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Pediatrics Clerkship > Aquifer - Cardiovascular and Hematology (Part 2) > Flashcards

Aquifer - Cardiovascular and Hematology (Part 2) Flashcards

1
Q

True or false - there is an association between iron deficiency in infancy and later cognitive defects.

A

True

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2
Q

How does ingestion of cow’s milk in young children increase the risk of iron deficiency anemia?

A 
Excessive ingestion (>24 oz/day)
Low concentration and bioavailability of iron
Risk fo occult intestinal blood loss
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3
Q

In the setting of mild anemia, what will many providers do first?

A

Trial iron rather than doing any further workup. If the Hgb recovers to the normal range, this is sufficient evidence of iron-deficiency anemia.

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4
Q

2 classification schemes for anemia?

A
  1. Size (MCV - micro/normo/macrocytic)

2. Mechanism (decreased production, increased destruction, blood loss)

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5
Q

Why is the size classification imperfect for anemia?

A

MCV values in children vary with age and certain conditions do not fit neatly into one category

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6
Q

DDx - microcytic anemia

A 
Iron deficiency
Thalassemia
Sideroblastic
Chronic inflammation/disease*
Lead poisoning*
*Can be normocytic
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7
Q

DDx - normocytic anemia

A 
Acute blood loss
Immune hemolytic anemia
Hereditary spherocytosis
G6PD deficiency
Sickle cell anemia
Renal disease
Transient erythroblastopenia of childhood (TEC)
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8
Q

DDx - macrocytic anemia

A 
Folate deficiency
B12 deficiency
Hypothyroidism
Neoplasms
Bone marrow failure syndromes (aplastic anemia, Diamond-Blackfan anemia, and congenital dyserythropoietic anemia)
Liver disease/failure*
*Can be normocytic
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9
Q

How does the reticulocyte count indicate mechanism of anemia?

A

Decreased production - low reticulocyte count
Increased destruction and blood loss - high reticulocyte count (patient is able to adequately make red cells and is trying to compensate for the anemia)

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10
Q

DDx - anemia due to decreased production

A 
Iron, folate, or B12 deficiency
Lead toxicity
Thalassemia
Aplastic anemia
Chronic inflammation
Neoplasms
TEC
DBA
Renal disease
Hypothyroidism
CDEA?
Sideroblastic anemia
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11
Q

DDx - anemia due to increased destruction

A 
Immune hemolytic disease
Hereditary spherocytosis
G6PD deficiency
Sickle cell disease
Thalassemia
DIC
Mechanical heart valves
Burns
Paroxysmal nocturanl hemoglobinuria (PNH)
Hypersplenism
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12
Q

DDx - anemia due to blood loss

A 
Acute hemorrhage
Dysfunctional uterine bleeding (heavy/prolonged menses)
Pulmonary hemosiderosis (hemorrhage)
Goodpasture's disease
GI blood loss (PUD, other GI conditions)
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13
Q

Lab findings of iron deficiency anemia?

A

Low reticulocyte count
Low iron levels
High iron-binding capacity

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14
Q

Risk factors for obesity in children?

A
  1. High birth weight
  2. Maternal diabetes
  3. Having an obese parent (strongest predictor before age 3)
  4. Low SES
  5. Certain genetic syndromes
  6. Early menarche
  7. Shorter extent/duration of breastfeeding
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15
Q

Sequelae of obesity in children?

A
  1. (Obstructive) Sleep apnea (cessation of breathing for at least 15 seconds while sleeping)
  2. Dyslipidemia
  3. Hypertension
  4. Slipped capital femoral epiphysis (SCFE) - displacement of the femoral head from the femoral neck through the physeal plate
  5. DM2
  6. Steatohepatitis
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16
Q

Characteristics of steatohepatitis in obese adolescents?

A

Mild increase in liver transaminases, hyperechoic liver on U/S, evidence of fatty infiltration and fibrosis on biopsy

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17
Q

When should an underling endocrinological disorder be suspected in the setting of weight gain in children/adolescents?

A

Endocrine diseases that cause weight gain usually limit growth and lead to short stature, whereas obesity stimulates stature growth and leads to tall stature for age. It also advances bone age and leads to early puberty.

Only 1% of overweight patients have endocrine problems.

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18
Q

Dx DM?

A

HbA1c 6.5+ % OR
Fasting plasma glucose of 126 mg/dL (no caloric intake for at least 8 hours) OR
Two-hour plasma glucose of 200+ mg/dL during an oral GTT following a load of 75 g glucose OR
Random plasma glucose of 200+ mg/dL in a patient with symptoms

(#1-3 must be repeated to confirm)

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19
Q

Compare the presentation of DM1 and DM2 in children.

A

DM2 - more indolent presentation, weight loss is less common, DKA is rare, accidental diagnosis is common

DM1 - more likely to present in early childhood, weight loss and DKA more common, rare to diagnose accidentally

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20
Q

Who should be screened for DM2 (children)?

A

Children who are overweight (BMI >85th percentile) PLUS 2 of the following:

Family history of DM2 in first or second degree relatives
Race/ethnicity
Signs of/conditions associated with insulin resistance (acanthosis nigricans, PCOS, HTN, dyslipidemia)
Maternal hx of DM or gestational DM during child’s gestation

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21
Q

Timing of screening for DM2 in children?

A

Initiate screening at 10 years of age or onset of puberty (whichever is earlier)
Screen every 3 years
Any test may be used

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22
Q

Causes of elevated BP measurements?

A
  1. White coat HTN
  2. Positioning (arm at side can elevate)
  3. Painful stimuli
  4. Cuff that is too small
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23
Q

Classification of HTN in children?

A

Normal: <90th percentile
Prehypertension: 90-95th percentile
Stage 1 HTN: 95th-99th percentile + 5 mmHg
Stage 2 HTN: >99th percentile + 5 mmHg

As with adults, adolescents with BP levels >120/80 but <95th percentile should be considered pre-hypertensive.

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24
Q

Management of prehypertension in children?

A

Therapeutic lifestyle changes
Follow-up in 6 months
No recommended diagnostic workup for a secondary cause unless there is a concern for an underlying cause in H&P or family history

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25
Q

Management of primary hypertension in children?

A

Medications (typically reserved for children with stage 2, secondary, or evidence of target-organ effects)
Dietary changes (less sweets, added sugars, fats, red meats, sodium)
Weight loss if overweight
Physical activity

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26
Q

Who should be screened for secondary HTN in children?

A

Umbilical artery or venous access during the perinatal period
UTI (renal scarring)
Catecholamine excess (pheochromocytoma or neuroblastoma)
Family hx of renal disease
Coarctation of the aorta

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27
Q

What is vasovagal syncope?

A

Fainting; caused by self-limited systemic hypotension due to altered neurocardiogenic reflexes leading to bradycardia and/or peripheral vasodilation

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28
Q

Prodromal symptoms of vasovagal syncope in chidlren?

A

Dizziness, lightheadedness, sweating, nausea, weakness, and visual changes; many children experience the prodromal symptoms without syncope

29
Q

What is syncope?

A

Transient, usually brief LOC and postural tone that results from inadequate cerebral perfusion; typically self-limited with unconsciousness for less than 1 minute, followed by gradual return of cerebral perfusino and awakening

30
Q

How should syncope be evaluated initially?

A

History (duration of symptoms, time of day, last meal, weight changes, activities leading up to the event, patient position, associated symptoms, drug history)
Physical: orthostatic BP measurement, detailed cardiac and neurological exams
EKG to rule out important arrhythmic causes of syncope such as WPW syndrome and QT syndrome

31
Q

Red flags for syncope?

A

Family history of seizures, sudden death, MI in family members <30 years of age
All syncope associated with exercise or exertion must be considered dangerous and requires a thorough cardiac evaluation
Association with chest pain or palpitations, an abnormal cardiac exam or history of cardiac diseaseFacial cyanosis, aura, frothing at the mouth, tongue biting, slow recovery, or postictal drowsiness and prolonged mental status changes or confusion after the event suggest a seizure
Syncope in the supine position, prolonged LOC (>5 minutes), convulsion before LOC, warm/flushed/cyanotic skin color rather than pallor and diaphoresis suggest a seizure

32
Q

Most common cause of sudden cardiac death in pediatric patients?

A

HCM

33
Q

EKG of a patient with HCM?

A

Left ventricular hypertrophy and/or ST/T wave changes indicative of repolarization abnormalities

Note - ~10% will have normal EKG’s

34
Q

If there are worrisome elements for HCM in the history of a pediatric patient with syncope or chest pain, what should be done?

A

Echo

35
Q

What is precordial catch syndrome?

A

Most common cause of chest pain in adolescents
Thought to be a form of MSK pain of unknown etiology
Benign condition characterized by sudden, sporadic onset of sharp pain, usually along the left sternal border, which is often exacerbated with deep inspiration
Brief, lasts seconds to a few minutes, resolves spontaneously
Pain can often be broken with a forced deep inspiration
Often not associated with exercise

36
Q

Presentation of costochondritis?

A

Benign cause of chest pain, but less common

Pain due to inflammation, lasts for hours or days

37
Q

Presentation of GI causes of chest pain (GERD, gastritis, esophagitis)?

A

Often retrosternal, burning, non-radiating, associated with meals

+medication history (non-prescription meds, OC’s, meds that cause gastric irritation)

Substance use

38
Q

DDx - Chest Pain

children and adolescents

A
  1. Cardiac cause (HCM, etc.)
  2. Precordial catch syndrome
  3. Costochondritis
  4. GI causes (GERD, gastritis, esophagitis)
  5. Asthma or exercise-induced bronchospasm
39
Q

Physical exam findings when assessing chest pain in children?

A

Vital signs
BP w/appropriately sized cuff
Palpate brachial and femoral pulses for possible coarctation
Auscultation supine and standing
Fever (infectious etiology - pericarditis, pneumonia, etc.)
Thrill, hyperdynamic precordium, murmurs
Body habitus suggesting a genetic disorder associated with cardiac disease (Marfan’s)
Chest wall inspection for signs of injury; reproducible pain implies MSK origin

40
Q

Symptoms and signs of cardiac chest pain in pediatric patients?

A 
Pain triggered by exertion or stress
Pressure or crushing sensation
10-15 minutes in length
Syncope, palpitations
Murmur, thrill, hyperdynamic precordium
41
Q

Murmurs that should be further evaluated?

A

Louder than III/VI
Diastolic
Increases with standing or Valsalva

42
Q

What is Kawasaki disease?

A

Acute inflammatory panvasculitis of unknown etiology that impacts any blood vessel, although there is a predilection for small and medium-sized vessels, especially the coronary arteries for unknown reasons

It is thought that it results from an AI response to a not-yet-identified infectious trigger

43
Q

Epidemiology of Kawasaki disease (age, timing, genetics)

A

Disease of childhood, with typical patients 15-80 months; 80% of patients with KD are under the age of 5 years

Outbreaks follow seasonal patterns

Children of Asian descent have a higher incidence

44
Q

Three distinct phases of Kawasaki disease?

A
  1. Acute phase (onset through 10 days) - fever, clinical findings, elevated APRs
  2. Subacute phase (10 days-3 weeks) - fever resolves, clinical findings largely subside often with peeling of hands and feet, elevated APRs
  3. Convalescent phase (3-6/8 weeks) - all clinical findings resolved, continued serologic evidence of inflammation
45
Q

Diagnostic criteria for Kawasaki disease?

A

High fever for at least 5 days + 4 of the following:

  1. Change in oral mucosa (i.e., strawberry tongue)
  2. Extremity changes (redness/swelling)
  3. Unilateral cervical lymphadenopathy (least likely to be present)
  4. Rash (non-specific, polymorphic)
  5. Conjunctivitis (bilateral, non-purulent)

Irritability is common
Consider other illnesses with similar features before diagnosing KD

46
Q

Lab evaluation of Kawasaki disease?

A
  1. CBC with differential (elevated WBCs, neutrophilic predominance, normochromic/normocytic anemia is common, thrombocytosis is common, usually starting in week 2)
  2. Liver enzymes (transaminases can be elevated)
  3. Serum albumin (frequently low)
  4. Acute phase reactants (ESR and CRP) - a negative ESR would argue strongly against KD; persistently elevated ESR after the fever supports KD
  5. UA - sterile pyuria secondary to sterile urethritis is associated with KD (clean-catch will show white cells, catheterized urine may not)
47
Q

Complications of KD?

A
  1. Aspetic meningitis or other CNS manifestations
  2. Coronary artery aneurysm (risk with greatest morbidity, main purpose of treatment is to minimize this risk) - all patients should receive a baseline echo during the acute phase
  3. Liver dysfunction
  4. Arthritis
  5. Hydrops of the gallbladder
48
Q

When is the greatest risk for the development of coronary artery aneurysms during KD?

A

In the subacute phase (beyond 10 days, almost always within 4 weeks of onset)

49
Q

Rx - Kawasaki Disease

A

Aspirin and IVIG (standard therapy)

High-dose aspirin for its anti-inflammatory properties (shortens the febrile course, no effect on development of aneurysms)

Low-dose aspirin following defervescence for its anti-paletlet effects - d/c after 6-8 weeks if no coronary artery changes are seen in follow-up echoes (if abnormalities - continue low-dose aspirin indefinitely)

IVIG to decrease the incidence of coronary artery aneurysm (single dose over 10-12 hours)

50
Q

Role of other antipyretics, antibiotics, and steroids in treating KD?

A

Other antipyretics are not usually effective for fever control
Ibuprofen antagonizes the irreversible platelet inhibition induced by aspirin
Antibiotics have no effect on clinical course
Role of steroids is unclear

51
Q

Follow-up care for KD?

A
  1. Cardiology follow-up visit at 1-2 weeks
  2. Aspirin: low-dose for 6-8 weeks after febrile phase, parents should watch for warning signs of GI bleeding, such as stomachache or blood in the stool
  3. Flu vaccine - children taking aspirin are at risk for Reye syndrome, a potentially fatal illness that causes multi-organ damage if infected with certain viruses, including influenza and varicella. Parents should avoid exposure to anyone with known flu or chicken pox and children should receive the IM flu vaccine.
52
Q

What does ESR measure?

A

Indirect measurement of fibrinogen elevation (levels of fibrinogen increase with inflammation) -> higher levels of fibrinogen lead to increased cohesion of erythrocytes and a faster sedimentation rate

53
Q

What does CRP measure?

A

Direct quantification of an acute phase reactant discovered in blood from patients with pneumococcal pneumonia and named because it reacted with the C-polysaccharide on the cell wall of S. pneumo

54
Q

Compare elevation time course of ESR and CRP.

A

ESR: rises comparatively slowly in response to an inflammatory stimulus and may not return to normal for weeks after clinical improvement

CRP: elevation is relatively quick, beginning at 4-6 hours after initial insult, peaking at 36-50 hours, and returning to normal within 3-7 days after the stimulus is withdrawn

55
Q

Compare the specificity of ESR and CRP.

A

ESR: not specific for inflammation, also abnormal in pregnancy and anemia; low to moderate reproducibility

CRP: more specific than ESR, high reproducibility

(Similar in cost)

56
Q

DDx - Fatigue

adolescent female

A
  1. Anemia
  2. Bleeding disorder
  3. Hypothyroidism
  4. Depression
  5. Substance abuse
57
Q

Causes of anemia leading to fatigue in an adolescent female?

A
  1. Bleeding disorder

2. Iron deficiency

58
Q

Presentation suggesting anemia due to a bleeding disorder in an adolescent female with fatigue?

A

Commonly cause menorrhagia (20% of women with heavy periods have a bleeding disorder)
Significant fatigue (rapid loss of Hgb)
Family hx of anemia
ROS negative unless there is severe systemic illness leading to DIC

59
Q

Presentation suggesting iron deficiency anemia in an adolescent female with fatigue?

A

Typically not as much fatigue (slow decline allows the body to decompensate)

60
Q

Lab tests to check for a bleeding disorder?

A 
CBC with platelets, RBC indices, and a smear, reticulocyte count
Pt/PTT
Platelet function test
Factor VIII activity
vWF antigen
Ristocetin cofactor (aka vWF activity)
61
Q

Presentation of hypothyroidism causing fatigue in adolescent female?

A

Menstrual abnormalities (menorrhagia, shorter cycles)

Constipation, weight gain, decreased appetite

Cold skin, slowness, fatigue, prefer hot weather to cold, doing poorly in school, coarse hair

[Rash on legs and edema of the feet are signs, but more often seen in adults)

62
Q

Most common hereditary bleeding disorder?

A

VW disease

63
Q

Inheritance pattern of VW disease?

A

AD w/variable penetrance (Type 1 and 2)

More rare Type 3 is AR

64
Q

Symptoms of VW disease?

A 
Ecchymoses
Epistaxis
Menorrhagia
Bleeding post-tonsillectomy and dental extractions
Gingival bleeds
65
Q

Most common type of VWD?

A

Type I (70%)

66
Q

Dx VW disease?

A

Careful clinical history is often the most sensitive indicator

Lab dx can be challenging - prolonged platelet function or bleeding time and mild prolongation of PTT point to this diagnosis, but this can be normal

To confirm, check VW factor Ag and/or platelet function analysis and factor VIII levels

67
Q

Rx - VW disease?

A

Intranasal or IV desmopressin

Sometimes can give human plasma-derived virally inactivated VWF concentrate

68
Q

Dx prediabetes?

A

Fasting blood glucose of 100-125 mg/dL OR

Hgb A1C 5.7-6.4%

Pediatrics Clerkship (14 decks)

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