AFP

In adults, high blood levels (over 500 nanograms/milliliter) of AFP are seen in only three situations:

• HCC
• Germ cell tumors (cancer of the testes and ovaries)
• Metastatic cancer in the liver (originating in other organs)

Several assays (tests) for measuring AFP are available. Generally, normal levels of AFP are below 10 ng/ml. Moderate levels of AFP (even almost up to 500 ng/ml) can be seen in patients with chronic hepatitis. Moreover, many patients with various types of acute and chronic liver diseases without documentable HCC can have mild or even moderate elevations of AFP.

The sensitivity of AFP for HCC is about 60%. In other words, an elevated AFP blood test is seen in about 60% of HCC patients. That leaves 40% of patients with HCC who have normal AFP levels. Therefore, a normal AFP does not exclude HCC. Also, as noted above, an abnormal AFP does not mean that a patient has HCC. It is important to note, however, that patients with cirrhosis and an abnormal AFP, despite having no documentable HCC, still are at very high risk of developing HCC. Thus, any patient with cirrhosis and an elevated AFP, particularly with steadily rising blood levels, will either most likely develop HCC or actually already have an undiscovered HCC.

An AFP greater than 500 ng/ml is very suggestive of HCC. In fact, the blood level of AFP loosely relates to (correlates with) the size of the HCC. Finally, in patients with HCC and abnormal AFP levels, the AFP may be used as a marker of response to treatment. For example, an elevated AFP is expected to fall to normal in a patient whose HCC is successfully removed surgically (resected).

There are a number of other HCC tumor markers that currently are research tools and not generally available. These include des-gamma-carboxyprothrombin (DCP), a variant of the gamma-glutamyltransferase enzymes, and variants of other enzymes (e.g., alpha-L-fucosidase), which are produced by normal liver cells. (Enzymes are proteins that speed up biochemical reactions.) Potentially, these blood tests, used in conjunction with AFP, could be very helpful in diagnosing more cases of HCC than with AFP alone.

portal vein thrombosis./ obstruction

Pathophysiology

The portal vein forms at the junction of the splenic vein and the superior mesenteric vein behind the pancreatic head, and it can become thrombosed or obstructed at any point along its course. In cirrhosis and hepatic malignancies, the thromboses usually begin intrahepatically and spread to the extrahepatic portal vein. In most other etiologies, the thromboses usually start at the site of origin of the portal vein. Occasionally, thrombosis of the splenic vein propagates to the portal vein, most often resulting from an adjacent inflammatory process such as chronic pancreatitis.

Inherited and acquired disorders of the coagulation pathway are frequent causes of portal vein thrombosis. Inherited disorders include mutations in the prothrombin gene G20210A as well as deficiencies of various intrinsic anticoagulation factors, such as protein C and protein S, and activated protein C resistance. Acquired disorders include antithrombin III deficiency resulting from malnutrition, sepsis, disseminated intravascular coagulation, inflammatory bowel disease, liver disease, or estrogen use.

Stasis can be another major category for portal vein thrombosis. The global resistance to hepatic blood flow produced by cirrhosis is a common cause. Sclerotherapy for esophageal varices has been postulated as a possible mechanism though not proven thus far. The portal vein or its tributaries can be obstructed by adjacent tumor compression or invasion. Infectious and inflammatory processes may also lead to venous thrombosis.

Portal vein obstruction does not affect liver function unless the patient has an underlying liver disease such as cirrhosis. This is partially due to a rapid arterial buffer response, with compensatory increased flow of the hepatic artery maintaining the total hepatic blood flow. Formation of collaterals occurs rather rapidly as well, and they have been described as early as 12 days after acute thrombosis, though the average time to formation is approximately 5 weeks.

The development of a collateral circulation, with its attendant risk of variceal hemorrhage, is responsible for most of the complications and is the most common manifestation of portal vein obstruction. Other sequelae of the subsequent portal hypertension, such as ascites, are less frequent. Rarely, the thrombosis extends from the portal vein to the mesenteric arcades, leading to bowel ischemia and infarction.

portal vein obstruction

• • causes-
    
  • In adults, cirrhosis is the major etiology, accounting for 24-32% of cases of portal vein thrombosis.
  • Neoplasms are another major cause, accounting for 21-24% of cases of portal vein obstruction, with hepatocellular carcinoma and pancreatic carcinoma causing most of these cases. These tumors can cause compression or direct invasion of the portal vein and lead to thrombosis by inducing a hypercoagulable state. Local ablative therapies for hepatocellular or metastatic disease have been linked to its development.
  • Although less common than in children, infections (predominantly intra-abdominal) still play an important role, with a particular association to Bacteroides fragilis bacteremia.
  • Myeloproliferative disorders and inherited or acquired coagulation disorders account for 10-12% of cases in adults.
  • Approximately 8-15% of cases have been reported to be idiopathic in the recent literature. For other less common etiologies, such as abdominal trauma, surgery, and inflammatory bowel disease

    Physical findings-
    

    • Splenomegaly is found in 75-100% of patients, most presenting in the chronic stage. Mild hepatomegaly is often present, as is right upper quadrant epigastric tenderness, especially in the acute setting.
    • Ascites is found infrequently. Stigmata of chronic liver disease, such as spider angiomata or palmar erythema, are usually found in the presence of underlying liver disease.
    • The presence of caput medusae indicates posthepatic or intrahepatic portal hypertension because it forms by recanalization of the umbilical vein, which connects with the left hepatic branch of the portal vein. It should not be observed in isolated extrahepatic portal vein obstruction because the obstruction is below the origin of the umbilical vein.
    • In children, growth retardation may be present.
    • Abnormalities of the extrahepatic biliary tree may occur in 80% of cases due to compression by choledochal or periportal varices or from ischemic stricturing. These findings manifest by jaundice, cholangitis, hemobilia, cholecystitis, or a hilar mass that can be mistaken for a cholangiocarcinoma.

    
    

    ,

renal failure

Q: What do you think is the cause of renal failure
A:Being of Asian descent Diabetes is highest on my list but could also be due to hypertension, glomerulonephritis, adult polycystic kidney dse, nephrocalcinosis

Skin

A straw-yellow hue is found in cancer cachexia.

Paleness may be from anemia, dysemia, leukemia, amyloid degeneration, or Bright's disease.

Articular rheumatism is marked by paleness, and profuse sweats with strong acid odor.

Anger, fear, and jealousy cause paleness. The cause is vascular spasm. Fainting causes pallor.

Plethoric people are too red in color. A florid complexion means the sanguinous temperament and does not mean too much blood.

Unconsciousness may be from syncope (fainting). The face is pale; either no pulse or very light; the breathing very low and quiet. There are no signs of distress; the face is usually composed.

2. Appearance Of Patient

2. Appearance Of Patient

The patient's appearance will tell whether or not he is able to meet the requirements of existence. He looks able to carry on his work--his particular occupation- or he does not. If he does not, he will give the appearance of being sick with either acute or chronic disease.

At the bedside the patient may look robust, sick, collapsed, bluish or cyanosed, thin, fat, with thick and short neck, or long and slender; he is on his back with legs extended, or with the legs drawn up; or on the side with legs drawn up against the abdomen.

The patient may be unable to give a history or describe his symptoms.
Decubitus (Lying Down)

The manner of lying is significant. On the back means exhaustion. This is the position when a patient has lost consciousness.

In a faint or anemia of the brain, the head drops; in congestion of the brain, the head must be supported on several pillows; in asthma of the lungs, bronchi, or caused by the heart, the patient must have much pillow support.

In heart disease the patient lies upon the right side. A normal person can lie on either side equally well.

When heart disease is advancing to the fatal state, the position is sitting, with head and shoulders supported by pillows.

Pain in the abdomen will cause the sufferer to press upon it, or lie on a pillow. Pressure gives some relief. When the pain is intense there will be twisting and writhing.

In peritonitis, appendicitis, cystitis, gallstones, cancer of the stomach and bowels, the tendency is to draw the legs on the abdomen. In peritonitis, the patient will usually be on the back, with legs drawn up.

In gastric ulcer, when suffering with pain, if the ulcer is in the front wall of the stomach, the patient will lie on his back; if the posterior wall is the location of the ulcer, the patient's position will be lying on the abdomen; or upon the right or left side, if the disease is of the right or left side. These positions relieve pressure on the ulcer.

In tubercular meningitis, the child lies on the side, with legs strongly drawn up against the thighs.

Facial Expressions

Disease as expressed in the face and posture.

Facies cardiac (heart): An anxious expression seen in the early stages of chronic valvular disease.

A purple or bluish appearance of the face, especially about the eyes, temples, and ears, with veins showing on the nose and sometimes on the cheeks, intensified by lying down: Caused by high blood pressure and an approaching dangerously plethoric state of the body.

Hepatic face: An earthy appearance; yellow tinge, jaundice.

Hippocratic face: Indicating rapid approach of death--pinched nose; hollow temples; eyes sunken; ears leaden and cold; lips relaxed; skin livid, and if the skin is pinched it returns slowly to the plane from which it was pinched or drawn.

Ovarian face: Features emaciated and sunken; anxious expression; forehead furrowed; eyes hollowed; nostrils open and sharply drawn; lips full and compressed; angles of mouth drawn and wrinkled, puckered but protruding"fish mouth."

The stupid face is that of typhoid.

Gastric face in children: A white line around the mouth, extending up by the side of the nose, shows irritation from improper feeding. Add to this sign pungent breath and vomiting, and the child has gastritis.

Gastric face in adults: Chronic irritation of the stomach in adults is indicated by a dragging-down of the comers of the mouth. Add to this drooling or driveling of saliva, and the indication is of starch poisoning; and if there is a broad, pallid tongue, the evidence is strong for overeating on starch.

Hysteria is marked by staring and an ecstatic expression.

Epilepsy is marked by a stupid face after an attack.

Protruding eyes and expressionless face in Graves' disease.

They lypermaniac has sadness written in his face. In general paralysis the countenance is composed and satisfied. The enebriate has trembling bps and a wandering expression.

The child with enlarged tonsils and adenoid growths has a stupid expression; the mouth is open, the lips hanging; the nose is expressionless.

The red nose, enlarged veins, bluish lips, cyanosed cheeks, and puffiness of face of the drinking man are called the mitral face. Where the aorta is diseased there is intense pallor. In Bright's disease the face is swollen and white.

The signs of croup are well known, but the type of disease is not so easily told. There are coughing and suffocating when a foreign body is in the air-passage.

Expiratory disturbance is marked by flushed face, puffed and bluish; the eyes are suffused, and the veins stand out.

In marasmus the features are drawn, the furrows deepened, the neck hollow; emaciation is marked, and, when profound, the whole appearance is that of the monkey.

The consumptive appearance is that of emaciation; protruding, flushed cheeks; pinched nose, with flaring nostrils; short, quick, jerky breathing; halting speech, and more or less suppressed voice.

When the face looks smaller--shrunken--and the nose is thin, long, and drawn, the bones prominent, the skin pale and covered with cold sweat, and, when drawn or pinched, the fold remains for some time, this is the facies of peritonitis, intestinal obstruction, renal and hepatic colic.

Fainting: The heart stops; the patient turns pale and falls motionless, but there is no distortion of the face; breathing is suspended.

Apoplexy: The patient is motionless and lies on the back; all animation is suspended; only breathing and pulse continue; the breathing is noisy, and gradually grows more stertorous. If the patient does not react and improve, the breathing and heart action gradually decline, the skin becomes drawn, the nose thinner and longer, the eyes dull, partially closed, glassy. The breathing stops, starts and continues, until it finally ends with a slight bodily convulsive movement.

Physical appearance must be noted--all deviations from the normal mean something.

Deformities, such as rickets, shorten the stature and cause the head to appear too large; the spine is incurved, the pelvis is deformed, the limbs are curved, the ribs project forward.

When the muscles become atrophied they cause general deformity.

Alterations of the heart or lungs cause deformities of the chest.

The bowels are often too large and distended from gas, fat, or ascites; in fevers, from tympanitis and inflammations.

Enlargement of the liver or spleen causes a large abdomen in the upper region; in the lower abdomen, enlargement may come from tumors, distended bladder, or a gravid uterus.

A large swelling at the base of the great toe, with the toe pointing outward, indicates a bunion. This deformity usually means that there is a slight rheumatism. Deformity of the third joint of the fingers--nodes of Heberden--means arthritis deformans. The nodes of Bouchard on the second joints of the fingers indicate dilation of the stomach--a disturbed nutrition from overeating of the carbohydrate foods. Joint distortions indicate gout, rheumatism, or injury; not infrequently they mean all of these. Frequently injury is complicated by rheumatism.

Hippocratic fingers (clubbing of finger-tips, with incurving nails) indicate heart or lung disease--scrofulous diathesis.

face,mrcp

Synovial Fluid Analysis The most important reason for performing joint fluid analysis is to rule out septic arthritis. Synovial fluid analysis can demonstrate local inflammatory response, infection and the presence of crystals. Synovial fluid effusions are classified into five general etiologic categories: noninflammatory responses, inflammation, sepsis, crystal induced and hemorrhage. The most common diseases associated with each category are summarized in the following table. Effusion Diseases Noninflammatory osteoarthritis, trauma, osteochondritis, pigmented villonodular synovitis, sickle cell disease, neuropathic Inflammation rheumatoid arthritis, SLE, Reiters syndrome, ankylosing spondylitis, ulcerative colitis, psoriasis Infection bacteria, fungi, mycobacteria Crystal gout, pseudogout Hemorrhage trauma, hemophilia, hemangioma, pigmented villonodular synovitis, anticoagulant therapy, tumors The following tests can be performed on synovial fluid. Visual examination Cell Count Gram stain & culture Polarizing microscopic crystal exam Normal synovial fluid is a clear, yellowish fluid and transparent enough to read newsprint through. The following table summarizes the typical laboratory findings for each category of joint disease. Test Normal Non-inflam Inflam Sepsis Crystal Hemo Clarity Clear Slightly turbid Turbid Turbid Turbid Bloody Color Yellow Yellow Yellow Gray -green Yellow-milky Red-Brown Viscosity High Reduced Low Low Low Reduced Mucin clot Firm Firm to friable Friable Friable Friable Friable Clotted no occasional occasional often occasional yes WBC/uL 0 - 200 0 - 2000 2000 - 100,000 50,000 - 200,000 500 - 200,000 50 - 10,000 %Polys <25 <30 >50 >90 <90 <50 Glucose difference 0 - 10 0 -10 0-40 20-100 0-80 0-20 Crystals Absent Absent Absent Absent Present Absent Culture Sterile Sterile Sterile Positive Sterile Sterile Synovial fluid protein concentration is usually 25% of serum (1-3 g/dL). Synovial fluid glucose is normally within 10 mg/dL of plasma glucose. Neither synovial fluid glucose nor protein provides much useful diagnostic information. White cell counts (WBC) are normally less than 200/uL with fewer than 25% neutrophils. A WBC count of 2,000/uL and a neutrophil count of 75% serve as useful cutoff points to distinguish inflammatory from noninflammatory disease. However, there is much overlap in synovial fluid WBCs between the inflammatory, crystal-induced, and sepsis categories. WBC is greater than 50,000/uL in 70% of patients with septic arthritis, 15% with gout, 10% with pseudogout, and 4% with rheumatoid arthritis. Acute septic arthritis is usually caused by bacterial infection of the joint. Tuberculosis and fungi are less commonly involved. Infection can occur by hematogenous spread, direct innoculation during surgery or trauma or from osteomyelitis. Septic arthritis is usually characterized by an acute onset of monoarticular joint pain. Staph aureus is responsible for the majority of cases of bacterial infection. Neisseria gonorrhea is common in adolescents and young adults. E. coli is most commonly seen in neonates. Other gram positive rods are associated with immunocompromised patients. Specimen requirement for cell count and differential is 1 mL of synovial fluid transferred to a lavender top (EDTA) tube. Bacterial cultures require 2-3 mL of fluid in a yellow top tube.

mrcp,rheumatology

30 years old male got acute left knee arthritis with swelling.it gradually resolving for 2 months and now he got acute swelling and tenderness in right knee.no history of eye redness or dysuria.no history of gonococcal urethritis.no back pain.