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Pediatrics 2 > general 4 > Flashcards

general 4 Flashcards

1
Q

what level of dehydration is suggested by the following clinical exam finding:
skin turgor good

A

mild

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2
Q

what level of dehydration is suggested by the following clinical exam finding:
alert, irritable child

A

moderate

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3
Q

what level of dehydration is suggested by the following clinical exam finding:
parched/cracked buccal mucosa/lips

A

severe

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4
Q

what level of dehydration is suggested by the following clinical exam finding:
dry/sunken eyes

A

severe

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5
Q

what level of dehydration is suggested by the following clinical exam finding:
tears present when crying

A

mild

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6
Q

what level of dehydration is suggested by the following clinical exam finding:
urine output significant diminished

A

moderate

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7
Q

what level of dehydration is suggested by the following clinical exam finding:
urine output oliguric

A

severe

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8
Q

what level of dehydration is suggested by the following clinical exam finding:
urine output diminished

A

mild

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9
Q

what level of dehydration is suggested by the following clinical exam finding:
flat fontanel

A

mild

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10
Q

what level of dehydration is suggested by the following clinical exam finding:
mild skin tenting

A

moderate

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11
Q

what level of dehydration is suggested by the following clinical exam finding:
cap refill above 3seconds

A

severe

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12
Q

what level of dehydration is suggested by the following clinical exam finding:
fontanel sunken

A

severe

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13
Q

what level of dehydration is suggested by the following clinical exam finding:
buccal musoca/lips moist or tacky

A

mild

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14
Q

what level of dehydration is suggested by the following clinical exam finding:
present tears, but reduced on crying

A

moderate

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15
Q

what level of dehydration is suggested by the following clinical exam finding:
dry skin to touch

A

moderate

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16
Q

what level of dehydration is suggested by the following clinical exam finding:
unremarkable skin to touch

A

mild

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17
Q

what level of dehydration is suggested by the following clinical exam finding:
soft, slightly depressed fontanelle

A

moderate

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18
Q

what level of dehydration is suggested by the following clinical exam finding:
slightly dry, deep set eyes

A

moderate

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19
Q

what level of dehydration is suggested by the following clinical exam finding:
dry, sunken eyes

A

severe

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20
Q

what level of dehydration is suggested by the following clinical exam finding:
increased pulse

A

severe

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21
Q

what level of dehydration is suggested by the following clinical exam finding:
age appropriate or slightly increased pulse

A

mild…mild/moderate

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22
Q

what level of dehydration is suggested by the following clinical exam finding:
cap refill 2-3 seconds

A

moderate

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23
Q

what level of dehydration is suggested by the following clinical exam finding:
lethargic

A

severe

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24
Q

what level of dehydration is suggested by the following clinical exam finding:
alert, consolable or irritable

A

mild

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25
Q

why do kids have a higher risk for dehydration

A

have higher surface area:body mass ration–greater relative area for evaporation

higher basal metabolic rates than adults which generates heat and expends water

higher % body weight that is water (infants are 70%, kids 65%, adults 60%)

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26
Q

why is diffuse abdo pain characteristic of DKA

A

ongoing acidosis

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27
Q

how does toxic ingestion often present

A

vomiting
altered mental status
obtundation

  • aspirin overdoses may present with tachypnea
  • may have abdo pain i.e with iron ingestion
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28
Q

ddx of vomiting and altered mental status

A
  1. DKA
  2. toxic ingestion
  3. GI obstruction
  4. increased ICP
  5. gastroenteritis
  6. appendicitis
  7. bacteria pna
  8. pyelonephritis
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29
Q

what is cushings triad

A

sign of increased ICP

  1. hypertension (progressive), widening pulse pressure
  2. bradycardia
  3. irregular breathing
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30
Q

what are the diagnostic criteria for DKA

A
  1. random blood glucose of over 11.1 mmol/L
  2. a venous pH below 7.3 or serum bicarb less than 15mmol/L
  3. moderate or large ketouria or ketonemia
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31
Q

how do you manage insulin in DKA

A

insulin drip 0.1 unite/kg/hour started after patient received initial volume expansion

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32
Q

should you give bicarb to manage DKA

A

no

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33
Q

what is the most common cause of diabetes associated death in kids

A

cerebral edema

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34
Q

should you give an insulin bolus in kids? why or why not?

A

no

increased risk of cerebral edema from rapid correction

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35
Q

why might you have a white count in DKAq

A

left shift from stress of DKA alone or from precipitating infection

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36
Q

do you get DKA only in T1DM

A

most commonly but can get it also in T2DM

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37
Q

what symptoms might make you think DKA

A 
vomiting
weight loss
dehydration
shortness of breath
abdominal pain
change in level of consciousness
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38
Q

how would the following be affected in DKA:

pH on venous blood gas

A

decreased

due to metabolic acidosis due to ketoacids

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39
Q

how would the following be affected in DKA:

serum sodium

A

decreased

hyponatremia from osmotic movement of water into the extracellular space in response to hyperglycemia and hyperosmolarity (dilutional hyponatremia) as well as from increased renal sodium losses

calculate corrected sodium and monitor with therapy

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40
Q

how would the following be affected in DKA:

potassium

A

lab value–often normal
total body sodium–depleted

acidosis and low insulin drive K out of cells into blood–as you correct the acidosis her serum K will drop leading to hypokalemia

must anticipate this drop and monitor K

usually add K to IVF after initial volume expansion and after urine output is established unless there are ECG changes suggestive of hyperkalemia

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41
Q

how would the following be affected in DKA:

bicarbonate

A

decreased

due to metabolic acidosis

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42
Q

how would the following be affected in DKA:

creatinine

A

elevated

even in context of normal renal function, can be elevated due to severe dehydration (prerenal azotemia)

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43
Q

how would the following be affected in DKA:

serum ketones

A

elevated

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44
Q

how would the following be affected in DKA:

urine ketones

A

elevated

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45
Q

what are the three types of dehydration

A

isotonic/isonatremic

hypotonic/hyponatremic

hypertonic/hypernatremic

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46
Q

what is isotonic/isonatremia dehydration

A

most common type in kids

occurs when sodium and water losses are balanced (including those with acute gastroenteritis and diarrhea)

typically deficit can be replaced within 12 hours

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47
Q

what is hypotonic/hyponatremic dehydration

A

occurs when sodium losses exceed those of water

usually when patients consume diluted fluids or water in the face of dehydration

hyponatremia may be the result of adrenal insufficiency

typically replaced over 12 hours

*rapid correcttion of hyponatremia is associated with central pontine myelinosis

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48
Q

what happens is you correct hyponatremia too quickly

A

central pontine myelinosis

–> damage to myelin sheath of CNS nerve cells in brainstem

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49
Q

what is hypertonic/hypernatremic dehydration

A

when water losses exceed that of sodium

associated with the highest mortality

can be due to breastfeeding failure, use of inappropriate rehydration solutions (boiled milk) and diabetes insipidus

typically replaced over 24 hours

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50
Q

what happens if you correct hypernatremia too fast

A

cerebral edema

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51
Q

what are the steps of fluid management

A
  1. provide bolus to restore intravascular volume
  2. correct dehydration
  3. provide maintenance fluids
  4. replace ongoing losses
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52
Q

how do you bolus to restore intravascular volume in a dehydrated patient

A

10-20 mL/kg bolus of 0.9% saline (NS)

NOT DKA–> serial boluses until patient urinates

IN DKA–> urinate very quickly due to osmotic diuresis, therefore monitor vital signs (normalized HR and BP) and mental status

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53
Q

how do you correct dehydration in a dehydrated patient

A

dictated by your assessment of severity of dehydration

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54
Q

how do you provide maintenance fluids in a dehydrated patient

A

replace daily insensible losses

1/4 normal saline or 1/2 normal saline with 5-10% dextrose usually used

approx 2 mL/kg/hr for kids under 15 kg and 1mL/kg/hr for kids above 15kg

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55
Q

list signs/symptoms of cerebral edema

A
  1. headache
  2. recurrence of vomiting
  3. bradycarida
  4. rising BP
  5. hypoxia
  6. restlessness, irritability
  7. increased drowsiness (lethargy)
  8. CN palsies–> CN VI
  9. abnormal pupillary response–> unequal, fixed dilated, absent responses unilaterally or bilaterally
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56
Q

what should admit orders include for DKA

A
  1. continuous monitoring of vitals
  2. hourly neuro checks
  3. monitor ins and outs
  4. insulin orders
  5. serum glucose every 60 minutes
  6. serum calcium, magnesium, and phosphorous now
  7. check serum pH (VBG) every 60 minutes
  8. urine dipstick for ketones
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57
Q

patients with T1DM are at risk for what other diseases?

A

other autoimmune related diseases with autoimmune thyroid disease and celiac disease being the most common

should have annual thyriod fxn test, screen for celiac at diagnosis

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58
Q

what do all insulin regimens consist of

A
  1. basal insulin–intermediate to long acting to suppress hepatic glucose production and maintain normoglycemia in fasting state
  2. prandial insulin–short acting to take before meals to cover carbohydrate load from food intake
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59
Q

peak age of T2DM dx

A

ages 12-16

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60
Q

what bruises raise the suspicion of non accidental bruising

A

bruising over well-cushioned areas of the body–buttocks, back, genitals

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61
Q

can bruises be aged based on color

A

no

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62
Q

what causes lyme disease

A

tick borne Borrelia burgdorferi

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63
Q

what is the characteristic rash associated with lyme disease

A

erythema migrans –> looks like a bullseye

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64
Q

symptoms of lyme disease

A

erythema migrans plus fever, malaise, fatigue, headache

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65
Q

how do you dx lyme disease

A

clinically, with rash etc…

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66
Q

what are the complications of lyme disease

A

arthritis is second most common manifestation of lyme disease–begins about 4 weeks after skin lesion

large joints closest to rash are most commonly affected

may relapse or recur only once

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67
Q

risk factors for DDH

A

female
breech delivery
family history of DDH

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68
Q

list 4 predictors of septic arthritis of the hip

A

fever
non weight bearing
ESR above 40
WBC above 12

1 predictor is 10% probability
4 predictors is 93% probability

fever was the best predictor
CRP above 20 was a strong risk factor

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69
Q

how do you dx septic arthritis of the hip

A

US of hip useful for ID of effusion and for guiding needle aspiration

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70
Q

most common causative organisms for septic arthritis

A

staph aureus

strep

Hib in unimmunized kids

N. gonorrhea

kingella kingae

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71
Q

tx of septic arthritis

A

empiric IV abx coverage should begin right after joint aspiration

may require surgical incision and drainage to remove debris and reduce pressure

requires prolonged abx and may require repeat arthrocentesis or surgical drainage

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72
Q

what is transient synovitis of the hip

A

relatively common condition resulting from inflammation and swelling of the tissues around the hip joint and can often be seen in kids who have recently had a cold

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73
Q

what causes transient synovitis of the hip

A

unknown

most have an URTI with it–?post infectious viral syndrome

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74
Q

tx for transient synovitis of the hip

A

rest and ibuprofen

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75
Q

duration of symptoms of transient synovitis of the hip

A

3-10 days

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76
Q

ddx of acute refusal to walk

A 
more likely--
leukemia
osteomyelitis
reactive arthritis
septic arthritis
transient synovitis
trauma
less likely--
JIA
SCFE
legg calve perthes 
avascular necrosis of the femoral head
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77
Q

what should always be considered in a child refusing to walk

A

leukemia

replacement of bone marrow by leukemia cells can cause bone pain that presents as limp, refusal to walk or localized discomfort of the jaw/long bones/vertebral column/hip/scapula or ribs

may preceed systemic signs such as fever and weight loss

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78
Q

most common cause of OM

A

staph aureus

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79
Q

what is reactive arthritis

A

inflammatory process assoc with infection outside of the joint–most often GI or GU

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80
Q

what are the infections outside the joint most commonly assoc with reactive arthritis

A

GI

GU

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81
Q

what is the typical presentation of transient synovitis

A

acute onset of hip pain with prehaps no other constitutional symptoms

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82
Q

what is JIA

A

group of disorders characterized by chronic inflammation of the joints

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83
Q

what are the diagnostic criteria for JIA

A
  1. less than 16 years old

2. arthritis in at least one joint for more than 6 weeks

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84
Q

what are the subtypes of JIA

A
  1. systemic–> constitutional sx such as fever and rash
  2. oligoarthritis–> usually knee
  3. polyarthritis (Rh positive and Rh negative)
  4. psoriatic arthritis
  5. enthesitis related arthritis

other arthritis

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85
Q

what is the most common hip disorder in adolescents

A

SCFE

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86
Q

what is the most common presentation for SCFE

A

months of vague hip or knee symptoms and limp with or without an acute exacerbation

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87
Q

what is legg calve perthes

A

avascular necrosis of the capital femoral epiphysis

most commonly affects boys between ages of 4 and 10

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88
Q

typical presentation of legg calve perthes

A

indolent or chronic pain rather than acute

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89
Q

natural history of legg calve perthes

A

typically self resolving but may lead to complications includng femoral head deformity and degenerative arthritis

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90
Q

treatment for legg calve perthes

A

refer to ortho

prevent damage to hip by containing femoral head within acetabulum

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91
Q

what avascular necrosis of the femoral head

A

necrosis of the bone due to loss of blood supply

traumatic or non traumatic

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92
Q

ibuprofen pediatric dose

A

10mg/kg q6-8h max dose 40mg/kg/24 hour PO

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93
Q 
what type of headache presents as:
episodic
worsens thru day
mild to moderate intensity
band around the head or occipital area with accompanying tenderness to posterior muscle of the neck
A

tension headache

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94
Q

what are the most common cause of recurrent headache in kids

A

migraine

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95
Q

what should be considered in a child with
cyclical vomiting
benign parxysmal vertigo

A

migrains

can also have abdominal migraines

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96
Q

common migraine precipitants

A

stress
bright lights
odors like perfumes
foods

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97
Q

are migraines relieve by sleep

A

yes commonly

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98
Q

what should you be concerned about in a patient with headaches that occur agyer a period of recumbency (i.e early morning) and may be accompanied by and relieved after forceful vomiting?

A

increased ICP

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99
Q

what should you be concerned about in a patient with headaches that awaken them from sleep

A

increased ICP

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100
Q

what should you be concerned about in a patient with headaches, photophobia and fever

A

infectious etiology like meningitis or encephalitis

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101
Q

what should you be concerned about in a patient with headaches that worsen with cough or valsalva

A

increased ICP

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102
Q

what should you be concerned about in a patient with headaches that progressively worsen

A

red flag for serious pathology

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103
Q

list findings associated with allergies

A
  1. allergic shiners
  2. allergic salute
  3. dennie’s lines
  4. cobblestoning
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104
Q

define allergic shiners

A

darkness and swelling beneath the eyes due to sinus congestion

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105
Q

define allergic salute

A

frequent upward rubbing of the nose to alleviate itching leads to transverse nasal crease along lower third of nose

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106
Q

define dennie’s lines

A

infraorbital transverse creases–> assoc with mild chronic inflammation of the conjunctivae

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107
Q

define cobblestoning

A

fine granular appearance of the palpebral conjunctivae resulting from edema and hyperplasia of the papillae

cobblestoning of the pharynx occurs with chronic nasopharyngeal drainage of allergic rhinitis –> lymphocytic hyperplasia

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108
Q

ddx acquired ataxia

A
  1. post infectious cerebellitis
  2. infectious cerebellitis
  3. meds or toxins
  4. intracranial mass
  5. opsoclonus-myoclonus syndrome
  6. migraine headache
  7. hydrocephalus
  8. metabolic disease
  9. neurodegenerative disease
  10. psychiatric illness
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109
Q

what is the most common cause of acute ataxia in kids

A

post infectious cerebllitis

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110
Q

what is post infectious cerebellitis

A

causes ataxia

diagnosis of exclusion in kids 1-3

autoimmune response leading to cerebellar demyelination

several weeks after viral infection i.e varicella

onset sudden–> ataxia, vomiting, nystagmus in about half of patients, dysarthria in some

CSF may be normal or have pleocytosis… protein may be elevated

majority recover within a few months

most typically assoc with fevers or other systemic manifestation

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111
Q

what is infectious cerebellitis

A

causes ataxia

viral or bacterial

fever often

mental status changes seen

i.e pumps, enteroviruses, EBV

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112
Q

where might a tumour be located causing ataxia

A

cerebellum or frontal lobe

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113
Q

what is opsoclonus-myoclonus syndrome

A

paraneoplastic syndrome that occurs most often with neuroblastoma–> usually in younger kid 6mo - 3 years

ataxia accompanied by intermittent jerking movements and erratic, jerky conjugate movements of the eyes (opsoclonus)

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114
Q

what migraines can cause ataxia

A

basilar artery or hemiplegic migraines –> intermittent episodes of acute ataxia

may also have intermittent loss of vision, speech change, headache, vomiting

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115
Q

how does hydrocephalus present

A

ataxia that is generally insidious and chronic with increasing loss of coordination over weeks to months

often with headache and vomiting

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116
Q

what metabolic disturbances can cause ataxia

A

PKU

maple syrup urine disease

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117
Q

what neurodegenerative diseases of childhood cause ataxia

A

ataxia-telangiectasis

friedrich ataxia

most kids are younger than 10 and sx are loss od devel milestones, ataxia and other neuro sx

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118
Q

what do lesions in the vermis of the cerebellum cause?

A

vermis is midline

causes truncal ataxia, dysarthria, gait abnormalities

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119
Q

what do lesions in the cerebellar hemispheres cause?

A

ipsilateral limb abnormalities, nystagmus, tremor/dysmetria and tend to spare speech

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120
Q

what do lesions in the deep nuclei of the cerebellum cause?

A

resting tremor, myoclonis, opsoclonus (similar to neuroblastoma)

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121
Q

what is the most common childhood cancer

A

leukemia

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122
Q

what is the second most common childhood cancer

A

brain tumour –> highest among childhood cancer deaths

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123
Q

in what age range are brain tumours most common

A

younger age group–less than 7

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124
Q

when are the peaks of incidence for brain tumours

A

first decade of life and 8th decade

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125
Q

what are the risk factors for childhood brain tumours

A

exposure to ionizing radiation

certain genetic syndrome–tuberous sclerosis, neurofibromatosis, li-fraumeni syndrome

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126
Q

what are the most common brain tumours

A
  1. medulloblastoma–20%
  2. juvenile pilocytic astrocytoma–20%
  3. low grade astrocytoma–15%
  4. high grade astrocytoma–7%
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127
Q

what is a medulloblastoma

A

most common pediatric brain tumous

malignant tumour that may spread throughout the CNS and is capable to metastasizing to extracranial sites

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128
Q

tx for medulloblastoma

A

treatment generally includes surgical resection, radiation and chemo

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129
Q

prognosis for medulloblastoma

A

dependent on size and dissemination of the tumour

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130
Q

what is an astrocytoma of the cerebellum

A

best prognosis of all intratentorial tumours in kids

often have cystic component

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131
Q

tx for astrocytoma of the cerebellum

A

surgical resection

radiation reserved for patients with high grade astrocytomas, partial resections or with post op progression

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132
Q

prognosis for astrocytoma of the cerebellum

A

5 year survival is 90% with complete resection

drop to 50-70% with partial resection

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133
Q

what is an ependymoma

A

arise from within fourth ventricle (ependymal lining) and cause symptoms related to hydrocephalus

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134
Q

treatment for ependymoma

A

surgical resection, then radiation

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135
Q

prognosis ependymoma

A

5 year survival approx 50%

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136
Q

what is a brain stem glioma

A

may be either quite aggressive–> diffuse infiltration of the pons//or low grade–> focal tumour in midbrain or medulla

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137
Q

treament brain stem glioma

A

surgical resection alone for low grade gliomas

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138
Q

prognosis brain stem glioma

A

quite grave to quite good–range

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139
Q

most common complications of brain tumours

A 
neurocognitive defects 
ADD
learning disabilities
endocrine abnormalities
stroke
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140
Q

best imaging for brain tumour

A

MRI

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141
Q

best imagine for cranial hemorrhage

A

CT

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142
Q

why do we care about testicular torsion

A

urologic emergency in which the goal is to save the affected testes

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143
Q

when does testicular torsion usually occur

A

early adolescence

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144
Q

how does testicular torsion present

A

acute onset of severe hemi scrotal pain with N/V

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145
Q

physical exam findings in testicular torsion

A

enlarged tender testis, scrotal edema, absence of cremasteric reflex

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146
Q

treatment of testicular torsion

A

surgical exploration and detorsion promptly

irreversible changes to the testis can occur within hours

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147
Q

what is the most common condition requiring emergency surgery in the pediatric population

A

appendicitis

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148
Q

is appendicitis common in children under 2

A

no

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149
Q

what fraction of paeds patients have atypical presentations of appendicitis

A

1/3–therefore high incidence of perforation in this pop

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150
Q

who is at highest risk for PID

A

sexually active females between 15-19

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151
Q

why are sexually active females between 15-19 at highest risk for PID

A

fewer protective antibodies in the vagina compared to older women

cervical ectropion (transition zone between columnar and squamous epithelium) not fully matured–> cells here are particularly prone to STDs and thus cervix easier to infect

behavioural–multiple sexual partners, intercourse during menses, infrequent or no condom use

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152
Q

which organisms most commonly cause PID

A

N. gonorrhea and C. trachomatis (more than 50% of all cases)–lower tract infection with these leads to alteration in the normal vaginal flora and allows bacteria like ecoli, bacteroides and other anaeobes, mycoplasma or ureaplasma access to the uterus and fallopian tubes

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153
Q

how do you dx PID

A

cervical motion tenderness

abdo pain

cervical discharge

cx for bacteria

molecular dx testing on urine or cervical discharge for chlamydia and gonorrhea

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154
Q

complications from PID

A

increased rates of infertility

sepsis

tubo-ovarian abscess

intra-abdominal abscesses

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155
Q

when should you think about doing a rectal exam

A

if there is an abdo complaint

part of an in depth neuro exam

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156
Q

ddx of abdo pain and vomiting

A
  1. appendicitis
  2. cholecystitis
  3. ectopic pregnancy
  4. hepatitis
  5. pancreatitis
  6. PID
  7. UTI
  8. acute gastroenteritis
  9. incarcerated hernia
  10. mesenteric adenitis
  11. ovarian torsion
  12. pneumonia
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157
Q

classic pattern of appendicitis

A

periumbilical pain followed by generalized RLQ pain

vomiting very common, diarrhea uncommon

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158
Q

descrieb cholecystitis pain

A

RUQ, steady, may radiate to shoulder

usually worse after eating, especially fatty foods

may be intermittent/colicky and accompanied by low appetite and N/V

less common in kids than adults

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159
Q

what should you always consider in a sexually active female with abdo pain

A

ectopic pregnancy because it is an emergency

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160
Q

how does ectopic pregnancy present

A

lower abdo pain, vaginal bleeding, abnormal menstual hx

fever and diffuse abdo pain are uncommon

vomiting without diarrhea suggests extra-intestinal pathology

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161
Q

what does band-like abdo pain radiating to the back suggest

A

pancreatitis

N/V almost always present

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162
Q

what is an incarcerated hernia

A

hernia that can no longer be reduced to its usual position with manipulation

most present before 1 year of age, slightly more in girls

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163
Q

what is mesenteric adenitis

A

inflamm of mesenteric lymph nodes

often presents like appendicitis

164
Q

typical presentation of mesenteric adenitis

A

RLQ pain with fever, vomiting and diarrhea

165
Q

when would you hospitalize a patient with PID

A

pregnant

previous noncompliance

high fever

intractable vomiting

inability to exclude a surgical emergency

166
Q

when is fever an emergency

A

infants younger than 6-8 weeks

167
Q

list the exam findings of bacterial meningitis

A

nuchal rigidity–57-92%

fever–66-100%

altered mental status–44-96%

kernigs or brudzinskis–61%

168
Q

do you diagnose shock in kids based on BP?

A

no–kids can maintain normal BP until in profound shock

169
Q

how do kids compensate for shock

A
  1. increased HR
  2. increased systemic vascular resistance–vasoconstriction
  3. increased heart contractility, with more complete emptying of ventricles
  4. increased venous tone–> more blood return to heart
  5. increased resp rate–compensate for metabolic acidosis from decreased oxygen perfrusion of cells and tissues
170
Q

signs of early shock in kids

A

elevated HR and RR

peripheral vasoconstriction (cool, clammy extremities and delayed cap refill)

decreased peripheral pulses

**hypotension is sign of late shock

171
Q

name 2 types of distributive shock

A

neurogenic

anaphylactic

172
Q

characteristics of distributive shock

A

intravascular hypovolemia due to vasodilation, increased capillary permeability and third space fluid loss

173
Q

what is the most common type of shock

A

hypovolemic

174
Q

what causes hypovolemic shock

A

inadequate fluid intake to compensate for fluid output

175
Q

signs of hypovolemic shock

A

mental status change

tachypnea

tachycardia

hypotension

cool extremities

oliguria

176
Q

what conditions are associated with cardiogenic shock

A

severe CHD

dysrhythmias

cardiomyopathy

tamponade

177
Q

signs of cardiogenic shock

A

cool extremities

delayed cap refill

hypotension

tachypnea

increasing obtundation

decreased urine output

178
Q

what causes septic shock

A

infectious organisms release toxins that affect fluid distribution and cardiac output

can be bacterial, viral or fungal in immunocompromised patient

179
Q

how do you treat septic shock

A

require repeat fluid bolusing

may also need pressors and dopamine

180
Q

symptoms of warm shock

A

warm extremities

bounding pulses

tachycardia

tachypnea

adequate urination

mild metabolic acidosis

181
Q

complications of meningococcal disease

A

hearing loss

neurologic disability

digit or limb amputations

skin scarring

182
Q

what is a sensitive measure of volume status

A

HR

tachycardia is the first and most subtle sign of possible inadequate perfusion

183
Q

what is a sensitive sign of hypovolemia

A

cap refill

184
Q

ddx lethargy

A
  1. sepsis
  2. meningitis
  3. encephalitis
  4. toxic ingestion
  5. pneumonia
  6. CNS tumour
  7. DKA
  8. hypoglycemia
  9. renal failure
185
Q

what often causes encephalitis in kids

A

virus

186
Q

what diagnosis must be at the top of the list in a patient with fever and petechiae

A

meningococcal sepsis

blood cx must always be done until disease ruled out

187
Q

describe the mucocutaneous leasions of kawasaki disease

A

associated with fever and rash

  1. “strawberry” tongue
  2. dry, red, cracked lips
  3. diffuse erythema of the oral cavity
  4. erythema and/or edema of the hands/feet
  5. polymorphic truncal rash
188
Q

what disease is associated with strawberry tongue

A

kawasaki

189
Q

presentation of toxic shock syndrome

A

fever with sun-burn looking rash that is rough to touch like sandpaper

190
Q

where are the petechiae of rocky mountain spotted fever

A

palms and soles

191
Q

how does scarlet fever start

A

finely punctate pink-scarlet exanthem

rash appears on upper trunk 12-48 hours after onset of fever

as exanthem spreads to extremities, becomes confluent and feels like sandpaper

fades in 4-5 days followed by desquamation of the skin

linear petechiae evident in body folds–> pastia’s sign

192
Q

what are the linear petechiae found in body folds in scarlet fever called

A

pastia’s sign

193
Q

describe the appearance of the pharynx in scarlet fever

A

beefy red and tongue is initially white and rough (strawberry tongue also)–> white coating sloughs in 4-5 days and tongue is bright red

194
Q

what is the priority in the management of shock

A

intravascular fluid replacement with ISOTONIC (NS) solutions

195
Q

when should you place an IO line

A

if you cant get IV access when needed within 90 sec

196
Q

apart from repeat fluid boluses, how can you manage shock

A

with inotropes to increase contractility and pressors to increase BP

197
Q

list common procedures for kids with sickle cell

A
  1. tonsillectomy

2. cholecystectomy

198
Q

why do kids with SCD get tonsillectomies

A

lymphoidal tissue hypertrophy involving waldeyer’s ring is common in kids with SCD

may see excessive snoring or OSA

tonsillectomy with adenoidectomy will improve the obstructive apnea for most patients

199
Q

why do kids with SCD get cholecystectomies

A

bilirubin gallstones form frequently in all patients with hemolytic anemias because of increased Hb breakdown

more common in adolescents

only for those who are symptomatic

preferably elective

200
Q

why are infants and young kids with SCD at increased risk of sepsis? what do you do about it?

A

decreased splenic function leads to decreased resistance to infection with encapsulated organisms (strep pneumo, Hib, neisseria meningitidis)

given penicillin as decreases risk of death from overwhelming sepsis in kids with SCD/sickling disorders

201
Q

list expected complications for kids with SCD

A
  1. jaundice
  2. anemia
  3. stroke
  4. resp problems
202
Q

what is the risk of stroke with SCD

A

10% by age 15

203
Q

what is acute chest syndrome

A

vaso-occlusion in the lung parenchyma from SCD

med emergency

give supplemental O2 and transfusion therapy

204
Q

why might growth be impaired in a kids with sickle cell

A 
chronic anemia
poor nutrition
painful crises
endocrine dysfunction
poor pulmonary function
205
Q

what should you look for in particular in the exam for a kid with SCD

A
  1. splenic enlargment
  2. sclera (icterus from hemolysis)
  3. neuro exam (stroke)
206
Q

what is splenic sequestration crisis

A

in kids with SCD

indicated by a massive enlargement or rapid change in size of spleen

accompanied by increased pallor, fatigue, irritability

life threatening

occurs when blood pools in spleen and leads to severe anemia and shock

207
Q

what happens to the spleen over time in SCD

A

progressively fibrotic

by time 4-6 years old, no longer palpable (kids with hemoglobin SC or Sbeta thalassemia can have splenic enlargment into teens)

208
Q

what is a typical baseline Hb in SCD

A

60-90

209
Q

what should you think in a kid with SCD and cough/breathing difficulty

A

pneumonia
intrapulmonary sickling
pulm fat embolism

–all of these are covered by the term acute chest syndrome

must address possibility of infection, pulm and resp complaints and the pain

210
Q

acute chest syndrome on xray

A

multilobal infiltrates

effusions

atelectasis

211
Q

pericarditis on xray

A

effusion and infiltration

212
Q

what is the only way to directly reduce or reverse the sickling process that is the undelrying cause of acute chest syndrome

A

rbc transfusion

213
Q

when do you transfuse in acute chest syndrome in SCD

A

consider when…

  1. fall in hb from baseline
  2. increasing resp rate
  3. worsening chest symptoms
  4. declining O2 sat
  5. progressive infiltrates on CXR
214
Q

when do you seek emergency care for kids with SCD

A
  1. fever–medical emergency in kid with SCD because sometimes only sign of serious infection
  2. splenic enlargment
  3. slurred speech–stroke?
  4. chest pain
  5. rapid breathing
  6. increased pallor
  7. increased jaundice
  8. priapism
215
Q

how does seasonal allergic conjunctivitis present

A

periorbital swelling

may be associated with pruritis and mucoid discharge

often assoc with sneazing, itchy nose, clear rhinorrhea

look for allergic shiners, dennie’s lines, cobblestoneing of conjunctiva

216
Q

what is the most prominent symptom of nephrotic syndrome

A

edema

217
Q

what is a common presenting finding of nephrotic syndrome

A

periorbital edema that improves when upright

edema then becomes more generalized–leads to pitting edema, ascites, weight gain

218
Q

what causes the edema in nephrotic syndrome

A

more due to interstitial fluid accumulation rather than intravascular fluid overload (which happens in acute glomerulomephritis)

hypertension thus does NOT usually occur

219
Q

do you expect hypertension in nephrotic syndrome

A

no

220
Q

do you expect hypertension in acute glomerulonehpritis

A

yes

221
Q

what is the most common form of nephrotic syndrome in kids

A

minimal change disease –90% of cases under age 10

222
Q

what is the characteristic histologic finding in kids with minimal change disease

A

fusion and diffuse effacement of the epithelial cell foot processes on electron microscopy

nephron appears relatively normal on light microscopy

223
Q

what are benign causes of proteinuria

A

fever
significant exertion

orthostatic proteinuria can be found in teens and doesnt mean renal disease–protein excretion only when standing, not recumbent (first morning urine is negative for protein)

224
Q

what are the mechanisms for proteinuria in nephrotic syndrome

A
  1. loss of polyanion charge characteristic of a normal capillary wall–> loss of charge permits large negatively charged proteins like albumin (previously repelled) to leak through the membrane of the glomerulus
  2. shift in capillary wall pore size in a direction permitting increased leaking of large molecules
  3. change in hemodynamic characteristics of capillary flow so greater filtration of larger molecules
225
Q

what diseases can cause proteinuria

A

any disease causing inflammation of the renal parenchyma (nephritis) can cause proteinuria

pyelonephritis
acute glomerulonephritis
interstitial nephritis

226
Q

if you saw tea coloured urine what might you think if the cause of renal disease in that patient

A

acute glomerulonephritis (i.e post strep)due to RBCs and red blood cell casts

227
Q

what lab test abnormalities would you expect in nephrotic syndrome

A

hypoalbuminemia (major loss of albumin in urine)

hyperlipidemia–> in reaction to decreased albumin, liver stimulated to make lipoproteins as well as albimun–> hyperlipidemia and hypercholesterolemia (also decreased clearance of lipids from blood)

228
Q

how do you classify minimal change disease

A

steroid responsive or relapsing/steroid dependent or
steroid resistant

95% are in first two groups

229
Q

how do you manage nephrotic syndrome in kids

A

kids between ages of 1-10 without gross hematuria and normal serum complement get trial of corticosteroids

most of them will be minimal change disease

230
Q

where can generalized edema best be seen in the male and female patients

A

male-scrotum

female-labia

231
Q

common features of down syndrome

A
  1. upslanting palpebral fissures
  2. small ears
  3. flattened midface
  4. epicanthal folds
  5. redundant skin on back of neck (nuchal skin)
  6. hypotonia (most consistent finding)
  7. predisposition to leukemia
  8. heart defects
  9. intestinal stenosis
  10. umbilical hernia
232
Q

which form of down syndrome geentics is most likely

A

trisomy (versus translocation and mosaic)

233
Q

how do you TEST for downs prenatally

A

chromosome analysis of amniotic fluid and chorionic villus sampling are both direct and diagnostic tests for downs because cells are of fetal origin

234
Q

how do you SCREEN for downs prenatally

A

maternal serum screening and fetal US can potentially screen for them but not definitive

235
Q

what is fragile X disease

A

caused by inheritance of abnormal number of CGG repeats in FMR1 gene

236
Q

physical features of fragile X

A

long face with large mandible

large prominent ears

large testicles after puberty

237
Q

what are the two most common genetic causes of intellectual disability

A

downs then fragile x

238
Q

what is the sex chromosomal disorder most likely to be assoc with physical differences at birth

A

turners

239
Q

what process happens in utero with turners girls

A

lymphedema

240
Q

features of trisomy 13/patau

A 
microcephaly
microphthalmia
severe intellectual disability 
polydactyly
cleft lip and palate
cardiac and renal defects
umbilical hernia
cutis aplasia
241
Q

features of trisomy 18/edwards

A 
severe intellectual disability
prominent occiput
micrognathia
low set ears
short neck 
overlapping fingers
heart defects
renal malformations
limited hip adbuction
rocker-bottom feet
242
Q

what endocrine abnormality is common in downs

A

hypothyroid

243
Q

ddx hypotonia in a newborn

A
  1. downs
  2. benign neonatal hypotonia
  3. zellweger syndrome
  4. family resemblance
244
Q

what is zellweger syndrome

A

peroxisomal disorder

generally hypotonic and poorly responsive

245
Q

test for downs

A

lymphocyte karyotype

246
Q

define macule

A

flat, circumscribed discoloration less than 1cm

ie freckle

247
Q

define patch

A

larger flat lesion of color change of the skin greater than 1cm

248
Q

define papule

A

elevated, circumscribed solid lesion

less than 1cm
ie mole

249
Q

define plaque

A

broad, elevated lesion (or confluence of papules)

greater than 1cm

250
Q

define vesciel

A

circumscribed, elevated lesion containing clear colored fluid

less than 1cm

251
Q

define bulla

A

larger, circumscribed, elevated fluid containing lesion greater than 1cm

252
Q

define pustule

A

exudate containing lesion

variable size

253
Q

define nodule

A

circumscribed elevated lesion that involves the dermis and may extend into the subcutaneous tissue

majority of nodules is below skin

254
Q

define wheal

A

a blanching, edematous, thin, erythematous papule or plaque, often with a ring of hypopigmentation

may be white to ale red and often appears and disappears over a period of hours

255
Q

define telangiectasia

A

dilation of superficial venules, arterioles or capillaries visible under the skin or mucous membrane

256
Q

define petechiae

A

tiny, red or purple macules caused by capillary hemorrhage under the skin or mucous membrane

petechiae do not blanch with pressure

257
Q

define purpura

A

larger, purple lesion caused by bleeding under the skin

may be palpable and do not blanch

258
Q

what is kawasaki disease

A

fever of at least 5 days duration–> high, spiking, not responsive to antimicrobial or antipyretic agents

presence of at least 4 of the following principal clinical factors:

  1. polymorphous exanthem (face, trunk, extremities, perineal region)
  2. bilateral conjunctivitis (nonexudative, bulbar)
  3. changes in lips and oral cavity (dry, cracked lips and strawberry tongue)
  4. changes in extremities (erythema of palms and soles, edema of hands and feet, followed by 1-3 weeks later of desquamation of fingers, toes and perineal region in infants)
  5. cervical lymphadenopathy
259
Q

in what kids should you consider kawasaki

A

child with persistent and unabating fever and

  1. no focus of infection
  2. no response to antimicrobial tx-or-
  3. other clinical and lab findings of kawasaki
260
Q

what is erythema toxicum

A

idiopathic, asymptomatic, benign self limiting cutaneous eruption of full term newborns

blotchy, macular erythema

progresses to 1-3mm yellow/white papules and pustules

present from day 2-10 of life

no treatment needed

261
Q

what is neonatal acne

A

assoc with saprophytic Malassezia species

not true acne

located on cheeks, chin, forehead

no tx necessary (topical antifungals can help)

262
Q

what is milia

A

clustered small white papules over the nose

small retention cysts resulting from keratin within dermis

seen in 40-50% of infants

cheeks, nose, chin, forehead

newborn milia resolves in 3-4 weeks

263
Q

what is neonatal herpes simplex

A

ranges from mild, self limiting illness to devastating neuro consequences

3 patterns:
SEM (skin eyes mucous membranes)
neuro disease
disseminates herpes

264
Q

what is transient neonatal pustular melanosis

A

benign self limiting disorder of unknown etiology

superficial vesciculopustular lesions

rupture easily and evolve into hyperpigmented macules

most common in infants with black skin

inferior chin, forehead, neck, lower back, shins

pustular lesions disappear within 24-48 hours

hyperpigmented macules fade gradually over weeks to months

265
Q

what is roseola

A

common childhood disease caused by HHV type 6 or 7

266
Q

what is the classic presentation of roseola

A

high fever last 3-5 days

otherwise well infant

with reduced fever–> classic exanthem appears–> initially on trunk, spreads to extremities, neck, face

267
Q

what infection has a slapped cheek appearance

A

erythema infectiosum

caused by parvovirus B19

268
Q

how does erythema infectiousum present

A

prodrome of 5-7 days of headaches, fever, chills

rash

269
Q

what disease causes a “dewdrops on a rosepetal” rash

A

varicella

270
Q

how does varicella present

A

prodrome of fever, chills, malaise, headache, arthralgia, myalgia

skin lesions occur 24-48 hours after

red macules/papules that rapidly evolve into vesicles

older lesions crust over
v
various stages present at same time

271
Q

how does the measles rash present

A

intensely erythematous patched of the face with cephalocauded spread onto the trunk and extremities

272
Q

what causes measles

A

single stranded RNA virus in family paramyxoviridae

273
Q

what is the measles prodrome

A

fever and the 3Cs: cough, coryza, conjunctivitis

koplik spots

274
Q

what are koplik spots

A

punctuate, gray-white to erythematous papules distributed on the buccal mucosa

275
Q

how does measles spread

A

cephalocaudad

276
Q

what are some complications of measles

A 
pneumonia
bronchitis
otitis
gastroenteritis
myocarditis 
encephalitis
277
Q

what might you think in a patient with nonspecific “rose pink” macules and papules on the trunk of an adolescent male associated with lymphadenopathy and arthralgia

A

rubella

278
Q

what causes rubella

A

RNA virus in the togaviridae family

279
Q

what is the rubella prodrome

A 
low grade fever
headache
malaise
eye pain
myalgias
sore throat
rhinorrhea
cough

progresses to…
rash
generalized lymphadenopathy (suboccipital, postauricular, cervical regions)
arthralgias and arthritis common

280
Q

describe the rubella rash

A

rose pink macules and papules becoming confluent

cephalocaudal spread and resolution

281
Q

why do we vaccinate against rubella

A

prevent fetal infection

282
Q

what is sturge-weber syndrome

A

facial bright red rash with glaucoma and seizures

neuroectodermal syndrome

triad:

  1. port wine stain in V1 distribution
  2. seizures
  3. glaucoma

requires multidisciplinary tx

283
Q

what are the 7 diagnostic features of NF1

A
  1. six cafe au lait macules that measure 0.5cm or more before puberty or 1.5 cm or more in diameter in adults
  2. freckling of the axillary and/or inguinal areas
  3. plexiform neurofibroma or two or more dermal neurofibromas
  4. two or more lisch nodules
  5. optic nerve glioma
  6. pathognomonic skeletal dysplasia (tibial or sphenoid wing dysplasia)
  7. affected first degree relative
284
Q

what is tuberous sclerosis

A

autosomal dominant disorder

characterized by development of hamartomas of the skin, brain, eye, heart, kidneys, lungs and bone

285
Q

list the major criteria for tuberous sclerosis dx

A 
facial angiofibroma
ungual fibroma
shagreen patch
hypomelanotic macule
cortical tuber
subependymal nodule
subependymal giant cell tumour
retinal hamartoma
cardia rhambomyoma
renal angiomyolipoma
lymphangiomyomatosis
286
Q

what is ataxia telangiectasia

A

can present with dilated vessels over the conjunctiva associated with progressive ataxia and immunodeficiency

287
Q

what is ataxia telangiectasia

A
  1. ataxia
    - -begins in infancy
    - -truncal ataxia progresses to axial ataxia
  2. telangiectasias
    - -characteristically conjunctival
  3. other features
    - -immunodeficiency
    - -predisposition to malignancies
288
Q

what is incontinentia pigmenti

A

x linked disorder that affects the skin, CNS, eyes and skeletal system

affects only women

289
Q

what are the 4 distinct phases of incontinentia pigmenti

A
  1. inflammatory vesicles or bullae
  2. verrucous lesions
  3. streaks of hyperpigmentation
  4. streaks of atrophy/hypopigmentation

may have cicatricial alopecia and nail dystrophy

also dental, ocular and CNS manifestations

peripheral eosinophilia in 70% of patients

lasts 4-5 months

290
Q

what is the most common form of allergic contact to metal

A

nickel dermatitis

291
Q

where do you often see nickel dermatitis

A

subumbilical eruption; earring or other piercing

292
Q

tx of nickel dermatitis

A

contact avoidance

text solution of dimethylglyoxime in a 10% aqueous solution of ammonia

293
Q

what is eczema herpeticum

A

a severe, disseminated HSV infection that occurs in individuals with atopic dermatitis

294
Q

complications of eczema herpeticum

A

keratoconjunctivitis

sercondary bacterial superinfection

fluid loss

viremia

295
Q

how do you treat eczema herpeticum

A

recognition and systemic acyclovir

296
Q

what is pityriasis alba

A

circumscribed scaly hypopigmented lesions on the cheek associated with atopic dermatitis

asymptomatic

face, neck, upper trunk, proximal extremities

non specific dermatitis with residual post inflammatory hypopigmentation

commonly seen in atopic dermatitis patients

297
Q

what is wiskott-aldrich syndrome

A

rare x linked recessive disorder

classic features:
recurrent pyogenic lesions

bleeding from thrombocytopenia and platelet dysfunction

recalcitrant dermatitis

most patients die by 3 years of age without transplantation…low levels of IgM

298
Q

what two hormones control the release of growth hormone

A

GHRH and somatostatin

299
Q

how is GH secreted

A

in a pulsatile manner, occurring at stage 4 sleep

300
Q

where does GH act

A

growth hormone receptor and causes some direct metabolic effects as well as the transcription of the IGF1 gene

301
Q

where is IGF1 produced

A

liver and target tissues

302
Q

what is IGF1 bound to in circulation

A

IGFBP

303
Q

how does IGF1 act

A

binds to IGF receptors, activating tyrosine kinases and specific cell pathway

leads to cell growth by inducing the cell cycle machinery, inhibiting apoptosis and inducing cellular differentiation

304
Q

list the growth hormone target tissues

A 
liver
growth plate
adipose tissue
muscle
lymphocytes
gonads
305
Q

what does GH do in the muscle and liver

A

insulin antagonism

306
Q

what does GH do in adipocytes

A

lipolysis

307
Q

how does thyroid hormone affect growth

A

direct effect on epiphyseal cartilage

TH needed in order to release growth hormone from the pituitary

TH needed for POST natal growth only

308
Q

how do sex steroids affect growth

A

act by augmenting GH pulses

do not play major role prior to puberty

early exposure to sex steroids results in rapid linear growth, skeletal maturation and premature fusion of the growth plates

309
Q

define familial short stature

A

childs height falls on percentil appropriate for his mid parental height

normal growth velocity

bone age equal to the chronological age

310
Q

define constitutional growth delay

A

children have growth deceleration between 18 months and 3 years

at 3 years they grow at normal rate

puberty is delayed as is their bone age

often history of later puberty or prolonged growth in a family member

311
Q

name the common bone/cartilage disorders that affect growth

A

achondroplasia

hypochondroplasia

spondylo-epiphyseal dysplasia

312
Q

name the chromosomal disorders associated with short stature

A 
down syndrome
turner syndrome
noonan syndrome
russel silver syndrome
chromosomal deletion syndromes
313
Q

define IUGR

A

height and weight less than 2 SD for the mean for gestational age

15% of these kids fail to achieve catch up growth

normally do not have abnormalities of the growth hormone axis

314
Q

are IGF1 levels high, normal or low in malnutrition

A

low

315
Q

how does hypopituitarism present in neonates

A
  1. hypoglycemia that requires 6-8 mg/kg/min of IV glucose to maintain euglycemia
  2. micropenis with or without undescended testes
  3. liver dysfunction secondary to giant cell hepatitis
  4. temperature instability
  5. associated midline defects (i.e cleft lip palate)
316
Q

how does hypopituitarism present in childhood

A
  1. growth failure
  2. difficulty handling illnesses necessitating hospitalization for dehydration
  3. hypoglycemia
  4. polyuria and polydipsia
  5. symptoms of increased intracranial pressure if tumour is present
  6. visual disturbance
317
Q

how do you assess for possible GH deficiency

A 
stimulation tests to assess GH reserve:
hypoglycemia
arginine
glucagon
dopamine
clonidine
318
Q

how do you test ACTH reserve

A

stimulation tests:
glucagon stimulation
hypoglycemia
low dose ACTH stimulation

319
Q

how do you test TSH reserve

A

free T4 or TRH test

320
Q

how do you test ADH reserve

A

water deprivation

321
Q

what are suprasellar tumours

A

cause hypopituitarism by invading the pituitary or stalk

craniopharyngiomals, gliomas of the optic nerve or hypothalamus and germinomas are most frequently seen

322
Q

how do germ cell tumours often present

A

with diabetes insipidus in both sexes, or with precocious puberty in males

323
Q

how can a UTI present in infants

A

N/V
irritability
poor feeding
sepsis

324
Q

what bug usually causes UTI

A

ecoli

325
Q

what other bugs can cause UTI

A

KEEPPSS

klebsiella
ecoli
enterococcus
proteus
pseudomonas
strep
staph saprophyticus
326
Q

how does glomerular hematuria present

A

brown or “tea colored” urine

RBC casts, cellular casts

tubular casts

proteinuria on dipstick if no gross hematuria

dysmorphic erythrocytes

327
Q

how does non glomerular hematuria present

A

red/pink urine

blood clots

no proteinuria on dipstick if no gross hematuria

normal erythrocytes

328
Q

definition of hematuria

A

more than 5 RBC/hpf on urine microscopy

329
Q 
what are the 
1. non renal
2. lower urinary tract
3. renal, non glomerular
4. renal, gomerular
etiologies of hematuria
A
  1. non renal–fever, drugs, exercise, menses, coagulopathy
  2. lower urinary tract–infection, trauma, stones
  3. renal, non glomerular–hypercalciuria, stones, sickle cell, cysts
  4. renal, glomerular–post infectious glomerulonephritis, IgA nephropathy, HSP, HUS, SLE, familial thin basement membrane disease, alports
330
Q

define proteinuria

A

more than 100mg/m2/day

331
Q

what causes proteinuria generally

A
  1. increased glomerular permeability
  2. inadequate tubular reabsorption
  3. overflow proteinuria
332
Q

what things can cause transient proteinuria

A

fever, exercise, seizures, stress

333
Q

what things can cause glomerular proteinuria

A 
minimal change disease
FSGS
membranous 
membranoproliferative 
SLE 
drugs
diabetes
334
Q

definition of nephrotic syndrome

A

proteinuria above 50mg/kg/day

hypoalbuminemia

hyperlipidemia

edema

335
Q

list the examples of end organ damage from hypertension

A
  1. hypertensive encephalopathy
  2. cerebral infarction or hemorrhage
  3. retinal infarction or hemorrhage
  4. CHF with pulm edema
  5. acute renal failure
336
Q

renal causes of HTN

A

glomerulonephritis

renovascular

acute and chronic renal failure

fluid volume overload

337
Q

endocrine causes of HTN

A

CAH, cushings

hyperaldosteronism

pheochromocytoma

hypo/hyperthyroid

338
Q

CV causes of HTN

A

coarctation

339
Q

CNS causes of HTN

A

infections

neoplasm

340
Q

drug causes of HTN

A

steroids

stimulants

341
Q

what is acute urticaria

A

a rash that comes and goes changing almost as one watches

“hives”

often caused by a histamine release triggered by allergens like drugs, foods or pollen

can also be caused by viruses, or temperature

often dont know trigger

342
Q

what is the atopic triad

A

family history of any of all three of the following

atopic dermatitis (eczema)
asthma
allergic rhinitis (hayfever)
343
Q

what is seborrheic dermatitis

A

very common skin condition for infants

little to no harm from it and most grow out of it

in older patients is caused by fungus (malassezia)

344
Q

treatment for seborrheic dermatitis in infants

A

baby oil and small brush to remove scales

frequency (daily) shampooing with gentle baby shampoo or prescription shampoo with hetoconazole or pyrithione zinc

low potency topical steroid cream or ketoconazole cream

345
Q

what are the stages of acne

A

usually starts as comedones (open–blackheads, closed–whiteheads)

then become inflamed, which may lead to larger, erythematous lesions called papules and pustules

can continue to progress in severe cases and become nodulo-cystic acne

346
Q

list 4 acne triggers

A
  1. make up (unless noncomedogenic)
  2. mechanical factors such as manipulation
  3. occlusion (i.e with some sports gear)
  4. overzealous cleaning

?high glycemia diets and acne

347
Q

what type of hypersensitivity reaction is chronic nickel contact dermatitis

A

delayed type IV hypersensitivity

348
Q

where is the most common site for impetigo

A

right below the nates (because of rubbing and colonization) but it can be anywhere

red sores that pop easily and leave a yellow crust

349
Q

what bug causes impetigo

A

most common is staph aureus and staph pyogenes (GAS)

350
Q

tx of impetigo

A

mild, localized–> treat with topical abx like mupirocin

watch out for abscess formation from MRSA

351
Q

what genus of plant often causes acute contact dermatitis

A

toxicodendron genus–poison ivy, poison oak and poison sumac

352
Q

list 4 side effects of topical steroid use

A

skin atrophy
telangiectasias
hypopigmentation
suppression of the hypothalamic pituitary axis

353
Q

first line tx for head lice

A

1% permethrin lotion

354
Q

what causes scabies

A

mmite–>sarcoptes scabiei

355
Q

when is the most intense time of itching for scabies

A

at night

356
Q

what is the common distribution pattern for scabies

A

wrists, elbows, fingers, toes

357
Q

describe the common scabies lesion

A

5-10 mm curvilinear thread-like lesion (burrow) –infants often do not have burrows on presentation

358
Q

tx for scabies

A

two applications of permethrin 5% cream one full week apart for all affected household members

cream applied at night before bed and washed off in morning

adults apply from neck down, infants from hairline down including behind the ears

359
Q

what bug causes ringworm

A

fungus tinea corporis

360
Q

describe the classic lesion of ringworm/tinea corporis

A

annular, well circumscribed, scaly plaque with raised border and a center that is brown or hypopigmented

lesions gradually enlarge and may coalesce with surrounding lesions

may be mildly pruritic or asymptomatic

361
Q

dx of tinea corporis

A

clinical or with KOH wet mount exam of skin scrapings –> classic branches and rod-shaped septated hyphae

362
Q

what causes tinea versicolor

A

yeast form of fungus malassezia globosa and others

363
Q

what does tinea versicolor look like

A

rash of pink, brown or white lesions depending on the background color of the skin

fine scale

changes color

can be contagious –> some people are more susceptible than others

excess heat and humidity predispose to the infection

364
Q

treatment of tinea versicolor

A

selenium sulfide lotion

365
Q

tx for tinea capitis

A

griseofulvin over 6-8 week

366
Q

what should you watch out for when treating tinea capitis?

A

significant allergic reaction called KERION–inflamed, weeping, boggy lesion that often requires treatment with oral steroids

367
Q

what are the common causes of diaper rash

A
  1. irritant dermatitis
  2. diaper candidiasis
  3. bacterial infection
368
Q

what is the most common cause of diaper rash

A

irritant dermatitis –> irregular areas of erythema with skin maceration on the convex surfaces of skin

369
Q

treatment for irritant dermatitis diaper rash

A

keep diaper area clean and dry and use zinc oxide creams or ointments (barrier)

370
Q

tx for diaper candidiasis

A

nystatin

371
Q

name 3 conditions that can present as diaper rash

A
  1. seborrhea and other common inflammatory conditions
  2. zinc deficiency
  3. langerhans cell histiocytosis
372
Q

focused hx for a rash

A 
duration
rate of onset
location
associated sx
family history of similar sx
whether the patients has any allergies 
any new exposures
any previous treatments
373
Q

on what skin surfaces does eczema usually present

A

extensor surfaces

374
Q

ddx for pustular rashes

A
  1. staph folliculitis
  2. acne vulgaris
  3. hidradenitis suppurativa
  4. rosacea
  5. perioral dermatitis
375
Q

where do you often find staph folliculitis

A

below waist or in groin area

376
Q

which form of hyperbilirubinemia causes the most problems

A

unconjugated

377
Q

define kernicterus

A

pathological term used to describe staining of the basal ganglia and cranial nerve nuclei by bilirubin

also described the clinical condition that results from the toxic effects of high levels of unconjugated bilirubin

378
Q

what may happen to kids with kernicterus

A

lose suck reflex

become lethargic

develop hyperirritability and seizures

ultimately die

can also develop…
opisthotonus

rigidity

oculomotor paralysis

temors

hearing loss

ataxia

379
Q

what is opisthotonus

A

abnormal posturing that involves rigidity and severe arching of the back with the head thrown backward

assoc with kernicterus

380
Q

where does most of the bilirubin formed by the healthy newborn come from

A

75% from physiological breakdown of RBCs

hemoglobin from RBCs–> unconjugated bilirubin–> INsoluble in aqueous solutions–> binds to albumin on bloodstream

in liver–> bilirubin extracted by hepatocytes–> binds to cytosolic proteins and is then conjugated with glucoronide by uridine diphosphate glucoronyl transferase

conjugated bilirubin is soluble in aqueous solution and excreted into bile

**newborn infant lacks GI flora to metabolize bile which allows B-glucoronidase present in meconium to hydrolyze the conjugated bili back to unconjugated –> reabsorbed into blood stream –> binds to albumin (enterohepatic recirc)

381
Q

define physiologic jaundice

A

total bili below 257 in full term infants who are otherwise healthy and have no other demonstratable cause for elevated bili

*almost all newborns have hyperbili but it is benign and self limited

usually noticed on day 2 or 3–> bili levels reach peak at day 3/4

382
Q

what factors can promote increased enterohepatic circulation that results in physiologic jaundice

A
  1. increased bili production from breakdown of short lived fetal cells
  2. relative deficiency of hepatocyte proterins and UDPGT
  3. lack of intestinal flora to betabolize bile
  4. high levels of B-glucuronidase in meconium
  5. minimal oral intake in first 2-4 days of life–> low meconium excretion (especially with breastfed kids)
383
Q

what is breastfeeding jaundice

A

happens early in first week of life and occurs when milk supply is relatively or absolutely low–> limited PO intake

“lack of breast milk jaundice” / “breastfeeding assoc jaundice”

low intake–> decreased GI motility–> promotes meconium retention

B-glucuronidase in meconium deconjugates bili –> unconj bili is reabsorbed via enterohepatic recirculation

breast milk production increases eventually

384
Q

what is breast-milk jaundice

A

occurs in first 407 days but may not peak until day 10-14

NOT result of low breast milk volume

cause not completely understood–> ?B-glucuronidase present in breast milk deconjugates bili in intestinal tract

can persist for up to 12 weeks but total bili rarely concerning levels

385
Q

what are the most common DAT (antibody) positive hemolysis conditions

A

Rh incompatibility

ABO incompatibility

incompatibilities with minor blood group antigens (less common)

386
Q

when do infants get antibody negative hemolysis?

A

infants who have RBC membrane defects (spherocytosis) or RBC enzyme defects (G6PD or pyruvate kinase deficiency)

387
Q

how does non-hemolytic red cell breakdown cause jaundice

A

same way as hemolysis but not hemolysis

occurs in extensive bruising from birth trauma, large cephalohematomas or other hemorrhage, polycythemia or swallowed blood during delivery

388
Q

name metabolic errors that can cause neonatal jaundice

A
  1. Crigler-Najjar syndrome–> hyperbilirubinemia from decreased bili clearance from deficienct or absent UDPGT
  2. galactosemia
  3. hypothyroidism
389
Q

in what populations is hyperbili most ocmmon

A

asian newborns then white then black

390
Q

what other factors can contribute to hyperbili

A

prematurity
bowel obstructon
birth at high altitude

391
Q

main carb in breast milk and formula

A

lactose

392
Q

what % of calories in human milk is lipids

A

50%

393
Q

what types of protein are in breast milk

A

whey and casein

394
Q

what should you suspect in a healthy-appearing infant who develops jaundice, dark urine, and pale (acholic) stools between 3-6 weeks of age

A

biliary atresia

eval with fractionated bili (total and direct)

395
Q

tx for biliary atresia

A

surgically when caught early–> Kasai procedure (anastamosis of the intrahepatic bile ducts to a loop of intestine to allow bile to drain directly into intestine)

396
Q

normal urination on

  1. day 3
  2. day 6
A
  1. 3-4 times a day

2. 6-8 times a day

397
Q

by what day should meconium have passed

A

day 3–> stools begin to appear yellow once meconium passed

398
Q

normal stooling for day 6/7

A

3-4 stools per day tho some have more

399
Q

signs of untreated congenital hypothyroid

A 
prolonged jaundice
lethargy
large fontanelles
macroglossia
umbilical hermia
constipation
abdominal distention
severe devel delay
400
Q

what is gilbert’s syndrome and what symptom does it cause

A

reduced activity of the enzyme glucuronyltransferase

relatively common cause of harmless jaundice

401
Q

enterovirus rash description

A

erythematous and maculopapular

palms and soles

can be petechial

late summer early fall

402
Q

infectious causes of generalized LAD

A
  1. measles (marked generalized LAD and splenomegaly that may last several weeks)
  2. infectious mononucleosis–EBV or CMV
  3. HIV
  4. histoplasmosis
  5. toxoplasmosis
  6. mycobacteria (can also be localized)
403
Q

noninfectious causes of generalized LAD

A
  1. lymphomas
  2. leukemia
  3. histiocytosis
  4. metastatic neuroblastoma
  5. rhabdomyosarcoma
404
Q

what can cause unilateral cervical LAD

A
  1. kawasaki
  2. reactive node
  3. bacterial cervical adenitis
  4. cat scratch disease
  5. mycobacteria
405
Q

in what diseases do you see strawberry tongue

A

strep pharygnitis
kawasaki
toxic shock

Pediatrics 2 (19 decks)

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