Nutrition and Health Issues in Pregnancy

Study Notes

Consume only cooked seafood to avoid parasites and bacteria
Avoid fish with high mercury levels (e.g., swordfish, shark, bigeye tuna, king mackerel) as mercury is toxic to fetal neurodevelopment.

Results from hypothalamic-pituitary-ovarian axis suppression due to strenuous exercise, calorie restriction, increased stress, or chronic illness.
Reduced GnRH secretion due to calorie deficiency and stress leads to abnormal FSH/LH pulses and low estrogen levels.
Confirm low estrogen levels with a progesterone challenge test.
Estrogen deficiency increases risk of decreased bone mineral density due to increased bone resorption.

Endometrial hyperplasia is a result of unopposed estrogen stimulation from chronic anovulation.
Withdrawal bleeding occurs from a progesterone challenge test due to high levels of estrogen that cause endometrial proliferation.

Associated with prothrombotic conditions (ex: postpartum).
Presentation varies and may include headache, increased intracranial pressure (ICP), seizures, and/or stroke.
Diagnosis involves obstructed venous flow on MR venography.
Risk factors include thrombophilia (factor V Leiden), pregnancy and postpartum, oral contraceptives (OCPs), malignancy, and infection.
Clinical presentation includes headache (HA), increased ICP, focal neurologic symptoms, seizures, and encephalopathy
Treatment includes anticoagulants (unfractionated heparin or low-molecular-weight heparin [LMWH]).

Pathogenesis includes ectopic implantation of endometrial glands.
Clinical features include dyspareunia, dysmenorrhea, chronic pelvic pain, infertility, dyschezia, cyclic dysuria, and hematuria.

Can involve immobile uterus, cervical motion tenderness, adnexal masses, rectovaginal septum, posterior cul-de-sac, and uterosacral ligament nodules.
Diagnosis includes direct visualization and surgical biopsy.
Treatment involves medical options (oral contraceptives, nonsteroidal anti-inflammatory drugs [NSAIDs]) and surgical resection.
Chronic pelvic inflammation and adhesion formation can lead to infertility.
Distorted pelvic anatomy can also result from the above conditions.

Severe nausea and vomiting during pregnancy, leading to weight loss greater than 5% of pre-pregnancy weight.
Risk factors include multiple gestation and hydatidiform mole.

Risk factors include prolonged rupture of membranes (≥18 hours), preterm premature rupture of membranes (PPROM), prolonged labor and internal fetal/uterine monitoring devices, and repetitive vaginal exams.
Diagnosis requires maternal fever combined with at least one of the following: fetal tachycardia (≥160 bpm), maternal leukocytosis, and/or purulent amniotic fluid.

Widening of the pubic symphysis, often due to fetal macrosomia, multiparity, or precipitous labor.
Presentation includes pain, pubic symphysis tenderness, and difficulty ambulating.
Management is typically conservative, with NSAIDs and physical therapy, and pelvic support.

Results from injury to internal iliac artery branches during delivery.
Clinical manifestations include hemodynamic instability and a palpable mass, possible fever.

Failure of paramesonephric duct development leading to missing/abnormal uterus, cervix, and upper third of vagina.
Clinical features include primary amenorrhea, normal female external genitalia, closed vaginal pouch, absent or rudimentary uterus, and normal functioning ovaries (normal FSH).
Management involves monitoring renal tract for abnormalities, such as via renal ultrasound, and potentially vaginal dilation (surgical or nonsurgical procedures).

46,XY genotype, impaired conversion of testosterone to dihydrotestosterone (DHT).
Impaired virilization during embryogenesis despite normal male testosterone and estrogen levels.
Clinical features include external female genitalia (e.g., blind-ending vagina) in males, genital ambiguity, and virilization at puberty.
Typical features include cliteromegaly, increased muscle mass, and male pattern hair development.
Nodulocystic acne can also be seen in patients with this genetic disorder.

A developmental failure causes a vaginal dimple or complete absence of a vaginal opening without affecting the presence of a uterus and fallopian tubes.

Excessive fluid accumulation in interstitial spaces (pericardial and pleural effusions).

Pathogenesis involves human papillomavirus (HPV) infection (types 16 and 18).
Clinical Presentation includes asymptomatic conditions, postcoital or intermenstrual bleeding, increased vaginal discharge, inguinal lymphadenopathy, and pelvic or low back pain.
Diagnosis through cervical biopsy during colposcopy.