#alk phos

[mcatmemoranda]

Stuff discussed on rounds today:

Hyperglycemic Hyperosmolar Non-Ketotic Coma can cause dehydration and hypernatremia-> AMS.

When blood cultures are drawn, 2 are done to account for the fact that you may get a contaminant in the sample. For example, one of my pt's blood cultures grew coagulase negative staph, which is likely a contaminant.

In hypernatremia, correct Na+ by 0.5 mEq/hour.

Thiamine can be given IV at 500 mg for Wernicke's encephalopathy. Fromt UTD:

Patients with suspected WE require immediate parenteral administration of thiamine. A recommended regimen is 500 mg of thiamine IV infused over 30 minutes three times daily for two consecutive days and 250 mg IV or IM once daily for an additional five days, in combination with other B vitamins

Stress dose of steroids should be given for a pt on chronic prednisone going for surgery. The attending today said to give hydrocortisone 50 mg q8 for a pt we have who is on prednisone 5 mg qd.

Steroids, EtOH, and HIV are the most common causes of avascular necrosis.

One of our pts has a prostate abscess. The prostate is hard to access and it has poor vascularity. It has fat, so a fat-soluble antibiotic is necessary for prostate abscess. The pt we have is on Zosyn.

Lithium toxicity can cause irreversible kidney damage. Can cause nephrogenic diabetes insipidus. You can dialyze it off acutely to prevent this.

Avoid morphine in pts with renal disease. Dilaudid and fentanyl are good for pain control in pts with renal disease.

Albumin less than 1.5, GI bleed, 2nd episode of SBP are indications for prophylactic antibiotics. Enterobacter has inducible resistance to ceftriaxone, so you don't give ceftriaxone to treat enterobacter. Use cefepime or higher.

Biliary obstruction first presents with elevated alk phos. Alk phos is in the cells of the biliary tree

[badaxefamily]

More medical nonsense incoming, feel free to skip though there's nothing gross/graphic in here. I do mention the existence of bones though.

I put as many of my maintenance doctor appointments in the winter time as I can, due to garden season being a busy time I don't want to interrupt for my chauffeur (read: my mom) and I also don't do well traveling in the heat. So winter is also when I Learn Things. Recently I had my six month followup with New Rheumy, whom I like a great deal more than Old Rheumy (the one that didn't think a score of 20% on a QoL survey was a bad thing). We discussed some things, adjusted some meds, all pretty standard. Then at the end she said "Your alkaline phosphatase was low on your last test. I only have this one test to look at but that's not normal..." and I interrupted with "Oh yeah, it's been like that for years. It's always low." And she gave me this side eye like

The thing with alkaline phosphatase (ALP on a blood test, or alk phos depending on who did it) is that for years doctors didn't pay attention to low numbers, only high ones. Doctors know the body uses it to build bones and process vitamin B6, but otherwise they don't really know much about it. High levels indicate liver problems, but unless you're a baby with soft bones low numbers don't raise alarms. My doctor said though that in just the last ten years or so, scientists have realized that even moderately low ALP causes weakness, headaches, brain fog, and extreme fatigue. You know, all the things I've struggled with for years. The condition is called hypophosphatasia, and the more extreme forms cause bones to not mineralize properly, but less severe ones may only cause weak teeth, or no bone involvement at all. To my knowledge I've never broken a bone (though people with HPP sometimes get microfractures that they're not aware of) but all the other symptoms check out.

I can get the genetic testing needed for diagnosis, but if it does turn out to be HPP I'm not sure about getting the treatment. In the US, the one medication available is only approved for use in people with the childhood forms of the disease (insert rant about how the US views illness in adulthood as a personal moral failing). I have to hope that the fact that I had these problems as a kid too will be enough. I'm currently waiting on the endocrinologist referral, my rheumy said he specializes in HPP so he should be able to put the pieces together and determine if that's what this is.

As strange as it is to say, I hope it is HPP. Treatment involves replacing the missing enzyme with multiple subcu injections every week, but nothing else works for me. Every condition we've checked for, every treatment I've tried, nothing works for long. It's like a bandaid. Eventually the bandaid falls off and the problem is still there.

[soapdishglitter]

omg went to the doctor today and my blood tests came back SO fucked up.... insanely low iron/super high white blood cell count/low alk-phos.... good to know i don't feel like my body is collapsing for no reason!

[moleculardepot]

Alkaline Phosphatase from Human Placenta

Alkaline Phosphatase from Human Placenta

Alkaline Phosphatase from Human Placenta Catalog number: B2012278 Lot number: Batch Dependent Expiration Date: Batch dependent Amount: 100 U Molecular Weight or Concentration: 10 U/mg Supplied as: Lyophilized Applications: molecular tool for various biochemical applications Storage: -20C Keywords: ALP, PLAP, Alk Phos Grade: Biotechnology grade. All products are highly pure. All solutions are made…

[mcatmemoranda]

The picture is algorithm 1. Evaluation of elevated serum alkaline phosphatase. Key: AMA: antimitochondrial antibodies; ERCP: endoscopic retrograde cholangiopancreatography; MRCP: magnetic resonance cholangiopancreatography; ULN: upper limit of normal.

My pt's AST is 66 and ALT is 64, so AST/ALT is 1.03 I'm reading the uptodate article about workup of transaminitis to figure out what to do first. He doesn't drink. I already thought to start with the hx and physical. The pt is a body builder, super healthy, except that the pt takes testosterone, steroids, and other drugs. Testosterone increases risk of thrombosis, so he should be on ASA. I remember answering a question yesterday about that that mentioned that transgender men (i.e., born female and transition to men) have increased risk of thrombosis because of the testosterone they take. I don't remember much about anabolic steroids and how they affect pts. I want to review it.

He's a competitive body builder. Takes testosterone 750 weekly, steroid Trenbolone acetate 300 weekly, HGH 6 IU qd, insulin glargine 60 qd, aromatase inhibitor 25 mg q.o.d.

PMH: 2017 echo for murmur showed trace regurg; high-arch palate

Meds: multivit, joint supplement, psyllium, essential FA, vit K w/ D3, melatonin, ramipril 10 mg, Zoloft 50 mg, others as above.

Meds on chart: insulin, examestane, Zoloft, lisinopril

Social: No EtOH or tobacco. Went to detox for opioids in May. Eats strict diet and exercises regularly.

Liver biochemical and function tests – Blood tests commonly obtained to evaluate the health of the liver include liver enzyme levels (alanine aminotransferase [ALT], aspartate aminotransferase [AST], alkaline phosphatase, gamma-glutamyl transpeptidase), tests of hepatic synthetic function (albumin, prothrombin time/international normalized ratio [INR]), and the serum bilirubin level.

Initial evaluation of abnormal liver biochemical and function tests – The initial evaluation includes obtaining a history to identify potential risk factors for liver disease and performing a physical examination to look for clues to the etiology and for signs of chronic liver disease. Subsequent testing is determined based on the information gathered from the history and physical examination as well as the pattern of liver test abnormalities (table 4 and algorithm 1). (See 'Initial evaluation' above.) Table 4: Initial evaluation:

Review possible links to medications, herbal therapies, or recreational drugs. Screen for alcohol abuse (history, screening instruments, AST/ALT ratio greater than 2:1) Obtain serology for hepatitis B and C (HBsAg, anti-HBs, anti-HBc, anti-HCV) Screen for hemochromatosis (Fe/TIBC greater than 45%)

[I also recall a question I answered yesterday that said hemochromatosis is associated with hepatocellular carcinoma.] Evaluate for fatty liver (AST/ALT usually less than 1, obtain RUQ ultrasonography)

Step 2: Second-line evaluation (if initial evaluation is unrevealing)

Consider autoimmune hepatitis, particularly in women and in those with a history of other autoimmune disorders (check serum protein electrophoresis; obtain ANA and ASMA [Anti-Smooth Muscle Antibody] if positive) Obtain thyroid function tests (TSH if hypothyroidism is suspected; otherwise, obtain serum TSH, free T4, and T3 concentrations) Consider celiac disease (especially in patients with a history of diarrhea or unexplained iron deficiency: serum IgA anti-tissue transglutaminase antibodies)

Step 3: Evaluation for uncommon causes (if second-line evaluation is unrevealing) Consider Wilson disease, especially in those less than 40 years of age (check serum ceruloplasmin, evaluate for Kayser-Fleischer rings) Consider alpha-1 antitrypsin deficiency, especially in patients with a history of emphysema out of proportion to their age or smoking history (obtain alpha-1 antitrypsin level) Consider adrenal insufficiency (8 am serum cortisol and plasma ACTH, high-dose ACTH stimulation test) Exclude muscle disorders (obtain creatine kinase or aldolase)

Step 4: Obtain a liver biopsy or observe (if no source identified after steps 1 to 3)

Observe if ALT and AST are less than twofold elevated Otherwise, consider a liver biopsy

●Patterns of liver test abnormalities – Liver biochemical test abnormalities can often be grouped into one of several patterns: hepatocellular, cholestatic, or isolated hyperbilirubinemia. Patients with a hepatocellular process generally have a disproportionate elevation in the serum aminotransferases compared with the alkaline phosphatase, while those with a cholestatic process have the opposite findings. The serum bilirubin can be prominently elevated in both hepatocellular and cholestatic conditions and therefore is not necessarily helpful in differentiating between the two. Abnormal tests of synthetic function may be seen with both hepatocellular injury and cholestasis.

●Patients with elevated serum aminotransferases – In the setting of hepatocyte damage, ALT and AST are released from hepatocytes, leading to increased serum levels. The differential diagnosis for elevated serum aminotransferases is broad and includes viral hepatitis, hepatotoxicity from drugs or toxins, alcoholic liver disease, hepatic ischemia, and malignant infiltration. The evaluation should take into account the patient's risk factors for liver disease as well as findings from the physical examination that may point to a particular diagnosis. The evaluation often involves testing for viral hepatitis and autoimmune disease (table 4). Occasionally, a liver biopsy may be required.

●Patients with cholestasis – Cholestasis may develop in the setting of extrahepatic or intrahepatic biliary obstruction (table 5). In patients with cholestasis, the alkaline phosphatase is typically elevated to at least four times the upper limit of normal. Lesser degrees of elevation are nonspecific and may be seen in many other types of liver disease, such as viral hepatitis, infiltrative diseases of the liver, and congestive hepatopathy. Patients with a predominantly cholestatic pattern typically undergo right upper quadrant ultrasonography to further characterize the cholestasis as intrahepatic or extrahepatic.

The presence of biliary dilatation on ultrasonography suggests extrahepatic cholestasis which may be due to gallstones, strictures, or malignancy. The absence of biliary dilatation suggests intrahepatic cholestasis. There are numerous possible causes of intrahepatic cholestasis (table 5), including drug toxicity, primary biliary cholangitis, primary sclerosing cholangitis, viral hepatitis, cholestasis of pregnancy, benign postoperative cholestasis, infiltrative diseases, and total parenteral nutrition. Subsequent testing to identify the underlying cause may include checking antimitochondrial antibodies, magnetic resonance cholangiopancreatography, computed tomography, endoscopic ultrasonography, and/or endoscopic retrograde cholangiopancreatography (algorithm 1).

●Patients with isolated hyperbilirubinemia – The evaluation of isolated hyperbilirubinemia begins with determining whether the hyperbilirubinemia is predominantly conjugated (direct hyperbilirubinemia) or unconjugated (indirect hyperbilirubinemia). An increase in unconjugated bilirubin in serum results from overproduction, impairment of uptake, or impaired conjugation of bilirubin. The evaluation of unconjugated hyperbilirubinemia typically involves evaluation for hemolytic anemia as well as obtaining a history to determine if the patient has Gilbert syndrome. In a patient with a history consistent with Gilbert syndrome (eg, the development of jaundice during times of stress or fasting), normal serum aminotransferase and alkaline phosphatase levels, and mild unconjugated hyperbilirubinemia (less than 4 mg/dL), additional testing is not required.

An isolated elevation in conjugated bilirubin is found in two rare inherited conditions: Dubin-Johnson syndrome and Rotor syndrome, as well as other genetic bile transport disorders in children. Dubin-Johnson syndrome and Rotor syndrome should be suspected in patients with mild hyperbilirubinemia (with a direct-reacting fraction of approximately 50 percent) in the absence of other abnormalities of standard liver biochemical tests. Normal levels of serum alkaline phosphatase and GGT help to distinguish these conditions from disorders associated with biliary obstruction. Differentiating between these syndromes is possible but clinically unnecessary due to their benign nature.

[moleculardepot]

Avidin Conjugated to Alkaline Phosphotase

Avidin Conjugated to Alkaline Phosphotase

Avidin Conjugated to Alkaline Phosphotase Catalog number: B2011819 Lot number: Batch Dependent Expiration Date: Batch dependent Amount: 1 mg Molecular Weight or Concentration: N/A Supplied as: Solution Applications: molecular tool for various biochemical applications Storage: -20 °C Keywords: Avidin protein (Alk Phos), Purified Avidin protein (Alk Phos) from hen egg white Grade: Biotechnology…

[mcatmemoranda]

Marked and early elevations of alkaline phosphatase is the earliest marker of metastatic liver cancers. Bilirubin and gamma glutamyl transferase (GGT) are the other two early indicators. Alkaline phosphatase provides for the most reliable liver function testing for demonstrating primary or metastatic tumors to the liver. Please note that increased levels of transaminases (AST or ALT) are the most sensitive markers for the liver cancers, but their levels do not rise as early or as abruptly as alkaline phosphatase.

[mcatmemoranda]

Alkaline phosphatase levels are high with gallbladder biliary obstruction and usually low or moderately elevated with hepatitis. The moderate rise of alkaline phosphatase in hepatitis is attributable to the extension of inflammation from the biliary ducts to the liver.

In alcoholic hepatitis (and also hepatocellular carcinoma) the ratio of AST to ALT is greater than 2:1 and both are elevated. Note that in cirrhosis the ratio of AST to ALT is more than 1 but less than 2. In viral hepatitis the ratio of AST to ALT is less than 1 but both are greatly increased. Also note that if AST and ALT are more than 1000, it indicates acetaminophen toxicity, OD, shock, and liver failure.

[mcatmemoranda]

The alkaline phosphatase is the most sensitive laboratory test for choledocholithiasis. It is usually the first of the liver function tests to be abnormal in choledocholithiasis and the degree of increase often correlates with the severity of obstruction. The WBC may be elevated with multiple hepatobiliary tract diseases. The lipase is usually normal unless pancreatitis is present which may indicate a stone has passed. In patients who are sick from biliary tract disease, the hematocrit may be elevated as a result of hemoconcentration. An increased AST and ALT usually indicates hepatic inflammation and is not specific to choledocholithiasis.

The differential diagnosis for abdominal pain after cholecystectomy includes bleeding, bile leak, missed enterotomy, and common bile duct injury. A CT scan, like an ultrasound, on post-op day 4 will likely show fluid but won’t help determine the source of the fluid. An ERCP is an invasive procedure that can be used to treat bile leaks but is not the best diagnostic test. MRCP may diagnose a ductal injury or a fluid collection but not the source. The HIDA scan will help to rule out a bile leak, clip across the duct, or a duct injury. Further studies can be ordered based on the results of the HIDA scan.

[mcatmemoranda]

Alkaline phosphatase (Alk. Phos.) comprises a group of related enzymes found in biliary tract epithelium, bone, and placenta. Elevated Alk. Phos. is normal in growing children (because their epiphyseal plates remain open) and pregnant women. If Alk. Phos. is elevated and there is doubt as to its source, concurrent elevations in 5'-nucleotidase (5-NT) and gamma-glutamyl transferase (GGT) establish a hepatic or biliary source since these enzymes are specific for hepatic origin. While serum Alk. Phos. may be elevated in any active liver disease it is most sensitive to biliary tract obstruction and serum levels generally correlate with the severity of obstruction. As discussed below, those processes confined to the gallbladder do not cause biliary obstruction and are thus associated with infrequent and mild Alk. Phos. elevations while those processes caused by stones in the common bile duct are usually associated with Alk. Phos. elevations, which can be severe. In uncomplicated cholelithiasis, any degree of Alk. Phos. elevation is rare, even in patients with severe symptoms. In acute cholecystitis mild elevations of bilirubin and Alk. Phos. with normal aminotransferases can often be documented. Significant Alk. Phos. elevation is not common and suggests choledocholithiasis with possible obstruction of the extrahepatic ducts. Most patients with choledocholithiasis have a significant degree of Alk. Phos. elevation. The amount of elevation depends on the degree of obstruction present, but Alk. Phos. is often the first of the liver function tests to become abnormal. Elevations of greater than 2.5x normal have been shown to be predictive of choledocholithiasis in patients with known cholelithiasis.(1) Approximately 78% of patients with cholangitis present with Alk. Phos. elevations due to obstruction of the common bile duct. (2) In gallstone pancreatitis Alk. Phos. elevation is common since the stone causing pancreatitis may also cause some degree of obstruction. The degree of Alk. Phos. elevation is related to the degree of common bile duct obstruction and not necessarily to the severity of pancreatitis. Alk. Phos. levels can be useful in distinguishing the aforementioned disease entities and, in conjunction with other liver function tests can also help distinguish them from other hepatocellular diseases or nonhepatobiliary processes.

[mcatmemoranda]

Alkaline phosphatase is found in bone, liver, placenta, and gut. It is elevated when there’s obstruction to bile flow anywhere in the biliary tree. If GGT is high, then the high ALK-P is coming from the liver.

[mcatmemoranda]

Osteoblasts use alkaline phosphatase to create an alkaline environment, which is necessary to mineralize osteoid. In osteomalacia, the osteoblasts are making osteoid, but the lack of calcium and phosphate (due to vitamin D deficiency) prevents proper bone mineralization. At any rate, the increased alk phos is because the bones are making osteoid.