Pregnancy Complications Flashcards
1
Q
hyperemesis Gravidarum
A
persistant and intractable vomiting > fluid and electrolyte imbalance
2
Q
Hyperemesis gravidarum risk factors
A
- Multiple pregnancy
- hydatiform mole
- family history
- femal foetus
- obstetric hx
- hx of motion sickness or migranes
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
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
5
Q
threatened miscarriage
A
PV bleeding 20/40. may be self limiting and not lead to abortiob. Cx remains closed
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
7
Q
Complete misscarriage
A
All products are expelled from uterus
8
Q
Incomplete misscarriage
A
Some conception products are retained
6-14/40
usually requires surgical removal
9
Q
Missed miscarriage
A
Foetus dies but is retained in the uterus
May be PV spotting
Conceptus must be removed
10
Q
Incompetent Cx
A
Dilation of Cx during 2nd/early 3rd trimester without labour or uterine contractions
11
Q
Polyhydramnios
A
Excessive volume of AF for dates (>1.5-2L at term)
12
Q
Polyhydramnios signs
A
- Large for gestation uterus
- Difficult to palpate foetus
- FHR difficult to auscletate
- breathlessness
13
Q
Polyhydramnios risk factors
A
- Multiple pregnancies
- Maternal diabetes
- rhesus isoimmunisation
- Infections
- foetal conditions: Chromosomal, genetic, neurological, GI, cardiac, haematological abnormalities
14
Q
polyhydramnios outcomes
A
- unstable lie
- PROM
- Prem labour
- cord porlapse
- placental abruption
- PPH (over stretching of living ligatures)
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
16
Q
Oligohydramnious Manifestations
A
- small for gestation uterus
- Reduced foetal movements
- Foetal parts easy to palpate
17
Q
Oligohydramnious risk factors
A
- amnion abnormalities
- placental ensufficiencies
- renal abnormalities
- IUGR
- PROM
- prolonged prengnancy
18
Q
(preterm) premature ROM
A
ROM before 37 weeks. slow leak or gush
19
Q
(preterm) premature ROM risk factors
A
- Polyhydramnious
- multiple pregnancy
- alterations in collegen levels within membranes
- infections
- smoking
- obstetrci Hx
20
Q
Cord prolapse
A
descent of cord through Cx alongside or before presenting part
21
Q
Hydatidiform Mole
A
development of tumor which has arised from trophoblastic tissue. caused by abnormal genetic material. Complete and Partial
22
Q
Complete hydatidiform mole
A
entirely androgenic - no foetal tissue development
23
Q
Partial hydatidiform mole
A
Conceptus is triploid with a foetus but abnormal depvelopment of placental tissue
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
25
Ectopic pregnancy
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
26
Twin-twin transfusion
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
27
twin-twin transfusion manifestations
- Smaller, hypovolaemic, anaemmic donor twin
| - larger hypervolaemic recipient twin
28
Implications for "donor" twin
- Hypovolaemia > dec CO > dec blood to tissue > ischemia
- Anaemia > dec capacity for O2 transportation > ischemia
- Dec CO > dec urine output > dec AF volume
29
Implications for "recipient" twin
- 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
30
Placenta Praevia 4 types
1. low lying
2. marginal
3. partial
4. complete
31
placenta praevia manifestations
- Painless bleeding during 2nd and 3rd trimester - worsening
- malpresentation
32
placenta praevia risk factors/potential causes
- Obstetric Hx
- Large Placenta
- high parity
- Maternal age
- Abnormal uterine shape
33
Placenta praevia pathophysiology
- 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
Placenta praevia and PPH link
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
Vasa Praevia is...
- Valamentous insertion of umbilical cord > foetal vessels corss over internal os
36
Vasa praevia manifestations
Profuse haemorrhage of feotal blood on ROM
37
Vasa praevia risk factors
- Placenta praevia
- Multiparity
- IVF conception
- multi-lobed or succenturiate-lobed placenta
38
Placental Abruption is
premature separation of the placenta causing bleeding
- Partial
- Complete
39
Placental abruption manifestations (4)
- PV blood loss (not always)
- abdominal/LBP
- Uterine tenderness
- Evidence of foetal compromise
40
Placental abruption risk factors/potential causes (8)
- 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
Placental abruption pathophysiology
Separation > bleeding in to decidua basalis > haematoma formation > further separation
42
Placental abruption implications for foetus
Dependant on degree of separation = extend to O2 and nutrient supply reduction
- decelerated growth
- possible IUD
43
Blood loss from placental abruption (3 types)
- 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
Placental abruption implications for mother
- depends on degree of blood loss
- maternal hypovolaemia > hypovolaemic shock
- also associated with DIC in severe cases
45
APH
Bleeding after mid pregnancy, before birth
46
Types of APH (2)
Inevitable: placental praevia
Accidental: placental abruption
47
APH Implications
depends on amount of blood loss: more blood loss = increased harm
48
Hypovolaemic Shock
State of shock due to reduced circulating blood volume > dec CO and insufficient supply to body tissue. 4 phases
49
Hypovolaemic shock causes
- Severe dehydration
| - haemorhhage
50
Hypovolaemic shock phase 1
- May go undetected
- Immediate response to blood loss
- Manifestations: vital signs drop
51
Hypovolaemic shock phase 2 Compensatory phase
- 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
Hypovolaemic shock Phase 3 decompensations
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
Hypovolaemic shock phase 4 irreversable
Widespread cell death > death
54
DIC in pregnancy is...
widespread coagulation and bleeding, clotting occuring throughout vascular tree using up clotting factors ulltimately leading to haemorrhage
55
DIC manifestations (4)
- Bruising
- Bleeidng from body openings/mucosal linings
- Hypotension
- Shock
56
DIC risk factors/causes
- Trauma
- Hypovolaemic shock
- Haemorrhage
- Infection
- IUD
- Retained porducts
- Placental abruption
- Pre-eclampsia
57
DIC pathophysiology
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
Pregnancy induced hypertension
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
PIH possible implications (4)
- IUGR
- Preterm birth
- Placental abruption
- Still birth
60
PET symptom pathophysiology: hypertension
poor uteroplacental perfusion > ishemic placental tissue > release of vasoconstrictive + procoagulant factors > followed by widespread vasospasm > inc BP
61
PET symptom pathophysiology: headache
Cerebral oedema
62
PET symptom pathophysiology: visual disturbacnes
oedema of the retina
63
PET symptom pathophysiology: epigastric pain
haemorrhages under the liver capsule (also attributed with nausea and vomiting)
64
PET symptom pathophysiology: Proteinuria/glucosuria
Increased glomerular permeability
65
PET symptom pathophysiology: Oedema and swelling
increased general capillary permeability
66
PET symptom pathophysiology: increased liver enzymes
Altered liver function
67
Eclampsia
Seizures occurring with pre-eclampsia due to changes in BBB resullting in vasospasm and oedema in the brain
68
HELLP
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
Rh blood group incompatibility
- 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
Obstetric Cholestasis pathophysiology
- 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
Obstetric Cholestasis manifestations (4)
- Pruritis
- Elevated bile acids
- Elevated liver enzymes
- Jaundice
72
Obstetric Cholestasis risk factors/causes
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Genetic predispopsition
family hx
multiple pregnancies
obstetric hx
gallstones
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73
Acute fatty liver of pregnancy
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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
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