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Bioscience Complications > Pregnancy Complications > Flashcards

Pregnancy Complications Flashcards

1
Q

hyperemesis Gravidarum

A

persistant and intractable vomiting > fluid and electrolyte imbalance

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2
Q

Hyperemesis gravidarum risk factors

A
  • Multiple pregnancy
  • hydatiform mole
  • family history
  • femal foetus
  • obstetric hx
  • hx of motion sickness or migranes
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3
Q

hyperemesis gravidarum pathophysiology

A

excessive vomiting > dec in fluid and electrolyte > prevents proper digestion/absorption of nutrients > loss of fluid > dec blood volume > dec urine output

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4
Q

Spontaneous loss of pregnancy

A

loss of pregnancy before viability of foetus. usually presents as PV blood loss before 20 weeks. may be accompanied by abdominal/LBP

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5
Q

threatened miscarriage

A

PV bleeding 20/40. may be self limiting and not lead to abortiob. Cx remains closed

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6
Q

Inevitable misscarriage

A

PV bleeding persists
Often associated with pain/uterine contractions
Pregnancy not viable
Spontaneous expulsion of conceptus or may need medical removal

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7
Q

Complete misscarriage

A

All products are expelled from uterus

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8
Q

Incomplete misscarriage

A

Some conception products are retained
6-14/40
usually requires surgical removal

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9
Q

Missed miscarriage

A

Foetus dies but is retained in the uterus
May be PV spotting
Conceptus must be removed

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10
Q

Incompetent Cx

A

Dilation of Cx during 2nd/early 3rd trimester without labour or uterine contractions

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11
Q

Polyhydramnios

A

Excessive volume of AF for dates (>1.5-2L at term)

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12
Q

Polyhydramnios signs

A
  • Large for gestation uterus
  • Difficult to palpate foetus
  • FHR difficult to auscletate
  • breathlessness
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13
Q

Polyhydramnios risk factors

A
  • Multiple pregnancies
  • Maternal diabetes
  • rhesus isoimmunisation
  • Infections
  • foetal conditions: Chromosomal, genetic, neurological, GI, cardiac, haematological abnormalities
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14
Q

polyhydramnios outcomes

A
  • unstable lie
  • PROM
  • Prem labour
  • cord porlapse
  • placental abruption
  • PPH (over stretching of living ligatures)
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15
Q

Oligohydramnious

A

Reduced AF (<500mL at term or less than half of expected volume throughout gestation).
Restricted space for movement and inhalation of AF.
Anatomical abnormalities due to position

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16
Q

Oligohydramnious Manifestations

A
  • small for gestation uterus
  • Reduced foetal movements
  • Foetal parts easy to palpate
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17
Q

Oligohydramnious risk factors

A
  • amnion abnormalities
  • placental ensufficiencies
  • renal abnormalities
  • IUGR
  • PROM
  • prolonged prengnancy
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18
Q

(preterm) premature ROM

A

ROM before 37 weeks. slow leak or gush

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19
Q

(preterm) premature ROM risk factors

A
  • Polyhydramnious
  • multiple pregnancy
  • alterations in collegen levels within membranes
  • infections
  • smoking
  • obstetrci Hx
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20
Q

Cord prolapse

A

descent of cord through Cx alongside or before presenting part

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21
Q

Hydatidiform Mole

A

development of tumor which has arised from trophoblastic tissue. caused by abnormal genetic material. Complete and Partial

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22
Q

Complete hydatidiform mole

A

entirely androgenic - no foetal tissue development

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23
Q

Partial hydatidiform mole

A

Conceptus is triploid with a foetus but abnormal depvelopment of placental tissue

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24
Q

hydatidiform mole manifestations

A
  • PV bleeding
  • Early onset PET
  • LGA uterus
  • no palpable foetus
  • hyperthermia
  • Hyperemesis gravidarum
  • elevated levels of hCG
  • multiple vesicles appear on ultrasound
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25
Q

Ectopic pregnancy

A

implatation outside of uterine cavity. depending on location along tube ectopic pregnancy will lead to: rupture of tube 5-7/40
expulsion of gestational sac from fibrated end of tube (Tubal abortion) 8-10/40

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26
Q

Twin-twin transfusion

A

Monozygotic twins sharing placental lobes. shared lobe is supplied by umbilical artery of one twin and drained by umbilical vein of other twin.
Can lead to death of both babies

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27
Q

twin-twin transfusion manifestations

A
  • Smaller, hypovolaemic, anaemmic donor twin

- larger hypervolaemic recipient twin

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28
Q

Implications for “donor” twin

A
  • Hypovolaemia > dec CO > dec blood to tissue > ischemia
  • Anaemia > dec capacity for O2 transportation > ischemia
  • Dec CO > dec urine output > dec AF volume
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29
Q

Implications for “recipient” twin

A
  • Hypervolaemia = inc CO = hypertrophy of myocardium
  • inc CO > inc urine output > polyhydramnios
  • Polycynthaemia = inc viscocity of blood > hyopertension
  • Hyperbilirubinaemia > inc bilirubin deposited in tissue and crossing BBB causing neurological damage
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30
Q

Placenta Praevia 4 types

A
  1. low lying
  2. marginal
  3. partial
  4. complete
31
Q

placenta praevia manifestations

A
  • Painless bleeding during 2nd and 3rd trimester - worsening
  • malpresentation
32
Q

placenta praevia risk factors/potential causes

A
  • Obstetric Hx
  • Large Placenta
  • high parity
  • Maternal age
  • Abnormal uterine shape
33
Q

Placenta praevia pathophysiology

A
  • Implantation occurs low in uterus (not fundus) > implantation deeper than normal to obtain adequate blood supply > migration occurs towards os (or away) later in pregnancy > increased elasticity in LUS not met by placenta > separation
    LUS changes increase throughout pregnancy > increased bleeding
34
Q

Placenta praevia and PPH link

A

After separation of placenta there is less living ligatures (no oblique muscle fibres) in the lower section of the uterus so blood flow is not controlled as easily

35
Q

Vasa Praevia is…

A
  • Valamentous insertion of umbilical cord > foetal vessels corss over internal os
36
Q

Vasa praevia manifestations

A

Profuse haemorrhage of feotal blood on ROM

37
Q

Vasa praevia risk factors

A
  • Placenta praevia
  • Multiparity
  • IVF conception
  • multi-lobed or succenturiate-lobed placenta
38
Q

Placental Abruption is

A

premature separation of the placenta causing bleeding

  • Partial
  • Complete
39
Q

Placental abruption manifestations (4)

A
  • PV blood loss (not always)
  • abdominal/LBP
  • Uterine tenderness
  • Evidence of foetal compromise
40
Q

Placental abruption risk factors/potential causes (8)

A
  • Hypertensive states
  • Conditions that increase intrauterine pressure ie. Polyhydramnios
  • Sudden decompression of uterus (ROM of polyhydramnios)
  • Preterm labour/preterm ROM
  • Obstetric Hx
  • Increased parity
  • Trauma
  • Smoking/drug use
41
Q

Placental abruption pathophysiology

A

Separation > bleeding in to decidua basalis > haematoma formation > further separation

42
Q

Placental abruption implications for foetus

A

Dependant on degree of separation = extend to O2 and nutrient supply reduction

  • decelerated growth
  • possible IUD
43
Q

Blood loss from placental abruption (3 types)

A
  • Concealed: occurs near centre of placental attachment site. Blood does not pass PV.
    Blood may infiltrate myometrium = swelling of uterus
  • Revealed: bleeding occurs at margin of placenta = blood loss occurs between membranes and decidua and passes PV
    Partially revealed: some blood loss PV some in haematoma
44
Q

Placental abruption implications for mother

A
  • depends on degree of blood loss
  • maternal hypovolaemia > hypovolaemic shock
  • also associated with DIC in severe cases
45
Q

APH

A

Bleeding after mid pregnancy, before birth

46
Q

Types of APH (2)

A

Inevitable: placental praevia
Accidental: placental abruption

47
Q

APH Implications

A

depends on amount of blood loss: more blood loss = increased harm

48
Q

Hypovolaemic Shock

A

State of shock due to reduced circulating blood volume > dec CO and insufficient supply to body tissue. 4 phases

49
Q

Hypovolaemic shock causes

A
  • Severe dehydration

- haemorhhage

50
Q

Hypovolaemic shock phase 1

A
  • May go undetected
  • Immediate response to blood loss
  • Manifestations: vital signs drop
51
Q

Hypovolaemic shock phase 2 Compensatory phase

A
  • Activation of sympathetic nervous system and renin angiotensin system to maintain homeostasis
    SYMPATHETIC NS: Inc HR, SV and TRP to maintain blood supply to organs
    R-A SYSTEM: Inc TPR and Na + H2O reabsorption to restore blood volume
52
Q

Hypovolaemic shock Phase 3 decompensations

A

Failing of negative feedback system mechanisms to maintain homeostasis > progression of shock exacerbating situation
Manifestations: sweating, cold and pale skin, no urinary loss, high HR + RR, low BP confusion and agitation
Survival is unlikely

53
Q

Hypovolaemic shock phase 4 irreversable

A

Widespread cell death > death

54
Q

DIC in pregnancy is…

A

widespread coagulation and bleeding, clotting occuring throughout vascular tree using up clotting factors ulltimately leading to haemorrhage

55
Q

DIC manifestations (4)

A
  • Bruising
  • Bleeidng from body openings/mucosal linings
  • Hypotension
  • Shock
56
Q

DIC risk factors/causes

A
  • Trauma
  • Hypovolaemic shock
  • Haemorrhage
  • Infection
  • IUD
  • Retained porducts
  • Placental abruption
  • Pre-eclampsia
57
Q

DIC pathophysiology

A

widespread endothelial damage = activation of clotting cascade >
coagulation throughout vascular tree alongside dec in fibrolytic activity >
microthrombi form in small vessels >
ischaemia >
release of more clotting factors >
clotting factors used up >
widespread bleeding occurs from damaged tissue > hypovolaemic shock >
organ failure and death

58
Q

Pregnancy induced hypertension

A

Elevated BP (diastolic >90mmHg) after 20/40.
May be essential that was masked in early pregnancy
Occurs without proteinuria
Often only diagnosed if PET does not develop

59
Q

PIH possible implications (4)

A
  • IUGR
  • Preterm birth
  • Placental abruption
  • Still birth
60
Q

PET symptom pathophysiology: hypertension

A

poor uteroplacental perfusion > ishemic placental tissue > release of vasoconstrictive + procoagulant factors > followed by widespread vasospasm > inc BP

61
Q

PET symptom pathophysiology: headache

A

Cerebral oedema

62
Q

PET symptom pathophysiology: visual disturbacnes

A

oedema of the retina

63
Q

PET symptom pathophysiology: epigastric pain

A

haemorrhages under the liver capsule (also attributed with nausea and vomiting)

64
Q

PET symptom pathophysiology: Proteinuria/glucosuria

A

Increased glomerular permeability

65
Q

PET symptom pathophysiology: Oedema and swelling

A

increased general capillary permeability

66
Q

PET symptom pathophysiology: increased liver enzymes

A

Altered liver function

67
Q

Eclampsia

A

Seizures occurring with pre-eclampsia due to changes in BBB resullting in vasospasm and oedema in the brain

68
Q

HELLP

A

Hemolysis
Elevated
Liver and
Low
Platelets
- Multisystem involvement kidey and liver failure and neurological problems
- Placental is involved and may lead to placental abruption
- progression of pre-eclampsia AND stand alone condition

69
Q

Rh blood group incompatibility

A
  • Rh - mother and Rh + foetus
  • D antigens present in RBC’s
  • if circulations mix it will stimulate production of Anti-D antibodies > subsequent pregnancies with Rh+ baby will stimulate maternal antibodies > antibodies cross placenta > inc risk of haemolysis of foetal RBC’s > severe foetal anaemia, tissue hypoxia > foetal demise
70
Q

Obstetric Cholestasis pathophysiology

A
  • increases in E + P during prengnancy = dec rate of bile passing through ducts of liver
  • E increases production of products in liver = congestion
  • P relaxes gall bladder and bile ducts
  • may lead to production of gallstones
    > increased bile > absorption in blood stream > pruritis > sleep disturbances > impact maternal condition
71
Q

Obstetric Cholestasis manifestations (4)

A
  • Pruritis
  • Elevated bile acids
  • Elevated liver enzymes
  • Jaundice
72
Q

Obstetric Cholestasis risk factors/causes

A 
Genetic predispopsition 
family hx 
multiple pregnancies 
obstetric hx
gallstones
73
Q

Acute fatty liver of pregnancy

A 
Accumulation of lipids in liver.  Aetiology uncertain:
Mitochondrial dysfunction (LCHAD deficiency) in O2 of fatty acids for ATP in foetus > accumulation of long chain fatty acids > return of fatty acids to maternal circulation > liver for lipolysis > eventually leads to hepatic fialure > hapatocytes undergo atrophy and lysis > liver failure > renal failure  > foetal mortality

Bioscience Complications (6 decks)

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