Immunodeficiency is present in all patients with chronic lymphocytic leukaemia (CLL), though it is often mild and not clinically significant. Infections are the leading cause of death in 25-50 percent of CLL patients, with respiratory tract, skin, and urinary tract infections being the most common.

Hypogammaglobulinemia is the most common cause of immunodeficiency in CLL patients, accounting for about 85 percent of all cases.

A refractory period follows each action potential. The absolute refractory time and the relative refractory period are two divisions of refractory periods. Because the sodium channels seal after an AP, they enter an inactive state during which they cannot be reopened regardless of membrane potential, this time occurs.

The sodium channels slowly come out of inactivation during the relative refractory period that follows. During this time, a stronger stimulus than that required to initiate an action potential can excite the cell. The strength of the stimulus required early in the relative refractory period is relatively high, and it steadily decreases as more sodium channels recover from the inactivation of the refractory period.

Nodes of Ranvier are periodic holes in a myelinate axon when there is no myelin and the axonal membrane is exposed. There are no gated ion channels in the portion of the axon covered by the myelin sheath, but there is a high density of ion channels in the Nodes of Ranvier. Action potentials can only occur at the nodes as a result of this.

An antidote for digoxin overdose is digoxin-specific antibody (Digifab). It’s a lyophilized preparation of digoxin-immune ovine Fab immunoglobulin fragments that’s sterile, purified, and lyophilized. These fragments were extracted from the blood of healthy sheep that had been immunised with a digoxin derivative called digoxin-dicarboxymethoxylamine (DDMA), a digoxin analogue that contains the functionally important cyclopentaperhydrophenanthrene:lactone ring moiety coupled to keyhole limpet hemocyanin (KLH).

Digifab has a higher affinity for digoxin than digoxin does for its sodium pump receptor, which is thought to be the site of its therapeutic and toxic effects. When given to a patient who is intoxicated, Digifab binds to digoxin molecules, lowering free digoxin levels and shifting the equilibrium away from binding to receptors, reducing cardio-toxic effects. The kidney and reticuloendothelial system then clear the Fab-digoxin complexes.

The following summarises the indications for Digifab in acute and chronic digoxin toxicity:
Acute digoxin toxicity
Chronic digoxin toxicity
Cardiac arrest
Life-threatening arrhythmia
Potassium level > 5 mmol/l
>10 mg digoxin ingested (adult)
>4 mg digoxin ingested (child)
Digoxin level > 12 ng/ml
Cardiac arrest
Life-threatening arrhythmia
Significant gastrointestinal symptoms
Symptoms of digoxin toxicity

M. tuberculosis is the causative agent of pulmonary tuberculosis (TB). The most commonly used diagnostic test for the diagnosis of pulmonary TB is the direct sputum smear microscopy (DSSM) wherein the presence of acid-fast bacilli (AFB) is tested.

The most common method is the hot method or also known as Ziehl-Neelsen method. This is a staining method special for Mycobacteria species because they are known to be acid-fast which means that they are not easily decolorized by acid alcohol. Once the DSSM tests positive for acid-fast bacilli, this indicates possible infection with tuberculosis. The gold standard for diagnosis is still culture but Mycobacteria species are slow-growers that is why DSSM is considered the best diagnostic method. A positive AFB smear and correlation with symptoms is usually used by physicians to create a final diagnosis of pulmonary tuberculosis.

Actions of adrenaline:
Cardiovascular system
– Increased rate and force of cardiac contraction
– Vasoconstriction of vessels in skin, mucous membranes and splanchnic bed
– Vasodilation of skeletal muscle vessels
– Increased cardiac output and blood pressure
Respiratory system
– Bronchodilation
– Increased ventilation rate
Gastrointestinal system
– Smooth muscle relaxation
– Contraction of sphincters
– Metabolism
– Decreased insulin release
– Increased glucagon release
– Increased thermogenesis
– Increased glycolysis
– Increased lipolysis
Eye
– Pupillary dilation

Heart Sound – Phase of Cardiac Cycle – Mechanical Event:
First heart sound – Start of systole – Caused by closure of the atrioventricular (mitral & tricuspid) valves
Second heart sound – End of systole – Caused by closure of the semilunar (aortic and pulmonary) valves
Third heart sound – Early diastole – Caused by rapid flow of blood from the atria into the ventricles during the ventricular filling phase
Fourth heart sound – Late diastole – Caused by filling of an abnormally stiff ventricle in atrial systole

Bacillus cereus = Gram-positive bacillus
Neisseria meningitidis = Gram-negative coccus
Salmonella enterica & Escherichia coli = Gram-negative bacilli

In Gram staining, crystal violet is a purple stain that is used to stain the bacteria first. The stained bacteria are decolorized and then stained with a red stain, which is safranin. Bacteria with thick cell walls keep the purple stain and are called Gram-positive. Thin-walled bacteria are easily decolorized so when safranin, the red stain, is placed on the organisms, they become red or Gram-negative.
The Staphylococci that are associated with infections in humans are colonizers of various skin and mucosal surfaces. Because the carrier state is common among the human population, infections are frequently acquired when the colonizing strain gains entrance to a normally sterile site as a result of trauma or abrasion to the skin or mucosal surface.

When the vagus nerve is damaged, the soft palate is paralyzed and the uvula is shifted away from the affected side. The vagus nerve innervates the uvulae muscle, which forms the uvula’s core. If only one side is innervated, contraction of the active muscle will draw the uvula towards it.

Clostridium tetaniis a Gram positive, rod shaped, obligate anaerobic bacterium.
The incubation period is quoted as anywhere between 4-21 days and can occur after several months but symptoms usually occur within the first 7 days after exposure.
Approximately 80% of patients develop generalised tetanus. The commonest presenting feature of generalised tetanus is trismus (lockjaw), occurring in approximately 75% of affected individuals. Other clinical features include:
Facial spasms (risus sardonicus)
Opisthotonus (characteristic body shape during spasms)
Neck stiffness
Dysphagia
Calf and pectoral muscle rigidity
Fever
Hypertension
Tachycardia
Spasms can occur frequently and last for several minutes, they can continue to occur for up to 4 weeks. Current mortality rates are between 10 and 15%.
Tetanic spasms are caused by the exotoxin tetanospasmin. The effects of tetanolysin are not fully understood but it is not believed to have clinical significance.
Localised tetanus is a rare form of the disease, occurring in around 1% of affected individuals. Patients have persistent contraction of muscles in the same anatomic area as the injury. It may precede generalised tetanus.

The only mechanism by which insulin facilitates uptake of glucose into cells is by facilitated diffusion through a family of hexose transporters.

The major transporter used for glucose uptake is GLUT4. GLUT4 is made available in the plasma membrane by the action of insulin.
When insulin concentrations are low, GLUT4 transporters are present in cytoplasmic vesicles, where they are cannot be used for transporting glucose.