Biochemistry Pregnancy and Fertility Flashcards by tish bullman

Definition of sub-fertility →

Cumulative conception rates:

4 Months 65%
9 Months 82%
12 Months 85%

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Causes of Subfertility →

Ovulatory failure 21%
Tubal damage 14%
Endometriosis 6%
Mucus defect 3%
Sperm defects 24%
Other male 2%
Coital failure 6%
Unexplained 28%
Others 11%

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Assessment of Ovulation →Progesterone (nmol/L)

> 30 ovulation (not sub-fertile)
<30 reduced conception rate
Low level repeat next cycle

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“day 21” progesterone
7 days before menses

Note → Variability in period together → change in follicular phase not luteal phase.
Timing

“day 21” progesterone
7 days before menses

Note → Variability in period together → change in follicular phase not luteal phase.

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Primary Ovarian Failure →

Impaired follicular development >
a. Low oestradiol
b. High LH/FSH (better marker) – PCOS or irregular ovulation – can alter LH levels.

→ No negative feedback to hypothalamus.

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Causes of Ovarian Failure

➢	Premature ovarian Failure
➢	Post menopausal
➢	Autoimmune damage
➢	Surgery
➢	Irradiation (late effects of childhood or early adult cancer)
➢	Dysgenesis (Turners Syndrome)

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Secondary Ovarian Failure

➢ Impaired LH/FSH production
➢ Low LH/FSH – not completely suppressed *
➢ Impaired follicular development > low estradiol

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Causes of secondary Ovarian Failure

LHRH deficiency (Kalmann’s syndrome)
Pituitary tumours (prolactinoma)
Secondary hypopituitarism e.g. irradiation, infiltrative and vascular disorders
Function – weight loss, stress, exercise, starvation
Systemic disease – e.g. thyroid, adrenal

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Kallmann’s Syndrome:

Absent sense of smell

2. Won’t go into puberty

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Polycystic Ovarian Syndrome → Epi

87-90% oligomenorrhea, 26-37% amenorrhoea

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Polycystic Ovarian Syndrome → Diagnosis

Ultrasound → 15 cysts arranged around cortex, echogenic stromal compartment.
Or Endocrine studies (less time consuming)

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Polycystic Ovarian Syndrome → Characteristic features of PCOS

Obesity
Insulin resistance – independent from obesity contribution
Increased cardiovascular risk
Hirsutism
Oestrogenisation – from multiple follicles

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Polycystic Ovarian Syndrome → Serum Levels

LH increased
FSH normal
LH:FSH ratio abnormal
Testosterone increased (free testosterone is a better discrimination

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Polycystic Ovarian Syndrome → Abnormal

Not all patients show the pattern
LH 12.6 93.1-26.0) 1-10 iu/L
• Sensitivity (positivety in disease)-60%
• Specificity (negativity in health)-94%

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Hormonal Assessment of the infertile male:

Semen Analysis
Abnormal
Testicular Problem

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Semen Analysis

Normal – no endocrine tests

Abnormal

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Abnormal

LH/FSH, prolactin testosterone
• Testicular problem
• Hypothalamic pituitary

Testicular Problem

Normal endocrinology

Abnormal endocrinology

Hypergonadotrophic hypogonadism (testicular failure)

serum levels

Low Testosterone
High LH
High FSH

Isolated germinal compartment failure serum levels

Normal testosterone
Normal LH (acting on Leydig)
High FSH (abnormal sertoli cell function)

Non-Endocrine – impaired sperm serum levels

Obstructive azoospermia
Retrograde ejaculation
→ Normal Testosterone
→ Normal LH
→ Normal FSH

Hypogonadotrophic hypogonadism → serum levels

Low Testosterone, LH, FSH

Chemical

Increases – Alk phos, hormone binding proteins

Decreases – Albumin, creatinine, urea

Physiological

Increases – plasma volume, cardiac output, weight gain, GFR early pregnancy
Deceases – Fasting BG early pregnancy, renal threshold for glucose

Endocrine

Increase – Oestrogen, progesterone, prolactin, hCG | Decrease – LH and FSH

Gestational diabetes → Epi

1-2% women develop gestational diabetes

Gestational diabetes → Diagnostic problem

15% women develop g;ycosuria | No accepted reference ranges

Gestational diabetes → Diagnostic tests

Blood glucose, random/fasting | GTT (glucose tolerance)

Gestational diabetes → Risk Factors for gestational diabetes

* BMI >30 kg/m2 * Previous macrosomic baby weighing >4.5 kg * Previous gestational diabetes * Family history diabetes (first degree relative) * Family origin with a high prevalence of diabetes

Gestational diabetes → Diagnostic tests

Blood tests: U and E, urate, urine protein, clotting, LFT | HELLP

Gestational diabetes → HELLP

Haemolysis, Elevated Liver enzymes, low Platelets

Gestational diabetes → HELLP diagnosis

Abnormality seen with raised ALT/AST

Gestational diabetes → Urate in gestational diabetes

Independent raise in pregnancy not explained by the change in renal function associated with pregnancy Increase urate = worse prognosis

Pregnancy related liver disease “Big 5”

1. Pre-eclampsia 2. HELLP 3. Hyperemesis Gravidarum 4. Acute Fatty Liver of Pregnancy 5. Obstetric Cholestasis

Pregnancy Unrelated Liver Disease

6. Pre-existing liver disease | 7. Liver disease co-incident with pregnancy

Obstetric Cholestasis → Definition

Usually occurs in the 3rd trimester | Significant peri-natal mortality and maternal morbidity

Obstetric Cholestasis → Cardinal feature

Generalised puritis (not specific)

Obstetric Cholestasis → Biochemical tests

Serum bile acids (sensitive but not specific) ALT and AST often raised Alkaline phosphatase and bilirubin – no significant contribution

Second Trimester

Triple or quadruple test which provides the current standard of a detection rate above 75% and a false-positive rate of less than 3%

New Guidance First trimester

The “combined test” (nucal translucency, hCG, pregnancy associated plasma protein A) should be offered between 11-13 weeks 6 days

Down’s Syndrome Screening Markers – 2nd Trimester

``` AFP hCG Free-beta hCG Alpha hCG Unconjugated estriol (uE3) Inhibin – A ```

Down’s Syndrome Screening Markers – 1st Trimester

Pregnancy associated plasma protein A nuchal translucency