Hyponatremia

Hyponatremia (<135 mEq/L) is a common electrolyte abnormality caused by an excess of total body water in comparison to that of the total body sodium content. Measuring the serum osmolality, urine sodium concentration and urine osmolality helps to differentiate among the possible causes. The severity of this electrolyte abnormality ranges from asymptomatic to seizures, coma and death as a consequence of cerebral swelling.

Pseudohyponatremia is due to hypertriglyceridemia or multiple myeloma. In regular subjects, the plasma water is 93% of the plasma volume. Plasma water part falls lower than 80% in cases with noticeable hyperlipidemia (triglycerides >1500 mg/dL) or hyperproteinemia (protein >10 mg/dL). Rise in blood urea causes the hyponatremia in renal failure.

True hyponatremia is having a fall in serum osmolality and is divided into hypervolemic, hypovolemic, and euvolemic based on volume status. 

Osmoreceptors in the hypothalamus detect the plasma osmolality. If Posm >285 mOsm/kg, osmoreceptors stimulate the release of anti-diuretic hormone (ADH) from the posterior pituitary into the circulation, as well as stimulate thirst. ADH release is also stimulated in states of low effective circulating volume. Circulating ADH binds to receptors on the principal cells of the collecting duct in the kidneys and activates a cellular pathway which ultimately results in water reabsorption. This results in a decrease in the serum osmolality and an increase in the urine osmolality (Uosm).  In certain states, ADH can be released inappropriately or ectopically, meaning that ADH is released without an osmotic or hemodynamic stimulus. When ADH is suppressed, water is renally excreted. 

Another important physiological pathway is the renin-angiotensin-aldosterone system (RAAS). This pathway is activated in states of low effective circulating volume and/or when there is reduced sodium in the renal tubules. These conditions stimulate the release of renin from the juxtaglomerular cells, which are part of the afferent arterioles. The activation of RAAS ultimately results in increased sodium reabsorption, arteriolar vasoconstriction and release of ADH from the posterior pituitary. Measured urine sodium concentration (UNa) is a reflection of intravascular volume; UNa is elevated with volume expansion and reduced with volume depletion. 

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Para-neoplastic dermatoses (PD)

Para-neoplastic dermatoses (PD):

• Heterogeneous, rare, acquired diseases characterized by the presence of an underlying neoplasia.
• Usually develop simultaneously with the underlying cancer, but they can also occur before or after the development of the neoplasia.
• Their recognition can lead to a prompt cancer detection and to an early start of the appropriate therapy.

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Diabetic Ketoacidosis (DKA)

Diagnostic Criteria:

• Serum glucose >250 mg/dL
• Arterial pH <7.3
• Serum bicarbonate <18 mEq/L
• At least moderate ketonuria or ketonemia.

10% to 30% of DKA cases occur in patients with type 2 diabetes, in situations of extreme physiologic stress or acute illness.

Infection is a very common trigger for DKA in patients who have new-onset diabetes and previously established diabetes. If there is any suspicion of infection, antibiotics should be administered promptly.

2.6% to 3.2% of DKA admissions are Euglycemic Diabetic ketoacidosis (EDKA).

Pregnancy is a risk factor for EDKA because of the physiologic state of hypoinsulinemia and increased starvation.
Alcoholic ketoacidosis may have a similar presentation to EDKA, with anorexia, vomiting, dyspnea, and significant anion gap metabolic acidosis and ketonemia.

Common, early signs of ketoacidosis include nausea, vomiting, abdominal pain, and hyperventilation.

Patients with DKA usually present with a serum anion gap greater than 20 mEq/L (normal 3 to 10 mEq/L). However, the increase in anion gap is variable, being determined by several factors: the rate and duration of ketoacid production, the rate of metabolism of the ketoacids and their loss in the urine, and the volume of distribution of the ketoacid anions.

Continue insulin infusion until ketoacidosis is resolved, serum glucose is below 200 mg/dL, and subcutaneous insulin is begun. Treatment with IV fluid resuscitation should continue until the anion gap closes and acidosis has resolved.

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Pemphigus

 Pemphigus vulgaris (PV) is an autoimmune, intraepithelial, blistering disease affecting the skin and mucous membranes. It is mediated by circulating autoantibodies against keratinocyte cell surfaces. Exposure to certain medications like penicillamine and captopril can trigger PV. Such a trigger can happen through the effects on binding to molecules involved in cell adhesion, influence on enzymes that mediate keratinocyte aggregation, and molecules involved in cell and by stimulating neoantigen formation. In addition, NSAID’s, penicillin, cephalosporins have been associated with drug-induced PV.

IgA pemphigus does not present with oral mucosa blisters. Direct and indirect immunofluorescence can both help to differentiate PV from IgA pemphigus.

Pemphigus foliaceus does not affect the oral mucosa and is less common than PV.

Paraneoplastic pemphigus presents with mucocutaneous vesicles and bullae and can be differentiated from PV using indirect immunofluorescence and immunoblot.

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Zephyr Endobronchial Valve

The Zephyr Endobronchial Valve is an endobronchial implant designed to occlude a hyperinflated lobe of the lungs with multiple valves, allowing air to escape while blocking airflow into the treated lobe. This is intended to result in a reduction in lung volume and hyperinflation in the targeted area. This one-way valve therapy leads to an improvement of lung function, exercise tolerance, and quality of life in patients with advanced emphysema.

Key inclusion criteria:

• Severe emphysema: forced expiratory volume in 1 second (FEV1) ≤ 45% of predicted, TLC ≥ 100% of predicted, RV ≥ 150% of predicted
• Resting partial pressure of arterial carbon dioxide (Paco2) ≤ 60 mm Hg
• Resting partial pressure of arterial oxygen (Pao2) on room air ≥ 45 mm Hg
• Body mass index ≤ 31 kg/m2 for men, ≤ 32 kg/m2 for women
• Abstinence from smoking for at least six months
• Completion of pulmonary rehabilitation.

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Diabetic foot infections (DFIs)

Diabetic foot infections (DFIs) is a common complication of longstanding diabetes, and it is associated with considerable morbidity, increased risk of lower extremity amputation, and a high mortality rate. The development of DFI derives from a complex interplay among peripheral neuropathy, peripheral arterial disease (PAD), and the immune system.

Most DFIs are polymicrobial, with aerobic gram-positive cocci, and especially staphylococci, the most common causative organisms. Aerobic gram-negative bacilli are frequently co-pathogens in infections that are chronic or follow antibiotic treatment, and obligate anaerobes may be co-pathogens in ischemic or necrotic wounds.

Empiric antibiotic therapy can be narrowly targeted at aerobic gram-positive cocci in many acutely infected patients, but those at risk for infection with antibiotic-resistant organisms or with chronic, previously treated, or severe infections usually require broader spectrum regimens. Imaging is helpful in most DFIs; plain radiographs may be sufficient, but magnetic resonance imaging is far more sensitive and specific.

Osteomyelitis occurs in 15% of ulcers, and 15% of those will go on to require amputation. Approximately 60% of patients undergoing lower extremity amputation have diabetic foot ulcers as the underlying cause. Following a lower extremity amputation, the 5-year mortality jumps to 60%.

Surgical interventions of various types are often needed, and proper wound care is important for the successful cure of the infection and healing of the wound. Patients with a DFI should be evaluated for an ischemic foot, and employing multidisciplinary foot teams improves outcomes.

The prognosis for a diabetic foot infection depends on many factors including vascular blood supply and the presence of neuropathy.

 

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Bleeding manifestation

Petechiae are small, flat, red, discrete areas of skin bleeding that are typically <2 mm in diameter. They are non-blanching, nonpalpable, and occur in dependent areas of the body Purpura results from coalesced petechiae. 

Purpura due to vasculitis is usually palpable and may be pruritic, and the distribution does not follow dependent areas. Wet purpura is the most predictive of serious bleeding in individuals with thrombocytopenia. 

Bruise (also called ecchymosis) is caused by the subcutaneous accumulation of extravasated blood. The skin is flat, and the color evolves over time from purplish blue to reddish brown to greenish-yellow, reflecting the metabolism (breakdown) of hemoglobin to biliverdin and bilirubin. 

Hematoma is a collection of blood in the extravascular space. Hematomas and hemarthroses (joint bleeding) are typical of coagulation factor deficiencies.

Von Willebrand factor

• Glycoprotein
• Synthesized in endothelial cells & megakaryocytes.
• Excessive bruising & prolonged bleeding
• Levels vary with stress; increase with estrogens, vasopressin, GH & adrenergic stimuli.
• Repeat tests at > 2 weeks
• Type O blood normally has the lowest levels
• Platelet levels tend to be normal, PT should be normal.

von Willebrand disease (Diagnosis)

• VWF antigen level VWF:Ag  (Quantity of VWF present in plasma; <50 are considered to be low)
• VWF ristocetin cofactor assay Efficacy of this plasma VWF in its ability to bind platelets in the presence of antibiotic ristocetin.
• Measurement of coagulation factor VIII (FVIII:C)
• Ratio of VWF:RCo/VWF:Ag (differentiate VWD type 1 and 2)

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Digoxin (Cardiac glycoside)

 The chemical formula of Digoxin is C41 H64 O14.

Digoxin (Cardiac glycoside) reversibly inhibits the sodium-potassium-ATPase, causing an increase in intracellular sodium and a decrease in intracellular potassium. The increase in intracellular sodium prevents the sodium-calcium antiporter from expelling calcium from the myocyte, which increases intracellular calcium. The net increase in intracellular calcium augments inotropy. Cardiac glycosides also increase vagal tone, which results in decreased conduction through the sinoatrial and atrioventricular nodes.

Life-threatening digoxin-induced arrhythmias and other toxic manifestations occur at a substantially increasing frequency as the plasma digoxin concentration rises above 2.0 ng/mL. However, toxicity is more likely in the presence of one or more comorbid conditions (eg, hypokalemia, hypomagnesemia, hypercalcemia, myocardial ischemia). Hypokalemia is a particularly important risk factor that can promote digoxin-induced arrhythmias.

PVCs are often the first sign of digoxin toxicity and are the most common arrhythmia due to digoxin toxicity. PVCs can be isolated or occur in a bigeminal pattern. The so-called "digitalis effect" on the ECG consists of T wave changes (flattening or inversion), QT interval shortening, scooped ST segments with ST depression in the lateral leads and increased amplitude of the U waves.

Early recognition of cardiac glycoside toxicity and prompt administration of Fab fragments is essential for the successful treatment of severe poisoning. Fab fragments are highly effective and safe and have transformed the management of cardiac glycoside poisoning.

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