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MoD-Exam 2 > 10.2 Disease of Infancy and Childhood > Flashcards

10.2 Disease of Infancy and Childhood Flashcards

1
Q

Why is Respiratory Distress Syndrome also known as hyaline membrane disease?

A. The lung parenchyma of infants with the condition resemble that of glassy collagenous hyaline

B. Hyaline proteinaceous material gets deposited on in the central air spaces of infants with the condition

C. Hyaline proteinaceous material gets deposited on in the peripheral air spaces (terminal alveoli and alveolar ducts) of infants with the condition

D. Elastase gets deposited in the peripheral airspaces of infants with the condition, that is often mistaken for hyalinization

A

C. Hyaline proteinaceous material gets deposited on in the peripheral air spaces (terminal alveoli and alveolar ducts) of infants with the condition

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2
Q

Which of the following is true in terms of the clinical findings of RDS in infants?

A. Recussitation is not needed at birth and after a few minutes breathing is normal and rhythmic, and color returns

B. 30 minutes later cyanosis is most evident even though there is no difficulty breathing

C. A few hours later cyanosis is the least evident and a chest xray reveals clear normal images

D.. 80% O2 via ventilation will usually fail to improve the situation, but if therapies stave off death for 3-4 days there is a great chance for recovery of the infant

A

D.. 80% O2 via ventilation will usually fail to improve the situation, but if therapies stave off death for 3-4 days there is a great chance for recovery of the infant

NOTE:

  • recessitation is needed at birth
  • few minutes later breathing is normal/rhythmic and no cyanosis
  • 30 minutes later there is breathing difficulty again
  • few hours later cyanosis is more evident and chest x-rays show reticulogranular densities
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3
Q

Characteristic clinical findings of infants with RDS include what 4 things excluding the timeline of presentation?

WMMC

A
  1. Preterm infant but still appropriate weight at birth
  2. Male
  3. Maternal diabetes
  4. C-section delivery
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4
Q

A few hours after delivery of an infant with RDS, chest x-rays often reveal densities of what cell type?

A. Neutrophilic densities producing ground-glass pictures

B. Granulocytes producing ground-glass pictures

C. Reticulogranular densities producing ground glass pictures

D. Basophilic densitiesproducing ground glass pictures

A

C. Reticulogranular densities producing ground glass pictures

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5
Q

Lung immaturity is the most important factor for which RDS develops. What is the RDS incidence % for infants born in the following weeks of gestation?

< 28 weeks

28-34 weeks

>34 weeks

A

< 28 weeks

60%

28-34 weeks

30%

>34 weeks

5%

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6
Q

What is the fundamental defect in infants who develop RDS?

A. Small lungs

B. Large lungs

C. Loss of alveoli

D. Surfactant deficiency

A

Surfactant deficiency

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7
Q

Which of the following components of surfactant primarily play a role in pulmonary host defense, as a component of innate immunity?

A. Lecithin (dipalmitoyl phosphatidylcholine)

B. Phosphatidyl glycerol

C. Hydrophilic glycoproteins SP-A and SP-D

D. Hydrophobic surfactant proteins SP-B and SP-C

A

C. Hydrophilic glycoproteins SP-A and SP-D

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8
Q

Which of the following components of surfactant primarily work with surfactant lipids to reduce surface tension within alveoli?

A. Lecithin (dipalmitoyl phosphatidylcholine)

B. Phosphatidyl glycerol

C. Hydrophilic glycoproteins SP-A and SP-D

D. Hydrophobic surfactant proteins SP-B and SP-C

A

D. Hydrophobic surfactant proteins SP-B and SP-C

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9
Q

True or False: The importance for surfactant protein is seen with the occurence of severe respiratory failure in infants with a congenital deficiency pf surfactant caused by mutation in SFTPB or SFTPC genes

True or False: Low levels of surfactant causes the lungs to collapse further with each successive breath, making every breath harder than the one before

A

True

True

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10
Q

Describe the pathophysiology of RDS starting with decreased alveolar surfactant and ending with the formation of hyaline membrane

A
  • Low surfactant –> increased surface tension –> stiffened lungs
  • Low perfusion and hypoventilation lead to low blood O2 and high CO2 –> acidosis and pulmonary vasoconstriction
  • Endothelial and epithelial damage cause plasma to leak –> fibrin necrotic cells rich exudate (hyaline membrane)
  • the hyaline membrane also feedsback into hypoxemia and CO2 retention as it increases the diffusion gradient
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11
Q

Upon gross examination of the lungs only lung size is considered normal, but what are 4 abnormal findings?

A

Airless

Solid

Reddish purple

Sink in water

Lungs of RDS are a solid, red-purple ship that sinks into the airless depths

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12
Q

Which of the following correctly describes the microscopic morphology seen in stillborn infants with RDS?

A. Necrotic cellular debris in terminal alveoli and alveolar ducts

B. Eosinophilic hyaline membranes that line respiratory bronchiols, ducts, and alveoli

C. Necrotic Type II alveolar cells intermixed with fibrin

D. Low to non-existant levels of neutrophils

E. None of the above

A

E. None of the above

What is described is NOT found in stillborns, but in infants that suffered from RDS post birth

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13
Q

What cell type are you most likely to see in the lungs of infants who survived past the 48 hour mark?

A. Neutrophils

B. Eosinophils

C. Macrophages

D. None of the above

A

Macrophages

  • macrophages tend to do the cleanup
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14
Q

What two substances are you most likely to see in the exudate of the infants suffering from RDS?

A. Neutrophils and Type I pneumocytes

B. Macrophages and Type I pneumocytes

C. Type I pneumocytes and Fibrin

D. Type II pneumocytes and Fibrin

A

D. Type II pneumocytes and Fibrin

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15
Q

Clinical features of RDS have since changed upon modern RDS therapies, and now include what two classic complications?

A
  1. Retinopathy of prematurity
  2. Bronchopulmonary dysplasia
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16
Q

Retinopathy of prematurity aka Retrolental Fibroplasia, is due to affects that arise during the hyperoxic phase 1 of therapy, followed by relatively hypoxic phase 2 of RDS therapy. Decreased levels of which of the following factors contributes to this retina pathology?

A. TNF and IL-1B

B. IL-6 and VEGF

C. VEGF

D. TGF-B

A

C. VEGF

17
Q

Bronchopulmonary dysplasia is believed to be implicated by an increase in pro-inflammatory cytokines like (TNF, IL-8, IL-6, IL-1B), which all contribute to dysplasia by which of the following mechanisms?

A. Promoting irreversible hyperactivity in the saccular stage of alveolar development

B. Promoting irreversible impairment of the saccular stage of alveolar development

C. Promoting reversible impairment of the “spectacular stage” of alveolar development

D. Promoting reversible impairment of the “saccular stage” of alveolar development

A

D. Promoting reversible impairment of the “saccular stage” of alveolar development

This impairment is why we see decreased alveolar seperation and dysmorphic capillary configuration

18
Q

Which of the following is true of the pathogenesis of necrotizing enterocolitis?

A. Unknown but likely multifactorial

B. Unknown but likely genetic

C. Unknown but likely environemental

D. None of the above

A

A. Unknown but likely multifactorial

19
Q

An male infant is brought in by there parents who are concerned with a recent onset of bloody stools. They are worried, as they know their child is at risk for a great number of clinical issues as he was born preterm. You note the infant’s abdomen is distended, and radiographs indicate gas within the intestinal wall (pneumostosis intestinalis). With the information you are able to diagnose the child with Necotizing Enterocolitis. Though not much is known of the pathogenesis of this disease, which of the following explanations would you be able to provide to the parents?

A. PAF is most likely implicated as it promotes enterocyte apoptosis and compormises tight junctions causing increased mucosa permeability

B. Decreased levels of TNF are most likely implicated as it promotes enterocyte apoptosis and compormises tight junctions causing increased mucosa permeability

C. The breakdown of the functionality of the mucosal barrier is probably what allowed migration of gut bacteria across the lumen leading to a cycle of inflammation and necrosis that is killing the enterocytes

D. A and B

E. B and C

F. A and C

G. All of the above are correct

A

A and C

A. PAF is most likely implicated as it promotes enterocyte apoptosis and compormises tight junctions causing increased mucosa permeability

C. The breakdown of the functionality of the mucosal barrier is probably what allowed migration of gut bacteria across the lumen leading to a cycle of inflammation and necrosis that is killing the enterocytes

20
Q

BElow is a depiction of necrotizing enterocolitis, where we are often able to grossly see distended, thin, congested and possibly gangrenous segments. While any segment can be affected, we most often see this in what 3 locations?

A

Terminal Ileum

Cecum

Right Colon

Ce**line thinks **TI** is al**Right

21
Q

Microsopic morphologies associated with Necrotizing Enterocolitis include ulceration, bacterial colonization, gas bubbles in the submucosa, and what type of necrosis in the mucosa or transmural surface?

A. Casceous necrosis

B. Fatty necrosis

C. Coagulative necrosis

D. Fibroi

A

C. Coagulative necrosis

below is a depiction of a kidney and relative histogram

22
Q

In general perinatal infections are acquired through 2 main routes. What are the 2 main routes?

A. AScending infections and Transcervical infections

B. HEmatologic infections and Transplacental infections

C. Hematologic and Ascending infections

D. TRanscervical Infections and Transplacental Infections

E. C and D are correct

A

C and D are correct

C. Hematologic and Ascending infections

D. TRanscervical Infections and Transplacental Infections

NOTE:

  • Transcervical = Ascending*
  • Transplacental = Hematologic*
23
Q

What is the name of the fetal accumulation of edema fluid during intrauterine growth?

A

Fetal Hydrops

24
Q

What is immune hydrops?

What are the major antigens that are known to induce clinical issues seen with immune hydrops?

A

Immune hydorops is a hemolytic disease where there is incompatibility of blood Ags between mom and baby

Rh Ags

ABO blood groups

25
Q

Which of the following leads to hydrops seen in immune hydrops?

A. Anemia that leads to extramedullary hematopoeisis

B. Anemia that leads to cardiac decompensation

C. Hemoglobin degredation that leads to increased bilirubin

D. Rh+ mother with an Rh+ fetus

A

B. Anemia that leads to cardiac decompensation

26
Q

In which of the following scenarios is the mother most likely to become immunized against Rh+ Ags?

A. Mother is Rh+ and is having a second pregnancy

B. ABO incompatibility between mother and fetus with A-Ag and B-Ag

C. Administration of RhIg with anti-D Abs administered to mother at 28 weeks and again within 72 hours of delivery

D. Rh- Mother experienced a transplancental bleed of > 1mL of Rh positive fetal RBCs during first child birth

A

D. Rh- Mother experienced a transplancental bleed of > 1mL of Rh positive fetal RBCs during first child birth

27
Q

What antigen is the major cause of Rh incompatibility?

A

D-Ag

28
Q

Which of the following has the best explanation of why most ABO hemolytic disease occurs if the mother is O and infants are A or B?

A. The A or B mother are unable to make IgM antibodies against their A or B infants

B. A or B group mothers care more about their babies

C. O group mothers are able to make IgG anti-A/B antibodies even without prior sensitization

D. O group mothers already have anti IgM anti-A/B antibodies, so first exposure the IgM is able to cross the placenta and wreck havoc

A

C. O group mothers are able to make IgG anti-A/B antibodies even without prior sensitization

29
Q

Explain how the anemia which results from excessive RBC destruction in neonates, leads to the edema we see in fetal hydrops

A

Progressive anemia leads to hypoxia of the liver and heart. THe hypoxic liver decreases protein synthesis, and the hypoxic heart undergoes cardiac decompensation; both result in decrease in oncotic pressure and increased hydrostatic pressure respectively, and edema is the result

30
Q

There are 3 major causes of nonimmune hydrops which include ______, ______, _______

A

Cardiovascular Defects

Chromosomal Anomalies

Fetal Anemia

31
Q

Which of the following is most likely indicated by the picture below?

A. Parvovirus B19 destruction of normoblasts which will lead to immune hydrops

B. Parvovirus B19 destruction of normoblasts which will lead to nonimmune hydrops

C. Erythropoetic cells of people with Turners syndrome, Downs syndrome, or Edwards syndrome

D. All of the above

A

B. Parvovirus B19 destruction of normoblasts which will lead to nonimmune hydrops

32
Q

What are main contributers to the cardiovascular defects which cause nonimmune hydrops?

What are main chromosomal anomalies which cause nonimmune hydrops?

A

Congenital Malformations and Arrhythmias

Turners (45XO), Trisomy 21 (Downs), Trisomy 18 (Edwards)

33
Q

Below is a depiction of cystic hygromas which is an accumulation of postnuchal fluid in the neck from lymphatic drainage. This finding is associated with nonimmune hydrops most often seen in those with…?

A. Congenital malformation of the heart or arrythmias

B. 45 XO (Turners)

C. Trisomy 21 (Downs) and/or Trisomy 18 (Edwards)

D. Fetal Anemia

A

45 XO (Turners)

NOTE: development of nonimmune hydrops in Trisomy 21 or 18 is usually due to heart defects associated with those disorders

34
Q

Below is a depiction of the most serious threat in fetal hydrops, what is it?

At what bilirubin blood level will it absolutely occur?

A

Kernicterus

bilirubin blood level > 20 mg/dL

NOTE: The brain will often be large and swollen, and a yellow color can be seen in the basal ganglia, thalamus, cerebellum, cerebral grey matter, and spinal cord

35
Q

Below is a picture depicting erythroblastosis fetalis that is often seen in hydrops associated with fetal anemia. Which of the following best explains when this occurs?

A. Parvovirus B19 destruction of erythroblast precursors increases the hematopoesis in the liver and spleen

B. Compensatory hyperplasia in the bone marrow is the only contributer to this

C. Extramedullary hematopoesis occuring in the liver, spleen, lymph nodes, kidneys, lungs, and heart

D. None of the above

A

C. Extramedullary hematopoesis occuring in the liver, spleen, lymph nodes, kidneys, lungs, and heart

NOTE: the picture is highlighting whats occuring in the liver

36
Q

Hydrops associated with fetal anemia the fetus and placenta are often described as…?

A. Eosinophilic

B. Edematic and swollen

C. Pale

D. Hypoplastic

A

Pale

37
Q

Which of the following is the most appropriate therapy for gravely ill infants with nonimmune hydrops?

A. Phototherapy only

B. Total transfusion and phototherapy

C. Partial Transfusion

D. Partial Transfusion and phototherapy

A

B. Total transfusion and phototherapy

38
Q

Which of the following are common clinical features seen in infants who are even minimally affected by nonimmune hydrops?

A. Generalized edema, intense jaundice, hepatosplenomegally

B. Pallor and hepatosplenomegaly

C. Signs of CNS injury

D. Generalized edema, signs of CNS injury, and intense jaundice

A

B. Pallor and hepatosplenomegaly

NOTE: Option D is usually seen in gravely ill infants

MoD-Exam 2 (11 decks)

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