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HD2 > HD2 Revision5 > Flashcards

HD2 Revision5 Flashcards

1
Q

What is normal weight range of baby? [1]

What is LBW range? [1]
What is VLBW? [1]
What is Exremely Low? [1]

A

Low birth weight (LBW) = 2,499g or less regardless of gestational age

Sub-category very low birth weight (VLBW) = less than 1,500g

Sub-category extremely low birth weight (ELBW) less than 1,000g

Normal weight at term 2,500-4,200g

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2
Q

What defines a baby as having Intrauterine growth restriction (IUGR)? [3]

A

Fetus with birth weight less than 10th percentile of those born at same gestational age

Two standard deviations below population mean are considered growth restricted

IUGR should strictly refer to fetus that is small for gestational age and that displays other signs of chronic hypoxia or failure to thrive

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3
Q

Growth rate of normal fetus: Weight gain is:
[] per day at 14-15 weeks of gestation
[] per day at 20 weeks
[] per day at 32-34 weeks
Then growth rate decrease

A

Weight gain
5g per day at 14-15 weeks of gestation
10g per day at 20 weeks
30-35g per day at 32-34 weeks
Then growth rate decrease

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4
Q

Which maternal mesaurement (height) height approx increases at 1cm per week between 14 and 32 weeks? [1]

How does abdominal girth change after 30 weeks, per week? [1]

A

Symphysiofundal height increases approx 1cm per week between 14 and 32 weeks

BUT if have polyhydramnios then this would cause inaccurate readings

After 30 weeks - increases by 2.5 cm per week

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5
Q

Explain the pathology behind Type 1 IUGR:

  • Is it caused by problem with mother or fetus? [1]
  • Is it symmetrical or asymmetrical? [1]
  • Between which weeks during pregnancy does it normally occur? [1]
A

Type 1 IUGR:

  • Problem with fetus growth during week 4-20 (when most of mitosis is occuring)
  • Everything is symmetrical / normal ration: but all parameters are below 10th percentile for gestational age
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6
Q

What are causes of type 1 IUGR? [4]

A

Etiology:
* Genetic: associated with trisomy 21, 18 and 13
* Infection (intrinsic to fetus; CMV)
* Multiple gestation
* Environmental toxins: fetal alcohol syndrome

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7
Q
  • Explain pathophysiology of Type 2 IUGR [1] Which maternal pathologies is it associated with? [3]
  • When does in pregnancy does it usually occur? [1]
  • How do neonates appear? [1]
  • WHat do neonates have reduced growth in? [2]
A
  • Caused by uteroplacental insufficiency: uterus not providing enough nutrition for fetus. Associated with: maternal HTN / pre-eclampsia; renal disease; vasculapathies
  • Growth restriction begins after week 28 in stage of hypertrophy : Fetus has near normal cell number but size reduced
  • Asymmetry seen: head sized normal, but redistribution of fetal CO causes reduced abdomen and splachnic growth, whilst brain is spared.
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8
Q

Mothers more at risk of giving birth to a IUGR baby have what wrong with them? [5]

A

Poor maternal nutrition: Low BMI at conception; Poor maternal weight gain during pregnancy

Pre-eclampsia

Renal disorders

Diseases causing vascular insufficiency

Infections (TORCH)

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9
Q

What measurement would use clinically to diagnosis IUGR? [1]

What is normal growth of ^? [1]
What would indicate IUGR? [1]
What would indicate severe IGR? [1]

A

Symphysio-fundal height:

  • Lag in fundal height of 4 weeks suggestive of IUGR
  • Lag of >6 weeks is suggestive of severe IUGR
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10
Q

Using a ultrasound to diagnose IUGR, what would you investigate? [3]

A

Head circumference
Abdominal circumference (AC) - AC highest sensitivity and greatest predictive value for diagnosis of IUGR
Amntiotic fluid volume

Can assess if type 1 or 2 by assessing differences in head vs abdomen

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11
Q

Fundal height is a measure between which two points? [2]

A

Fundal height: Pubic symphysis to top of where can palpate uterus / fundus Exam Q!

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12
Q

Explain the pathology that associated with lungs with pre-term birth? [5]

A

Respiratory distress syndrome

Hyaline membrane (fibrotic tissue) develops

Surfactant deficiency

Type II pneumonocytes

Results in decreased lung compliance, unstable alveoli

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13
Q

What are the 3 overiding factors that caues IUGR? [3]

A

Maternal factors (age / nutrition / stress / genotype / previous IUGR / HTN / substance abuse)

Placental and cord abnormalities (placental insuffiency - reduced AA transport, O2 delivery /; placental tumour / single umbilical artery / incorrect cord insertion)

Foetal factors (Congential heart disease / downs, turners, pataus syndrome)

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14
Q

How would you detect infection in placenta histologically? [1]

A

Presence of lymphocytes or plasma cells

Mother should be transferring antibodies, not lymphocytes into the placenta

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15
Q

What type of histocytes normally prevent vertical transmission of disease? [1]

A

Macrophages (histocytes) called Hofbauer cells prevent vertical transmission. Shouldn’t be found in choroinic villi

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16
Q

What complications of IUGR would you expect in antepartum period? [2]

A
  • Increased incidence of still births (52% of unexplained still births – die in utero)
  • Oligohydramnios (esp. type 2 - kidneys haven’t formed properly)
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17
Q

What complications of IUGR would you expect in intrapartum period? [2]

A

Higher incidence of meconium aspiration:: Fetal distress

Intrapartum fetal death

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18
Q

What complications of IUGR would you expect in neonatal period? [5]

A
  • Increased incidence of hypoxic ischemic encephalopathy: heart not developed so o2 to brain is insufficient
  • Persistent fetal circulation insufficiency (patent ductus arteriosus - all O2 blood is mixed with deO2 - leads to hypoxia)
  • Difficulty in temperature regulation: Absent brown fat and small body mass to surface area in type 2
  • Poor glycogen stores may predispose to hypoglycemia
  • Chronic intrauterine hypoxia lead to polycythemia, necrotizing enterocolitis, other metabolic abnormalities
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19
Q

What pathology is 4-6 x higher of occuring in childhood because of IUGR? [1]

A

Cerebral palsy

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20
Q

Which mothers at more risk of givng birth of IUGR babies? [5]

A
  • Poor maternal nutrition (low BMI at conception; underweight / overweight)
  • Pre-eclampsia
  • Renal problem
  • Vascular insufficiency
  • TORCH infections
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21
Q

For Type 1 & Type 2 IUGR, state if:

Cell number: Normal or Reduced? [2]
Cell size: Normal or Reduced? [2]

A

Type 1 IUGR:
* Cell number: reduced
* Cell size: normal

Type 2 IUGR:
* Cell number: normal
* Cell size: reduced

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22
Q

Which type of IUGR does this baby display? [1]

A

asymmetrical IUGR

Note loss of fat whole over the body, visible rib cage, excessive skin fold whole over the body and relatively large heads compared with rest of the body.

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23
Q

How would IUGR impact umblical and middle cerebral artery flow (especially type 2) [1]

A
  • Normal: no diastolic backflow (means that there is blood flow through all points of cardiac cycle)
  • IUGR (esp. type 2): umbilical flow restricted so that more blood is directed to brain. Vasodilation of the cerebral circulation causes brain sparing effect
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24
Q

What is normal v abnormal cerebral: placenta ratio? [2]

What does this indicate? [1]

A

cerebroplacental ratio: >1:1 is normal and <1:1 is abnormal
<1 = abnormal

Indicates more flow to cerebral atery than placenta (and therefore brain sparing)

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25
Q

in the normal situation the fetal MCA has a [high / low] resistance flow which means there is minimal antegrade flow in fetal diastole

in pathological states this can turn into a [high / low] resistance flow mainly as a result of the fetal head sparing theory

A

in the normal situation the fetal MCA has a high resistance flow which means there is minimal antegrade flow in fetal diastole

in pathological states this can turn into a low resistance flow mainly as a result of the fetal head sparing theory

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26
Q

Explain how you manage IUGR [5]

  • Maternal oxygen therapy? [1]
  • Bed rest position? [1]
  • Drugs? [1]
A

Identify etiology of IUGR then treatment of underlying cause:

Stop smoking, alcohol, protein energy supplementation, hypertension

Bed rest in left lateral position increases uteroplacental blood flow

Maternal oxygen therapy
55% O2 at 8L/min round the clock decreases perinatal mortality rate

No pharmacological therapy which can reverse IUGR
Delivery

Risk of prematurity versus risk of intrauterine death has to be judged

Antenatal steroids reduces incidence of respiratory distress syndrome, intraventricular hemorrhage and death for fetus of <1500g

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27
Q

Adequate vitamin D reduces which pathologies? [3]

A

Adequate vitamin D reduces:
- sepsis
- ROP
- delayed retinal maturation

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28
Q

Describe the pathology of Intraventricular hemorrhage / periventricular leukomalacia:

What birth weight babies most likely? [1]
What is pathophysiology? [1]
Which disease is a risk factor for this? [1]

A

Intraventricular hemorrhage / periventricular leukomalacia:

  • VLBW (less than 1500g) at greatest risk
  • Resp. distress syndrome 4x more likely
  • Pathology: blood vessels in the preterm may be more fragile and immature and cause small to large bleeds in brain ventricles
29
Q

What does Intraventricular hemorrhage / periventricular leukomalacia look like on ultrasound? [1]

A

Honeycombed

30
Q

Describe physiology of retinal blood vessels in normal fetus:

  • when does it normally start & complete by? [2]
  • Which directions do the retinal blood vessels grow? [1]
  • What condition within the eye controls normal retinal development? [1]
A

Retinal blood vessel development starts at around 16 weeks and is complete by 37 – 40 weeks gestation.

The blood vessels grow from the middle of the retina to the outer area.

This vessel formation is stimulated byhypoxiawhich is a normal condition in the retina during pregnancy

31
Q

Explain pathology behind retinopathy of prematurity

A

Normal conditions: vessel formation is stimulated byhypoxiawhich is a normal condition in the retina during pregnancy

Pre-term baby causes exposure to higher oxygen concentrations, particularly with supplementary oxygen during medical care, the stimulant for normal blood vessel development is removed

When the hypoxic environment recurs, the retina responds by producing excessive blood vessels (neovascularisation), as well as scar tissue.

These abnormal blood vessels mayregressand leave the retina without a blood supply. The scar tissue may causeretinal detachment

32
Q

What specific nutritional support do you give pre-term babies? [3]

A

Decreased activity compared to normal weight babies may decrease energy requirements.

Need lots of protein and calcium and phosphorous to build skeletons and muscles

33
Q

Which nutritional things would you screen for in pre-term babies? [2]

A

Hyperglycemia (poorly developed pancreas; immature insulin secretion)

Osteopenia (limited Ca & P in parentral nutrition)

34
Q

Explain pathophysiology of necrotising enterocolitis [2]

How serious? [1]

A

Part of the bowel becomes necrotic due to bacterial invasion of ischaemic bowell wall:

Causes large amount of gas in bowel: can cause perforation of bowel: leads to peritonitis & sepsis

It is a life threatening emergency

35
Q

Name a risk factor for necrotising enterocolitis? [1]

A

More common in babies fed cow’s milk formula

36
Q

Treatment of necrotising enterocolitis? [3]

A
  • Stop oral feeding
  • Broad spectrum antibiotics covering both aerobic and anaerobic species
  • Surgery to remove perforated sections
37
Q

Why do pre-term babies have increased fluid loss? [2]

What is important to consider when rehydrating? [1]

A

Have not developed skin with less keratin – so get more loss of water from skin. Easy to become dehydrated AND increased body surface to body mass ratio increases fluid loss

BUT don’t want to give too much water and disrupt electrolyte balance (can cause congestive heart failure, necrotising enterocolitis and mortality)

38
Q

Label A-D of this Doppler ultrasound of an artery [4]

A

A: Systole
B: Average
C: Diastole
D: Diastolic notch

39
Q

Compare the flow between A & C of this doppler ultrasound.

A

A: showing normal flow

C: severely reduced flow with severe notch (see arrows).

40
Q

What does the pulsatility index (PI) of doppler ultrasound show [1] and measure? [1]

How does the PI differ between the MCA and umbilical artery in a normal & IUGR fetus? [2]

A

Pulsatility Index (PI):
* the difference between the peak systolic flow and minimum diastolic flow velocity, divided by the mean velocity recorded throughout the cardiac cycle.
* It is a non-invasive method of assessing vascular resistance with the use of Doppler ultrasonography.

Healthy fetus:
* PI of MCA greater than umbilical artery
* Creates ratio >1

IUGR:
* PI of MCA less than umbilical artery

41
Q

What does prescence of uterine artery notch after 22 weeks indicate? [1]

A

The presence of a notch after 22 weeks indicates increased uterine vascular resistance and warrants monitoring of the patient.

42
Q

How does the A-wave in a ductus venosus doppler ultrasound present in a normal and IUGR fetus? [2]

A

Normally ductus venosus shows positive A wave.

Reversal of the A wave may be seen in severe intrauterine growth restriction as well as in tricuspid regurgitation.

43
Q

What is the definiton of miscarriage? [1]

What is the definiton of stillbirth? [1]

What is early and late neonatal death? [2]

What is infant death? [1]

A

Miscarriage: pregnancy loss <24 weeks

Stillbirth: baby born >24 weeks with no signs of life

Neonatal death: baby born live but dies in first 28 days of life
- Early neonatal: 0-7 days death
- Late neonatal: 7-28 days death

Infant death: anytime in first year

44
Q

What are biggest global causes of neonate death? [3]

What are biggest global causes of stillbirths? [3]

A

Neonates:
* Preterm
* Infections
* Birth complications (e.g. birth ashpyxia /

Still births:
* Malaria
* syphilis
* Diabetes & obesity

45
Q

What are steps for a perinatal post mortem exam? [6]

A
  • Clinical history and circumstance of death
  • Radiology (XR)
  • Check identification
  • Body weight and measurements (IUGR)
  • External signs of injury (skin lacerations / bruises / torn frenula / perineum and anus)
  • External signs of disease (Dysmorphism and deformities rashes / oedema / jaundice)
46
Q

Which ancillary investigations would you conduct in a post-mortem exam? [4]

A

Bacteriology

Virology

Toxicology

Metabolic and genetic studies

47
Q

Ancillary investigations: which metabolic and genetic studies would you conduct if perinatal death has occured [4]

A

Vitreous humor (slow turn over – so stores problems)

Guthrie card: blood and bile spots

Skin for fibroblast culture

Frozen tissue: muscle, heart, liver, kidney for oil-red-O, to assess for abnormal fat accumulation

48
Q

What internal examinations would you conduct in post-moretm?

A

Sampling: blood, fluids, tissue samples,

  • Organ examination (weigh & exam); tissues samples from all organs
  • Open skull: remove and weigh the brain (fix in formalin for 1-2 weeks prior to dissection & sampling)
49
Q

How does respiratory syncytial virus cause infant death? [1]

How does this appear histologically? [2]

A

RSV accounts for many cases of pneumonia in children under 2

Histologically:
* giant cells / macrophages with intracytoplasmic inclusion
* massive infiltrate of lymphoid cells in walls of bronchi causing obstruction

50
Q

Which viruses is hand, foot and mouth disease commonly caused by? [3]

Describe pathology

A

Enterovirus 71 Virus
Coxsackie virus
Kawasaki virus

Causes neurological or cardiac complications including death

Kawasaki disease causes medium vessel vasculitis of children that can cause coronary artery aneursym

51
Q

Explain pathophysiology of Marfans syndrome causing sudden death (include gene mutation) [2]

A

Lack of Fibrillin covering elastin due to mutation in FBN1 gene.

Can cause aortic aneurysm which burst

52
Q

What is definiton of SIDs? [1]

A

Sudden unexpected death of an infant under 12 months of age. Death reamins unexplained after a thorough post-mortem examination

53
Q

Non-specific post mortem findings in SIDS? [8]

A
  • Thymus with petechiae (round spots that appear on the skin as a result of bleeding)
  • Petechiae in pleura
  • Epicardial petechiae
  • Full expansion of lungs
  • Liquid heart blood
  • Empty bladder
  • Prominent lymph nodes & Peyer’s patches
54
Q

What mechanism continues within the liver in SIDs children? [1]

A

Persistent haemopoiesis in the liver

55
Q

Lung changes in SIDs? [2]

A

Oedema / hemorrhaging

56
Q

Explain pathology behind shaken baby syndrome (caused by a triad off..) [3]

A

Caused by
* sub-dural hematoma - most common
* encephalopathy;
* retinal haemorrhages

57
Q

Which pathologies may cause fractures in newborns? [5]

A
  • Sometimes seen in vaginal delivery
  • Osteopenia of prematurity (neonatal ricket)
  • Vitamin D deficiency especially in breast fed babies
  • Osteogenesis imperfecta (brittle bone disease)
  • Resuscitation
58
Q

Explain the brain anomalies that are common in SIDs pathology

A
  • Alterations (decreases) in serotonin signalling
  • causes disturbances in medulla and ANS:
  • leads to underdevelopment of arctuate nucleus which controls neuroendrocine & physiological functions
  • Platelets carry around serotonin. More serotonin in platelets increases the stickiness.
59
Q

Explain subset of SIDS infants related to serum platelet anomolies

A

Subset of SIDS infants have elevated serum serotonin platelets carry >98% of 5HT in blood:

Causes constriction of damaged blood vessels and enhances platelet aggregation

60
Q

Which causative agent most likely caused this pneumonia? [1]

Cytomegalovirus
Parainfluenza virus
Respiratory syncytial virus
Adenovirus

A

Which causative agent most likely caused this pneumonia? [1]

Cytomegalovirus
Parainfluenza virus
Respiratory syncytial virus - Multinucleated giant cells can be seen within the bronchial epithelium and neighboring alveoli.
Adenovirus

61
Q

What type of virus caused this lung infection? [1]

A

RSV

. Multinucleated giant cell (MNGC) of respiratory syncytial virus infection
demonstrating a large intracytoplasmic inclusion (arrow); (H&E, 1000 ). MNGCs
are more commonly seen within alveoli than within bronchioles.

62
Q

What is the most common bacterial [1] and viral [1] cause of pneumonia in neonates? [2]

A

Respiratory syncytial virus (RSV)
streptococcus pneumoniae

63
Q

What is the causative agent of this CSF infection? [1]

A

Group B streptococcus

64
Q

What is the most likely cause of this neonatal pathology? [1]

A

Osteogenesis imperfecta

65
Q

A child presents to A&E and becomes siginifcantly unwell and dies. The biopsy reveals viral antigens.

What is the most likely cause of their death? [1]

A histological biopsy from their lung is shown below.

A

RSV - most likely cause of viral pneumonia in neonates

66
Q

Which SIDS pathology is depicted in this histopathological slide? [1]

A

Persistent haemopoiesis in the liver

67
Q

What is likely to be the cause of death from this infant? [1]

A

Unknown - lung petechiae are suggestive of SIDS

68
Q

What should normal symphysio-fundal height correspond to? [1]

A

In a normally growing fetus, the SFH measurement in centimetres it taken as corresponding to the gestation in weeks

69
Q

IUGR is associated with which congenital heart defect in neonates? [1]

A

Patent ductus ateriosus - causes hypoxia

HD2 (55 decks)

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