An action potential (AP) is initiated when the myocyte is depolarised to a threshold potential of about -65 mV, as a result of transmission from an adjacent myocyte via gap junctions. Fast voltage-gated Na+channels are activated and a Na+influx depolarises the membrane rapidly to about +30 mV. This initial depolarisation is similar to that in nerve and skeletal muscle, and assists the transmission to the next myocyte.

Hypoperfusion, renal failure, and the oligohydramnios sequence are all linked to ACE inhibitor use in the second and third trimesters.

The oligohydramnios sequence refers to a foetus’ or neonate’s atypical physical appearance as a result of oligohydramnios in the uterus. It’s also linked to aortic arch obstructive malformations and patent ductus arteriosus.

The inhibitory effects on the renin-angiotensin-aldosterone system appear to be the cause of these defects. To avoid these risks, ACE inhibitors should be stopped before the second trimester.

Aldosterone is a steroid hormone produced in the adrenal cortex’s zona glomerulosa. It is the most important mineralocorticoid hormone in the control of blood pressure. It does so primarily by promoting the synthesis of Na+/K+ATPases and the insertion of more Na+/K+ATPases into the basolateral membrane of the nephron’s distal tubules and collecting ducts, as well as stimulating apical sodium and potassium channel activity, resulting in increased sodium reabsorption and potassium secretion. This results in sodium conservation, potassium secretion, water retention, and a rise in blood volume and blood pressure.

Aldosterone is produced in response to the following stimuli:

Angiotensin II levels have risen.
Potassium levels have increased.
ACTH levels have risen.
Aldosterone’s principal actions are as follows:
Na+ reabsorption from the convoluted tubule’s distal end
Water resorption from the distal convoluted tubule (followed by Na+)
Cl is reabsorbed from the distal convoluted tubule.
K+ secretion into the convoluted distal tubule’s 
H+ secretion into the convoluted distal tubule’s 

Proton pump inhibitors (PPIs) have a variety of side effects, including:
Vomiting and nausea
Pain in the abdomen
Flatulence
Diarrhoea
Constipation
Headache

PPIs have been linked to a significant increase in the risk of focal tachyarrhythmias (link is external).
Low serum magnesium and sodium levels have been linked to long-term use of PPIs, according to the US Food and Drug Administration (link is external).

Long-term PPI use has also been linked to an increased risk of fracture, according to epidemiological evidence (link is external). Observational studies have discovered a slight link between hip, wrist, and spine fractures. However, there is no link between the two and an increased risk of pelvic fracture. For this reason, the MHRA recommends that patients at risk of osteoporosis who take PPIs maintain an adequate calcium and vitamin D intake.

Phenytoin Contraindications include:

Hypersensitivity
Sinus bradycardia
Sinoatrial block
Second and third degree A-V block
Adams-Stokes syndrome
Concurrent use with delavirdine
History of prior acute hepatotoxicity attributable to phenytoin

Sensory innervation to the external ear is supplied by both cranial and spinal nerves. Branches of the trigeminal, facial, and vagus nerves (CN V, VII, X) are the cranial nerve components, while the lesser occipital (C2, C3) and greater auricular (C2, C3) nerves are the spinal nerve components involved. The lateral surface of the tympanic membrane, the external auditory canal, and the external acoustic meatus are all innervated by nervus intermedius (a branch of CN VII), the auriculotemporal nerve (CN V3), and the auricular branch of the vagus nerve. The concha receives split innervation from nervus intermedius, the auricular branch of the vagus nerve, and the greater auricular (spinal) nerve. Beyond the concha, the anteromedial and anterosuperior parts of the pinna are innervated by the auriculotemporal nerve, and a portion of the lateral helix by the lesser occipital nerve. The greater auricular nerve provides innervation to the area of the pinna inferolateral to the lobule.

Tetanus is caused by Clostridium tetani, a bacterium. Tetanus can cause mild spasms to severe whole-body contractions, suffocation, and heart attack.

Gas gangrene and food poisoning are both caused by Clostridium perfringens.

Pseudomembranous colitis is caused by Clostridium difficile.

Urinary tract infections, respiratory infections, dermatitis, soft tissue infections, bacteraemia, bone and joint infections, gastrointestinal infections, and a variety of systemic infections are all caused by Pseudomonas aeruginosa.

Pharyngitis, skin infections, acute rheumatic fever, scarlet fever, poststreptococcal glomerulonephritis, toxic shock–like syndrome, and necrotizing fasciitis can all be caused by Streptococcus pyogenes infection.

Patellar dislocation is a disabling musculoskeletal disorder which predominantly affects younger people who are engaged in multidirectional physically active pursuits. Conservative (non-operative) treatment is the treatment of choice for FTPD (first time patellar dislocation). Quadriceps strengthening exercises are considered one of the principal management aims for people following FTPD. A United Kingdom (UK) survey of physiotherapy practice has shown that quadriceps strengthening and specific-vastus medialis obliquus (VMO) or distal vastus medialis (VM) muscle strengthening or recruitment exercises were two of the most frequently used interventions for this population. Specific VM exercises are favoured in some quarters based on the assumption that the VM has an important role in preventing excessive lateral patellar translation.

During or shortly after transfusion, febrile transfusion reactions, also known as non-haemolytic transfusion reactions, present with an unexpected temperature rise (38oC or 1oC above baseline, if baseline is 37oC). This is usually a one-off occurrence. The fever is sometimes accompanied by chills.

The most common type of transfusion reaction is febrile transfusion reactions, which occur in about 1 in every 8 transfusions.

The most common event leading to symptoms of febrile transfusion reactions is cytokine accumulation during storage of cellular components (especially platelet units). White cells secrete cytokines, and pre-storage leucodepletion has reduced this risk.

Recipient antibodies (raised as a result of previous transfusions or pregnancies) reacting to donor human leukocyte antigen (HLA) or other antigens can also cause febrile transfusion reactions. Donor lymphocytes, granulocytes, and platelets all contain these antigens.

Treatment is reassuring. Other causes should be ruled out, and antipyretics like paracetamol can help with fever relief. If another cause of fever is suspected, the transfusion should be stopped; however, if other causes of fever have been ruled out, it can be restarted at a slower rate.

Cortisol is a steroid hormone produced in the zona fasciculata of the adrenal cortex. It is released in response to stress and low blood glucose concentrations.
Cortisol acts to: raise plasma glucose by stimulating glycolysis and gluconeogenesis in the liver and inhibiting peripheral glucose uptake into storage tissues, increase protein breakdown in skeletal muscle, skin and bone to release amino acids, increase lipolysis from adipose tissues to release fatty acidsand at higher levels and mimic the actions of aldosterone on the kidney to retain Na+ and water and lose K+ ionssuppress the action of immune cells