Drug-induced gingival enlargement

Drug-induced gingival enlargement is a side-effect of certain drugs where the gingival tissue is not the intended target organ. The key offending drug classes are anticonvulsants, immunosuppressants, and calcium channel blockers. It is estimated that 50% of adults treated with phenytoin experience gingival enlargement, 30% with cyclosporine, and 20% with nifedipine. This overgrowth impedes proper dental hygiene and, apart from the cosmetic damage, causes painful chewing and eating. The common mechanism of action at the cellular level of all these three categories of dissimilar drugs appears to be inhibition of cation influx, particularly sodium and calcium ions. The modalities of treatment are medical and surgical. Medical management is the first line of therapy and includes discontinuing or changing the medication must be placed under consideration. Surgery is reserved for recurrences or cases that persist despite good medical treatment.

 

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Celiac disease

 

Celiac Disease (CD) is an immune-mediated, multisystem disorder that affects genetically susceptible individuals upon exposure to gluten-containing grains such as wheat, barley, and rye. Also known as gluten-sensitive enteropathy, CD is characterized by an inappropriate immune response to gluten, leading to inflammation and damage of the small intestinal mucosa.

CD is associated with various autoimmune and idiopathic conditions, including:

• Type 1 diabetes mellitus

• Hashimoto’s thyroiditis

• Selective IgA deficiency

• Alopecia areata

• Addison’s disease

• Connective tissue diseases (primarily Sjögren’s syndrome)

• Chromosomal disorders (e.g., Down syndrome, Turner syndrome, and Williams syndrome)

• Neurological disorders (e.g., cerebellar ataxia, peripheral neuropathy, epilepsy with or without occipital calcifications)

• Hepatic autoimmune diseases (e.g., primary biliary cholangitis, autoimmune hepatitis, and primary sclerosing cholangitis)

• Idiopathic dilated cardiomyopathy

Extraintestinal manifestations are common and may include:

• Anemia due to impaired absorption of vitamin B12, folate, or iron

• Coagulopathy due to vitamin K deficiency

• Osteoporosis

• Neurological symptoms such as muscle weakness, paresthesias, seizures, and ataxia

Dermatitis herpetiformis is a pathognomonic extraintestinal manifestation of CD. This papulovesicular, extremely pruritic rash appears on extensor surfaces including the elbows, knees, buttocks, and scalp. It represents an immunologic skin response to gluten and is often referred to as celiac disease of the skin.

Diagnosis involves serologic testing and histologic confirmation:

• Serologic tests include anti–tissue transglutaminase (tTG) antibodies (measured quantitatively by enzyme-linked immunosorbent assay, ELISA) and anti-endomysial antibodies.

• Esophagogastroduodenoscopy (EGD) with small bowel biopsy remains the gold standard for diagnosis, particularly in patients with negative serology but strong clinical suspicion.

• Genetic testing for HLA-DQ2 or HLA-DQ8 alleles may be considered in selected cases, especially when the diagnosis remains uncertain.

Management consists of strict lifelong adherence to a gluten-free diet, which is the cornerstone of treatment and typically results in clinical and histological improvement.

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Rhabdomyolysis

Creatine kinase (CK) is an intracellular enzyme present in skeletal muscle, myocardium & brain; smaller amounts in visceral tissues. Released after disruption of cell membranes due to hypoxia or other injury.

Sustained increases in these levels can be a sensitive indicator of underlying muscle damage.
CK may increase to as much as 30 times the upper limit within 24 hrs of strenuous physical activity, then slowly decline over next 7 days.
The definitive diagnosis of rhabdomyolysis is reliably made by serologic testing for creatine kinase (CK). Elevated levels of CK are the hallmark of rhabdomyolysis.
CK functions as an energy reservoir for ATP:
Creatine + ATP = creatine kinase + ADP (adenosine diphosphate).
CK has a half-life of 1.5 days; its level elevated in the first 12 hours, peaks during the first 3 days, and normalizes at around 5 days after injury.
CK level five times the upper limit of normal (≈1000 U/L), without apparent cardiac or brain injury, confirms the diagnosis.
Risk of developing AKI is usually low when the CK level is below 10,000 U/L.
AKI at lower levels of CK noted with coexisting conditions, such as sepsis, hypotension, or underlying CKD.
Myoglobin levels rise rapidly (within 3 hours) and peak prior to serum CK levels.
Myoglobin has a short half-life of 2 - 3 hours and is rapidly excreted by the kidneys.
Rapid and unpredictable metabolism makes serum myoglobin a less useful marker of muscle injury than CK, and is rarely used in assessing the risk of AKI.

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Biliary system and physiology

Bile acids are the end products of cholesterol catabolism. Cholic acid and chenodeoxycholic acid are the major primary bile acids synthesized in human livers and are conjugated with taurine or glycine for secretion into bile. Human liver synthesizes about 200 to 600 mg bile acids per day. The net daily turnover of bile acids is about 5% of a total bile acid pool of about 3 g. Conversion of cholesterol to bile acids involves 17 distinct enzymes located in the cytosol, endoplasmic reticulum, mitochondria, and peroxisome. After each meal, cholecystokinin secreted from the intestine stimulates gallbladder contraction to empty bile acids into the intestinal tract. When passing down the intestinal tract, small amounts of unconjugated bile acids are reabsorbed in the upper intestine by passive diffusion. Most bile acids (95%) are reabsorbed in the brush border membrane of the terminal ileum, trans diffused across the enterocyte to the basolateral membrane, and secreted into portal blood circulation to liver sinusoids and are taken up into hepatocytes. Bile acids lost in the feces (~0.5 g/day) are replenished by de novo synthesis in the liver to maintain a constant bile acid pool.

Bile acids stimulate glucagon-like peptide 1 (GLP1) production in the distal small bowel and colon, stimulating insulin secretion, and therefore, are involved in carbohydrate and fat metabolism. Bile acids through their insulin sensitizing effect play a part in insulin resistance and type 2 diabetes. Bile acid metabolism is altered in obesity and diabetes.

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Mercedes Benz sign

Radiological sign, a triradiate radiolucent shadow, characteristic of the automobile maker's trademark. In case of Gallstones, radiolucent lines represent gas accumulation within the body of a calculus. Center of calculus may contract more than its periphery, which would result in the radial fissures. Gas in the fissures typically comprises < 1% O2, 6–8% Co2 & the rest nitrogen.

The inverted Mercedes-Benz sign refers to the shape taken on by a spinal subdural hematoma on axial imaging at the level of the denticulate ligaments, best visualized on MRI. A pair of denticulate ligaments and the dorsal septum constitute the three radiating spikes of the sign, while blood expands and fills the three loculations in-between.

The Mercedes-Benz sign can be seen in aortic dissection on CT. It is seen as three distinct intimal flaps that have a triradiate configuration like the Mercedes-Benz logo. The appearances are postulated to represent secondary dissection in the wall of the dissected false lumen. It is also called a triple-barreled aortic dissection

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Warfarin induced skin necrosis

Warfarin induced skin necrosis is often heralded by paresthesia, or a sensation of pressure, associated with an erythematous flush that is usually poorly demarcated. The lesions are painful, sudden, well localized and initially hemorrhagic or erythematous. In women, the site of the lesion is random and unpredictable, but the breast is the most common site, followed by the buttocks and thighs. Occasionally, the trunk, face and extremities are also involved.

The mechanism is thought to be that, following the initiation of warfarin, both protein C antigen and activity levels drop rapidly, compared with levels of other vitamin K-dependent factors such as factors IX and X, and prothrombin. This observed rapid early fall in protein C level prompted the hypothesis that the administration of warfarin to protein C-deficient individuals causes a temporary exaggeration of the imbalance between pro- coagulant and anticoagulant pathways; that is, the early suppressive action of warfarin on protein C may not be counterbalanced by the anticoagulant effect created by the decline in other vitamin K-dependent factors, thereby leading to a relative hypercoagulable state at the start of treatment. This leads to thrombotic occlusions of the microvasculature with resulting necrosis.

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Exophthalmos

Exophthalmos (also known as proptosis) is the protrusion of one eye or both anteriorly out of the orbit. It derives from Greek, meaning 'bulging eyes. It occurs due to an increase in orbital contents in the regular anatomy of the bony orbit. Exophthalmos typically arises from an increase in orbital contents within the bony orbit, leading to forward displacement of the globe. The origin of the increased orbital content depends on the underlying cause. In Graves ophthalmopathy, enlargement of the extraocular muscles and expansion of the orbital adipose tissues occurs due to abnormal hyaluronic acid accumulation and edema collection into the retro-orbital space.

The etiological basis of proptosis can include inflammatory, vascular, infectious, cystic, neoplastic (both benign and malignant, metastatic disease), and traumatic factors. Some examples include infectious causations such as orbital cellulitis and subperiosteal abscesses. Traumatic causations could be orbital emphysema, retro-orbital hemorrhage, and carotid-cavernous fistula. Vascular causations not traumatically related would be orbital arteriovenous malformation (AVM) varices and aneurysms. Neoplastic causations include adenocarcinoma of the lacrimal gland, pleomorphic adenoma of the lacrimal gland, meningioma, lymphoma, and metastatic disease.

A ruptured lymphangioma can enlarge after its rupture and sequestering of heme, which pathologically is described as a chocolate cyst. Orbital varices can result in proptosis with increased venous pressure in the orbit, as seen with a Valsalva maneuver or change in postural position.

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Bladder outlet obstruction (BOO)

Functional obstruction may be caused by detrusor-sphincter dyssynergia (DSD), either at the level of the smooth muscle or rhabdosphincter; primary bladder neck obstruction, which may be functional and anatomic in character; or due to dysfunctional voiding, associated with learned voiding disorders or pelvic floor dysfunction associated with pain syndromes.

Anatomic obstruction in men results most commonly from benign prostatic enlargement (BPH) or urethral stricture.

Examination of historical and physical evidence of both onset and magnitude and severity of symptoms is critical in the primary evaluation of these patients. In men, benign prostatic obstruction (BPO) is the most common cause of BOO and stems from a variety of etiologies. Other causes of BOO include urethral stricture disease, dysfunctional voiding, neurogenic-based detrusor-sphincter dyssynergia (DSD), and primary bladder neck obstruction.

A normal flow rate in men does not preclude the possibility of obstruction. Concomitant analysis of flow rates and residual volumes is important to avoid misinterpretation of isolated data. Urodynamics, alternative radiologic procedures, or cystoscopy is recommended in the case of failed presumptive therapy, a complex presentation scenario, or when a diagnosis is in doubt. Formal urodynamic evaluation is usually reserved for complicated cases and is often performed in conjunction with a pressure flow evaluation.

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