CFB OG01 Physiology Of Pregnancy And Minor Ailments
Physiology of pregnancy encompasses the maternal anatomical and physiological adaptations—cardiovascular, respiratory, renal, endocrine, and hematological—that support fetal development, along with the common minor ailments such as nausea, heartburn, constipation, varicose veins, and backache that arise from these changes.
Physiology of Pregnancy & Minor Ailments
The Big Idea: A pregnant woman's body undergoes proactive, systematic physiological adaptations across every organ system — not as a response to pathology, but as a purposeful anticipatory strategy to provide energy, oxygen, and nutrition to the developing fetus while maintaining maternal safety. These changes alter lab values, cause common symptoms ("minor ailments"), and create clinical pitfalls that examiners love to test. Understanding "why" each change occurs from first principles is far more useful than memorising isolated numbers.
Learning Objectives (from the lecture slide): [1]
- Describe the effects of pregnancy on the major organ systems
- Discuss the clinical implications of these changes with reference to changes in laboratory test results and clinical features
- Manage common minor ailments of pregnancy and discuss the differential diagnoses
- Identify and interpret changes in body function due to the effect of pregnancy
- Counsel women on normal pregnancy and common obstetric problems
The physiological adaptations of pregnancy are proactive rather than reactive — they exist to maintain a safe environment for the fetus and to provide extra energy, nutrition, and oxygen needed to support fetal growth. [1]
Why 'Proactive' Matters for Exams
Examiners may ask you to explain why a healthy pregnant woman's blood pressure drops in the second trimester or why her pCO2 is lower than normal. The answer is never "because the body is trying to compensate for a problem" — it's because the body anticipates the need ahead of time. This framing is the key discriminator in MCQs about normal vs pathological findings.
From first principles: The placenta is metabolically greedy — it demands oxygen, glucose, and amino acids continuously. The mother's body cannot wait for the fetus to "ask" for these resources; by the time fetal distress signals arrive, it would be too late. So every system ramps up early — cardiac output rises sharply in the first trimester, GFR increases by 50% before the fetus is even large, and ventilation increases well before oxygen demand peaks.
Part 2: System-by-System Physiological Changes
2.1 Respiratory System
Mechanical effects: A combination of the enlarging uterus along with hormonal changes and increasing laxity of the thoracic ligaments affects the anatomy of the thoracic cage. [1]
| Change | Mechanism | Why it matters |
|---|---|---|
| Lifting of rib cage with upward flaring of ribs | Relaxin loosens ligamentous attachments → AP and transverse diameters ↑ → lower chest circumference ↑ by ~5 cm | Compensates for diaphragm elevation so vital capacity is preserved |
| Costal angle widens | Same mechanism | Allows thoracic expansion despite rising diaphragm |
| Elevation of diaphragm | Enlarging uterus pushes abdominal contents up ~4 cm | Despite elevation, diaphragmatic function remains normal and its excursion is not reduced — this is a common exam trap |
Exam Trap
Students often say "the diaphragm is pushed up so it moves less." The lecture explicitly states diaphragmatic excursion is NOT reduced. The rib cage compensates by widening. This is directly testable.
| Parameter | Change | Numbers | Mechanism |
|---|---|---|---|
| O2 consumption | ↑ 20% | 220 → 260-270 mL/min (30-40 mL/min increase) | To support extra cardiac, renal, respiratory work + uterine/breast development + feto-placental metabolism |
| Ventilation | ↑ 40% | — | Progesterone acts on medullary respiratory centre, lowering CO2 set point |
| Tidal volume | ↑ 40% | 500 → 700 mL | Progesterone-driven; the main way ventilation increases |
| Respiratory rate | No change | — | Ventilation increases entirely through tidal volume, NOT rate |
| Maternal pCO2 | ↓ | 4.8 → 3.7 kPa | Purpose: creates a larger CO2 gradient across the placenta so fetal CO2 (7.3 kPa) can diffuse to the mother more efficiently |
| FRC | ↓ | — | Diaphragm elevation compresses the residual volume |
| ERV | ↓ ~20% | — | Same mechanism |
| Inspiratory capacity | ↑ | — | Compensates for reduced ERV |
| Vital capacity | No change overall | — | ↑IC offsets ↓ERV |
Why pCO2 drops — the "CO2 gradient" concept: The fetus produces CO2 that must cross the placenta into maternal blood. If maternal pCO2 were 4.8 kPa (normal) and fetal pCO2 were 7.3 kPa, the gradient would be only 2.5 kPa. By dropping maternal pCO2 to 3.7 kPa, the gradient widens to 3.6 kPa — a 44% improvement in driving pressure for CO2 transfer. This is elegant physiology driven by progesterone's effect on the respiratory centre.
Dyspnoea during normal pregnancy is common, mechanism not entirely clear → progesterone-induced hyperventilation → dyspnoea during pregnancy correlated with a low pCO2 [1]
Why dyspnoea? The sensation of breathlessness is linked to the respiratory drive outstripping the actual need — the woman's brain is being told to breathe more by progesterone, and she perceives this heightened drive as dyspnoea. It is NOT from mechanical restriction (the diaphragm still moves fine). Important differential: exclude cardiac disease, PE, asthma exacerbation, and anaemia before attributing dyspnoea to normal pregnancy.
2.2 Cardiovascular System
↓ Systemic vascular resistance 35-40% of baseline - ↓ afterload [1] ↑ Plasma volume – ↑ preload [1] ↑ Heart rate progressively throughout pregnancy by 10-20 bpm, max in 3rd trimester [1] ↑ Stroke volume [1] ↑ Cardiac output by 30-50%; sharpest rise in cardiac output occurs by the beginning of the 1st trimester, and there is a continued increase into the 2nd trimester, further ↑ during labour [1]
| Parameter | Direction | Magnitude | Timing | Mechanism |
|---|---|---|---|---|
| SVR | ↓ | 35-40% | Early pregnancy | Progesterone + nitric oxide + prostacyclin from placenta → vasodilation |
| Plasma volume | ↑ | ~40-50% | Starts 6-8 weeks, peaks 30-34 weeks | RAAS activation; oestrogen stimulates hepatic angiotensinogen; also aldosterone ↑ |
| Heart rate | ↑ | 10-20 bpm | Progressive, max 3rd trimester | Compensatory for ↓ SVR; also sympathetic tone ↑ |
| Stroke volume | ↑ | ~25% | Peaks mid-pregnancy | Frank-Starling: ↑ preload from ↑ plasma volume |
| Cardiac output | ↑ | 30-50% | Sharp early ↑, continues into 2nd trimester, further ↑ in labour | CO = HR × SV; both increase |
| Blood pressure | ↓ then ↑ | See below | Nadir 2nd trimester | SVR drops more than CO rises early on |
↓ Systolic blood pressure (SBP), ↓ Diastolic blood pressure (DBP) to a nadir during the 2nd trimester (dropping 5-10 mmHg below baseline), then gradually ↑ during 3rd trimester to near pre-pregnant level at term [1]
Why the BP dip matters clinically:
- A woman with pre-existing hypertension may appear normotensive in the 2nd trimester → the "physiological dip" can mask chronic hypertension.
- Conversely, if BP rises in the mid-trimester (even if still < 140/90), that is unusual and should raise suspicion for pre-eclampsia or chronic hypertension. [1]
It is unusual if the BP starts to rise during the mid-trimester even though it is still below 140/90 mmHg [1]
This directly connects to the hypertension-in-pregnancy lectures and past paper Q10 (2020): a woman with BP 150/98 at 13 weeks → chronic hypertension (because gestational hypertension and pre-eclampsia are diagnosed after 20 weeks). [5]
Ejection systolic murmur may be detected from mid-trimester ("flow murmur") due to the hyperkinetic state of the CVS system [1]
- This is an innocent flow murmur — increased cardiac output, stroke volume, and heart rate create turbulence across a normal valve. It does NOT signify valvular disease.
- More common for gestational hypertension & preeclampsia to be diagnosed in the 3rd trimester — because BP naturally rises back towards baseline in the 3rd trimester, crossing the diagnostic threshold in susceptible women. [1]
High-Yield Connection: Supine Hypotension
The gravid uterus in late pregnancy can compress the IVC when the woman lies flat → ↓ venous return → ↓ cardiac output → hypotension, dizziness, syncope. This was directly tested in the 2023 SAQ Q2. Advise left lateral tilt position. This is a separate concept from the general vasodilation-related fainting.
2.3 Haematological System
↑ Plasma volume starting at 6 to 8 weeks and rising progressively until 30-34 weeks [1] ↑ Red blood cell mass by 20%, erythropoiesis is increased, provided that the mother has normal nutrition and sufficient iron and vitamin supplement [1] Plasma volume ↑↑ proportionally more than the red blood cell mass, resulting in a "physiological anemia" from hemodilution [1]
| Component | Change | Why |
|---|---|---|
| Plasma volume | ↑ ~40-50% | RAAS, oestrogen-driven |
| RBC mass | ↑ ~20% | Erythropoietin increases; BUT requires adequate iron/folate |
| Net effect | ↓ Hb, ↓ Haematocrit, ↓ RBC count | Dilutional — plasma rises MORE than RBC mass |
From first principles: The body increases plasma volume more than RBC mass because the primary goal is to reduce blood viscosity (making it easier to pump blood through the low-resistance placental circulation) and to provide a buffer for blood loss at delivery. The "cost" is a lower Hb concentration — but total oxygen-carrying capacity is actually increased because total RBC mass is up 20%.
Normal Hb threshold in pregnancy: Generally Hb > 11 g/dL in first trimester, > 10.5 g/dL in second trimester is acceptable. Below this → investigate for true iron deficiency, folate deficiency, thalassaemia etc.
| Parameter | Direction | Why |
|---|---|---|
| ↑ WBC (↑ neutrophil) | ↑ | Stress/cortisol; also demargination |
| ↓ Platelet count | ↓ | Haemodilution + ↑ consumption + increased fibrinolysis in uteroplacental circulation |
| ↑ Procoagulatory factors (VII, VIII, X, fibrinogen) | ↑ | Prepares for haemostasis at delivery — the placental bed has massive blood flow and needs rapid clotting when the placenta separates |
| ↓ Antithrombin III, ↓ Protein S | ↓ | Shifts balance towards clotting |
Pregnancy is a relatively pro-coagulatory state; need to watch out for venous thromboembolism esp. if other risk factors e.g. prolonged bed rest are present [1]
Clinical relevance points from the lecture: [1]
- Note Hb level at booking visit & repeat Hb later in pregnancy (26-30 weeks); the woman may become anaemic in later part of the pregnancy
- Expansion in plasma vol. is relatively less in women with preeclampsia; need to watch out if the woman has static/increasing haematocrit — this is a subtle but high-yield point: in pre-eclampsia, plasma leaks into the interstitium due to endothelial damage, so haemoconcentration occurs
- Thrombocytopenia due to pregnancy — 8-10% of normal pregnancy — gestational thrombocytopenia is benign, typically platelet > 70 × 10⁹/L, resolves postpartum
VTE in Pregnancy
Pregnancy increases VTE risk 5-fold. Risk is highest 6 weeks postpartum [3]. If anticoagulation is needed, the ONLY option antenatally is LMWH — it does not cross the placenta. Warfarin and DOACs are contraindicated in pregnancy. The 2022 MCQ Q13 and 2025 MCQ Q10 both tested post-CS DVT scenarios.
↑ Thyroxine-binding globulin [1] ↑ Total T4 and T3 rise by approximately 50 percent during the first half of pregnancy, plateauing at approximately 20 weeks of gestation [1] human chorionic gonadotrophin (hCG) has weak thyroid-stimulating activity (peaks at ~12 weeks) → ↓ TSH or ↑ free T4 and T3 [1]
From first principles:
- Oestrogen stimulates the liver to produce more TBG → more total T4/T3 bound → total T4/T3 goes up, but free T4/T3 may be normal.
- hCG shares structural similarity with TSH (both are glycoprotein hormones with a common alpha subunit). At high concentrations (peaking ~12 weeks), hCG weakly stimulates the TSH receptor → mild ↑ free T4 → feedback suppresses TSH.
- This produces transient subclinical hyperthyroidism in the first trimester.
The transient, usually subclinical, hyperthyroidism should be considered a normal physiologic finding [1] Use trimester-specific reference range during pregnancy [1]
Why this matters: If you measure TSH in the first trimester and see it slightly low with mildly elevated fT4 — this may be NORMAL, not Graves' disease. The clinical clue to pathological hyperthyroidism would be persistent symptoms, goitre, eye signs, or very suppressed TSH with markedly high fT4 beyond the first trimester.
Connection to antithyroid drug management in pregnancy: [4]
- If hyperthyroidism requires treatment in pregnancy → use PTU in the first trimester (less teratogenic than MMZ/CMZ)
- Switch to MMZ in the second trimester (PTU has hepatotoxicity risk)
Carbohydrate Metabolism (from senior notes) [2]
- Insulin resistance increases progressively, especially in the 2nd half of pregnancy
- Mechanism: placental hormones (human placental lactogen [hPL], cortisol, glucagon, progesterone) → antagonise insulin
- Purpose: shunt glucose/nutrients to the fetus ("facilitated anabolism" in early pregnancy → "accelerated starvation" in late pregnancy)
- In women with insufficient pancreatic reserve → gestational diabetes mellitus (GDM)
↑ Kidneys size (1 cm in length and volume increases by up to 30%) [1] Marked dilatation of calyces, renal pelvis & ureters in most pregnant women due to hormonal factors and in later pregnancy, the enlarging uterus [1] ↑ Renal plasma flow increased by 60-80% [1] ↑ Glomerular filtration rate (GFR) by 50% over nonpregnant women by the end of the 1st trimester [1] ↓ Serum creatinine and urea level [1] ↓ Reabsorption of glucose by kidney [1] ↑ Excretion of glucose across glomerulus by 10x [1]
Why GFR ↑ by 50%:
- Cardiac output ↑ 30-50% → more blood delivered to kidneys
- SVR ↓ → renal vascular resistance ↓ → more blood flows through glomeruli
- Progesterone + relaxin dilate afferent arterioles
- This increased GFR means the kidney filters more creatinine and urea per minute → serum creatinine and urea DROP. A "normal" creatinine in a non-pregnant woman might actually represent renal impairment in a pregnant woman.
Why glycosuria occurs:
- GFR ↑ 50% → more glucose filtered per minute
- ↑ Excretion of glucose across glomerulus by 10x — the tubular maximum for glucose reabsorption (Tm glucose) does not increase proportionally
- Result: glucose spills into the urine even at normal blood glucose levels
Glycosuria by dipstick testing is common in pregnancy — may be present in the absence of hyperglycaemia or renal disease [1]
Exam Trap: Glycosuria ≠ GDM
Finding glucose on urine dipstick in a pregnant woman does NOT automatically mean gestational diabetes. It may be physiological glycosuria due to increased GFR and reduced tubular reabsorption. However, persistent or heavy glycosuria warrants a 75g OGTT to exclude GDM. This is a classic MCQ discriminator.
Physiological hydronephrosis & hydroureters during pregnancy — usually more over the right side [1]
Why right > left? The dextro-rotated uterus preferentially compresses the right ureter against the pelvic brim. The left ureter is partly protected by the sigmoid colon. This is important because it can mimic obstructive uropathy on ultrasound — don't panic at "bilateral hydronephrosis" on an obstetric renal USS.
Physiological changes in pregnancy include relaxation of smooth muscle resulting in: [1]
- ↑ Intragastric pressure
- ↓ Lower oesophageal sphincter pressure
- ↓ Gastric peristalsis
- ↓ Gastric emptying
- ↑ Small and large bowel transit time (↑ water absorption from gut)
The "Progesterone on Smooth Muscle" Principle: Progesterone relaxes ALL smooth muscle — this is the single unifying mechanism behind most GI changes (and many other minor ailments):
- LES relaxation → reflux → heartburn
- ↓ Gastric motility → delayed emptying → nausea
- ↓ Colonic motility + ↑ water absorption → constipation
- Venous smooth muscle relaxation → varicosities
Gastro-oesophageal reflux, nausea and vomiting, and constipation are common in pregnancy [1]
Clinical relevance for anaesthesia: Delayed gastric emptying + ↓ LES tone → increased aspiration risk during general anaesthesia in pregnant women. This is why pregnant women undergoing emergency caesarean under GA receive sodium citrate (antacid) and rapid-sequence induction with cricoid pressure (Sellick's manoeuvre).
↑ Alkaline phosphatase (ALP) with gestation due to placental production (2-4 fold by term, max 400 U/L in the 3rd trimester) therefore may not be reliable [1] ↓ Gamma glutamyl transferase (GGT) [1] ↓ Albumin by 20-40%; this is partially dilutional due to increased total blood volume (contributes to most of the fall in total serum protein) [1] ↓ Bilirubin [1] No change in bile acid, aminotransferases (ALT, AST) [1]
| LFT Parameter | Change | Mechanism |
|---|---|---|
| ALP | ↑ 2-4 fold | Placental isoenzyme production (heat-stable ALP) |
| GGT | ↓ | Uncertain; may be dilutional |
| Albumin | ↓ 20-40% | Dilutional + ↑ catabolism for fetal amino acid supply |
| Bilirubin | ↓ | Dilutional |
| ALT, AST | No change | Any rise = pathological (investigate!) |
| Bile acids | No change | Any rise = suspect intrahepatic cholestasis of pregnancy |
Caution with interpretation of laboratory results e.g. alkaline phosphatase (ALP) during pregnancy may not be reliable, need specific tests (isoenzymes) to exclude liver or bone cause [1]
Key Exam Point: Unchanged LFTs in Pregnancy
ALT, AST, and bile acids do NOT change in normal pregnancy. If you see elevated transaminases → think HELLP syndrome, acute fatty liver of pregnancy, viral hepatitis. If you see elevated bile acids → think intrahepatic cholestasis of pregnancy (ICP). An elevated ALP alone is usually just placental and does NOT indicate liver disease. This is a frequently tested concept.
| System | Key Changes | Direction | Clinical Significance |
|---|---|---|---|
| Respiratory | O2 consumption, tidal volume, ventilation | ↑ | Dyspnoea may be normal |
| Respiratory | pCO2 | ↓ | Facilitates CO2 transfer from fetus |
| Respiratory | Respiratory rate, vital capacity | No change | Don't confuse tachypnoea with normal pregnancy |
| CVS | CO, HR, SV, plasma volume | ↑ | Flow murmur is normal |
| CVS | SVR, BP (nadir 2nd trimester) | ↓ | May mask chronic HTN; rising BP in mid-trimester is abnormal |
| Haematological | Plasma volume (> RBC mass) | ↑↑ vs ↑ | Physiological anaemia |
| Haematological | Factors VII, VIII, X, fibrinogen | ↑ | Pro-coagulatory state → VTE risk |
| Haematological | Protein S, Antithrombin III | ↓ | Same |
| Haematological | Platelets | ↓ | Gestational thrombocytopenia (8-10%) |
| Endocrine | TBG, total T4/T3 | ↑ | Don't diagnose hyperthyroidism on total T4 alone |
| Endocrine | TSH (1st trimester) | ↓ | hCG effect; use trimester-specific reference ranges |
| Renal | GFR, renal plasma flow | ↑ | ↓ creatinine/urea; glycosuria is common |
| Renal | Renal pelvis/ureters | Dilated | Physiological hydronephrosis (R > L) |
| GI | LES tone, gastric motility | ↓ | Reflux, N/V, constipation |
| GI | Gut transit time | ↑ | ↑ water absorption → constipation |
| Hepatobiliary | ALP | ↑ 2-4× | Placental; unreliable for liver/bone |
| Hepatobiliary | Albumin | ↓ 20-40% | Dilutional; affects drug binding |
| Hepatobiliary | ALT, AST, bile acids | No change | If elevated → pathological |
Part 3: Minor Ailments of Pregnancy
Not life-threatening but cause discomfort & distress to many pregnant women [1] Due to adaptation of the maternal body to provide a safe environment for the fetus [1] Many are caused by the effect of progesterone on the smooth muscles and connective tissues of the body [1]
The lecture lists 10 minor ailments. Each is linked to the physiological changes above.
Onset is always in the 1st trimester, usually till 12 weeks of gestation [1] Affects 70% of pregnant women [1] Severe – hyperemesis gravidarum [1] Aetiology: Unknown, various contributory factors been proposed; primarily thought to be associated with rising levels of hCG [1]
Why hCG? hCG rises exponentially until ~12 weeks, then declines — matching the timeline of morning sickness perfectly. hCG stimulates the chemoreceptor trigger zone (CTZ) in the area postrema. Higher hCG levels (e.g., multiple pregnancy, molar pregnancy) → worse nausea.
Prevention & Treatment: [1]
- Dietary change and lifestyle changes, avoid triggers
- Light snacks instead of large meals
- Avoid iron supplements (iron is very emetogenic)
- Seek medical advice if severe vomiting – may need to correct electrolytes & fluid imbalance
- Anti-emetics:
- H1 receptor antagonists (Dimenhydrinate)
- Dopamine antagonist (Promethazine)
- UGI motility stimulants (Metoclopramide)
Hyperemesis gravidarum = severe, intractable vomiting → dehydration, ketonuria, electrolyte disturbance, weight loss > 5%. May need IV fluids, thiamine supplementation (prevent Wernicke's), hospital admission.
Differential: Vomiting in 1st Trimester
If onset is NOT in the 1st trimester, or vomiting persists beyond 20 weeks without other explanation, consider alternative diagnoses: UTI, appendicitis, bowel obstruction, molar pregnancy, hyperthyroidism, intracranial pathology. Remember to check urine pregnancy test and thyroid function in any woman of childbearing age with vomiting [6].
Burning sensation felt behind sternum caused by reflux of acid gastric contents into the oesophagus [1] Affects 50% of pregnant women [1]
Aetiology: [1]
- Relaxing effect of progesterone on cardiac sphincter (LES)
- ↑ intragastric pressure from pressure due to growing uterus
- Flattening of diaphragm distorts the shape of the stomach & ↓ the angle at the gastroesophageal junction
The angle of His (the acute angle between the oesophagus and gastric fundus) normally acts as a flap valve preventing reflux. When the diaphragm is pushed up, this angle becomes more obtuse → reflux.
Prevention & Treatment: [1]
- Small, frequent meals, low in spices
- Avoid food that may lower the sphincter pressure e.g. chocolate, coffee, alcohol
- Sleeping in a more upright position by using additional pillows
- Antacids — taken after meals and at bed time
May lead to development of haemorrhoids, which in turn may increase constipation because of fear of pain [1]
Aetiology: [1]
- ↓ gut motility caused by progesterone
- ↑ water absorption from gut due to ↑ gut transit time
- Oral iron supplement (iron is constipating)
Prevention & Treatment: [1]
- Increase dietary fibre
- Adequate fluid intake
- Moderate exercise and maintain regular bowel habits
- Stool softener / laxative
Occurs when there is insufficient blood & oxygen to the brain [1]
Aetiology: [1]
- ↑ vasodilatation due to effect of progesterone on smooth muscle
- Standing erect for long period of time → venous pooling in lower limbs
Supine hypotension — ↓ cardiac output due to ↓ venous return caused by pressure of gravid uterus on vena cava when the patient is lying flat on her back [1]
This is the "aortocaval compression syndrome" — the heavy uterus (especially in late 2nd and 3rd trimester) compresses the IVC and sometimes the aorta when the woman lies supine. This reduces preload dramatically → ↓ CO → hypotension → syncope.
Prevention & Treatment: [1]
- Get up slowly after sitting or lying down
- If feel faint when standing still, find a seat quickly
- Avoid total supine position, turning to lie on side if starts to feel faint lying on back
2023 SAQ Q2 – Directly Tested!
A 36-year-old at 28 weeks with dizziness in the supine position. The expected answers were: (a) supine hypotension syndrome / aortocaval compression, (b) the underlying changes — enlarged gravid uterus compresses IVC → ↓ venous return → ↓ cardiac output → ↓ cerebral perfusion; also ↓ SVR from progesterone; (c) repeat Hb at 26-30 weeks to rule out anaemia; (d) avoid lying flat, lie on left side, get up slowly [7].
Include varicose veins, haemorrhoids, vulval varicosities [1]
Aetiology: [1]
- Relaxing effect of progesterone on the smooth muscles of the wall of the veins
- Aggravated by the growing uterus, which causes pelvic congestion & poor venous return
- Constipation (straining → haemorrhoids)
Prevention & Treatment: [1]
| Type | Management |
|---|---|
| Haemorrhoids | Prevention/treatment of constipation; topical Anusol suppositories/ointment; surgery NOT performed during pregnancy |
| Varicose veins | Avoid prolonged standing; exercise leg muscles; leg elevation; support stockings |
| Vulval varicosities | Sanitary pad/panty girdle for support; caution when cutting the episiotomy (risk of massive venous bleeding) |
Affects 50% of pregnant women [1]
Aetiology: [1]
- Increased lumbar lordosis causing strain on back muscles (the centre of gravity shifts forward as the uterus grows → compensatory lordosis)
- Ligamentous laxity due to hormone effects — progesterone and relaxin
Prevention & Treatment: [1]
- Comfortable chair supporting back and thighs
- Stand tall with abdomen & buttocks tucked in
- Wear flat shoes for even weight distribution
- Sleep on good mattress
- Use arms to push up into sitting position first (avoid straining the back)
- Avoid lifting heavy objects
Often occur at night and can be very painful, affecting sleep and daily activities [1] More common during the 3rd trimester [1] Exact reason unknown [1]
Prevention & Treatment: [1]
- Regular gentle exercise in pregnancy, particularly ankle and leg movements, to improve circulation
- Magnesium, calcium or non-pharmacological treatment options can be used based on a woman's preferences (WHO recommendation)
Numbness & tingling sensation in the fingers and hands [1] Worse at night, common in 2nd & 3rd trimesters [1] Fluid retention & swelling of connective tissues which compresses the median nerve as it runs through the carpal tunnel in the wrist [1]
Prevention & Treatment: [1]
- Elevate the hand
- Nocturnal wrist splinting
- Physiotherapy
Note from senior notes [2]: surgical decompression is rarely performed during pregnancy; symptoms usually resolve postpartum as fluid retention resolves.
Affects the pregnant women most during the 1st and 3rd trimester [1]
Aetiology: [1]
- Pressure from the growing uterus on the bladder
- ↑ glomerular filtration rate and urine output
- Fatigue and more time spent in bed at night
Why 1st AND 3rd but not 2nd? In the 1st trimester, the uterus is still in the pelvis and directly compresses the bladder. In the 2nd trimester, the uterus rises out of the pelvis → bladder pressure relieved. In the 3rd trimester, the fetal head descends ("lightening"/"engagement") and again compresses the bladder.
Prevention & Treatment: [1]
- Fluid restriction in the evening with ↑ fluid intake earlier in the day
- Limit intake of natural diuretics e.g. caffeine
Important Differential
Urinary frequency can also be from UTI (dysuria, haematuria, fever) or gestational diabetes (polyuria with polydipsia). Always check MSU and dipstick. Don't dismiss all urinary symptoms as "normal pregnancy."
| Ailment | Timing | Mechanism | Key Management |
|---|---|---|---|
| N/V | 1st trimester | hCG ↑ | Dietary modification; anti-emetics; avoid iron |
| Heartburn | Any, worse later | ↓ LES tone (progesterone) + ↑ intragastric pressure | Small meals; antacids; elevate head |
| Constipation | Any | ↓ gut motility (progesterone); ↑ water absorption; iron | Fibre, fluids, exercise; laxatives |
| Fainting | Any | Vasodilation; supine hypotension | Avoid supine; get up slowly; left lateral |
| Varicosities | 2nd-3rd trimester | Progesterone on venous wall; pelvic congestion | Support stockings; Anusol; NO surgery in pregnancy |
| Backache | Any, worse later | ↑ lordosis; ligament laxity | Flat shoes; posture; avoid heavy lifting |
| Leg cramps | 3rd trimester | Unknown | Exercise; Mg/Ca supplementation |
| CTS | 2nd-3rd trimester | Fluid retention → median nerve compression | Wrist splint; elevate hand |
| SPD | Usually 3rd trimester | Relaxin → pubic symphysis widening | Rest; pelvic support; analgesia |
| Urinary frequency | 1st and 3rd trimester | Uterine pressure on bladder + ↑ GFR | Fluid redistribution; limit caffeine |
Exam Intelligence
-
MCQ: "Which of the following is a normal finding in pregnancy?" → Answers: glycosuria, physiological anaemia, low pCO2, ejection systolic murmur, mild hydronephrosis (all correct — pick the one they ask about)
-
SAQ: "A 28-week pregnant woman has dizziness in supine position. Name the condition and underlying changes." → Supine hypotension / aortocaval compression; gravid uterus compresses IVC → ↓ venous return → ↓ CO (2023 SAQ Q2) [7]
-
MCQ: "BP 150/98 at 13 weeks, urine dipstick negative." → Chronic hypertension (NOT gestational HTN or pre-eclampsia, which require > 20 weeks) (2020 MCQ Q10) [5]
-
MCQ/SAQ: "What investigation at 26-30 weeks?" → Hb level to check for anaemia [1], or 75g OGTT for GDM screening (depending on risk factors) [5]
-
MCQ: "Which LFT is unreliable in pregnancy?" → ALP (placental production, 2-4× normal) [1]
| Trap | Correct Answer |
|---|---|
| "Respiratory rate increases in pregnancy" | No — tidal volume increases; rate is unchanged |
| "Diaphragm excursion is reduced" | No — diaphragm moves normally despite elevation |
| "Glycosuria = GDM" | No — may be physiological; needs OGTT to confirm |
| "Rising BP at 16 weeks but < 140/90 is normal" | No — unusual; should raise suspicion |
| "Low TSH = Graves' disease in 1st trimester" | No — may be physiological from hCG; use trimester-specific ranges |
| "Elevated ALP means liver disease" | No — placental ALP is the cause; check isoenzymes |
| "ALT/AST normally rise in pregnancy" | No — they are UNCHANGED; elevation is pathological |
High Yield Summary
- Summary
- Pregnancy causes proactive, anticipatory adaptations across all organ systems. Key testable changes: ↑ CO 30-50% (sharp early rise), ↓ SVR 35-40%, BP nadir in 2nd trimester, physiological anaemia (plasma volume ↑ > RBC mass ↑), ↓ pCO2 to 3.7 kPa (facilitates fetal CO2 transfer), ↑ GFR 50% (↓ creatinine, glycosuria), pro-coagulatory state (↑ factors VII/VIII/X, ↓ protein S/ATIII), hCG-driven transient subclinical hyperthyroidism (use trimester-specific reference ranges), and progesterone-mediated smooth muscle relaxation causing most GI symptoms and varicosities. ALT, AST, and bile acids do NOT change — elevation is always pathological. ALP rises 2-4× from placental production (unreliable for liver/bone disease). Minor ailments are not life-threatening but cause significant distress; management is primarily lifestyle modification with judicious pharmacotherapy. Supine hypotension (IVC compression by gravid uterus → ↓ venous return → ↓ CO) is a directly tested concept (2023 SAQ Q2).
Active Recall - Physiology of Pregnancy and Minor Ailments
[1] Lecture slides: CFB (OG01) Physiology of Pregnancy and Minor Ailments.pdf [2] Senior notes: Adrian Lui Obstetric Notes.pdf (Ch 2: Physiology of Pregnancy; Ch 5.1: Minor Ailments) [3] Senior notes: Block A - Leg swelling and chest pain_ deep vein thrombosis; pulmonary embolism; Thrombophilia.pdf (Pregnancy and VTE section) [4] Senior notes: Block A - I am losing weight and sweating all the time_ causes of severe, weight loss; thyrotoxicosis; hypothyroidism.pdf (Antithyroid drugs in pregnancy) [5] Past papers: 2020 Fourth Summative Assessment MCQ paper.pdf (Q10 - chronic hypertension at 13 weeks) [6] Senior notes: Block A - Indigestion and 'heartburn'_ nausea and vomiting; gastric motility problems; benign esophageal lesions.pdf (Workup for acute vomiting) [7] Past papers: 2023 Fourth Summative SAQ.pdf (Q2 - supine hypotension at 28 weeks)
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