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Hyperemesis gravidarum - definition, epidemiology, pathophysiology, complications, management

Definition: Mild to moderate nausea and vomiting are seen commonly until approximately 16 weeks in most pregnant ladies. Although nausea and vomiting tend to be worse in the morning, thus erroneously termed morning sickness, they frequently continue throughout the day. In some cases, however, it is severe and unresponsive to simple dietary modification and antiemetics. Hyperemesis gravidarum is defined as vomiting sufficiently severe to produce weight loss, dehydration, alkalosis from loss of hydrochloric acid and hypokalemia. Rarely, acidosis from partial starvation and transient hepatic dysfunction develop. Modified PUQE scoring index  (Pregnancy-Unique Quantification of Emesis and Nausea) can be used to quantify the severity of nausea and vomiting.  Epidemiology: There appears to be an ethnic or familial predilection. The hospitalization rate for hyperemesis is around 0.5 to 0.8%. Hospitalization is less common in obese women. In women hospitalized in a previous pregnan

Calcinosis cutis

Competitive, uncompetitive and non competitive enzyme inhibitors

(A) Enzyme–substrate complex;  (B) a competitive inhibitor binds at the active site and thus prevents the substrate from binding;  (C) an uncompetitive inhibitor binds only to the enzyme–substrate complex;  (D) a noncompetitive inhibitor does not prevent the substrate from binding.

Visceral and parietal layer of serous pericardium

Pericardium The pericardium is a fibroserous sac surrounding the heart and the roots of the great vessels. It consists of two components,  1) the fibrous pericardium and  2) the serous pericardium. The fibrous pericardium is a tough connective tissue outer layer that defines the boundaries of the middle mediastinum.  The serous pericardium is thin and consists of two parts: 1) The parietal layer lines the inner surface of the fibrous. 2) The visceral layer adheres to the heart and forms its outer covering. The parietal and visceral layers of serous pericardium are continuous at the roots of the great vessels. The narrow space created between the two layers of serous pericardium, containing a small amount of fluid, is the pericardial cavity. This is pictured in the diagram above as a fist in a filled balloon. This potential space allows for the relatively uninhibited movement of the heart. Fibrous pericardium The fibrous pericardium is a cone-shape

Diaxozide - mechanism of action

The diagram shows a beta cell of the islet of pancreas and will explain how local factors regulate secretion of insulin from it. Glucose enters the cell via the GLUT-2 transporter. Inside the cell there is metabolism with the generation of ATP. This causes the ATP-sensitive K+ channel to close, as shown in A. Closure of this channel leads to cell membrane depolarization. This in turn allows calcium ions to enter the cell via another calcium channel, shown in B. Increased intracellular calcium activates calcium dependent phospholipid protein kinase. This leads to exocytosis of insulin granules. Diaxozide acts by opening the K+ channel. This leads to loss of K+ and causing membrane hyperpolarization. This prevents Ca2+ from entering, protein kinases are not activated and thus there is no exocytosis of insulin granules...