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The space of Disse is the space between hepatocytes and sinusoidal lining endothelial cells heart attack or gas purchase cardura on line. The intrahepatic biliary system begins with the bile canaliculi interposed between the adjacent hepatocytes heart attack 18 year old male 2 mg cardura with visa. Manufacture of several major plasma proteins such as albumin blood pressure 80 60 buy cardura with a visa, fibrinogen and prothrombin hypertension treatment guidelines 2014 purchase genuine cardura online. Thus a battery of liver function tests is employed for accurate diagnosis, to assess the severity of damage, to judge prognosis and to evaluate therapy. Bilirubin pigment has high affinity for elastic tissue and hence jaundice is particularly noticeable in tissues rich in elastin content. Jaundice is the result of elevated levels of bilirubin in the blood termed hyperbilirubinaemia. Jaundice becomes clinically evident when the total serum bilirubin exceeds 2 mg/dl. A rise of serum bilirubin between the normal and 2 mg/dl is generally not accompanied by visible jaundice and is called latent jaundice. The remaining 15-20% of the bilirubin comes partly from non-haemoglobin haem-containing pigments such as myoglobin, catalase and cytochromes, and partly from ineffective erythropoiesis. Some of the absorbed urobilinogen in resecreted by the liver into the bile while the rest is excreted in the urine as urobilinogen. Accordingly, it is of 3 types; each type affecting respective zone is caused by different etiologic factors: i) Centrilobular necrosis is the commonest type involving hepatocytes in zone 3. Since zone 1 is most well perfused, it is most vulnerable to the effects of circulating hepatotoxins. Decreased excretion of bilirubin into bile Accordingly, a simple age-old classification of jaundice was to divide it into 3 predominant types: pre-hepatic (haemolytic), hepatic, and post-hepatic cholestatic. However, hyperbilirubinaemia due to first three mechanisms is mainly unconjugated while the last variety yields mainly conjugated hyperbilirubinaemia. Hence, currently pathophysiologic classification of jaundice is based on predominance of the type of hyperbilirubinaemia. The presence of bilirubin in the urine is evidence of conjugated hyperbilirubinaemia. There is increased release of haemoglobin from excessive breakdown of red cells that leads to overproduction of bilirubin. Laboratory data in haemolytic jaundice, in addition to predominant unconjugated hyperbilirubinaemia, reveal normal serum levels of transaminases, alkaline phosphatase and proteins. However, there is dark brown colour of stools due to excessive faecal excretion of bile pigment and there is increased urinary excretion of urobilinogen. This can occur in certain inherited disorders of the enzyme, or acquired defects in its activity. However, hepatocellular damage causes deranged excretory capacity of the liver more than its conjugating capacity. Morphologically, cholestasis means accumulation of bile in liver cells and biliary passages. The defect in excretion may be within the biliary canaliculi of the hepatocyte and in the microscopic bile ducts (intrahepatic cholestasis or medical jaundice), or there may be mechanical obstruction to the extrahepatic biliary excretory apparatus (extrahepatic cholestasis or obstructive jaundice). The features of intrahepatic cholestasis include: predominant conjugated hyperbilirubinaemia due to regurgitation of conjugated bilirubin into blood, bilirubinuria, elevated levels of serum bile acids and consequent pruritus, elevated serum alkaline phosphatase, hyperlipidaemia and hypoprothrombinaemia. Liver biopsy in cases with intrahepatic cholestasis reveals milder degree of cholestasis than the extrahepatic disorders. The biliary canaliculi of the hepatocytes are dilated and contain characteristic elongated greenbrown bile plugs. The common causes are gallstones, inflammatory strictures, carcinoma head of pancreas, tumours of bile duct, sclerosing cholangitis and congenital atresia of extrahepatic ducts. The features of extrahepatic cholestasis (obstructive jaundice), like in intrahepatic cholestasis, are: predominant conjugated hyperbilirubinaemia, bilirubinuria, elevated serum bile acids causing intense pruritus, high serum alkaline phosphatase and hyperlipidaemia. However, there are certain features which help to distinguish extrahepatic from intrahepatic cholestasis. In obstructive jaundice, there is malabsorption of fat-soluble vitamins (A,D,E and K) and steatorrhoea resulting in vitamin K deficiency.

Fibrous union may result instead of osseous union if the immobilisation of fractured bone is not done hypertension cdc generic cardura 1mg line. Non-union may result if some soft tissue is interposed between the fractured ends pulse pressure 62 buy cardura with visa. Delayed union may occur from causes of delayed wound healing in general such as infection hypertension 14090 purchase cardura without prescription, inadequate blood supply arrhythmia quizlet cheap cardura 4mg without prescription, poor nutrition, movement and old age. These fibrils grow along the track of degenerated nerve so that in about 6-7 weeks, the peripheral stump consists of tube filled with elongated Schwann cells. On injury, the cut ends of muscle fibres retract but are held together by stromal connective tissue. If the muscle sheath is intact, sarcolemmal tubes containing histiocytes appear along the endomysial tube which, in about 3 months time, restores properly oriented muscle fibres. If the muscle sheath is damaged, it forms a disorganised multinucleate mass and scar composed of fibrovascular tissue. However, in large destructive lesions, the smooth muscle is replaced by permanent scar tissue. This occurs by proliferation from margins, migration, multilayering and differentiation of epithelial cells. However, in parenchymal cell damage with intact basement membrane or intact supporting stromal tissue, regeneration may occur. Stem cells are the primitive cells which have 2 main properties: i) They have capacity for self renewal. Stem cells exist in both embryos and in adult tissues: In embryos, they function to generate new organs and tissues; their presence for organogenesis has been an established fact. In adults, they normally function to replace cells during the natural course of cell turnover. For example, stem cells in the bone marrow which sponateously differentiate into mature haematopoietic cells has been known for a long time. Some of the major clinical trials on applications of stem cells underway are in the following directions: 1. Bone marrow stem cells Haematopoieitc stem cells, marrow stromal cells and stem cells sourced from umbilical cord blood have been used for treatment of various forms of blood cancers and other blood disorders for about three decades. Neuron stem cells these cells are capable of generating neurons, astrocytes and oligodendroglial cells. Islet cell stem cells Clinical trials are under way for use of adult mesenchymal stem cells for islet cells in type 1 diabetes. Cardiac stem cells It is now known that the heart has cardiac stem cells which have capacity to repair myocardium after infarction. Skeletal muscle stem cells Although skeletal muscle cells do not divide when injured, stem cells of muscle have capacity to regenerate. Adult eye stem cells the cornea of the eye contains stem cells in the region of limbus. These limbal stem cells have a potential therapeutic use in corneal opacities and damage to the conjunctiva. Skin stem cells In the skin, the stem cells are located in the region of hair follicle and sebaceous glands. Brucellosis Which of the following type of leprosy is not included in RidleyJopling classification? By hydrolytic enzymes Main cytokines acting as mediators of inflammation are as under except: A. Chronic suppurative inflammation Tubercle bacilli cause lesions by the following mechanisms: A. Direct cytotoxicity the following statements are correct for tubercle bacilli except: A. More acid fast compared to tubercle bacilli 99 Chapter 5 Inflammation and Healing 100 Lepromin test is always positive in: A. They do not have capacity to multiply in response to stimuli throughout adult life 21. Connective tissue in scar is formed by the following types of fibrillar collagen: A.

As with glucose transport blood pressure 30 year old female order cardura 1 mg on-line, the Na -dependent carriers of the apical membrane of the intestinal epithelial cells are also present in the renal epithelium pulse pressure map discount cardura 4mg free shipping. Conversely hypertension and kidney disease buy cardura once a day, the facilitated transport carriers in the serosal membrane of the intestinal epithelia are similar to those found in other cell types in the body arteria umbilical unica 2012 cardura 2 mg amex. During starvation, the intestinal epithelia, like these other cells, take up amino acids from the blood to use as an energy source. Hartnup disease is another genetically determined and relatively rare autosomal recessive disorder. It is caused by a defect in the transport of neutral amino acids across both intestinal and renal epithelial cells. The signs and symptoms are, in part, caused by a deficiency of essential amino acids (see Clinical Comments). Cystinuria and Hartnup disease involve defects in two different transport proteins. In each case, the defect is present both in intestinal cells, causing malabsorption of the amino acids from the digestive products in the intestinal lumen and in kidney tubular cells, causing a decreased resorption of these amino acids from the glomerular filtrate. They may be transported through intestinal epithelial cells, probably by pinocytosis, or they may slip between the cells that line the gut wall. This process is particularly troublesome for premature infants, because it can lead to allergies caused by proteins in their food. These patients do not absorb the affected amino acids at a normal rate from the digestive products in the intestinal lumen. They also do not readily resorb these amino acids from the glomerular filtrate into the blood. Therefore, they do not have a hyperaminoacidemia (a high concentration in the blood). Normally, only a few percent of the amino acids that enter the glomerular filtrate are excreted in the urine; most are resorbed. In these diseases, much larger amounts of the affected amino acids are excreted in the urine, resulting in a hyperaminoaciduria. Transport of Amino Acids into Cells Amino acids that enter the blood are transported across cell membranes of the various tissues principally by Na -dependent cotransporters and, to a lesser extent, by facilitated transporters (Table 37. In this respect, amino acid transport differs from glucose transport, which is Na -dependent transport in the intestinal and renal epithelium but facilitated transport in other cell types. The Na dependence of amino acid transport in liver, muscle, and other tissues allows these cells to concentrate amino acids from the blood. These transport proteins have a different genetic basis, amino acid composition, and somewhat different specificity than those in the luminal membrane of intestinal epithelia. For instance, the N system for glutamine uptake is present in the liver but either not present in other tissues or present as an isoform with different properties. There is also some overlap in specificity of the transport proteins, with most amino acids being transported by more than one carrier. All proteins within cells have a half-life (t1/2), a time at which 50% of the protein that was synthesized at a particular time will have been degraded. Other proteins are present for extended periods, with half-lives of many hours, or even days. Thus, proteins are continuously being Cal Kulis and other patients with cystinuria have a genetically determined defect in the transport of cystine and the basic amino acids, lysine, arginine, and ornithine, across the brush-border membranes of cells in both their small intestine and renal tubules. However, they do not appear to have any symptoms of amino acid deficiency, in part because the amino acids cysteine (which is oxidized in blood and urine to form the disulfide cystine) and arginine can be synthesized in the body. Ornithine (an amino acid that is not found in proteins but serves as an intermediate of the urea cycle) can also be synthesized. The most serious problem for these patients is the insolubility of cystine, which can form kidney stones that may lodge in the ureter, causing bleeding and severe pain. Na -dependent carriers transport both Na and an amino acid into the intestinal epithelial cell from the intestinal lumen.

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Organic molecules containing a high proportion of electronegative atoms (generally oxygen or nitrogen) are soluble in water because these atoms participate in hydrogen bonding with water molecules (Fig blood pressure medication hydroxyzine cardura 2mg generic. In a similar fashion prehypertension hypertension stage 1 cardura 4 mg amex, the oxygen atom of water molecules interacts with inorganic cations such as Na and K to surround them with a hydration shell arteria hipogastrica effective cardura 1 mg. Although hydrogen bonds are strong enough to dissolve polar molecules in water and to separate charges hypertension organization discount cardura 1 mg mastercard, they are weak enough to allow movement of water and solutes. The strength of the hydrogen bond between two water molecules is only approximately 4 kcal, roughly 1/20th of the strength of the covalent O­H bond in the water molecule. Thus, the extensive water lattice is dynamic and has many strained bonds that are continuously breaking and reforming. The average hydrogen bond between water molecules lasts only about 10 psec (1 picosecond is 10 12 sec), and each water molecule in the hydration shell of an ion stays only 2. As a result, hydrogen bonds between water molecules and polar solutes continuously dissociate and reform, thereby permitting solutes to move through water and water to pass through channels in cellular membranes. Its heat of fusion is high, so a large drop in temperature is needed to convert liquid water to the solid state of ice. The thermal conductivity of water is also high, thereby facilitating heat dissipation from high energy-using areas such as the brain into the blood and the total body water pool. Water responds to the input of heat by decreasing the extent of hydrogen bonding and to cooling by increasing the bonding between water molecules. In the emergency room, Di Abietes was rehydrated with intravenous saline, which is a solution of 0. Osmolality and Water Movement Water distributes between the different fluid compartments according to the concentration of solutes, or osmolality, of each compartment. The osmolality of a fluid is proportionate to the total concentration of all dissolved molecules, including ions, organic metabolites, and proteins (usually expressed as milliosmoles (mOsm)/kg water). The semipermeable cellular membrane that separates the extracellular and intracellular compartments contains a number of ion channels through which water can freely move, but other molecules cannot. Likewise, water can freely move through the capillaries separating the interstitial fluid and the plasma. As a result, water will move from a compartment with a low concentration of solutes (lower osmolality) to one with a higher concentration to achieve an equal osmolality on both sides of the membrane. The force it would take to keep the same amount of water on both sides of the membrane is called the osmotic pressure. As water is lost from one fluid compartment, it is replaced with water from another to maintain a nearly constant osmolality. The blood contains a high content of dissolved negatively charged proteins and the electrolytes needed to balance these charges. As water is passed from the blood into the urine to balance the excretion of ions, the blood volume is repleted with water from interstitial fluid. When the osmolality of the blood and interstitial fluid is too high, water moves out of the cells. The loss of cellular water also can occur in hyperglycemia, because the high concentration of glucose increases the osmolality of the blood. Because her blood levels of glucose and ketone bodies are so high, these compounds are passing from the blood into the glomerular filtrate in the kidneys and then into the urine. As a consequence of the high osmolality of the glomerular filtrate, much more water is being excreted in the urine than usual. As a result of water lost from the blood into the urine, water passes from inside cells into the interstitial space and into the blood, resulting in an intracellular dehydration. The hydrogen ions are extensively hydrated in water to form species such as H3O, but nevertheless are usually represented as simply H. The concentration of hydrogen ions in a solution is usually denoted by the term pH, which is the negative log10 of the hydrogen ion concentration expressed in mol/L (Equation 4. Because water dissociates to such a small extent, [H2O] is essentially constant at 55. Acidic solutions have a greater hydrogen ion concentration and a lower hydroxide ion concentration than pure water (pH 7. Strong and Weak Acids During metabolism, the body produces a number of acids that increase the hydrogen ion concentration of the blood or other body fluids and tend to lower the pH (Table 4. These metabolically important acids can be classified as weak acids or strong acids by their degree of dissociation into a hydrogen ion and a base (the anion component).

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