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, 

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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, 

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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 

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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, 

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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.

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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, 

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