WEEK 1: MEDICAL DISORDERS IN PREGNANCY Flashcards

1
Q

What is hyperemesis gravidarum?

A

Hyperemesis gravidarum is a severe and potentially life-threatening condition of pregnancy characterized by extreme and persistent nausea and vomiting.

While nausea and vomiting are common symptoms during pregnancy, hyperemesis gravidarum goes far beyond typical morning sickness in terms of severity and duration.

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2
Q

Describe the 5 key features of hyperemesis gravidarum.

A

Key features of hyperemesis gravidarum include:

  1. Severe Nausea and Vomiting: Women with hyperemesis gravidarum experience relentless and severe nausea and vomiting that often leads to dehydration and malnutrition. These symptoms can occur throughout the day and night.
  2. Weight Loss: The frequent vomiting and inability to keep down food and fluids can lead to significant weight loss, electrolyte imbalances, and nutritional deficiencies.
  3. Dehydration: The excessive vomiting can cause dehydration, leading to symptoms such as dry mouth, dark urine, and reduced urine output.
  4. Ketosis: In severe cases, the body may start to break down fat for energy, resulting in the production of ketones. Ketosis can be detected in urine samples.
  5. Inability to Eat or Drink: Sufferers often find it nearly impossible to eat or drink without vomiting shortly afterward, leading to severe malnutrition and a decline in overall health.
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3
Q

Describe the 5 possible pathophysiology of Heartburn and GERD in pregnancy.

A
  1. Hormonal Changes:

Progesterone helps relax smooth muscles, including the lower esophageal sphincter (LES), which is the muscular ring that separates the esophagus from the stomach.

The relaxation of the LES allows stomach acid to flow back into the esophagus, leading to acid reflux. This weakening of the LES is a key contributor to both heartburn and GERD.

  1. Increased Intra-abdominal Pressure:

As the pregnancy progresses, the growing uterus puts pressure on the abdominal organs, including the stomach. This increased intra-abdominal pressure can promote the backflow of stomach contents into the esophagus.

  1. Delayed Gastric Emptying:

Pregnancy can lead to a slowing of the normal gastric emptying process. This can result in the stomach contents staying in the stomach for longer periods, allowing more time for acid to reflux into the esophagus.

  1. Growth of the Uterus:

The physical growth of the uterus can push the stomach upward, increasing the likelihood of acid reflux. As the pregnancy advances, the size and position of the uterus can exacerbate this effect.

  1. Dietary and Lifestyle Factors:

Pregnant women may experience changes in dietary habits, which can include consuming larger meals or eating close to bedtime. These behaviors can contribute to heartburn and GERD.
Other lifestyle factors, such as lying down after eating or being overweight, can also increase the risk of acid reflux.

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4
Q

Describe the pathophysiology of constipation in pregnancy.

A
  1. Hormonal Changes:

Progesterone has a muscle-relaxing effect, which can lead to reduced gastrointestinal motility. Slower intestinal transit times allow more water to be absorbed from the stool in the colon, resulting in firmer and harder stools that are more difficult to pass.

  1. Mechanical Pressure:

As the uterus enlarges during pregnancy, it can exert physical pressure on the intestines, particularly the colon. This mechanical pressure can compress and slow down the movement of stool through the colon, leading to constipation.

  1. Iron and Prenatal Supplements:

Pregnant women often take iron supplements to prevent or treat anemia. Iron supplements can have a constipating effect on some individuals. Prenatal vitamins, which often contain iron, may also contribute to constipation.

  1. Dietary Factors:

Changes in dietary habits during pregnancy, including consuming more processed or low-fiber foods, can contribute to constipation. Inadequate fluid intake and insufficient fiber in the diet can further exacerbate the problem.

  1. Dehydration:

Pregnancy increases the body’s demand for fluids, and dehydration can lead to harder stools. In some cases, pregnant women may not consume enough water to meet their body’s needs, which can contribute to constipation.

  1. Medications and Supplements:

Certain medications taken during pregnancy, such as calcium or iron supplements, can have constipation as a side effect.

7.Physical and Hormonal Changes in the Colon:

The colon undergoes certain physiological changes during pregnancy. The colon may become more sluggish, which can affect bowel movements.

  1. Pressure on the Rectum and Pelvic Floor:

The pressure from the growing uterus can also affect the pelvic floor muscles and rectum, making it more challenging to pass stools.

  1. Gastrointestinal Disturbances:

In some cases, pregnancy can lead to gastrointestinal disorders, such as irritable bowel syndrome (IBS) or functional constipation, which can contribute to constipation.

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5
Q

Hypertensive disorders in pregnancy

-Broadly considered as pre-existing or pregnancy induced hypertension

State the 5 categories of hypertensive disorders in pregnancy.

A

5 major categories
-Chronic HT in pregnancy
-Gestational HT (Non proteinuria)
-Pre-eclampsia (With and without severe features)
-Eclampsia
-Chronic HT with superimposed pre-eclampsia

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6
Q

What is gestational hypertension?

A

Gestational HT
Hypertension (BP ≥ 140/90mmHg at least 2 readings 4-6hours) without proteinuria or other signs/symptoms of end-organ dysfunction developing after 20 weeks of gestation

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7
Q

What is pre-eclampsia?

A

New onset hypertension and proteinuria or significant end-organ dysfunction (with or without proteinuria), typically after 20 weeks of gestation in a previously normotensive woman.

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8
Q

Pre-eclampsia is one the leading causes of maternal death both in Botswana and Globally.

State the ranking of pre-eclampsia in Botswana and globally.

A
  1. Globally
    *Second to PPH
  2. Third to hemorrhage of unsafe abortion and hypertensive disorders
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9
Q

A multisystem progressive disorder characterized by the new onset of hypertension and proteinuria or the new onset of hypertension and significant end-organ dysfunction with or without proteinuria in the last half of pregnancy or postpartum.
Close to 80% of cases present at term with good maternal and fetal outcomes.

These pregnancies are at increased risk for maternal and/or fetal serious morbidity or mortality.
A multisystem progressive disorder characterized by the new onset of hypertension and proteinuria or the new onset of hypertension and significant end-organ dysfunction with or without proteinuria in the last half of pregnancy or postpartum.

Close to 80% of cases present at term with good maternal and fetal outcomes.

These pregnancies are at increased risk for maternal and/or fetal serious morbidity or mortality.

20% of cases present before term and carry additional high risk for preterm birth. May also develop postpartum.

Name the disorder described above.

.

A

Pre-eclampsia

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10
Q

State the 6 severe features of pre-eclampsia.

A

1.Severe BP elevation
2.Symptoms of CNS dysfunction
3.Hepatic abnormality
4.Thrombocytopenia
5.Renal abnormality
6.Pulmonary oedema

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11
Q

State the 8 risk factors of pre-eclampsia.

A

Extremes of age( <20, >35)
Multiple pregnancy
Nullipara
Previous history
Pre-existing DM, HT, renal disease,vasculopathy
Connective tissue disorders
Molar pregnancy
Smoking

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12
Q

Describe the 2-stage theory of the PATHOPHYSIOLOGY /PATHOGENESIS of pre-eclampsia.

A

Stage 1: Inadequate Placentation
This stage is characterized by inadequate invasion of the maternal spiral arteries by trophoblast cells.

Normally, trophoblasts, which are cells derived from the fertilized egg, invade the maternal spiral arteries in the uterus and remodel them to ensure optimal blood flow to the placenta.

In pre-eclampsia, this process is compromised, leading to reduced placental perfusion. The inadequate blood supply to the placenta triggers a series of events, including:

*Hypoxia (Low Oxygen Levels): The impaired blood flow results in lower oxygen levels in the placenta, leading to a state of hypoxia.

*Release of Factors: Hypoxia induces the release of factors such as soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng) from the placenta. sFlt-1 is known to inhibit the action of vascular endothelial growth factor (VEGF), a key protein involved in blood vessel formation.

*Endothelial Dysfunction: The released factors contribute to endothelial dysfunction, which involves damage to the lining of blood vessels.

*There is then increased peripheral vascular resistance, capillary leakage.

Stage 2: Maternal Systemic Inflammatory Response

The second stage involves a systemic maternal inflammatory response triggered by the factors released from the poorly perfused placenta.

This inflammatory response affects multiple organs and contributes to the clinical manifestations of pre-eclampsia.

  1. Vasculopathy – Hypertension:

Hypertension is a hallmark feature of the second stage of pre-eclampsia. Endothelial dysfunction and vasoconstriction contribute to elevated blood pressure. The compromised blood vessels can lead to damage throughout the body.
Glomerular Endotheliosis – Proteinuria:

  1. Endothelial dysfunction, particularly in the glomeruli of the kidneys, results in glomerular endotheliosis. This condition contributes to proteinuria, were proteins, especially albumin, leak into the urine due to increased permeability of the damaged glomerular endothelium.
    Increased Pulmonary Alveolar Edema – Pulmonary Edema:
  2. Elevated blood pressure and endothelial dysfunction can lead to increased permeability of pulmonary capillaries. This may result in the accumulation of fluid in the lungs, causing pulmonary edema. This condition can lead to respiratory distress and is a serious complication of severe pre-eclampsia.
    Vasogenic/Cytogenic Edema – Cerebral Edema:
  3. Vasogenic and cytogenic edema refers to the accumulation of fluid in the extracellular and intracellular spaces of the brain, respectively. Endothelial dysfunction and hypertension can disrupt the blood-brain barrier, contributing to cerebral edema. This can manifest as headaches, visual disturbances, and in severe cases, may lead to seizures (eclampsia).
  4. Periportal Necrosis and Ischemia – HELLP Syndrome and Hepatic Rupture:

HELLP syndrome (Hemolysis, Elevated Liver enzymes, and Low Platelet count) is a severe form of pre-eclampsia that involves liver dysfunction. The periportal necrosis and ischemia are indicative of compromised blood flow to the liver, contributing to the features of HELLP syndrome. In severe cases, hepatic rupture can occur, although this is rare.

  1. Fetal Syndrome – IUGR, IUFD, Abruption:

The systemic effects of pre-eclampsia can impact the placenta and fetal well-being. Insufficient blood flow to the placenta can result in Intrauterine Growth Restriction (IUGR), Intrauterine Fetal Demise (IUFD), and placental abruption, where the placenta detaches from the uterine wall prematurely.

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13
Q

Describe the presentation (symptoms and signs) of pre-eclampsia in the following systems:

  1. General:
  2. CNS:
  3. GI:
  4. GUS:
  5. R/S:
  6. CVS:
  7. Hematological:
  8. Obstetric:
A

General: Swelling of feet, Facial puffiness, Rapid weight gain

CNS: Headache, Visual disturbances-blurring, double, blindness.

GI: Epigastric or RUQ pain, nausea vomiting

GUS: Altered urine volume and colour (tea/coke colour)

R/S: Shortness of breath, cough, pink frothy/blood-stained sputum.

CVS: Elevated BP

Hematological: Bleeding disorders (DIC)

Obstetric: Small for dates uterine size (IUGR)/oligohydramnios/IUFD

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14
Q

Define the following terms:
1. Chronic hypertension

  1. Superimposed Pre-eclampsia on chronic hypertension
A

Chronic hypertension

*Hypertension ≥140/90 occurring before pregnancy or is present on at least two occasions before the 20thweek of gestation or persists longer than 12 weeks postpartum.

Superimposed Pre-eclampsia on chronic HT.

*Worsening or resistant hypertension, the new onset or worsening proteinuria and/or significant new end-organ dysfunction after 20 weeks of gestation in a woman with chronic hypertension

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15
Q

Define eclampsia.

A

Eclampsia
New-onset, generalized, tonic-clonic seizures or coma in a woman with preeclampsia or gestational hypertension that are not attributable to any other neurological condition.

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16
Q

State the pregnancy complications and Sequelle associated with hypertensive disorders on the mother.

A

*Long term, women with preeclampsia are at increased risk for cardiovascular, renal, and chronic hypertensive disease

*Multisystemic complications as listed in severe features above-renal, liver, cardiac failure, stroke

*Recurrence in subsequent pregnancy

*Abruptio placenta-APH

*PPH- (Atony and coagulopathy)

*Pulmonary oedema

*Progression to eclampsia

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17
Q

State the pregnancy complications and Sequelle associated with hypertensive disorders on the foetus.

A

Fetal
*IUGR and Oligohydramnios secondary to placental insufficiency
*IUFD
*Preterm birth
*Increased perinatal morbidity and morbidity

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18
Q

Outline general management principles for hypertensive disorders.

A

-Early detection and treatment are critical

-BP control with antihypertensives more so for severe hypertension

-Close Maternal and fetal monitoring

-Prevent seizures

-Delivery planning

-Postpartum follow up

19
Q

Describe the management of eclampsia.

A

Mgt:
*Patient safety
*Control and prevent recurrence of fits with Magnesium Sulphate
*Control BP with antihypertensive treatment
*Close maternal and fetal monitoring
*Stabilize patient and aim to deliver within 6hrs
*Induce abortion if the fetal is unlikely to survive

20
Q

Outline ways of preventing pre-eclampsia

A

*Avoid modifiable risk factors: smoking, poor diet, obesity
*Good control of HT
*Close monitoring of BP during ANC
*Low dose Aspirin to high-risk patients

21
Q

How many % of pregnancies are prone to gestational diabetes?

Describe the pathogenesis of gestational diabetes.

At how many weeks of gestation is it usually common?
WHY?

A

-Affects 3-10% of pregnancies

-Secondary to receptor insensitivity due to pregnancy related hormones such as Cortisol, HPL: Human Placental Lactogen, also known as human chorionic somatomammotropin (HCS), progesterone, Estradiol.

-Common after 20w, once the placenta has formed

-Asymptomatic patient

22
Q

State the 6 predisposing factors to gestational diabetes.

A

*Advancing age 40+
*Family history- first degree relative
*Obesity
*History of macrosomia: having delivered a baby more than 4kg
*Unexplained IUFD at term: “IUFD” stands for “Intrauterine Fetal Demise.” In simple terms, IUFD refers to the death of a fetus inside the uterus before the delivery. It is also commonly known as stillbirth.
*History of gestational diabetes

23
Q

Describe the screening process for gestational diabetes.
*One step test
*Two step test

A
  1. 1 -step test
    *You do the oral glucose tolerance test only.
  2. 2-step test

*50g load following normal diet
*1hr later blood glucose test is done
*Cut off 130 (7.2)-140mg/dl (7.7)

Those above thresholds are subjected to step 2, oral glucose tolerance test (OGTT)

24
Q

Describe the procedure for doing the oral glucose tolerance test.

A

-Patient comes in the morning after an overnight fast after 8-14hr fasting
-Patient given 2h 75g glucose load versus 3h 100g glucose load

-Readings taken hourly.

-For 2h 75g glucose load 1 abnormal reading is needed for diagnosis.

-For 3h 100g glucose load, 2 abnormal readings are needed for diagnosis

25
Q

Describe the management of gestational diabetes management.

A

*Glycemic control preconception for Preexisting Type 1 and 2 DM Hb A1C <6%

*Multidisciplinary care

*Good control during pregnancy and labor

*Anomaly screening and for other pregnancy complications

*Screening for GDM in pregnancy

*Antepartum surveillance

*Deliver preferably at 39w if controlled

*Postpartum follow up

*Care of newborn

26
Q

State the 10 effects and risks associated with gestational diabetes.

A

Increased risk of miscarriage
Increased risk of anomalies
*Increased risk for Pre-eclampsia, UTI etc.
*Macrosomia
*Polyhydramnios-preterm birth
*IUFD
*Birth injuries
*Neonatal hypoglycemia and seizures
*Perinatal mortality
*Long term type 2 DM from GDM

27
Q

State the 4 WHO Strategies for elimination of MTCT.

A

Disease burden-
380,000 PLWHIV(2017)
High prevalence in females 15-49(26.3% vs 17..6%) with peak in reproductive years upto 50% among 35-39 yr olds
In pregnancy 37% (2005) 30.4% (2011) more recent survey July 2020 17%
Risk of MTCT with no intervention upto 40%
Risk greatest intrapartum though can occur antenatally and postpartum
Reduced to <2% with appropriate interventions
High ART coverage
WHO Strategies for elimination of MTCT

-Eliminate HIV in would be parents.
-Avoid unplanned pregnancies among HIV positive.
-PMCT
-Holistic care for mother and family

28
Q

State the Current recommendations for HIV in pregnancy.

A

-Screen and treat all for life (Option B+) irrespective of CD4 count

-Routine testing first visit and ideally repeated every 3 months

-Also screen for STI’s

29
Q

State the 5 significances for HIV treatment and screening in pregnancy.

A

*Elimination of Pediatric HIV

*Promotion of safe infant feeding

*Promotion of planned pregnancy

*Minimizing morbidity and mortality

*Worker safety in OBGY practice

30
Q

Cardiac diseases are one of the lethal medical diseases in pregnancy.

They have low incidences but are more complicated.

State the 3 types of Cardiac diseases in pregnancy.

A

i) Congenital
ii) Acquired cardiac disease
-valvular
-myocardial
-pericardial
iii) Peripartum cardiomyopathy

31
Q

Why is there need for checking for cardiac diseases in pregnancy.

State the effects of cardiac diseases on the fetus.

State the effects of cardiac diseases on the mother.

A

Significance: Aggravated by physiological changes in pregnancy such as increase in blood volume, increase in heart rate due to increase demand hence there is often decompensation.

*Intrauterine fetal hypoxia and IUGR due to poor placenta perfusion
*Preterm delivery
*IUFD

Maternal
*High risk of maternal morbidity
*Cardiac failure
*Maternal mortality
*Difficult labor
*Contraception

32
Q

State the Vascular and hemorrhagic disorders significance in pregnancy.

A

*Transplacental passage of drugs
*Transfer of HIV from mother to child
*Placentates
*Autoimmune Thrombocytopenia- intracranial hemorrhage

33
Q

One of the major hematological disorders in pregnancy is anemia.

State the main cause of anemia in 95% of pregnancies.

A

Anemia- Hb less than 11g/dl in first and third trimester and less than 10g/dl in 2nd trimester

95% Fe deficiency anemia in etiology
Increased demand of pregnancy

34
Q

State 8 risk factors of anemia in pregnancy.

A

Risk factors-
*Age: teenagers
*Menorrhagia,
*Short inter pregnancy interval LESS THAN 24 MONTHS interval
*GIT disease,
*Low dietary intake,
*Low socioeconomic status,
*Preexisting anemia
*Lack of ANC supplementation

35
Q

State the 6 significances of anemia in pregnancy.

A

Significance:
*IUGR/Low BWT
*Preterm births
*IUFD
*PPH: The uterus cannot contract well
*Transfusion demand and risks
*Genetic transmission and genetic counselling e.g., SCD

36
Q

State the prevention methods of anemia in pregnancy.

A

Prevention
*Diet, supplements, pre-pregnancy optimization

37
Q

UTIs are also common in pregnancy.

State the 4 complications of UTI in the pregnant woman.

Why are pregnant women prone to UTIs.

.

A

Genital urinary:
-Asymptomatic bacteriuria
-Cystitis; Bladder inflammation
-Pyelonephritis: upper urinary system
inflammation
- renal failure

Increased risk due to physiological changes in pregnancy.

-Progesterone result in relaxation of smooth muscles in the Genitourinary system especially in the collecting duct. There is stasis of urine for a long time which provides breeding environment for bacteria and prone to UTI.

38
Q

State some of the risk factors for UTIs

A

-Short urethra
-Unhygienic practices: front to back wiping
-STIs: Neisseria

39
Q

State the prevention methods of UTIs.

A

Prevention
- Plenty of oral fluids more urinating to flash the urinary system
-Avoiding holding urine for a long time.

40
Q

State the complications on the fetus associated with UTIs.

A

Complications:
*Preterm labor
*Preterm PROM: premature rapture of membranes
*Fetal compromise or IUFD with high fever

41
Q

State respiratory disorders in pregnancy.

A

*Asthma
*Bronchopneumonia
*Pulmonary tuberculosis

42
Q

State endocrine disorders in pregnancy.

A

*Hypothyroidism
*Hyperthyroidism
*Diabetes

43
Q

Viral Hepatitis B

What is its significance to the foetus?

A

Transmission to fetus

44
Q

State the significance of CNS lesions and seizure disorders e.g., Epilepsy.

A

Significance:
Recurrent seizures cut blood supply to the foetus IUGR.

-Congenital anomalies-teratogenicity with treatment( neurotube defects)

-Pre-pregnancy optimization and drug/dose review

-Folate supplementation

-Pregnancy planning

-Risks of neonatal hemolysis