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FINALS > Neonatology > Flashcards

Neonatology Flashcards

1
Q

<p>what are causes of a prem baby</p>

A

<p>idiopathic</p>

<p>infections</p>

<p>iugr</p>

<p>congenital abnormalities</p>

<p>preeclampisa</p>

<p>interuterine bleed</p>

<p>cervicle weakness</p>

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2
Q

<p>what is the management of an at risk prem baby</p>

A

<p>antenatal corticosteroids (reduces risk of prem ROM)</p>

<p>glucocorticoids (reduce rds risk)</p>

<p>antibiotics</p>

<p>tocolysis (suppress prem labour)</p>

<p>magnesium sulphate (reduce CP risk)</p>

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3
Q

<p>what are complications of prematurity</p>

A

<p>RDS</p>

<p>pneumothorax</p>

<p>PDA</p>

<p>necrotising enterocolitis</p>

<p>retinopathy</p>

<p>bronchopulmonary displasia</p>

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4
Q

<p>how do you staibalise a prem baby</p>

A

<p>resp breaths</p>

<p>incubator</p>

<p>O2 on high flow nasal cannula/CAPAP</p>

<p>periferal and umbillical lines</p>

<p></p>

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5
Q

<p>what is gestational diabetes</p>

A

<p>previous non diabetic developing high blood sugars during pregnancy</p>

<p>due to carbohydrate intolerance and insulin resistant state of pregnancy</p>

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6
Q

<p>what are the RF for gestational diabetes</p>

A

<p>PCOS</p>

<p>pre diabtes</p>

<p>increased maternal and paternal age</p>

<p>overweight</p>

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7
Q

<p>how do you chech for gestational diabetes in pregnancy</p>

A

<p>glucose tolerence test at 28 weks in high risk women</p>

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8
Q

<p>describe the glucose tolerence test</p>

A

<p>nin fasting + 50g glucose load</p>

<p>testes one hour later</p>

<p>2 or more abnormal tests = diabetes</p>

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9
Q

<p>what is the management of gestational diabetes</p>

A

<p>insulin = aim to prevent fetal macrosomia</p>

<p>c section if macrosomia</p>

<p>GTT 6 weeks post partum</p>

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10
Q

<p>what complications does maternal hyperthyroidism pose to baby</p>

A

<p>prem</p>

<p>iugr</p>

<p>higher risk of perinatal mortality</p>

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11
Q

<p>what are maternal complications of hyperthyroidism</p>

A

<p>infertility</p>

<p>miscarrige</p>

<p>cardiac failure</p>

<p>thyroid storm</p>

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12
Q

<p>how do you manage maternal hyperthyroidism</p>

A

<p>propythiouracil (better than carbimazole in pregnancy)</p>

<p>regular fetal US to chech tachycardia (thyroid dysfunction) after 32 weeks</p>

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13
Q

<p>what features of pregestational diabetes would indicate a poor prognosis</p>

A

<p>uncontrolled diabetes</p>

<p>DKA</p>

<p>Pyleonephritis</p>

<p>vasculopathy</p>

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14
Q

<p>what is the management of poorly controlled pre diabetes</p>

A

<p>good control prior to conception</p>

<p>check HBA1C</p>

<p>in labour: IV glucose and 1-2hrly BMs</p>

<p>insulin</p>

<p>metformin</p>

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15
Q

<p>what fetal complications may arise due to pregestational diabetes</p>

A

<p>congenital malformations (like CHD)</p>

<p>iugr</p>

<p>macrosomia</p>

<p>birth asphixia</p>

<p>shoulder dystocia</p>

<p>nerve paulseys</p>

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16
Q

<p>what is the presentation of fetal hypoglycaemia</p>

A

<p>sweating</p>

<p>irritability (due to abdo pain)</p>

<p>pallor</p>

<p>hunger</p>

<p>lethargy</p>

<p>seizures</p>

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17
Q

<p>why is fetal hypoglycemiacommon in first day of life</p>

A

<p>fetal hyperinsulinism</p>

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18
Q

<p>what are RF for fetalhypoglycemia</p>

A

<p>IUGR</p>

<p>prem</p>

<p>T1+2DM maternal</p>

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19
Q

<p>why do prem babys have higer risk of becominghypoglycemic</p>

A

<p>low / no glycogen stores</p>

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20
Q

<p>why do babys with DM T1+2 have higher risk ofhypoglycemia</p>

A

<p>due to hyperplasia of islat cells causing hyperinsulinism</p>

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21
Q

<p>how do you diagnosehypoglycemia</p>

A

<p>x2 low readings</p>

<p>or</p>

<p>x1 very low reading</p>

<p>or symptomatic</p>

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22
Q

<p>how do you treat fetalhypoglycemia</p>

A

<p>iv glucose + glucagon/hydrocortisone</p>

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23
Q

<p>how do you treat an a granuloma (umbilical )</p>

A

<p>silver nitrate topical</p>

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24
Q

<p>what cab GBS cause</p>

A

<p>early or late sepsis</p>

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25
Q

<p>describe the early presentation of sepsis</p>

A

<p>RDS</p>

<p>pneumonia</p>

<p>septicemia</p>

<p>meningitis</p>

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26
Q

<p>describe the presentationof late onset sepsis</p>

A

<p>meningitis: irritability, neck stiffess, unlwell</p>

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27
Q

<p>when does late onset sepsis occur</p>

A

<p>7days-3months post delivery</p>

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28
Q

<p>how does late onset sepsis occur</p>

A

<p>BS carried on skin or mucosa</p>

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29
Q

<p>what are RF for sepsis</p>

A

<p>prolonged ROM</p>

<p>maternal fever</p>

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30
Q

<p>when do you check for GBS</p>

A

<p>35-38w</p>

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31
Q

<p>a pregnant lady is positive for GBS at 35w what is her management</p>

A

<p>proflactic intrapartum abx</p>

<ul> <li>penicillin</li> <li>vancomycin</li></ul>

<p>and give same ABx to child within 2-4h of birth</p>

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32
Q

<p>what is RDS</p>

A

<p>surfactant deficiency causes a decrease in surface tension causing alveolar collapse and inadequate gas exchange</p>

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33
Q

<p>what is surfactant</p>

A

<p>phospholipids and protein excreted by T2 pneumocytes</p>

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34
Q

<p>what are the RF for RDS</p>

A

<p>prem <28weeks</p>

<p>male has worse severity</p>

<p>maternal diabetes</p>

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35
Q

<p>what is the presentation f RDS</p>

A

<p>tachyopnea</p>

<p>laboured breathing</p>

<p>chest wall recession</p>

<p>nasal flaring</p>

<p>expiratory grunting</p>

<p>cyanosis</p>

36
Q

<p>how do you manage RDS</p>

A

<p>if suspected premature antenatally give glucocorticoids</p>

<p>then:</p>

<p>O2/CPAP</p>

<p>surfactant therapy via trachyal tube</p>

37
Q

<p>what is bronchopulmonary displasia</p>

A

<p>lung damage due to trauma from o2 therapy, infections, artificial ventilation.</p>

<p>this lung damage means infants have high o2 requirements past 36 weeks</p>

38
Q

<p>what is the diagnosis of<strong>bronchopulmonary displasia</strong></p>

A

<p>clinical</p>

<p>x ray = wide spread opacification and cystic changes</p>

39
Q

<p>what is tha management ofbronchopulmonary displasia</p>

A

<p>reduce o2 conc on CPAP>O2 therapy>nothing over the course of months</p>

<p>short corse of corticosteriods</p>

<p></p>

40
Q

<p>what do long courses of corticosteroids in infants cause (when treatingbronchopulmonary displasia )</p>

A

<p>CP</p>

<p>neurodevelopmental delay</p>

41
Q

<p>why is pertusis + RSV dangerous for kids withbronchopulmonary displasia</p>

A

<p>severe disease causing: pulmonary HTN and resp failure</p>

<p>often requiring ICU</p>

<p></p>

42
Q

<p>what type of conjunctivtis is normal in infants</p>

A

<p>sticky eyes but clear discharge with no redness</p>

<p>washing with saline is all requried</p>

43
Q

<p>what is abnormal conjunctivitis</p>

A

<p>red eyes with purulent discharge</p>

44
Q

<p>what pathogen usually causes conjuntivitis in neonates</p>

A

<p>staph or strep</p>

45
Q

<p>what is the treatement for staph or step conjunctivitis</p>

A

<p>neomycin eye drops</p>

46
Q

<p>what are signs of a ghonnococcal eye infection</p>

A

<p>within 48 hrs of birth</p>

<p>red eyes and purlulent discharge</p>

47
Q

<p>what must you do if you suspect a ? ghonnococcal conjunctivitis</p>

A

<p>gram stain and swab</p>

<p>blood cultures</p>

48
Q

<p>what is the management of gonnococcal conjunctivitis</p>

A

<p>cefalexin</p>

<p>penicinnin IV</p>

49
Q

<p>what is the presentation of chlamydia conjuntivitis</p>

A

<p>eye swelling!</p>

<p>purulent discharge</p>

<p>can present upto 2 w post birth</p>

50
Q

<p>what is the treatement for chlamydia conjunctivitis</p>

A

<p>erythromycin x2 weeks</p>

51
Q

<p>how is listeria transmitted</p>

A

<p>listeria myogenes i stransmitted via foods like unpasteurised chese or undercooked paultry</p>

52
Q

<p>what is maternal presentation oflisteria</p>

A

<p>flu like</p>

53
Q

<p>what are consequenses oflisteria infections to baby</p>

A

<p>spontaneous abortion</p>

<p>prem baby</p>

<p>fetal / neonatal sepsis</p>

54
Q

<p>what is the just born presentation of listeria</p>

A

<p>meconium stained liquor</p>

<p>rash</p>

<p>septicemia + meningitis (although this can have late onset)</p>

<p></p>

55
Q

<p>how do you treatlisteria</p>

A

<p>ampicillin + gentaycin</p>

56
Q

<p>what is a PDA</p>

A

<p>a left to right shunt in prem babies as ductus rteriosis hasnt closed yet</p>

57
Q

<p>what is the presentation of a PDA</p>

A

<p>mainly asymptomatic but:</p>

<p>apnoea</p>

<p>bradycardia</p>

<p>cynosis</p>

<p>HF if severe</p>

58
Q

<p>what are the cardiac signs of a PDA</p>

A

<p>Bounding pulse</p>

<p>systolic murmur</p>

59
Q

<p>what is used to investigate a PDA</p>

A

<p>an echo</p>

60
Q

<p>how would you manage a PDA</p>

A

<p>prostaglandin synthase inhibitors = indomatacin or ibruprofen</p>

<p>surgery</p>

61
Q

<p>what causes HIE to occur</p>

A

<p>compramised cardiac function or decreased perfusion to brain causing barin injury</p>

62
Q

<p>what can trigger the events leading to HIE</p>

A

<p>prolonged contractions</p>

<p>placental abruption</p>

<p>umbillical cord compression</p>

<p>shoulder dystocia</p>

<p></p>

<p>maternal hypotension/hypertension</p>

<p>IUGR</p>

<p>failure to breathe at birth</p>

63
Q

<p>what is the presentation of HIE</p>

A

<p>must be within 48hrs of birth!!</p>

<p>mild=</p>

<p>irritable, hyperventilative, staring of eyes</p>

<p>mod =</p>

<p>fluctuating hyper + hypotonia. May have seizures</p>

<p>severe =</p>

<p>no response to pain, fluctuating tone, multiorgan failure, seizures</p>

64
Q

<p>what is the management of HIE</p>

A

<p>resp sopport</p>

<p>+/- anticinvulstants</p>

<p>EEG</p>

<p>fluid restriction</p>

<p>inotrope (digoxin)</p>

<p>hypoglycaemia support</p>

<p>hypocalcaemia support</p>

<p>manage hypothermia</p>

65
Q

<p>what is retinopathyof immaturity</p>

A

<p>vasular proloferation causinf retinal detachement</p>

66
Q

<p>what are Rf for retinopathy of prematurity</p>

A

<p>high o2 therapy</p>

<p>low birth weight (1500g)</p>

<p>prem (<32)</p>

<p>and if under 28 weeks theres risk of bilaterap retinopathy of prematurity</p>

67
Q

<p>what is the management of at risk patients ofretinopathy of prematurity</p>

A

<p>weekly fundoscopy</p>

<p>lazer surgery</p>

68
Q

<p>what is necrotising enterocolitis</p>

A

<p>bacterial invasion of ischemic bowel wall upon bowel death</p>

69
Q

<p>how does necrotising enterocolitis present</p>

A

<p>feeding intolerence</p>

<p>abdo pain and distension</p>

<p>shiny skin on abdomen</p>

<p>bloody stools</p>

<p>bile stained vomit</p>

<p>shock</p>

70
Q

<p>what investigations are used in necrotising enterocolitis</p>

A

<p>x ray</p>

<p>transillumination of abdomen</p>

71
Q

<p>what findings on Xray would there be fornecrotising enterocolitis</p>

A

<p>distended bowel loops</p>

<p>thickened bowel walls</p>

<p>intermural gas</p>

<p>gas under duaphragm and in billary tree</p>

72
Q

<p>how do you managenecrotising enterocolitis</p>

A

<p>stop feeds</p>

<p>parenteral nutrition</p>

<p>abx</p>

<p>ventilation</p>

<p>surgery</p>

73
Q

<p>is an infant hasnecrotising enterocolitis what are they at risk of getting in later ife</p>

A

<p>strictures and malabsorbtion</p>

74
Q

<p>what are the types of cleft lip and pallette</p>

A

<p>unilateral]bilateral</p>

75
Q

<p>what is the pathophysiology of cleft lip/pallette</p>

A

<p>failure of fusion of frontonasal + maxillary process as well as failure to fuse palatine process and nasal septum</p>

76
Q

<p>what causescleft lip/pallette</p>

A

<p>folic acid deficiency</p>

<p>chromosomal</p>

<p>maternal anticonvulstant therpay</p>

77
Q

<p>what is the management ofcleft lip/pallette</p>

A

<p>surgery erly in life</p>

78
Q

<p>describe caput succedaneum</p>

A

<p>bruising of presenting part of baby</p>

79
Q

<p>describe cephalohaematoma</p>

A

<p>bleeding below periosteum</p>

<p>usually on parietal bone</p>

80
Q

<p>when can a chingon ocur</p>

A

<p>ventrose delivery</p>

81
Q

<p>what can scalp electrodes do to baby</p>

A

<p>cause abrasions</p>

82
Q

<p>why would a brachial paulsey occur</p>

A

<p>breech</p>

<p>shoulder dystocia</p>

83
Q

<p>what nerve does erbs paulsey affect</p>

A

<p>C5+6</p>

<p>'waiters arm'</p>

84
Q

<p>why wuld a facial nerve pasley occur</p>

A

<p>compression during birth</p>

85
Q

<p>what may you need to help manage facial nerve palsey</p>

A

<p>hydrating eye drops</p>

<p>mathylcellulose</p>

86
Q

<p>when do palseys usually reverse by</p>

A

<p>2-3 months</p>

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