New-onset Medical Disorders Flashcards

1
Q

What is gestational diabetes?

A

-Carbohydrate intolerance of variable severity with onset or first recognition during the current pregnancy
-The diagnosis is arbitrary depending on where the cut-off is placed on the normal spectrum of glucose intolerance in pregnancy

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2
Q

Risk factors for gestational diabetes

A

-Obesity (BMI > 30 kg/m2)
-Family origin with high prevalence of diabetes (South Asian, Caribbean, Middle Eastern)
-Family history of type 2 diabetes or GDM in a 1st degree relative
-Previous macrosomic baby > 4.5kg
-PCOS
-Multiple pregnancy
-Increasing maternal age

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3
Q

Global prevalence of GDM

A

-SEA: 25.9%
-Northern America: 20.7%
-Europe: 15%
-Africa: 13%

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4
Q

Clinical features of GDM

A

-Asymptomatic
-Develops in 2nd or 3rd trimester
-Diagnosed by screening (1 or more risk factors)
-No increase in congenital anomaly

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5
Q

Why does GDM matter?

A

-Increases risk of type 2 diabetes in later life (40-60% in10-15 years)
-A small number identified with GDM will actually have pre-existing diabetes
-Women with GDM have a higher chance of macrosomia and adverse pregnancy outcome
=There is no threshold effect
=We know treatment improves outcomes
=Birth weight has life-long implications for the offspring
=Linear relationship between maternal hyperglycaemia and adverse outcome with no threshold

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6
Q

Overall GDM management

A

-Dietary modification
-Exercise
-Metformin
-Insulin

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7
Q

GDM diet

A

-Choose healthier carbs
-Reduce sugar
-Limit carbohydrate portion size
-Choose sensible snacks
-Understand Glycaemic Index (GI)
=How quickly foods affect your blood sugar

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8
Q

Exercise in GDM

A

-A brisk walk after meals will lower blood sugar –even just 2 minutes!
-Ideally 30 mins at least 3times per week

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9
Q

Pharmacotherapy in GDM

A

-In addition too, not instead of, dietary modification
-1st line metformin (no difference in perinatal outcomes, women prefer oral therapy to insulin_
-2nd line insulin (in addition to metformin, not tolerated instead of)
-Always discontinued after birth

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10
Q

Postnatal management of GDM

A

-Contraception
-Breast feeding support
-HbA1C or OGTT 3 months after birth
-Encourage weight loss and maintenance of healthy eating
-Advise of risk of recurrence of GDM and of future risk of T2DM

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11
Q

Classification of gestational hypertension

A
  1. Gestational hypertension (without proteinuria)
  2. Gestational proteinuria (without hypertension)
  3. Gestational proteinuric hypertension (pre-eclampsia)
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12
Q

What is pre-eclampsia?

A

-Hypertension developing after 20 weeks’ gestation with one or more of the following: proteinuria, maternal organ dysfunction or fetal growth restriction.
-This new definition means that proteinuria is no longer essential for diagnosis.

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13
Q

Potential forms of maternal organ dysfunction in pre-eclampsia

A

-Renal insufficiency (creatinine >90 µmol/L)
-Liver involvement (elevated transaminases—at least twice the upper limit of normal ± right upper quadrant or epigastric abdominal pain)
-Neurological complications (examples include eclampsia, altered mental status, blindness, stroke or, more commonly, hyperreflexia when accompanied by clonus, severe headaches when accompanied by hyperreflexia, persistent visual scotomata)
-Haematological complications (thrombocytopenia—platelet count below 150,000/dL, disseminated intravascular coagulation, haemolysis).

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14
Q

Epidemiology of chronic hypertension and pre-eclampsia

A

-Chronic hypertension is estimated to affect 1% to 5% of pregnant women and is frequently diagnosed for the first time during antenatal care.
-The prevalence of pre-eclampsia varies with the definition used and the population studied; however, pre-eclampsia occurs in less than 5% of an average antenatal population.
-The incidence of non-proteinuric PIH is approximately three times greater

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15
Q

Features of superimposed pre-eclampsia

A

-A rapid rise in hypertension
-New onset or doubling of proteinuria
-Other laboratory parameters, for example, low platelets, or raised liver enzymes or creatinine

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16
Q

Risk factors for pre-eclampsia

A

-First pregnancy
-Family history—mother/sister (x4-8 risk)
-Extremes of maternal age (40+)
-Obesity

-Medical factors:
=Pre-existing hypertension (20%)
=Renal disease
=Acquired thrombophilia—antiphospholipid antibodies
=Inherited thrombophilia
=Connective tissue disease (e.g., systemic lupus erythematosus)
=DM

-Obstetric factors
=Multiple pregnancy
=Previous pre-eclampsia (particularly requiring delivery before 37 weeks: 20% chance redeveloping)
=Hydatidiform mole
=Triploidy
=Hydrops fetalis (immune and non-immune)
=Inter-pregnancy interval of >10 years

17
Q

Symptoms of pre-eclampsia

A

-Severe headache
-Severe right upper quadrant and epigastric abdominal pain
-Sudden swelling of the face, hands or feet
-Visual disturbances, including blurring, flashing or scotoma
-Vomiting
-Restlessness or agitation

18
Q

Signs of pre-eclampsia

A

-Hypertension and proteinuria
-Hyperreflexia
-Serum creatinine raised
-Platelet count decreased
-Clonus
-Haemolytic anaemia
-Elevated liver enzymes
-Retinal haemorrhages and papilloedema

19
Q

Assessment/ investigation of pre-eclampsia

A

-BP

-Urinary protein
=exceeds 30 mL/dL, a level that usually correlates with 1+ on a urine dipstick
=Gold standard confirmation of the diagnosis would be 24-hour collection of urine (with >300 mg proteinuria in 24 hours being considered elevated).
=Albumin:creatinine ratio (ACR) and protein:creatinine ratio (PCR) are commonly used in clinical practice to quantify urinary protein, with 30 mg/mmol used as a threshold for significant proteinuria.

-Blood test
=FBC (reduced platelets, haemoglobin, haemolysis)- HELLP
=Renal function (reduced UO, increased urate, urea, creatinine)
=Coagulation system (prolonged coagulation indices)
=Hepatic (elevated ALT and AST)

-Fetal assessment
=Fundal height
=Fetal movements
=Fetal growth ultrasound

20
Q

Pre-eclampsia prophylaxis

A

-Low-dose aspirin (100-150mg daily from 12 weeks- 15% reduction in incidence)
-Possibly of Value: Calcium supplementation
-Not of Value
=Diet with high protein content
=Restriction of salt in diet
=Restriction of weight gain
=Vitamins C and E

21
Q

Clinical management of pre-eclampsia

A

-Fetal advantages to conservative management before 34 weeks if the blood pressure, laboratory values and fetal condition are stable
-Control maternal blood pressure
-Assess maternal fluid balance
-Prevent seizures/ eclampsia
-Consider delivery
-Optimise postnatal care

22
Q

Controlling maternal BP in Pre-eclampsia

A

-Reduce the diastolic blood pressure to <100 mmHg using labetalol, nifedipine, hydralazine or methyldopa
-Effective control of hypertension is essential to prevent cerebrovascular accidents.
=As intracerebral haemorrhage contributes to a significant proportion of deaths, systolic blood pressure should always be <150 mmHg and treated aggressively if not.
-Labetalol is now recommended as first-line treatment. Regimens vary, but NICE guidelines now recommend a standard approach to hypertensive management.

23
Q

Assess maternal fluid balance in pre-eclampsia

A

-Pre-eclampsia is associated with an increased vascular permeability and a reduced intravascular compartment.
=Administering too little fluid risks maternal renal failure and giving too much fluid may cause pulmonary oedema.
-Fluid input and urine output should be monitored.
-In severe pre-eclampsia, the maternal oxygen saturation (SaO 2 ) should also be monitored, along with serum urea and electrolytes, liver function tests, haemoglobin, haematocrit, platelets and coagulation.
-If there is marked oliguria, central venous pressure monitoring may be helpful to differentiate intravascular volume depletion from renal impairment.

24
Q

Preventing eclampsia

A

-The use of magnesium sulphate (MgSO 4 ) in severe pre-eclampsia halves the risk of subsequent eclampsia and may reduce the risk of maternal death.
- MgSO 4 given to those who have had an eclamptic seizure prevents further seizures.

25
Q

Timing of delivery in pre-eclampsia

A

-Depends on the maternal condition, fetal condition and gestational age.
-Maternal indications for delivery include
=gestation ≥37 weeks
=an inability to control hypertension
=deteriorating liver or renal function
=progressive fall in platelets
=Neurological complications.

-Fetal indications include
=abnormal fetal heart rate monitoring or a fetal condition that is clearly deteriorating.

-If pre-term delivery is being considered at <34 weeks’ gestation, corticosteroids should be administered to the mother to reduce the risks associated with prematurity unless there is acute compromise requiring immediate delivery

26
Q

Optimising postnatal care in pre-eclampsia

A

-Women with pre-eclampsia who remain hypertensive in the initial postpartum period are still at risk of pre-eclampsia-related complications, particularly for the initial 72 hours following delivery when the blood pressure often peaks.
-Continued vigilance is advisable during this period, as an inpatient if necessary.

27
Q

Maternal complications of pre-eclampsia

A

-Placental rupture
-Disseminated intravascular coagulation
-HELLP syndrome
-Pulmonary oedema
-Aspiration
-Eclampsia
-Liver failure or haemorrhage
-Stroke
-Death
-Long-term cardiovascular morbidity

28
Q

Neonatal complications of pre-eclampsia

A

-Pre-term delivery
-Intrauterine growth restriction
-Hypoxia-neurological injury
-Perinatal death
-Long-term cardiovascular morbidity (associated with low birth weight)

29
Q

What is HELLP?

A

-HELLP syndrome (which affects 10%–20% of eclamptic pregnancies) is defined by the presence of haemolysis, elevated liver enzymes and a low platelet count.
-Associated morbidity commonly includes disseminated intravascular coagulation, placental abruption and acute renal failure.
-It is also associated with maternal mortality in between 1.1% and 25% of cases (with the most common causes of mortality being haemorrhage and stroke).

30
Q

Long term implications of pre-eclampsia

A

-3x risk of hypertension (6x if recurrent pre-eclampsia)
-2x risk IHD
-2-3x risk of T2DM

31
Q

Presentation of obstetric cholestasis

A

-Usually presents after 30 weeks’ gestation, possibly due to a genetic predisposition to the cholestatic effect of oestrogens.
-Pruritus affects the limbs and trunk, and it is often severe.
-Pale stools, dark urine

32
Q

Investigation and diagnosis of obstetric cholestasis

A

-There may be a positive family history in up to 35% of cases.
-Serum total bile acid concentration is increased early in the disease and is the optimum marker for the condition.
-Transaminases may be increased (<3-fold).
-Bilirubin is usually <100 µmol/L

33
Q

Risks and management of obstetric cholestasis

A

-There are no serious long-term maternal risks, but there is a risk of pre-term birth, fetal distress, and intrauterine fetal death.
-Birth at 37–38 weeks should be discussed with the woman, if bile acids are markedly elevated, in an effort to prevent fetal death.