Hepatitis A usually doesn’t pose a special risk to a pregnant woman or her baby. Maternal infection doesn’t result in birth defects, and a mother typically doesn’t transmit the infection to her baby. HAV is almost always transmitted by the faecal-oral route and is usually acquired through close personal contact or via contaminated food.

When a woman has chickenpox in the first 20 weeks of pregnancy, there is a 1 in 50 chance for the baby to develop a set of birth defects. This is called the congenital varicella syndrome. It includes scars, defects of muscle and bone, malformed and paralyzed limbs, small head size, blindness, seizures, and intellectual disability.

TORCH Syndrome refers to infection of a developing foetus or newborn by any of a group of infectious agents. “TORCH” is an acronym meaning (T)toxoplasmosis, (O)ther Agents, (R)ubella (also known as German Measles), (C)ytomegalovirus, and (H)erpes Simplex.
Infection with any of these agents may cause a constellation of similar symptoms in affected newborns. These may include fever; difficulties feeding; small areas of bleeding under the skin, causing the appearance of small reddish or purplish spots; enlargement of the liver and spleen (hepatosplenomegaly); yellowish discoloration of the skin, whites of the eyes, and mucous membranes (jaundice); hearing impairment; abnormalities of the eyes; and other symptoms and findings.

Many medications, including warfarin, require cytochrome P450 enzymes for their metabolism. When co-prescribing cytochrome p450 enzyme inducers and inhibitors with warfarin, it’s critical to be cautious.

Inhibitors of the cytochrome p450 enzyme potentiate the effects of warfarin, resulting in a higher INR. To remember the most commonly encountered cytochrome p450 enzyme inhibitors, use the mnemonic O DEVICES:

O– Omeprazole
D– Disulfiram
E– Erythromycin (And other macrolide antibiotics)
V– Valproate (sodium valproate)
I– Isoniazid
C– Ciprofloxacin
E– Ethanol (acute ingestion)
S- Sulphonamides

Digoxin directly inhibits membrane Na+/K+ ATPase, which is responsible for Na+/K+ exchange across the myocyte cell membrane. This increases intracellular Na+ and produces a secondary increase in intracellular Ca2+ that increases the force of myocardial contraction. The increase in intracellular Ca2+ occurs because the decreased Na+ gradient across the membrane reduces the extrusion of Ca2+ by the Na+/Ca2+ exchanger that normally occurs during diastole. Digoxin and K+ ions compete for the receptor on the outside of the muscle cell membrane, and so the effects of digoxin may be dangerously increased in hypokalaemia.

The following structures are the layers of the anterior abdominal wall from the most superficial to the deepest layer:

Skin
Fatty layer of the superficial fascia (Camper’s fascia)
Membranous layer of the superficial fascia (Scarpa’s fascia)
Aponeurosis of the external and internal oblique muscles
Rectus abdominis muscle
Aponeurosis of the internal oblique and transversus abdominis
Fascia transversalis
Extraperitoneal fat
Parietal peritoneum

PO43-renal excretion is regulated several mechanisms. These include:
-parathyroid hormone – increases excretion by inhibiting reabsorption in the proximal tubule
-acidosis – increases excretion
-glucocorticoids – increases excretion
-calcitonin – increases excretion
-activated vitamin D – decreases excretion by increasing reabsorption in the distal tubule

Acetazolamide is a non-competitive, reversible inhibitor of carbonic anhydrase found in the cytosol of cells and on the brush border of the proximal convoluted tubule. Bicarbonate and hydrogen ions are converted to carbonic acid by carbonic anhydrase, which then converts carbonic acid to carbon dioxide and water. As a result, acetazolamide reduces the availability of hydrogen ions, causing sodium and bicarbonate ions to accumulate in the renal tubule, resulting in diuresis.
The mechanism of action of the various types of diuretics is summarised below:

1) Loop diuretics, e.g. furosemide, bumetanide
Act on the Na.K.2Cl co-transporters in the ascending loop of Henlé to inhibit sodium, chloride and potassium reabsorption.

2) Thiazide diuretics, e.g. Bendroflumethiazide, hydrochlorothiazide
Act on the Na.Cl co-transporter in the distal convoluted tubule to inhibit sodium and chloride reabsorption.

3) Osmotic diuretics, e.g. mannitol
Increases the osmolality of the glomerular filtrate and tubular fluid, increasing urinary volume by an osmotic effect.

4) Aldosterone antagonists, e.g. spironolactone
Acts in the distal convoluted tubule as a competitive aldosterone antagonist resulting in inhibition of sodium reabsorption and increasing potassium reabsorption.

5) Carbonic anhydrase inhibitors, e.g. acetazolamide
Inhibit the enzyme carbonic anhydrase preventing the conversion of bicarbonate and hydrogen ions into carbonic acid.

Primary adrenal insufficiency, also known as Addison’s disease, occurs when the adrenal glands cannot produce an adequate amount of hormones despite a normal or increased corticotropin (ACTH) level.

Amiodarone has a chemical structure that is similar to that of thyroxine and can bind to the nuclear thyroid receptor. It can cause both hypothyroidism and hyperthyroidism, though hypothyroidism is far more common, with 5-10% of patients suffering from it.

Glucagon is a peptide hormone that is produced and secreted by alpha cells of the islets of Langerhans, which are located in the endocrine portion of the pancreas. The main physiological role of glucagon is to stimulate hepatic glucose output, thereby leading to increases in glycaemia. It provides the major counter-regulatory mechanism to insulin in maintaining glucose homeostasis.
Hypoglycaemia is the principal stimulus for the secretion of glucagon but may also be used as an antidote in beta-blocker overdose and in anaphylaxis in patients on beta-blockers that fail to respond to adrenaline.
Glucagon then causes:
Glycogenolysis
Gluconeogenesis
Lipolysis in adipose tissue
The secretion of glucagon is also stimulated by:
Adrenaline
Cholecystokinin
Arginine
Alanine
Acetylcholine
The secretion of glucagon is inhibited by:
Insulin
Somatostatin
Increased free fatty acids
Increased urea production

Glycolysis is the metabolic pathway that converts glucose into pyruvate. The free energy released by this process is used to form ATP and NADH. Glycolysis is inhibited by glucagon, and glycolysis and gluconeogenesis are reciprocally regulated so that when one cell pathway is activated, the other is inactive and vice versa.

Glucagon has a minor effect of enhancing lipolysis in adipose tissue. Lipolysis is the breakdown of lipids and involves the hydrolysis of triglycerides into glycerol and free fatty acids. It makes fatty acids available for oxidation.

Haemoglobin is composed of four polypeptide globin chains each with its own iron containing haem molecule. Haem synthesis occurs largely in the mitochondria by a series of biochemical reactions commencing with the condensation of glycine and succinyl coenzyme A under the action of the key rate-limiting enzyme delta-aminolevulinic acid (ALA) synthase. The globin chains are synthesised by ribosomes in the cytosol. Haemoglobin synthesis only occurs in immature red blood cells.
There are three types of haemoglobin in normal adult blood: haemoglobin A, A2 and F:
– Normal adult haemoglobin (HbA) makes up about 96 – 98 % of total adult haemoglobin, and consists of two alpha (α) and two beta (β) globin chains. 
– Haemoglobin A2 (HbA2), a normal variant of adult haemoglobin, makes up about 1.5 – 3.5 % of total adult haemoglobin and consists of two α and two delta (δ) globin chains.
– Foetal haemoglobin is the main Hb in the later two-thirds of foetal life and in the newborn until approximately 12 weeks of age. Foetal haemoglobin has a higher affinity for oxygen than adult haemoglobin. 
Red cells are destroyed by macrophages in the liver and spleen after , 120 days. The haem group is split from the haemoglobin and converted to biliverdin and then bilirubin. The iron is conserved and recycled to plasma via transferrin or stored in macrophages as ferritin and haemosiderin. An increased rate of haemoglobin breakdown results in excess bilirubin and jaundice.