Amylase LEC

What is the EC of Amylase?

E.C. 3.2.1.1

What is the other name of Amylase?

1,4-D-Glucan Glucanohydrolase

Breakdown of starch and glycogen to oligosaccharides/maltose

Amylase

Activators of Amylase

calcium and chloride

Released by the pancreas in response to chyme in the duodenum

Pancreatic juice

Isoenzyme of Amylase?

P-type isoamylase

S-type isoamylase

Is located in the Acinar cells of the pancreas

More powerful than S-type

Also known as ptyalin

P-type isoamylase

Located in:

Salivary gland

Lungs

Fallopian tubes

S-type isoamylase

Chewing: ?

food + salivary amylase

In chewing, not more than 5% is hydrolyzed. (Y/N)

Yes.

P-amylase is blocked by the stomach acidity. (Y/N)

No. (S-amylase is blocked by the stomach acidity)

2 Intestinal Hormones of Amylase?

Secretin

Cholecystokinin

Secretin is produced by the _____ in duodenum

S cells

Secretin is released in the presence of ______ (with HCl) in the small intestine/change in pH

Chyme

Secretin initiates increased ______________ secretion by the pancreas to neutralize acidity

Bicarbonate ion

Cholecystokinin is produced by the ________ of the duodenum

Ito cells

Cholecystokinin is released if _______ is present in the SI

Chyme

Cholecystokinin initiates bile and ________________ release

Pancreatic enzyme

In the SI, pancreatic amylase will begin gigestion of all carbohydrates within ?

15-30 minutes

P-amylase will convert starch to ?

oligosaccharides and maltose

Brush border enzymes convert amylase products into water-soluble monosaccharides. (Y/N)

Yes.

What enzyme will convert Maltose into Glucose?

Maltase

What are the diagnostic significance of Amylase?

Acute Pancreatitis

Salivary gland lesions (parotitis, mumps)

Intra-abdominal diseases

Acute Pancreatitis:

Rise: ?

Peak: ?

Normalize: ?

Rise: 5-8 hours after the onset of an attack

Peak: 24 hours

Normalize: 3-5 days

Inflammation of the pancreas

ACUTE PANCREATITIS

2 major causes of Acute Pancreatitis

– Gallstones (30-60%)

– Acute and chronic alcoholism (15-30%)

3 Diagnosis of Acute Pancreatitis

– Epigastric pain that may radiate to the back

– 3X ULN pancreatic enzymes

– Confirmatory findings in abdominal imaging (ultrasound, CT scan): objective evidence

Chronic alcohol ingestion results in the?

– Secretion of protein-rich pancreatic fluid that leads to the deposition of thickened protein plugs and obstruction of small pancreatic ducts

– Transient increase in the pancreatic exocrine secretion and contraction of the sphincter of Oddi

– Direct toxicity in the acinar cells

Intrapancreatic digestive enzyme activation and acinar cell injury (trypsin activation by cathepsin B)

Initial phase of AP

Activation, chemoattraction, and sequestration of WBCs and macrophages causing increased inflammatory reaction

Second phase of AP

Activated proteolytic enzymes not only digest the pancreas but also activate other enzymes

Third phase of AP

Digestion of membranes leading to hemorrhage and necrosis and eventually multi-organ failure

Third phase of AP

First sign of Acute Pancreatitis

Abdominal pain

Physical examination of Acute Pancreatitis

– Low-grade fever

– Tachycardia

– Hypotension

– Cullen’s sign

– Turner’s sign

Persistent increase in serum amylase is seen without clinical symptoms can be because of?

Macroamylasemia

AMS molecule combines with immunoglobulin, especially IgA

Macroamylasemia