Bacteriostatic antibiotics include erythromycin and other macrolide antibiotics. They work by attaching to the bacterial ribosome’s 50S subunit, preventing translocation and thereby protein synthesis. Macrolide antibiotics are actively concentrated inside leukocytes and delivered to the infection site as a result.

Erythromycin is an orally active antibiotic that can also be given intravenously. It is metabolized in the liver and eliminated in the bile and has a biological half-life of 1.5 hours.

It has a similar antibacterial spectrum to benzylpenicillin (i.e., a narrow spectrum, primarily against Gram-positive pathogens) and can be used as a penicillin substitute in people who are allergic to penicillin.
Erythromycin is unsuccessful in the treatment of meningitis because it does not penetrate the central nervous system well enough. It is efficient against a variety of unusual pathogens, unlike penicillin.

The biceps brachii muscle is one of the chief muscles of the arm. The origin at the scapula and the insertion into the radius of the biceps brachii means it can act on both the shoulder joint and the elbow joint, which is why this muscle participates in a few movements of the arm. It derives its name from its two heads which merge in one unique distal body, defining the unusual structure of the muscle.

The biceps brachii muscle is supplied by the musculocutaneous nerve (C5-C6), a branch of the brachial plexus.

Arterial supply to the biceps brachii muscle varies considerably, coming from up to eight vessels originating from the brachial artery in the middle third of the arm.

In the shoulder joint both muscle heads partially enforce opposite movements. The long head pulls the arm away from the trunk (abduction) and turns it inwards (inward rotation) whereas the short head pulls the arm back towards the trunk (adduction). When both heads contract simultaneously it leads to an arm bend (flexion). In the elbow joint the muscle bends the forearm (flexion) and rotates it outwards (supination). The supination is most powerful in a flexed elbow. In addition to the movement functions, the biceps has the important task to support the humeral head within the shoulder joint. Its antagonist is the triceps brachii in the posterior compartment of the arm.

An overdose of levothyroxine can happen by accident or on purpose. Intentional overdosing is sometimes done to lose weight, but it can also happen in patients who are suicidal. The development of thyrotoxicosis, which can lead to excited sympathetic activity and high metabolism syndrome, is the main source of concern. The time between ingestion and the emergence of clinical features associated with an overdose is often quite long.

After a levothyroxine overdose, the majority of patients are asymptomatic. Symptoms and signs are usually only seen in patients who have taken more than 10 mg of levothyroxine in total.

The following are the most commonly seen clinical features in patients developing clinical features:
Tremor
Agitation
Sweating
Insomnia
Headache
Increased body temperature
Increased blood pressure
Diarrhoea and vomiting
Less common clinical features associated with levothyroxine overdose include:
Seizures
Acute psychosis
Thyroid storm
Tachycardia
Arrhythmias
Coma

The continued absorption of the ingested levothyroxine causes a progressive rise in both total serum T4 and total serum T3 levels in the first 24 hours after an overdose. However, in some cases, the biochemical picture is completely normal. Thyroid function tests are not always recommended after a thyroxine overdose. Although elevated thyroxine levels are common, they have little clinical significance and have no impact on treatment. Following a levothyroxine overdose, the following biochemical features are common:
T4 and T3 levels in the blood are elevated.
Free T4 and Free T3 levels are higher.
TSH levels in the blood are low.
If the patient is cooperative and more than 10 mg of levothyroxine has been consumed, activated charcoal can be given (i.e., likely to become symptomatic)
Within an hour of ingestion, the patient presents.

The treatment is mostly supportive and aimed at managing the sympathomimetic symptoms that come with levothyroxine overdose. If beta blockers aren’t an option, try propranolol 10-40 mg PO 6 hours or diltiazem 60-180 mg 8 hours.

Beta-thalassaemia major is caused by a complete or almost complete failure of β-globin chain synthesis, severe imbalance of α:β-chains with deposition of α-chains in erythroblasts, ineffective erythropoiesis and extramedullary haemopoiesis. The severe anaemia becomes apparent at 3 – 6 months when the switch from γ-chain to β-chain synthesis normally occurs. Beta-thalassaemia minor is a variable syndrome, milder than thalassaemia major, with later onset and characterised by moderate hypochromic microcytic anaemia with raised haemoglobin A2. Beta-thalassaemia trait is characterised by mild hypochromic, microcytic anaemia with raised red cell count and raised haemoglobin A2.

Cortisol levels fluctuate throughout the day, with the greatest levels occurring around 0900 hours and the lowest occurring at 2400 hrs during sleep.

The diurnal swing of cortisol levels is lost in Cushing’s syndrome, and levels are greater throughout the 24-hour period. In the morning, levels may be normal, but they may be high at night-time, when they are generally repressed.

The obturator internus is innervated by the obturator internus nerve (L5–S2), a branch of sacral plexus.

Codeine phosphate is a weak opioid and can be used for the relief of mild to moderate pain where other painkillers such as paracetamol or ibuprofen have proved ineffective.Codeine is metabolised to morphine which is responsible for its therapeutic effects. Codeine 240 mg is approximately equivalent to 30 mg of morphine. The capacity to metabolise codeine can vary considerably between individuals; there is a marked increase in morphine toxicity in people who are ultra rapid metabolisers, and reduced therapeutic effect in poor codeine metabolisers. Codeine is contraindicated in patients of any age who are known to be ultra-rapid metabolisers of codeine (CYP2D6 ultra-rapid metabolisers).Codeine is also contraindicated in children under 12, and in children of any age who undergo the removal of tonsils or adenoids for the treatment of obstructive sleep apnoea due to reports of morphine toxicity.

Non-Hodgkin’s lymphoma (NHL) refers to a group of lymphoproliferative malignancies (about 85% of B-cell and 15% of T or NK (natural killer) cell origin) with different behavioural patterns and treatment responses. This group of malignancies encompasses all types of lymphoma without Reed-Sternberg cells being present. The Reed-Sternberg cell is classically seen in Hodgkin’s lymphoma.
NHL is five times as common as Hodgkin’s lymphoma. The peak incidence of NHL is in the 50-70 years age group, it affects men and women equally, but affects the Caucasian population more commonly than black and Asian ethnic groups.
The following are recognised risk factors for NHL:
Chromosomal translocations and molecular rearrangements
Epstein-Barr virus infection
Human T-cell leukaemia virus type-1 (HTLV-1)
Hepatitis C
Congenital and acquired immunodeficiency states
Autoimmune disorders, e.g. Sjogren’s syndrome and Hashimoto’s thyroiditis
The most common clinical features at presentation are:
Lymphadenopathy (typically asymmetrical and painless)
Weight loss
Fatigue
Night sweats
Hepatosplenomegaly
For clinical purposes, NHL is divided into three groups: indolent, high-grade, and lymphoblastic.
Indolent (low-grade) NHL:
The cells are relatively mature
Disease follows an indolent course without treatment
Often acceptable to follow a ‘watch and wait’ strategy
Local radiotherapy often effective
Relatively good prognosis with median survival of 10 years
High-grade NHL:
Cells are immature
Disease progresses rapidly without treatment
Significant number of patients can be cured with intensive combination chemotherapy regimens
Approximately 40% cure rate
Lymphoblastic NHL:
Cells are very immature and have a propensity to involve the CNS
Treatment and progression are similar to that of acute lymphoblastic leukaemia (ALL)

During the AP plateau, Ca2+enters the cell and activates Ca2+sensitive Ca2+release channels in the sarcoplasmic reticulum allowing stored Ca2+to flood into the cytosol; this is called Ca2+-induced Ca2+release. In relaxation, about 80% of Ca2+is rapidly pumped back into the SR (sequestered) by Ca2+ATPase pumps. The Ca2+that entered the cell during the AP is transported out of the cell primarily by the Na+/Ca2+exchanger in the membrane which pumps one Ca2+ion out in exchange for three Na+ions in, using the Na+electrochemical gradient as an energy source. Increased heart rate increases the force of contraction in a stepwise fashion as intracellular [Ca2+] increases cumulatively over several beats; this is the Treppe effect. Factors that affect intracellular [Ca2+] and hence cardiac contractility are called inotropes.

Ectopic pregnancy most commonly occurs in the ampulla (70% of cases).