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Pediatrics 2 > Block 2 > Flashcards

Block 2 Flashcards

1
Q

proposed a clinical
classification utilizing both the temporal pattern of
child’s headache plotted against its severity over
time.

A

Winner and Rothner

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2
Q

Single event with no history of previous similar

event.

A

Acute Headache

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3
Q

Periodic headaches that are separated by painfree

intervals

A

Acute Recurrent Headache

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4
Q

Ex. migraine

A

Acute Recurrent Headache

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5
Q

Headaches that worsen in frequency and severity

over time.

A

Chronic Progressive Headache

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6
Q

The progression may be rapid or slow

A

Chronic Progressive Headache

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7
Q

May be accompanied by symptoms and signs of
increased intracranial pressure or progressive
neurologic disease

A

Chronic Progressive Headache

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8
Q

The neurologic exam is usually abnormal

A

Chronic Progressive Headache

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9
Q

Organic process is usually present

A

Chronic Progressive Headache

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10
Q

Chronic Progressive Headache is also known as?

A

Also known as tension-type headaches,
muscle contraction headaches, chronic daily
headaches

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11
Q

Generalized or localized

A

Acute Headache

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12
Q

Maybe associated with neurologic symptoms and
signs or seen in the absence of neurologic
symptoms

A

Acute Headache

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13
Q

Intracranial Sources of Headache Pain

A
  1. Cerebra and dural arteries
  2. Dura mater at the base of the brain
  3. Large veins and venous sinuses
  4. Blood vessels
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14
Q

Main pain-sensitive structures inside the skull

A

Blood vessels

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15
Q

Mechanisms of pain from the blood vessels:

A
  1. Vasodilation
  2. Inflammation
  3. Traction-displacement
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16
Q

Mechanism of pain transmission in intracranial source of headache pain

A

• Pain transmission from supratentorial intracranial
vessels is via Trigeminal nerve (specifically V1-
ophthalmic, which results in referred pain)
• Pain transmission from infratentorial vessels is by
the first 3 cervical nerves.

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17
Q

Extracranial sources of headache pain

A
  1. Cervical Roots
  2. Cranial Nerves
  3. Extracranial arteries
  4. Muscles attached to the skull
  5. Periosteum/ sinuses
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18
Q

Neurological injury caused by the occlusion or

rupture of cerebral blood vessels

A

Stroke

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18
Q

Neurological injury caused by the occlusion or

rupture of cerebral blood vessels

A

Stroke

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19
Q

Two categories of stroke in children

A
  1. Perinatal stroke

2. Childhood stroke

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20
Q

MENINGITIS

Classified into 2 syndromes:

A
  1. Septic or Purulent meningitis

2. Aseptic meningitis

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21
Q

bacterial or fungal.

A

Septic or Purulent meningitis

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22
Q

viral, spirochetal, protozoal, metazoal,

neoplastic, or other non-septic causes.

A

Aseptic meningitis

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23
Q

Refers to the inflammation of the
leptomeninges (pia and arachnoid), the
connective tissue layers in close proximity to
the surface of the brain.

A

Leptomeningitis

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24
Q

Bacterial organisms reach the meningeal

region by one of 4 routes:

A
  1. Direct hematogenous spread.
  2. Passage through the choroid plexus
    (infection is already inside the brain).
  3. Rupture of superficial cortical abscesses.
  4. Contiguous spread of an adjacent infection
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25
Q

 Occurs during bacteremia
 Through the passive transfer of organism by
infected leukocytes.
 Through damaged or malformed blood vessels
or because of neurosurgical procedures.
 In cases of neurosurgical procedures

A

Direct Hematogenous Spread

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26
Q

 Abscess, osteomyelitis (especially in the
temporal bone) of the skull or the head and
spine.
 Otitis media (mastoiditis), sinusitis
 Developmental anomalies and penetrating
injuries of the skull.
 Develop after bacterial attachment and invasion
of the nasopharyngeal mucosa.

A

Contiguous spread of adjacent infection:

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27
Q

Bacterial organisms secrete IgA

proteases that neutralize IgA.

A
  1. S.pneumoniae
  2. H. influenza
  3. N. meningitides
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28
Q

Blood Brain Barrier composed of:

A
  1. Arachnoid membrane
  2. Choroid plexus epithelium
  3. Endothelial cells of the cerebral
    microvasculature
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29
Q

BBB is disrupted by?

A

nitric oxide and metabolites

of the arachidonic pathway

30
Q

Upon entering the ______, bacteria encounter few host defenses because it lacks antibody complement and opsonic activity.

A

CSF

31
Q

hyperemia of the meningeal vessels.

A

1st stage

32
Q

migration of neutrophils into the

subarachnoid space.

A

2nd stage

33
Q

rapidly increases over
hours and extends into the sheaths of blood vessels and along cranial and spinal nerves PMNs that contain phagocytized bacteria predominate

A

Subarachnoid exudate

34
Q

begin to degenerate and

are removed by macrophages.

A

Neutrophil leukocytes

35
Q

Fibrinogen and other blood proteins are exuded, and more plasma cells appear

A

(2nd week)

36
Q

The exudate beneath the arachnoid consists of

an outer layer of?

A

neutrophils and fibrin

37
Q

The exudate beneath the arachnoid consists of an inner layer composed of?

A

lymphocytes, macrophages, and plasma cells.

38
Q

Endothelial cells swell, proliferate, and crowd into the vessel lumen in?

A

48 to 72 hours

39
Q

________ and ________ develop that

partially or totally occlude the lumen.

A

Focal necrosis and mural thrombi

40
Q

In _______, venous thrombosis is much more frequent than arterial thrombosis.

A

bacterial meningitis

41
Q

Venous thrombosis is common in?

A

subdural empyema

42
Q

________ persist for months

A

Lymphocytes, plasma cells and macrophages

43
Q

GOLD STANDARD in diagnosis meningitis

A

CSF culture by doing Lumbar Puncture

44
Q

Are soluble proteins that are released by host cells in response to bacterial products such as endotoxin, cell walls, and toxins.

A

Cytokines

45
Q

In excess amounts they contribute to

parenchymal injury because it will:

A
  1. Directly affect the function of the endothelial cells.
  2. Increase the blood-brain barrier permeability.
  3. Decrease autoregulation of cerebral blood flow.
  4. Induce cytotoxic edema.
  5. Induce recruitment of leukocytes into the infected compartment.
46
Q

Proinflammatory cytokines

A
  1. Tumor necrosis factor-alpha (TNF-a)
  2. Interleukine-1B (IL-1B)
  3. Interleukin-6 (IL-6)
  4. Interleukin-8 (IL-8)
47
Q

Anti-inflammatory cytokines

A
  1. IL-10

2. Transforming growth factor B (TGF-B)

48
Q

 Increases the permeability of the blood-brain barrier.
 Induces cell lysis.
 Mediates myelin and oligodendrocyte damage.
 If you have destruction of myelin, this will affect the action of your axons and will lead to motor dysfunctions.

A

TNF-a

49
Q

 Highly potent inducer of neutrophil accumulation and procoagulant (can cause thrombosis, infarction and stroke-like phenomenon).
 Stimulates the release of other cytokines such as TNF and IL-6 and of hypothalamic corticotrophin-releasing factor

A

IL-1B

50
Q

 a pyrogen

 Plays a role in the induction and propagation of inflammatory responses

A

IL-6

51
Q

 A leukocyte chemotactic agent that promotes leukocyte adherence ( increase in meningococcal meningitis)
 Downregulates inflammation and may contribute to chronicity of disease

A

IL-8

52
Q

 Downregulate inflammation and may contribute to chronicity of disease.
 Not present in serum but is elevated in CSF in the first 48 to 72 hours of viral meningitis

A

IL-10

53
Q

hydrocephalus

A

Fibrinopurulent exudate accumulates in large quantities → obstruction of the foramina of Luschka and Magendie or the aqueduct of Sylvius → hydrocephalus

54
Q

Result from inflammation of exudate in the subarachnoid space around the brainstem and over the cerebral convexity.

A

Communicating Hydrocephalus

55
Q
  • —Induced by components of the neutrophil membrane

- —Can depolarize neuronal membranes and lead to seizure activity

A

Brain edema

56
Q

2 types of brain edema in meningitis

A
  1. Cytotoxic

2. Vasogenic

57
Q

→ Marked by increased brain water, cellular swelling.
→ Increased intracellular sodium.
→ Loss of intracellular potassium.

A

Cytotoxic edema

58
Q

→ Caused by opening of tight junctions between cerebral capillary endothelial cells
→ Can result from the presence of bacteria as well as inflammation.

A

Vasogenic edema

59
Q

Early signs of bacterial meningitis:

A

Low-grade fever, poor feeding, somnolence, irritability

60
Q

Later signs of bacterial meningitis:

A

vomiting, lethargy, seizure

61
Q

 Streptococcal meningitis

A

78% -

62
Q

 H. influenza meningitis

A

44% -

63
Q

 S. pneumonia

A

25% -

64
Q

 Meningococcal infections

A

10% -

65
Q

Complications – Acute Bacterial Meningitis

A
  1. Ventriculitis
  2. Subdural effusion/subdural empyema
  3. Electrolyte disturbance
  4. Recurrent bacterial meningitis
66
Q

 Infections of the ventricular system can be primary
 Can develop secondary to the spread of organism from the subarachnoid space caused by the flow of CSF or by migration of bacteria

A

Ventriculitis

67
Q

 Caused by increased efflux of intravascular fluids
 Consequence of thrombophlebitis of the veins bridging the subdural space
 Abnormal vascular permeability at the arachnoid-dura infertace
 Spread of infection from arachnoditis

A

Subdural effusion / subdural empyema

68
Q

 Most common cause of subdural effusion/ subdural empyema:

A

H. influenza (45%)
 Pneumococcus (30%)
 Meningococcus (9%)

69
Q

 Management for Subdural effusion / subdural empyema:

A
  1. Conservative treatment of subdural effusions.
  2. Multiple subdural aspirations or surgical
    intervention no longer recommended.
70
Q

 Indications for subdural tap

A
  1. Patients suspected of subdural empyema.
  2. If the effusion becomes hemorrhagic.
  3. If large enough to cause a significant
    ventricular shift
71
Q

Hyponatremia is secondary to:

A
  1. Inflammation
  2. Syndrome of inappropriately high secretion of antidiuretic hormone (SIADH)
  3. Increased release of atrial natriuretic peptide.
72
Q

Gold standard for the diagnosis of bacterial meningitis –

A

identification by culture and gram

stain of CSF

73
Q

Expected CSF findings:

A
  1. Fluid is cloudy, increased pressure.
  2. Acute stage: PMNs, mononuclear later stage.
  3. Cell count: 1,000 to 10,000 per uL.
  4. Glucose decreased (bacterial/TB)
    o Less than 40% (bacterial).
  5. Protein is increased 100 mg/dl and higher.

Pediatrics 2 (2 decks)

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