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B.Pharm Lab. Instruction Manuals

Pharmacology I

APHE Anatomy, Physiology, and Health Education

Pharmaceutical Analysis

Pharmacy study material

General Pharmacology

Bones and Skeleton System

Bone disease (Gout) (Rheumatoid arthritis) (Osteoarthritis) (Osteoporosis)

Cancer and music therapy

Memory of water

Phenomena associated with liver cirrhosis

Ascites associated with liver cirrhosis

Alcoholol induced necrosis of hepatocytes causes the impaired physiological functions of liver as well as blood vessel damage in the liver. Therefore, total blood supply towards inferior vena ceva is diminished and it affects the cardiac output. The incident caused the decreased blood supply to kidney. As a result, "renin-angiotensin-aldosterone system" and "sympathetic system" become activated that cause sodium and water retention from convoluted distal tubule, followed by the accumulation of excess fluid in inter-tissue spaces (ascites). Decreased album and other plasma proteins by liver are also impaired that causes the decreased ommotic pressure and more water retention via. kidney. It favours the ascites [Barbara 2009],[emedicine].

Varices associated with liver cirrhosis

Varices is the dilated blood vessel (usually veins) with haemorrhage. Esophageous and gastric varices are commonly associated with liver cirrhosis. As we discussed previously, normal portal vein pressure is upto 9 mmHg and it is 2-6 mmHg in inferior "vena ceva". Therefore, the pressure gradient between the two is 3-7 mmHg. If portal pressure rises above 12 mmHg, the gradient rises above 7-10 mmHg, causing portal hypertension. The shunting of hepatic vein redirects the portal vein blood towards lower pressure areas like lower parts of esophagous (esophageal varices), abdominal wall, stomach (gastric varices) and rectum (rectum varices). Therefore, the blood vessels of these areas become dilated and varices [emedicine].

Clinical representation and management of liver cirrhosis

Hepatic encephalopathy (HE)

As we have discussed, hepatocytes are matrix for the detoxification of ammonia, ketone bodies and other nitrogenous substances. Due to cirrhosis, these products return in blood and travel to body tissues including brain. Ketone bodies and ammonia have capability to induce nerve cell damage. It must have to add further that, thiamine (vitamin $B_1$) is stored in skeletal muscle, brain, liver and kidney. Apart from dietary sources, these are utilised by the body for the metabolism of pyruvic acid into $CO_2$ and water. Vitamin $B_1$ is essential for the synthesis of acetylcholine. Vitamin $B_1$ is mostly utilised by CNS. Therefore, deficiency of vitamin $B_1$ due to liver cirrhosis leads to degeneration of myoline sheeth, impaired function of brain followed by impaired reflex, sense of touch etc. Impaired production of ATP in muscle due to vitamin $B_1$ deficiency leads to smooth muscle paralysis of gastro intestinal tract and digestive disturbance, skeletal muscle paralysis and atrophy of limbs.

Coagulation defects

Most of the clotting factors (fibrinogen (I), prothrombin (II), proaccelerin or labile factor (V), serum prothrombin conversion accelerator or stable factor (VII), anti haemophilic factors A, B (VIII, IX), stuart factor or thrombokinase (X), plasma thromboplastin antecetent or anti haemophilic factor C (XI), glass factor or contact factor or anti haemophilic factor D (XII), fibrin stabilizing factor (XIII) are synthesized in liver. So, cirrhosis promotes to the impaired synthesis of these proteins followed by bleeding diathesis or haemorhage [Barbara 2009].

Reference

[Barbara 2009] Barbara GW, Joseph TD, Terry LS, Cecily VD, Pharmacotherapy Handbook, $7^{th}$ Edition, Mc Growhill, 239-320, 2009.
[emedicine] http://emedicine.medscape.com/article/170907-overviewa4.

Anatomy and Physiological roles of liver

Classification of liver cirrhosis

Phenomena associated with liver cirrhosis

Clinical representation and management of liver cirrhosis