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The most common cause of hyperparathyroidism is Parathyroid adenoma. Another cause is hyperplasia of the parathyroid glands.

Parathyroid hormone (PTH) increases serum calcium by

·         Enhancing distal tubular calcium reabsorption

·         Rapidly mobilizing calcium and phosphate from bone (bone resorption)

·         Increasing intestinal absorption of calcium by stimulating conversion of vitamin D to its most active form, calcitriol

Hyperparathyroidism is characterized as:

·         Primary: Excessive secretion of PTH due to a disorder of the parathyroid glands

·         Secondary: Hypocalcemia due to non-parathyroid disorders leads to chronic PTH hypersecretion

·         Tertiary: Autonomous secretion of PTH unrelated to serum calcium concentration in patients with long-standing secondary hyperparathyroidism

Primary hyperparathyroidism: excessive secretion of PTH by one or more parathyroid glands. Incidence increases with age and is higher in postmenopausal women. Primary hyperparathyroidism causes hypercalcemia, hypophosphatemia, and excessive bone resorption (leading to osteoporosis).

Secondary hyperparathyroidism occurs most commonly in advanced chronic kidney disease when decreased formation of active vitamin D in the kidneys and other factors lead to hypocalcemia and chronic stimulation of PTH secretion. Hyperphosphatemia that develops in response to chronic kidney disease also contributes. Other less common causes of secondary hyperparathyroidism include

·         Decreased calcium intake

·         Poor calcium absorption in the intestine due to vitamin D deficiency

·         Excessive renal calcium loss due to loop diuretic use

·         Inhibition of bone resorption due to bisphosphonate use

Tertiary hyperparathyroidism results when PTH secretion becomes autonomous of serum calcium concentration and generally occurs in patients with long-standing secondary hyperparathyroidism, as in patients with ESRD of several years’ duration.

Indications of surgery:

·         Serum calcium 1 mg/dL greater than the upper limits of normal

·         Calciuria > 400 mg/day

·         Creatinine clearance < 60 mL/minute

·         Peak bone density at the hip, lumbar spine, or radius 2.5 SD below controls (T score = −2.5)

·         Age < 50 years

·         The possibility of poor adherence with follow-up

Secondary hyperparathyroidism in patients with renal failure can result in a number of symptoms, including

·         Osteitis fibrosa cystica with arthritis, bone pain, and pathologic fractures

·         Spontaneous tendon rupture

·         Proximal muscle weakness

·         Extra-skeletal calcifications, including soft tissue and vascular calcification

·         Pruritis


Total O2 content is expressed by the following equation:

O2 content (CaO2) = (Hgb x 1.34 x SaO2) + (0.0031 x PaO2)

where Hgb is hemoglobin concentration and SaO2 is hemoglobin saturation at the given PO2. 

The principal form of oxygen transport in blood is as hemoglobin-bound.

Each gram of hemoglobin can maximally bind 1.34 mL of oxygen.

The oxygen-carrying capacity of the blood is calculated as = [Hb] x 1.34.

In a healthy person, with a hemoglobin concentration of 15 g / dL blood, the oxygen carrying capacity is 20.1 mL O2 / dL blood.

 

Oxygen transport is dependent on both respiratory and circulatory function.

Total O2 delivery (DO2) to tissues is the product of arterial O2 content and cardiac output (CO).

DO2 = CaO2 x CO

Note that arterial O2 content is dependent on PaO2 as well as hemoglobin concentration. As a result, deficiencies in O2 delivery may be due to a low PaO2, a low hemoglobin concentration, or an inadequate cardiac output.

 

The Fick equation of O2 consumption

VO2 = CO x (CaO2 – CvO2)


Oxy-hemoglobin Dissociation Curve

With a normal O2 consumption of approximately 250 ml/min and cardiac output of 5000 ml/min the normal arteriovenous difference is calculated to be about 5 ml O2/dl blood. The normal extraction ratio is approximately 25%, thus the body normally consumes only ~25% of the O2 carried on hemoglobin. When O2 demand exceeds supply, the extraction fraction exceeds 25%, and conversely, if O2 supply exceeds demand, the extraction fraction falls below 25%.

When DO2 (oxygen delivery) is moderately reduced, VO2 usually remains normal because of increased O2 extraction (meaning mixed venous O2 saturation decreases). With further reductions in the DO2, a critical point is reached beyond which VO2 becomes directly proportional to DO2. This state of supply-dependent O2 is typically associated with progressive lactic acidosis caused by cellular hypoxia.


An acute ST-elevation myocardial infarction occurs due to occlusion of one or more coronary arteries, causing transmural myocardial ischemia which in turn results in myocardial injury or necrosis. MI in general can be classified from Type 1 to Type 5 MI based on the etiology and pathogenesis.

·         Type 1 MI is due to acute coronary atherothrombotic myocardial injury with plaque rupture. Most patients with STEMI and many with NSTEMI comprise this category.

·         Type 2 MI is the most common type of MI encountered in clinical settings in which is there is demand-supply mismatch resulting in myocardial ischemia. This demand supply mismatch can be due to multiple reasons including but not limited to presence of a fixed stable coronary obstruction, tachycardia, hypoxia or stress. Other potential etiologies include coronary vasospasm, coronary embolus, and spontaneous coronary artery dissection (SCAD).

·         Type 3 MI include patient with Sudden cardiac death who succumb before any troponin elevation comprise.

·         Types 4 and 5 MIs are related to coronary revascularization procedures like PCI or CABG.

The American College of Cardiology, American Heart Association, European Society of Cardiology, and the World Heart Federation committee established the following ECG criteria for ST-elevation myocardial infarction STEMI:

·         New ST-segment elevation at the J point in 2 contiguous leads with the cutoff point as greater than 0.1 mV in all leads other than V2 or V3

·         In leads V2-V3 the cutoff point is greater than 0.2 mV in men older than 40 years old and greater than 0.25 in men younger than 40 years old, or greater than 0.15 mV in women

Patients with a pre-existing left bundle branch block can be further evaluated using Sgarbossa's criteria:

·         ST-segment elevation of 1 mm or more that is concordant with (in the same direction as) the QRS complex

·         ST-segment depression of 1 mm or more in lead V1, V2, or V3

·         ST-segment elevation of 5 mm or more that is discordant with (in the opposite direction) the QRS complex


 Cardiomyopathies are a heterogeneous group of diseases of the myocardium associated with mechanical and/or electric dysfunction that usually (but not invariably) exhibit inappropriate ventricular hypertrophy or dilatation and are due to a variety of causes that frequently are genetic. Cardiomyopathies either are confined to the heart or are part of generalized systemic disorders.

John F. Goodwin developed a classification based on structural and functional changes.

·         Congestive cardiomyopathy, now referred to as dilated cardiomyopathy (DCM),

·         Hypertrophic cardiomyopathy (HCM), and

·         Constrictive (now referred to as restrictive) cardio myopathy (RCM).

·         Arrhythmogenic right ventricular cardiomyopathy (arrhythmogenic cardiomyopathy),

Each of these categories was further subdivided by pathogenesis, such as secondary to a systemic disorder, an infection, inflammation, an inherited disorder, or idiopathic cardiomyopathies.




 In patients with heart failure (HF), the goals of treatment are to improve their clinical condition, functional capacity, quality of life, and to prevent the events of hospital readmissions and mortality. GDMT includes the following drug therapies: renin-angiotensin-aldosterone system inhibitors (RAAS-I), with or without a neprilysin inhibitor, β-blockers, and mineralocorticoid-receptor-antagonists (MRA).

Recently, sodium-glucose cotransporter-2 inhibitors (SGLT2i) demonstrated efficacy as an important fourth pillar of GDMT. Together, this combination can add over six additional years of lifespan for HFrEF patients compared to the traditional approach of RAAS-I and β-blockers alone. However, studies highlight that many eligible HFrEF patients are not receiving one or more of the recommended medications, in the absence of contraindications or intolerance. Even among patients who are treated, less than half receive optimal doses of GDMT. Additionally, time to initiation and optimization of dosing may be exceedingly slow in the outpatient setting.




 

Iron deficiency develops in stages. In the first stage, iron requirement exceeds intake, causing progressive depletion of bone marrow iron stores. As stores decrease, absorption of dietary iron increases in compensation. During later stages, deficiency impairs RBC synthesis, ultimately causing anemia. Severe and prolonged iron deficiency also may cause dysfunction of iron-containing cellular enzymes.

Iron deficiency anemia is classically described as a microcytic anemia. The differential diagnosis includes thalassemia, sideroblastic anemias, some types of anemia of chronic disease, and lead poisoning. Serum ferritin is the preferred initial diagnostic test. Total iron-binding capacity, transferrin saturation, serum iron, and serum transferrin receptor levels may be helpful if the ferritin level is between 46 and 99 ng per mL (46 and 99 mcg per L); bone marrow biopsy may be necessary in these patients for a definitive diagnosis.

 

The diagnosis of IDA requires that a patient be anemic and show laboratory evidence of iron deficiency. Red blood cells in IDA are usually described as being microcytic (i.e., mean corpuscular volume less than 80 μm3 [80 fL]) and hypochromic, however the manifestation of iron deficiency occurs in several stages. Patients with a serum ferritin concentration less than 25 ng per mL (25 mcg per L) have a very high probability of being iron deficient. The most accurate initial diagnostic test for IDA is the serum ferritin measurement. Serum ferritin values greater than 100 ng per mL (100 mcg per L) indicate adequate iron stores and a low likelihood of IDA




Tumor lysis syndrome is a clinical condition that can occur spontaneously or after the initiation of chemotherapy associated with the following metabolic disorders: hyperkalemia, hyperphosphatemia, hypocalcemia, and hyperuricemia leading to end-organ damage. It is most common in patients with solid tumors. Tumor lysis syndrome usually develops after the initiation of chemotherapy treatment. However, there are more cases of spontaneous development of tumor lysis syndrome with high-grade hematology-oncology malignancies.

Hallmarks of this condition

  • Potassium >6.0 meq/L or a 25% increase from baseline
  • Phosphorous >4.5 mg/dL or a 25% increase from baseline
  • Calcium <7 mg/dL or a 25% decrease from baseline
  • Uric acid >8 mg/dL or a 25% increase from baseline

Clinical tumor lysis syndrome:

  • Creatinine greater than 1.5 times normal
  • Cardiac arrhythmia/sudden death
  • Seizure

Most of the symptoms seen in patients with tumor lysis syndrome are related to the release of intracellular chemical substances that cause impairment in the functions of target organs. This can lead to acute kidney injury (AKI), fatal arrhythmia, and even death.

In patients at low risk for developing TLS, management includes hydration and close monitoring of volume status and renal function. The use of urine alkalinization to promote elimination of urate is not recommended because it can induce calcium phosphate deposition and therefore aggravate TLS.
In patients at intermediate risk with uric acid levels lower than 8 mg/dl, a xanthine oxidase inhibitor such as allopurinol also should be started 2 days before chemotherapy, whereas rasburicase should be used in patients with uric acid levels higher than 8 mg/dl. 

Rasburicase should not be used in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency. For high-risk patients, a single dose of rasburicase (up to 0.2 mg/kg, although a lower dose is usually prescribed) is recommended, followed by close monitoring of uric acid levels. If uric acid normalizes, allopurinol treatment can be started. If urine output decreases despite adequate fluid administration, a loop diuretic should be added, and RRT will be required if oliguria persists.


 

An inguinal hernia is a protrusion of abdominal or pelvic contents through a dilated internal inguinal ring or attenuated inguinal floor into the inguinal canal and usually, but not always, out of the external inguinal ring, causing a visible or easily palpable bulge.

Presents with visible or easily palpable swelling in the groin, often with discomfort during strenuous exercise or heavy lifting.

Complications are rare but include incarceration, bowel obstruction, and strangulation.

Diagnosis is usually clinical; imaging may be helpful where there is doubt about diagnosis, but also identifies many clinically insignificant apparent hernias.

Surgical repair remains the mainstay of therapy, although watchful waiting is reasonable in adults with minimally symptomatic or asymptomatic inguinal hernia.





 Model for End-Stage Liver Disease (MELD) score is a prognostic scoring system, based on laboratory parameters, used to predict 3-month mortality due to liver disease

MELD scores range from 6 to 40; the higher the score, the higher the 3-month mortality related to liver disease

The MELD score does not accurately predict survival in all patients with cirrhosis; conditions such as liver cancer, hepatopulmonary syndrome, and porto-pulmonary hypertension, are associated with a higher mortality rate than MELD score would reflect. Therefore, patients with these conditions may receive additional MELD points when listed for liver transplantation

Recommendations

  • Calculate a MELD score every 3-6 months in all patients with cirrhosis to repeatedly assess their score
  • Consider referral for liver transplantation in patients with MELD score of 10 or higher
  • Consider using MELD score to assess mortality in patients with acute liver failure or acute variceal bleeding
  • Calculate MELD scores for patients who have:
    • cirrhosis and are undergoing surgery (abdominal, orthopedic, cardiac, etc.)
    • cirrhosis and are being considered for TIPS
    • alcoholic hepatitis and are being considered for steroids
    • acute liver failure or acute variceal bleeding

Appropriate Use of the MELD

  • The original MELD calculator was used to predict mortality in those undergoing placement of a transjugular intrahepatic portosystemic shunt (TIPS)
  • The MELD score has been validated to predict short-term survival in patients with cirrhosis waiting for liver transplantation, but it also was found to be useful in predicting liver-related mortality in patients with alcoholic hepatitis, acute liver failure, acute variceal hemorrhage, or postsurgical procedures
  • MELD is useful in determining when a patient should be evaluated for transplant; the benefit of liver transplantation outweighs the risk once MELD score is 15 or higher
  • In patients with alcoholic hepatitis, MELD score of >20 identifies severe disease, when steroid treatment should be considered
  • Patients listed for liver transplantation will have their MELD scores updated at regular intervals (from every 7 days if 25 or greater, to every 1-3 months

Understanding the MELD Score Calculation

  • When inputting values, laboratory values of less than 1 are rounded to 1
  • A score of 40 is set as the upper limit regardless of how high the inputted laboratory values may be.

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In 1890, Ludwig Courvoisier described his observation that patients with painless jaundice and a palpable gallbladder often have a malignant obstruction of the common bile duct; this is known as “Courvoisier's law.” Painless jaundice and a palpable gallbladder are present in 50%–70% of patients with periampullary cancer or carcinoma of the head of pancreas. The gallbladder with stones is usually chronically fibrosed and so, incapable of enlargement.


 


 The prevalence of asymptomatic microscopic hematuria in adults ranges from 0.19 to 21 percent. Patients with asymptomatic microscopic hematuria or with hematuria persisting after treatment of urinary tract infection also need to be evaluated. Because upper and lower urinary tract pathologies often coexist, patients should be evaluated using cytology plus intravenous urography, computed tomography, or ultrasonography. When urine cytology results are abnormal, cystoscopy should be performed to complete the investigation.

Microscopic hematuria generally is defined as one to 10 red blood cells per high-power field of urine sediment. The American Urological Association (AUA) defines clinically significant microscopic hematuria as three or more red blood cells per high-power field on microscopic evaluation of urinary sediment from two of three properly collected urinalysis specimens. May be associated with urologic malignancy in up to 10 percent of adults.


 Antiarrhythmic Medications - Vaughan-Williams Classification

 • Class I (Ia, Ib, Ic)

 • Class II

 • Class III

 • Class IV

 • Other anti-antiarrhythmic drugs: Adenosine, Digoxin, Ivabradine

Satyendra Dhar, MD 



D-dimer is the smallest fibrinolysis-specific degradation product found in the circulation. The D-dimer is very sensitive to intravascular thrombus and may be markedly elevated in disseminated intravascular coagulation, acute aortic dissection, and pulmonary embolus. Because of its exquisite sensitivity, negative tests are useful in the exclusion venous thromboembolism. Elevations occur in normal pregnancy, rising two- to fourfold by delivery. D-dimer also rises with age, limiting its use in those > 80 years old. There is a variable rise in D-dimer in active malignancy and indicates increased thrombosis risk in active disease. Elevated D-dimer following anticoagulation for a thrombotic event indicates increased risk of recurrent thrombosis. 


Satyendra Dhar MD



 

Lactic acid was first found & described in sour milk by Karl Wilhelm Scheele in 1780. German physician–chemist Johann Joseph Scherer (1841–1869) demonstrated the occurrence of lactic acid in human blood under pathological conditions in 1843 & 1851.

Lactic acid is essentially a carbohydrate within cellular metabolism and its levels rise with increased metabolism during exercise and with catecholamine stimulation. Glucose-6-phosphate is converted anaerobically to pyruvate via the Embden-Meyerhof pathway. Pyruvate is in equilibrium with lactate with a ratio of about 25 lactate to 1 pyruvate molecules. Thus, lactate is the normal endpoint of the anaerobic breakdown of glucose in the tissues.

The causes of lactic acidosis can generally be divided into those associated with obviously impaired tissue oxygenation (type A) and those in which systemic impairment in oxygenation does not exist or is not readily apparent (type B). However, there is frequently overlap between type A and type B lactic acidosis. In sepsis, for example, there is both an increase in lactate production resulting from microcirculatory failure and also a decrease in lactate clearance that is not solely due to diminished oxygen delivery.

Satyendra Dhar MD, 


 Monkeypox is a viral zoonotic infection that results in a rash similar to smallpox. However, person-to-person spread outside the household and mortality from a monkeypox infection are significantly less than for smallpox. The rash of monkeypox can also be similar in appearance to more common infectious rashes, such as those observed in secondary syphilis, herpes simplex infection, and varicella-zoster virus infection.

WHO has activated its highest alert level for the growing monkeypox outbreak, declaring the virus a public health emergency of international concern.

Monkeypox is a rare disease caused by infection with the monkeypox virus. Monkeypox virus is part of the same family of viruses as variola virus, the virus that causes smallpox. Monkeypox symptoms are similar to smallpox symptoms, but milder, and monkeypox is rarely fatal. Monkeypox is not related to chickenpox.

Symptoms of monkeypox can include:

  • ·         Fever
  • ·         Headache
  • ·         Muscle aches and backache
  • ·         Swollen lymph nodes
  • ·         Chills
  • ·         Exhaustion
  • ·         Respiratory symptoms (e.g. sore throat, nasal congestion, or cough)
  • ·         A rash that may be located on or near the genitals (penis, testicles, labia, and vagina) or anus (butthole) but could also be on other areas like the hands, feet, chest, face, or mouth.

o   The rash will go through several stages, including scabs, before healing.

o   The rash can look like pimples or blisters and may be painful or itchy.

Source : CDC/WHO


Satyendra Dhar MD


 Candida glabrata was considered a relatively nonpathogenic commensal fungal organism of human mucosal tissues. However, with the increased use of immunosuppressive agents, mucosal and systemic infections caused by C. glabrata have increased significantly, especially in the human immunodeficiency virus-infected population. A major obstacle in C. glabrata infections is their innate resistance to azole antimycotic therapy, which is very effective in treating infections caused by other Candida species. Candida glabrata, formerly known as Torulopsis glabrata, contrasts with other Candida species in its nondimorphic blastoconidial morphology and haploid genome. C. glabrata currently ranks second or third as the causative agent of superficial (oral, esophageal, vaginal, or urinary) or systemic candidal infections, which are often nosocomial.

Satyendra Dhar MD,

Acute limb ischemia (ALI)

Rapid decrease in lower limb blood flow due to acute occlusion of a peripheral artery or bypass graft and etiology are broadly divided into embolism and thrombosis with various comorbidities. The symptoms of ALI are abrupt with pain, numbness, and coldness of the lower limb, and paresthesia, contracture, and irreversible purpura will appear with the exacerbation of ischemia.

Critical Limb ischemia

Etiology: obstructive atherosclerotic disease; atheroembolic or thromboembolic disease, vasculitis, in situ thrombosis related to hypercoagulable states, thromboangiitis obliterans, cystic adventitial disease, popliteal entrapment, or trauma.

pathophysiology: chronic & complex process that affects the macrovascular, microvascular systems & surrounding tissues.

The twin Saints Comas and Damian were ascribed to have saved a gangrenous limb in the 13th century and became patrons of future surgeons. In the 1960s, Charles Dotter developed techniques to image diseased arteries during a recanalization procedure. The development of guide wires, angioplasty balloons, & stents quickly followed.

Satyendra Dhar MD, 


 HYPOMAGNESEMIA

If unsure, the distinction between gastrointestinal losses and renal losses can be made by measuring the 24-hour urinary magnesium excretion. In addition, one can calculate the fractional excretion of magnesium (on a random urine specimen) with the following formula where U and P refer to the urine and plasma concentrations of magnesium (Mg) and creatinine (Cr).

FEMg  = [(UMg x PCr) / (PMg x UCr x 0.7)] x 100

If the fractional excretion of magnesium is above 2% in someone with normal renal function, the hypomagnesemia is likely secondary to renal magnesium wasting from drugs such as diuretics, aminoglycosides, or cisplatin.

2 grams of IV magnesium sulfate increased serum levels by a paltry median of 0.2 mg/dL.  

Rechecking too soon may give a false sense of security.

  • If the Magnesium level is 1.7 to 2, give 2 grams of MgSO4 IV.
  • If the Magnesium level is 1.3 to 1.7 give 4 grams of MgSO4  IV.

Parenteral (IV or IM): Magnesium Sulfate (MgSO4)

Magnesium Sulfate is 10% elemental (1 gram of Magnesium per 100 ml solution)

  • One gram of MgSO4 contains 8.12 meq of Magnesium
  • One ml MgSO4 50% Solution = 4 meq Magnesium
  • One ml MgSO4 10% Solution = 0.8 meq Magnesium


Satyendra Dhar MD, 


 INSULIN CONVERSION

A total daily dose of insulin (TDD) =

             N X Wt in Kg

(N= 0.5-1.0 for obese, resistant & most type 2 DM)

Administer:

 ½ as Basal (Long acting) & ½ in 3 divided doses a day before each meal

Target pre-meal BG < 140 & random BG < 180 in non-ICU pts

For patients who aren’t transitioning from IV insulin or who aren’t on an insulin regimen at home, many experts offer these rules of thumb for estimating the total daily dose:

* 0.3 units/kg/day for patients who are lean, on hemodialysis, frail and elderly, insulin-sensitive, or at risk for hypoglycemia;

* 0.4 units/kg/day for a patient at normal weight;

* 0.5 units/kg/day for overweight patients; and

* 0.6 units/kg/day or more for patients who are obese, on high-dose steroids, or insulin-resistant.

Satyendra Dhar MD, 


 UROLITHIASIS

80% of stones are composed of calcium oxalate or phosphate. Others include uric acid (9%), struvite (10%), & cystine (1%) stones. Struvite stones can form into a staghorn or large calculus that overwhelms the renal collecting system; are Mg ammonium phosphate; secondary to elevated urine pH, & urease forming Proteus or Klebsiella species.

Urea breakdown yields ammonia as a by-product, which increases the urinary pH (typically to more than 8), and facilitates struvite stone formation.

Uric acid stone formation is related to low urinary uric acid levels, low urine pH, and low urinary volume. Most commonly, these patients will present as idiopathic uric acid stone formers; however, metabolic disorders such as diabetes and obesity will also increase the risk of uric acid stones.

Cystine stones are rare and occur due to an inborn congenital disorder causing mutations in 2 genes, SLC3A1, and SLC7A9. These mutations cause defective cystine metabolism and transport, resulting in cystinuria and stones.

Satyendra Dhar MD,


 GRADING in clinical medicine

The grading system is often used in Clinical medicine to indicate the severity scale of a disease or a pathology. Below are some of the grading systems used often in daily practice. Please comment & add if you know of any other grading systems.

Satyendra Dhar MD,

 


 ACUTE COMPARTMENT SYNDROME

The definitive surgical therapy for compartment syndrome is emergent fasciotomy (compartment release), with subsequent fracture reduction or stabilization and vascular repair, if needed. The goal of decompression is the restoration of muscle perfusion within 6 hours.

The original description of the consequences of unchecked rising intra-compartmental pressures is widely attributed to Richard von Volkmann.

In acute compartment syndrome, especially with trauma, consider performing a workup for rhabdomyolysis, with measurement of the following:

* Creatine phosphokinase (CPK)

* Renal function studies

* Urinalysis

* Urine myoglobin

Satyendra Dhar MD, 


 The mechanism of action of lithium is not known. It is rapidly absorbed, has a small volume of distribution, and is excreted in the urine unchanged (there is no metabolism of lithium).
Toxic levels > 2 mEq/L

Satyendra Dhar MD,


Statins & Recommendations:

Word Cholesterol came from Cholesterine, named by French chemist Michel E. Chevreul (‘solid bile’ in Greek: ‘chole’ for bile and ‘stereos’ for solid). The exact formula of cholesterol was established in 1888 by Friedrich Reinitzer. Merck Labs found the first statin, in 1978, in a fermentation broth of Aspergillus terreus, named mevinolin & later lovastatin.

Statins inhibit the critical step of cholesterol synthesis in which 3-hydroxy-3-methylglutaryl coenzyme A (HMGC) is transformed to mevalonate by the enzyme HMGC reductase. By doing so, they have a potent lipid-lowering effect that reduces cardiovascular risk and decreases mortality. Since the mevalonate pathway also influences endothelial function, the inflammatory response, and coagulation, the effects of statins reach well beyond their cholesterol-lowering properties. As with all drugs, statins may have adverse effects; these include musculoskeletal symptoms, increased risk of diabetes, and higher rates of hemorrhagic stroke. However, the frequency of adverse effects is extremely low and, in selected patient populations, the benefits of statins considerably outweigh the potential risks.

Satyendra Dhar MD, 


 SKIN RASHES

Skin rashes can occur from a variety of factors, including infections, heat, allergens, immune system disorders, and medications.

A rapid and accurate diagnosis is critically important to make treatment decisions, especially when mortality or significant morbidity can occur without prompt intervention.

Rashes can be divided into petechial/purpuric, erythematous, maculopapular, and vesiculobullous. After this differentiation, the presence of fever and systemic signs of illness should be assessed. Through the breakdown of rashes into these classes, emergency providers can ensure deadly conditions are considered.

Satyendra Dhar MD, 


 Nail Findings & Associated Conditions

Change in color, texture, or shape can be harmless, but may suggest an underlying systemic disease.

 • Muehrcke's Lines

 • Melanoma

 • Terry's Lines

 • Onychogryphosis

 • Clubbed Fingernails

 • Mees' lines

 • Koilonychia

 • Pterygium Unguis

 • Green Nail Syndrome

 • Leukonychia

 • Beau's Lines

 • Yellow Nail Syndrome

 • Onycholysis

 • Transverse Ridging

 • Nail Plate Crumbling

 • Nail Pitting

 • Central Nail Canal

 • Periungual Telangiectasia

 Satyendra Dhar, MD 


 LUDWIG’S ANGINA

This condition was named after a German physician, Wilhelm Friedrich von Ludwig, who first described it in 1836.

Although traditionally associated with pain of cardiac origin, the term “angina” is derived from the Latin word for choke (angere) and the Greek word for strangle (ankhone). In the case of Ludwig’s angina, it refers to the feeling of strangling and choking secondary to lingual airway obstruction, which is the most serious potential complication of this condition.

Ludwig angina is a bilateral infection of the submandibular space that consists of two compartments in the floor of the mouth, the sublingual space, and the submylohyoid (also known as submaxillary) space.

Ludwig's angina usually originates from dental infections in the mandibular molars, particularly the second and third molars, accounting for over 90% of cases.

Satyendra Dhar MD, 


 Tongue Pathology

Geographic tongue, fissured tongue, and hairy tongue are the most common tongue problems and do not require treatment. Median rhomboid glossitis is usually associated with a candidal infection and responds to topical antifungals. Atrophic glossitis is often linked to an underlying nutritional deficiency of iron, folic acid, vitamin B12, riboflavin, or niacin and resolves with correction of the underlying condition. Oral hairy leukoplakia, which can be a marker for underlying immunodeficiency, is caused by the Epstein-Barr virus and is treated with oral antivirals. Tongue growths usually require a biopsy to differentiate benign lesions (e.g., granular cell tumors, fibromas, lymphoepithelial cysts) from premalignant leukoplakia or squamous cell carcinoma. Burning mouth syndrome often involves the tongue and has responded to treatment with alpha-lipoic acid, clonazepam, and cognitive behavior therapy in controlled trials. Tongue lesions of unclear etiology may require biopsy or referral to an oral and maxillofacial surgeon, head and neck surgeon, or a dentist experienced in oral pathology.

Recognition and diagnosis of tongue abnormalities require examination of tongue morphology and a thorough history, including onset and duration, antecedent symptoms, and tobacco and alcohol use. A complete head and neck examination, with careful assessment for lymphadenopathy, is essential.

Satyendra Dhar MD, 

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