Tongue Pathologies (Differential Diagnosis)

 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, 

Infographics

Nuclear myocardial perfusion imaging (MPI)

 Nuclear myocardial perfusion imaging (MPI) may be performed by either single-photon emission CT (SPECT) or positron emission tomography (PET). As with stress echocardiography, MPI stress testing may be exercise or pharmacologically induced. MPI involves IV administration of radioactive tracers. A gamma camera detects radio emissions from the tracer that perfuses the myocardium. Tracer uptake depends on flow dynamics as well as myocyte membrane integrity. Color-coded images of myocardial perfusion pre- and post-stress are generated in different axes to allow assessment for each coronary distribution.

Pharmacologic stress testing is an alternative modality in patients who are unable to exercise and with the following conditions:

Patients presenting with unstable angina.

History of heart failure which is not well controlled, and there is a concern for deterioration.

Poorly controlled blood pressure with systolic blood pressure significantly higher (>200 mmHg at rest).

Patients with a history of aortic stenosis which is significantly worse on echocardiogram (aortic valve area <1.0 cm2 and mean gradient >40 mmHg) and have ongoing symptoms.

Myocardial infarction in the last week.

Acute pulmonary embolism

Acute inflammation of the pericardium or myocardium

Severe pulmonary hypertension

The exercise stress test is not useful when baseline EKG is abnormal such as with left ventricular hypertrophy (LVH), left bundle branch block (LBBB), paced rhythm, Wolff Parkinson White (WPW) syndrome, or greater than 1 mm ST-segment depression. These patients are suitable candidates for testing involving pharmacologic agents.

Regadenoson is a pharmacological stress agent that has been widely used since its approval by the Food and Drug Administration (FDA) in 2008. For many years, dipyridamole and adenosine, which are non-selective adenosine receptor agonists, were more popular. However, these agents are less preferred now due to their undesirable adverse effects as compared to regadenoson. 

Satyendra Dhar MD, 

Infographics

Diuretics - Pharmacology

 Diuretics - Pharmacology

Thiazides diuretics:

 • Inhibit Na+ Cl- cotransporter in distal tubule

 • Chlorothiazide, Chlorthalidone, Indapamide, Hydrochlorothiazide, Methyclothiazide, Metolazone

 

Loop diuretics:

 • Inhibit Na+K+Cl2- cotransporter in thick ascending limb

 • Bumetanide, Furosemide, Ethacrynate, Torsemide, Piretanide

 

Potassium sparing diuretics:

 • Inhibit Na+ reabsorption in the collecting duct

 • Amiloride, Spironolactone (Aldactone), Triamterene

 

Carbonic anhydrase inhibitors:

 • Inhibit Na+ and HC03- in the proximal tubule

 • Acetazolamide, Methazolamide

 

Osmotic diuretics:

 • Promote Na+ and water loss through the nephron by excretion of non-reabsorbable filtrate

 • Glycerin (Glycerol), Isosorbide, Mannitol, Urea

Vasopressin receptor antagonists (also called Vaptans):

 • Aquaretics (not a diuretic as no effect on sodium reabsorption)-promote water excretion by inhibiting antidiuretic hormone (ADH)-mediated water reabsorption in the collecting duct

 

Satyendra Dhar, MD 

Infographics

Adrenal Crisis

 Adrenal Crisis

Do not confuse acute adrenal crisis with Addison’s disease. In 1855, Thomas Addison described a syndrome of long-term adrenal insufficiency that develops over months to years, with weakness, fatigue, anorexia, weight loss, and hyperpigmentation as the primary symptoms. In contrast, an acute adrenal crisis can manifest with vomiting, abdominal pain, and hypovolemic shock. When not promptly recognized, adrenal hemorrhage can be a cause of the adrenal crisis. Administration of glucocorticoids in supraphysiologic or stress doses is the only definitive therapy for adrenal crisis.

In 1856, Trousseau termed adrenal insufficiency as "bronze Addison disease," which became known widely as Addison disease. With the discovery of cortisone by Hench, Kendall, and Reichstein in the late 1940s, the life expectancy of patients with adrenal insufficiency dramatically improved, and initial data suggested that life expectancy was normalized. Tuberculosis was the most common cause (70%) during the 1930s. Currently, autoimmune adrenalitis is the most common cause of primary adrenal insufficiency in developed countries, and tuberculosis is still the leading cause of adrenal insufficiency in developing countries.

Satyendra Dhar MD, 

Infographics

Anterior cerebral artery (ACA) strokes

ACA infarcts are rare because of the collateral circulation provided by the anterior communicating artery. ACA infarct can present as contralateral hemiparesis with loss of sensibility in the foot and lower extremity, sometimes with urinary incontinence. This is due to the involvement of the medial paracentral gyrus. If the lesion is very proximal, it is possible that there may be cognitive impairment due to lesions in the prefrontal cortex.

Anterior cerebral artery strokes occur in the territory of the anterior cerebral artery which involves the superior and medial part of the parietal lobe along with the midline of the frontal lobe. These are uncommon causes of ischemic infarctions, making up about 0.3%-4.4% of stroke cases in series reports. The clinical presentation of this stoke is variable as it depends on whether the anterior cerebral artery or one of its branches is involved.

Infographics

Mean arterial pressure (MAP)

 Mean arterial pressure (MAP)

 A common method used to estimate the MAP is the following formula:

* MAP = DP + 1/3(SP – DP) or

* MAP = DP + 1/3(PP)

Where DP is the diastolic blood pressure, SP is the systolic blood pressure, and PP is the pulse pressure.

To perfuse vital organs requires the maintenance of a minimum MAP of 60 mmHg. If MAP drops below this point for an extended period, end-organ manifestations such as ischemia and infarction can occur. If the MAP drops significantly, blood will not be able to perfuse cerebral tissues, there will be a loss of consciousness, and neuronal death will quickly ensue.

Satyendra Dhar MD, 

Infographics

Posterior cerebral artery (PCA) strokes

Posterior cerebral artery (PCA) strokes can be challenging to diagnose, due to the variability in symptoms, which may be nonspecific and inconsistent upon initial presentation.

The incidence of PCA strokes can be estimated between 5% to 10%.

Patients may present in a comatose state via ambulance or may walk to an emergency department without assistance. Patients with a PCA stroke may present with only a headache and mild visual changes such as vision loss, diplopia, inability to see half of the view, or difficulty reading perceiving colors, or recognizing familiar faces.

Satyendra Dhar MD, 

Infographics

Middle Cerebral Artery (MCA) territory CVA

The middle cerebral artery territory is the most commonly affected territory in a cerebral infarction, due to the size of the territory and the direct flow from the internal carotid artery into the middle cerebral artery, providing the easiest path for thromboembolism.

The neurological deficit will depend on the extent of the infarct and hemispheric dominance, and include:

• contralateral hemiparesis
• contralateral hemisensory loss
• hemianopia
• aphasia: if the dominant hemisphere is involved; may be expressive in anterior MCA territory infarction, receptive in posterior MCA stroke, or global with extensive infarction
• neglect: non-dominant hemisphere.

Infographics

ProBNP (pro B-type natriuretic peptide)

 ProBNP (pro B-type natriuretic peptide) is secreted by cardiomyocytes in response to stretch and is quickly cleaved into 2 circulating fragments—the biologically active 32-amino acid C-terminal BNP (B-type natriuretic peptide) and the inert 76-amino acid NT-proBNP (N-terminal pro-BNP). Both fragments are routinely used to aid diagnosis of heart failure, predict outcomes, and to monitor the effects of therapy.

Differences between BNP and NT-proBNP on a biological level really relate to the fact that one is biologically active as a hormone, BNP, whereas NT-proBNP is cleared passively from the body and is not biologically active.

BNP has a much shorter half-life, and NT-proBNP has a longer half-life. NT-proBNP, as a consequence, circulates in higher concentrations in the bloodstream, therefore, more likely to be more sensitive for detecting earlier forms of heart failure because it circulates at somewhat higher levels.

BNP and NT-proBNP are extracted by the kidneys to a comparable extent of only about 15–20%. The calculated biological half-lives of BNP range from 13 to 20 minutes and of NT-proBNP from 25 to 70 minutes.

BNP and NT-proBNP are cleared differentially: BNP is actively removed from the bloodstream (binding to clearance receptors and a much lesser extent by enzymatic degradation by neutral endopeptidase) and also has passive clearance mechanisms, including renal clearance; NT-proBNP is cleared more passively by organs with high rates of blood flow (e.g. muscle, liver, kidneys).

Satyendra Dhar MD,

Infographics

Pancreatic pseudocysts

 Pancreatic pseudocysts are fluid collections in the pancreatic tissue or the adjacent pancreatic space. It is surrounded by a well-defined wall and contains essentially no solid material. Most pancreatic pseudocysts occur as a consequence of acute pancreatitis. However, they can also occur in the setting of chronic pancreatitis, postoperatively, or after pancreatic trauma. Pseudocysts may be asymptomatic or may present with a variety of symptoms such as pain, satiety, upper gastrointestinal bleeding, nausea, and vomiting. The maturation period of pancreatic pseudocysts is reported to be approximately 2 to 6 weeks, and during this time, 33% of cysts are expected to spontaneously resolve. However, a substantial number of persistent cysts require treatment, owing to potential complications such as infection, hemorrhage, and cyst rupture.

Satyendra Dhar MD, 

Infographics

Circle of Willis and brain circulation

 Circle of Willis and brain circulation

Herophilus of Chalcedon (335-280 BC), “Father of Anatomy,” described the vascular structure at the base of the brain which he named the rete mirabile (Latin for “wonderful net”).  Although works of Herophilus were tragically destroyed on Julius Caesar’s invasion of Alexandria, some of his teaching can be found in the writings of Galen, who was said to have possessed all his work. Thomas Willis (1621–1675), a physician and Professor of Natural Philosophy at Oxford in the mid-17th century, demonstrated with great precision both the structure and the function of one major anastomotic arterial system. For this reason, the name of this structure is interchangeable, either as Willis’ circle or as Willis’ polygon, being one of the most famous eponymous structures in human anatomy. Hippocrates, “father of medicine” first recognized CVA > 2400 years ago & called it apoplexy, Greek term - "struck down by violence". Name described sudden changes occurring in stroke but didn’t necessarily convey what’s actually happening in the brain.

Satyendra Dhar MD, 

Infographics

C-REACTIVE PROTEIN

 C-REACTIVE PROTEIN

Discovered by Tillett & Francis in 1930. First identified as a substance in the serum with acute inflammation that reacted with the "c" carbohydrate Ab of the capsule of pneumococcus.

CRP is a pentameric protein synthesized by the liver, whose level rises in response to inflammation. CRP is an acute-phase reactant protein that is primarily induced by the IL-6 action on the gene responsible for the transcription of CRP during the acute phase of an inflammatory/infectious process.

Lab values vary, and there is no standard at present.  However, in general, the result is reported in either mg/dL or mg/L. Hs-CRP is usually reported in mg/L.

Interpretation of CRP levels:

• Less than 0.3 mg/L: Normal (level seen in most healthy adults).
• 0.3 to 1.0 mg/L: Normal or minor elevation (can be seen in obesity, pregnancy, depression, diabetes, common cold, gingivitis, periodontitis, sedentary lifestyle, cigarette smoking, and genetic polymorphisms).
• 1.0 to 10.0 mg/L: Moderate elevation (Systemic inflammation such as RA, SLE, or other autoimmune diseases, malignancies, myocardial infarction, pancreatitis, bronchitis).
• More than 10.0 mg/L: Marked elevation (Acute bacterial infections, viral infections, systemic vasculitis, major trauma).
• More than 50.0 mg/L: Severe elevation (Acute bacterial infections).

Certain medications, such as NSAIDs will falsely decrease CRP levels. Statins, as well, have been known to reduce CRP levels falsely. Recent injury or illness can falsely elevate levels, particularly when using this test for cardiac risk stratification. Magnesium supplementation also can decrease CRP levels.

As mentioned above, mild elevations in CRP can be seen without any systemic or inflammatory disease. Females and elderly patients have higher levels of CRP. Obesity, insomnia, depression, smoking, and diabetes can all contribute to mild elevations in CRP, and the results shall be interpreted with caution in individuals with these comorbidities.

Satyendra Dhar MD, 

Infographics