Symptomatic treatment: beta blockers (propanolol)
Radioactive iodine ablation: potential first line treatment in patients >10y
Surgery (near-total thyroidectomy): in children >5y not improved with antithyroid drugs

101
Q

Define neonatal hyperthyroidism

A

Transplacental passage of maternal TSH receptor antibodies from mother with Graves’ disease to its babies. Occurs in approx. 5% of babies born with mother having Graves’ disease.

102
Q

When does symp. of hyperthyroidism in neonates appear?

A

May appear at birth or be delayed for 10 days (bc. of maternal antithyroid medication passing transplacental to the baby).

103
Q

Symptoms of neonatal hyperthyroidism

A

Irritable, restlessness, tachycardia, poor weight gain, diffuse goiter, microcephaly (bc. of premature fusion of cranial sutures)

104
Q

Complications of untreated neonatal hyperthyroidism

A

Cardiac failure and intellectual disability

105
Q

Treatment of neonatal hyperthyroidism

A

usually resolves within 1-3 months. If not, treat symptomatic infants with methamizol and propanolol.

106
Q

Hypocalcemia etiology

A

Vitamin def., diabetes, acute renal failure, prematurity, DiGeorge syndrome

107
Q

Hypocalcemia clinical features

A

Usually asymp., but spasms, seizures and tetanus can occur

108
Q

Hypocalcemia treatment

A

In asymp infants: initiate feeding is enough
If not: Ca substitution

109
Q

Hypercalcemia etiology

A

Idiopathic infantile hypercalcemia, hyperparathyroidism, Williams syndrome, hypercalcemia of malignancy, Vit D intoxication, renal failure, Addisons disease, iatrogenic (e.g. thiazide diuretics).

110
Q

Hypercalcemia clinical features

A

Anoreia, nausea/vomit, constipation, abdominal pain, polyuria, polydypsia, drowsiness, depression

111
Q

Hypercalcemia treatment

A

Treat underlying condition

112
Q

Hyperparathyroidism

A

PTH –> bone resorption –> release Ca and P in blood AND increase P excretion in kidneys. Therefore hyperPTH gives high PTH in blood, high Ca in blood and low plasma P. It’s uncommon in children.

Etiology: Rickets, MEN1 and 2, parathyroid adenoma

113
Q

HypoPTH

A

Etiology: failure in prathyroid development (agenesis, dysgenesis), magnesium deficiency (failure in PTH secretion)

Clinical: low plasma Ca and PTH, high plasma P

114
Q

Define Rickets

A

Disorder of impaired mineralization of cartilaginous growth plates due to Vit D deficiency. Only occurs in children bc. the growth plates haven’t yet fused. (the adult version would be osteomalacia)

115
Q

Etiology of Rickets

A

Vitamin D deficiency. Breast milk has low amounts of it and therefore newborns need supplementation.

116
Q

Pathophys of Rickets

A

Vitamin D deficiency –> hypocalcemia –> defective growth plate mineralisation. Hypocalcemia –> incr. PTH –> decr. P –> also impaired mineralisation

117
Q

Clinical features of Rickets

A

Bone deformities
– bending of long bones
– distension of bone-cartilage junctions: rachitic sign, marfan sign, craniotabes, genu varum
– increased fracture risk
– late closing of fontanelles
– impaired growth

118
Q

Diagnosis of Rickets

A

Lab: decr. Ca and P, incr. PTH and ALP
Imaging: bone deformities
Bone biopsy

119
Q

Diagnosis of growth disorders

A

– Sex, background, genetics
– Bone age
– Calculation of mid-parental height
– Calculation of target heigh channel

120
Q

What is target height channel?

A

Determination wether child is growing according to familys genetic background.

Boys: (fathers height + mothers height)/2 + 13cm
Girls: (fathers height + mothers height)/2 - 13cm

121
Q

Etiologies of short stature

A

Non-pathological family short stature

Endocrine etiologies
– Hypothyroidism
– GH deficiencies
– Glucocorticoid excess
– DM1

Genetic etiologies
– Turner syndrome
– Downs syndrome
– Williams synrome
– CF

Psychosocial etiologies
– Maternal substance use
– Psychoscoial short stature
– Psychiatric conditions (anorexia)

122
Q

Etiologies of tall stature

A

Non-pathological family tall stature

Endocrine etiologies
– Hyperthyroidism
– Obesity
– GH excess

Genetic etiologies
– Fragile X syndrome
– Marfan syndrome
– Klinefelter
– Triple X syndrome

123
Q

Pubertal stages

A

Tanner stages:
– breast development
– genital development
– pubic hear development

124
Q

What is considered precocious puberty?

A

Appearance of secondary sexual characteristics before the age of:
Girls – 8 years
Boys – 9 years

125
Q

Classification of precocious puberty

A

Central (true) precocious puberty: gonadotropin dep.
Peripheral precocious puberty: gonadotropin indep.
Benign pubertal variants

126
Q

Define central precocious puberty

A

Elevated GnRh (gonadotropin) levels. Most commonly idiopathic, but can be due to CNS problems, obesity etc.
It leads to an early activaiton of hypothalamo-hypophysial axis and abnormally early onset of puberty. Follows normal pattern of puberty, it’s just early.

127
Q

Diagnosis of central precocious puberty

A

Serum LH and FSH increased
GnRh stimulation test, Gn should increase
Brain MRI/CT: rule out CNS lesion

128
Q

Treatment of central precocious puberty

A

GnRH agonist

129
Q

Define peripheral precocious puberty

A

Indep of GnRH. Due to peripheral synthesis or exogenous exposure to sex hormones. Either due to incr. androgen production or estrogen production or increased b-hCG production.

May not follow normal pattern of puberty.

130
Q

Diagnosis of peripheral precocious puberty

A

Serum LH and FSH decreased
GnRH stim. doesnt lead to incr. Gn
Incr. serum testo/estrogen

131
Q

Define disorders of delayed pubertal growth and sexual maturation

A

Absent or incomplete developemnt of secondary sexual characteristics by age of 14 in boys and 13 in girls

132
Q

Etiologies of delayed pubertal growth

A

Hypergonadotropic hypogonadism
– primary gonadal insufficiency (kinefelter, turner, androgen insensiticity)
– secondary gonadal insufficiency (chemother., infection, trauma, autoimmune)

Hypogonadotropic hypogonadism
– CNS lesion
– Kallmann syndrome
– Prader-Willi syndrome

133
Q

Define Henoch-Schonlein purpura/IgA vasculitis

A

Autoimmune complex-mediated small vessel vasculitis. Most commonly occurs in children > 5y. Often preceeded y an URTI.

134
Q

What is the mechanism of Henoch-Schonlein purpura?

A

Exposure to allergen/antigen (e.g. infection/drugs) –> stimulation of IgA production –> deposition of IgA immune complexes in vascular walls –> activation of complement system –> vascular inflammation and damage

135
Q

Symptoms of Henoch-Schonlein purpura

A

Typical triad:
– palpable purpura
– arthritis/arthralgia
– abdominal pain
– renal disease (hematuria)

136
Q

Treatment of Henoch-Schonlein purpura

A

Usually self-limiting, which only requires supportive care (NSAIDS for pain, rest, hydration)
Severe disease: systemic glucocorticoids, acute dialysis, antihypertensives, renal transplantation, IV fluids,

137
Q

Define Kawasaki syndrome

A

Acute necrotizing vasculitis of unknown etiology. Primarily affects children <5y, more common in asian population.

138
Q

Clinical diagnosis of Kawasaki syndrome

A

Requires at least 5d of fever + one of:
– 4 or more other specific symptoms
– under 4 specific system + coronary artery involvement

Specific symptoms:
– erythema + edema of hans and feet
– desquamation of fingertips and toes
– polymorphous rash originating from trunk
– conjuctivitis without exudate
– oropharyngeal mucositis: strawberry tongue
– vercival lymphadenopathy

139
Q

Treatment of Kawasaki syndrome

A

IVIG: reduce risk of coronary artery aneurysms
Oral aspirin high dose: anti-inflam. effect
Oral aspirin low dose later: for anticoag. effect
IV glucocorticoids: lower the risk of coronary involvement

!!! Kawasaki syndrome is a rare exception to the CI of giving aspirin to children

140
Q

Complications of Kawasaki syndrome

A

Coronary artery aneurysm, AMI, myocarditis, ventricular dysfunction, arrythmias

141
Q

What is MISC?

A

Complication of COVID-19 manifesting with severe illness, hyperinflammation, multi organ failure etc.

Symp: fever, GI symp., etc

Criteria:
– Age <21y
– fever
– + inflam. markers
– involvement of 2+ organs
– severe illness requiring hospitalization

Tr: not sure yet what is most effective
- steroids
- antithrombotic treatment
– immunomodulators

142
Q

Treatment of UTI

A

3rd gen cephalosporins
Aminoglycosides
!!50% are resistant against ampicillin and amoxicillin

Neonates: ampicillin + gentamycin

143
Q

List kidney malformations

A

Renal agenesis
Renal hypoplasia
Horseshoe kidney
Kidney dysplasia
Multicystic dysplastic kidney
Ectopic kidney
Hydronephrosis
Duplex kidney

144
Q

Ureter development disorders

A

Pyelouretral junction stenosis
Ureter-vesicular stenosis
Uterocele
Vesico-ureteral reflux

145
Q

Bladder malformations/disorders

A

Bladder extrophy
Bladder diverticulum
Urachus persistens

146
Q

Urethra malformations

A

Posterior urethral valve
Hypspadius
Epispadius

147
Q

Define glomerulonephritis

A

Damage to the gomeruli. It’s often caused by your immune system attacking healthy body tissue. Glomerulonephritis does not usually cause any noticeable symptoms. It’s more likely to be diagnosed when blood or urine tests are carried out for another reason.

148
Q

Clinical signs of glomerulonephritis

A

Hematuria
Oliguria
Edema
Hypertension
Variable proteinuria

149
Q

Etiology of glomerulonephritis

A

Post infectious (most common)
- Bacterial (strep., staph.,)
- Viral (herpesvirus: EBV, varicella, CMV)
- Fungi (candida, aspergillus)
- Parasites (toxoplasma, malaria)

Others (less common)
- MPGN
- IgA nephropathy
- SLE

150
Q

Treatment of glomerulonephritis

A

Treat all life-threathening conditions:
– hyperkalemia, HT, acidosis, seizures, hypocalcemia

Supportive treatment and monitoring:
– fluid balance
– HT: CCB, a-block., DO NOT USE ACEi
– Ab if bacterial cause (penicillin against strep)

151
Q

Diagnosis of glomerulonephritis

A

Urinalysis (hematuria, proteinuria, RBC casts
Blood (CBC, autoAb, albumin)
Renal US

152
Q

Most common cause of glomerulonephritis

A

Post-streptococcal glomerulonephritis
– Strep. pyogenes (GAS)

153
Q

Define nephrotic syndrome

A

Proteinuria > 3g/day
Hypoalbuminemia <25g/L
Edema
Hyperlipidemia

154
Q

Etiology of nephrotic syndrome

A

Primary: congenital, infantile

Secondary:
– minimal change disease (85%)
– focal segmental glomerulosclerosis
– membrane proliferative glomerulonephritis
– membranous glomerulonephritis

155
Q

Clinical features of nephrotic syndrome

A

Edema: initially preorbital, then becoming generalized with pitting edema)
Foamy urine
Hypercoaguable state
HTN

156
Q

Diagnosis of nephrotic syndrome

A

Urinalysis: protein+++
Microscopy: hematuria/RBC casts
Culture
Protein:creatinin ratio (>300mg/mmol)
Lipids (hyperlipidemia)

157
Q

Treatment of nephrotic syndrome

A

Fluid resuscitation + prevention of hypovolemia
Oral steroids
Prophylaxis against bacterial infection (esp. pneumococci)
Immunosupressants (cyclophosmamide)

158
Q

Complications of nephrotic syndrome

A

Infection (bc of decr. IgG)
Thrombosis (hypercoag. state)
Hypovolemia
Acute renal failure

159
Q

Cyanotic congenital heart defects types

A

R-L shunt: tetralogy of fallot
Separate circulations: transposition of great arteries
Complete mixing: tricuspid atresia, truncus arteriosus, hypoplastic left heart syndrome, TAPVR

160
Q

Tetralogy of fallot

A
  1. Pulmonary stenosis
  2. Ventricular septal defect
  3. Misplaced aorta
  4. Right ventricular hypertrophy
161
Q

Clinical features of tetralogy of fallot

A

Boot-shaped heart on XR
Cyanosis
Shortness of breath

162
Q

Diagnosis of tetralogy of fallot

A

Ultrasound
Echocardiogram

163
Q

What is transposition of great vessels?

A

Pulmonary artery is rising from LV and aorta is arising from RV. It’s associated w. maternal DM

164
Q

Clinical features and treatment of transposition of great vessels

A

Signs: cyanosis
Tr: Shunting (ASD), PGE (prostaglandin) adm. to maintain PDA until surgery.

165
Q

Tricuspid atresia

A

Absent tricuspid valve resulting in no blood flow between RA and RV. This leads to RV hypoplasia and RA dilation due to volume overload.

Clinical: cyanosis, diminished peripheral pulses

Tr.: surgery (making shunting)

166
Q

Define truncus arteriosus

A

Underdeveloped aorticopulmonary septum, trunkis arteriosus not diveded into aorta and pulm. trunk. This results in a mixture of ox. and deox. blood.

167
Q

Which disease is truncus arteriosus associated with?

A

DiGeorge syndrome

168
Q

Symptoms and treatment of truncus arteriosus

A

Cyanosis, resp. distress, systolic murmur, bounding peripheral pulses.
Tr.: surgery.

169
Q

Non-cyanotic congenital heart defects

A

L-R shunts: ASD, VSD, AVSD, PDA
Obstructive lesions: AS, PS, aortic coarctation

170
Q

Atrial septal defect (ASD)

A

– Defect in atrial septum.
– Associated with Down’s and fetal alcohol syndrome
– L-R shunt
– Split S2
– Paradoxical emboli

171
Q

Ventricular septal defect (VSD)

A

– Defect in ventricular septum
– Most common congenital heart defect
– Ass. with Down’s syndrome, TORCH, maternal DM
– L-R shunt: dilation of LV bc of incr. preload)
– Tr.: Loop diuretics, ACEi, surgery

172
Q

Patent ductus arteriosus (PD)

A

– Failure of the closure (usually close within 12-24h)
– Associated with Rubella
– L-R shunt

In utero, DA shunts blood from right to left in order to bypass the lungs. If DA stays open, the blood starts to shunt the other way bc. of increased systemic circulation.

– Ascultation: machine like murmurs, continous over systole + diastole
– Complication: eisenmenger syndrome
– Tr.: indomethacine (decrease prostaglandin and closure of DA)

173
Q

Coarctation of aorta

A

Narrowing of the aorta. Divided into infantile and adult form.

Infantile: ass. with PDA, lower extr. cyanosis
Adult: not ass. with PDA, HT in upper extr. and hypotension in lower extr.

Important to due 4 limb oxymetry to look for this. If decreased in legs –> possible coarctation that needs to be double checked

174
Q

Classification of malabsorption

A

Impaired intraluminal digestion
Intestinal malabsorption
Malabsorption due to fermentation (maldigestion of cbh)

175
Q

Define malabsorption

A

Malabsorption is difficulty in the digestion or absorption of nutrients from food. Malabsorption can affect growth and development, or it can lead to specific illnesses

176
Q

Leading cause of malabsorption

A

Cystic fibrosis

177
Q

Etiology of malabsorption

A

Coeliac disease, cystic fibrosis, cow’s milk protein intolerance, cholestatic liver disease,
short gut syndrome, post-necrotising enterocolitis (NEC)

178
Q

Malabsorption manifest as:

A

– abnormal stools
– failure to thrive or poor growth in most but not all
cases
– specific nutrient deficiencies, either singly or in
combination.

179
Q

Define celiac disease

A

Immune mediated systemic disorder elicited by gluten. The gliadin fraction of gluten provokes a damaging immunological response in the proximal small intestinal mucosa. The villi becomes shortened and flattened.

180
Q

Symptoms of celiac disease

A

– Profound malabsorptive syndrome at 8–24 months of age after the introduction of wheat-containing weaning foods.
– Failure to thrive, abdominal distension and
buttock wasting abnormal stools and general irritability

181
Q

Diagnosis of celiac disease

A

– Clinical suspiction or high risk group
– Measure transglutaminase antibodies and total IgA
– Biopsy by endoscopy (not done unless highly necessary, then taken from distal duodenum)
– Endomysial antibdoies

182
Q

Respiratory distress syndrome caused by

A

surfactant deficiency

183
Q

Symptoms of respiratory distress syndrome

A

Cyanosis, tachypnea, grunting, dyspnea

184
Q

What can happen if giving prolonged ventilation and ox. therapy in newborn

A

Bronchopulmonary dysplasia

185
Q

Prevention of respiratory distress syndrome

A

Corticosteroids given to mother 1-7 days before delivery

186
Q

Acute neonatal respiratory diseases

A

Transient tachypnea of newborn
Congenital pneumonia
Meconium aspiration syndrome
Milk aspiration
Persistant pulmonary HT of newborn

187
Q

Conse of congenital pneumonia

A

Aspiration of infected amniotic fluid

188
Q

TORCH

A

Toxoplasmosis, rubella, CMV, herpes, others (HIV, syphilis, hepatitis B, herpes zoster).

189
Q

Normal bilirubin vs. hyperbilirubinemia

A

Normal: 0,1-1,2mg/dl
Hyper: >5mg/dl

190
Q

Etiology of physiological neonatal jaundice

A

Hemolysis of fetal hgb and immature hepatic metabolism of bilirubin

191
Q

How can you differ between unconjugated and conjugated hyperbilirubinemia?

A

– Bilirubin in urine: suggest conjugated
– Serum bilirubin <15% of total bilirubin: unconj.
– Serum bilirubin >20% of total bilirubin: conj.

192
Q

Define retinopathy of prematurity

A

Retina with abnormal vessel proliferation

193
Q

Define necrotizing enterocolitis

A

hemorrhagic inflammation of the intestinal wall

194
Q

define SIRDS

A

Abrupt and unexplained death of an infant less than 1 year

195
Q

Pediatric etiologis of fever

A

Infections
Malignancy
Autoimmune

196
Q

Etiology of respiratory acidosis

A

Respiratory type II (hypercapnic)

197
Q

Symptoms of respiratory acidosis

A

Decreased inotropy, hypoxia, hyperkalemia, emesis, coma, insulin resistance, hypervenitaltion (compensation), increased symp. activity (incr. HR, BP, hyperthermia)

198
Q

Etiology of respiratory alkalosis

A

Primary of secondary hyperventilation.
– Hypoxic resp. failuer
– Salicylate intoxication
– Early sepsis

199
Q

Etiology of metabolic acidosis

A

Incr. anion gap: increased acid (lactic, keto) + renal failure
non-anion gap: loss of HCO3 (renal tubular acidosis, GI acidosis, iatrogenic acidosis, diarrhea)

200
Q

Define cholestasis

A

Impaired bile flow: accumulation in liver and serum of subsances that normally are secreted in the bile – bilirubin, bile acids, cholesterol

201
Q

Etiology of cholestasis

A

Intrahepatic and/or extrahepatic

– biliary atresia
– alagille syndrome
– alpha-1-antitrypsin deficiency

202
Q

Define biliary atresia

A

Closed/discontinous biliary tracts. Affects both intra- and extrahepatic bile ducts

203
Q

Complications of biliary atresi

A

Early liver cirrhosis (at approx. 9 weeks of age), high mortality.

204
Q

Forms of biliary atresia

A

Congenital (10%)
Postnatal/parinatal (90%)

205
Q

Clinical presentation of biliary atresia

A

Prolonged jaundice, hepatomegaly, bleeding, portal HT, cirrhosis

206
Q

Treatment of biliary atresia

A

Creating connection between liver and small intestines to allow bile drainage.
Liver transplant in case of liver cirrhosis

207
Q

Define Allagille syndrome

A

Genetic condition char. by intrahepatic biliary duct aplasia or hypoplasia.

208
Q

Clinical manifestation of Alagille syndrome

A

Hepatic: jaundice, chirrosis
Facial dysmorphisms
Congenital heart defects
Butterfly vertebrae
Renal dysplasia

209
Q

Diagnosis of Alegille syndrome

A

5 major criteria, 3 required:
– interlobular bile duct absence/cholestasis
– cardiac malformation
– spine deformity
– characteristic face
– ocular abonrmality

Diagnosis done by genetic testing of JAG1 gene

Pediatrics 5th year (1 decks)

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