Mrs. Ashley Medical Assistant Science. PANCREAS ANATOMY stomach esophagus ductus choledocus duodenum...

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Mrs. Ashley Medical Assistant Science

Transcript of Mrs. Ashley Medical Assistant Science. PANCREAS ANATOMY stomach esophagus ductus choledocus duodenum...

Page 1: Mrs. Ashley Medical Assistant Science. PANCREAS ANATOMY stomach esophagus ductus choledocus duodenum duct of Santorini duct of Wirsung pancreas.

Mrs. AshleyMedical Assistant Science

Page 2: Mrs. Ashley Medical Assistant Science. PANCREAS ANATOMY stomach esophagus ductus choledocus duodenum duct of Santorini duct of Wirsung pancreas.
Page 3: Mrs. Ashley Medical Assistant Science. PANCREAS ANATOMY stomach esophagus ductus choledocus duodenum duct of Santorini duct of Wirsung pancreas.

PANCREAS ANATOMY

stomach

esophagus

ductus choledocus

duodenum

duct of Santorini

duct of Wirsung

pancreas

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Exocrine and endocrine cells 90% of pancreas related to exocrine

(digestive function) 10% endocrine (homeostasis for glucose

levels in the body)

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◦ Both an exocrine and endocrine organ◦ Cells with exocrine function release

an alkaline fluid containing sodium bicarbonate and enzymes → pancreatic duct → small intestine

◦ Pancreatic “juice” aids in breakdown and digestion of food in the small intestine

◦ Pancreatic exocrine cells = acinar cells

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Acinar cells - exocrine cells of the pancreas that produce and transport digestive enzymes

Amylase, lipase, phospholipase, proteases (trypsinogen, chymotrypsinogen)

Page 8: Mrs. Ashley Medical Assistant Science. PANCREAS ANATOMY stomach esophagus ductus choledocus duodenum duct of Santorini duct of Wirsung pancreas.

PANCREATIC SECRETIONS

1. PROTEASES (70%)

Endopeptidases (trypsin, chymotrypsin, elastases)

Exopeptidases (carboxypeptidases)

trypsinogen trypsin activates all other precursors

enterokinase(duct walls)

2. NUCLEASES (DNAase, RNAase)

3. PANCREATIC AMYLASE (hydrolyse starch and gl;ycogen)

4. PANCREATIC LIPASE (triglycerides fatty acids and glycerol)

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PANCREAS (PANORAMIC)

pancreatic acini

islet ofLangerhans

islet ofLangerhans

BV

pancreatic lobe

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Islets of Langerhans - endocrine cells of the pancreas that produce and secrete hormones into the bloodstream

Glucagon - Alpha cells (A cells) - raises the level of glucose (sugar) in the blood by causing liver to break down stored glycogen

Insulin - Beta cells (B cells) - stimulates cells to use glucose and reduce glucose levels in blood

Antagonistic Hormones

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Endocrine Function :Cells of the Islet of Langerhans synthesize and release hormones into the circulation.

Hormones travel through the bloodstream to target tissues (especially liver and muscle)

At the target cells, hormones bind specific receptors and cause cell changes that control metabolism

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Chemically – high levels of glucose and amino acids in the blood

Hormonally – beta cells are sensitive to several hormones that may inhibit or cause insulin secretion

Neurally – stimulation of the parasympathetic nervous system causes insulin to be secreted.

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Transported through the blood to target tissues where it binds to specific receptors

The binding of insulin to target cells:◦ Acts as a biochemical signal to the inside of the cell Overall, cell metabolism is stimulated There is increased glucose uptake into the cell Regulation of glucose breakdown within the

cell Regulation of protein and lipid breakdown

within the cell

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Blood glucose is decreased because insulin causes glucose to leave the bloodstream and enter the metabolizing cells.

With the exception of brain, liver and erythrocytes, tissues require membrane glucose carriers.

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Inflammation of the pancreas

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Pancreas suddenly becomes inflamed Causes: Gallstones Ethanol Trauma

Steroids Mumps Autoimmune Scorpion venom Hyperlipidaemia, hypothermia ↑Ca2+

Drugs

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Symptoms epigastric and central abdominal pain vomiting and nausea swollen and tender abdomen fever dehydration and low blood pressure

Diagnosis medical history and physical exam blood test: ↑ amylase, lipase abdominal ultrasound, Endoscopic

Ultrasound, CT scan

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Treatment nothing to eat or drink intravenous fluids analgesia ERCP and gallstone removal

Complications shock, Acute respiratory distress

syndrome, renal failure, Disseminated intravascular coagulation, sepsis, ↓Ca2+

pancreatic necrosis, pseudocyst, abscesses, bleeding, thrombosis

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inflammation of the pancreas - gets worse over time and leads to permanent damage

Causes: many years of alcohol use hereditary disorders of the

pancreas cystic fibrosis haemochromatosis autoimmune conditions

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Symptoms nausea and vomiting weight loss diarrhea steatorrhea

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Treatment drugs - analgesia, lipase, fat-soluble

vitamins diet surgery – pancreatectomy pancreaticojejunostomy

Complications pseudocyst, diabetes, biliary obstruction,

local arterial aneurysm, splenic vein thrombosis

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The single most common endocrine disorder – group of glucose intolerance disorders

Incidence is estimated at 8.3% of the North American population

35% are pre-diabetic Many of these cases are undiagnosed

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Historically ‑ distinguished by weight loss, excessive urination, thirst, hunger

Excessive urination = polyuriaExcessive thirst = polydipsiaExcessive hunger = polyphagia

Modern characterization is by hyperglycemia and other metabolic disorders

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increased level of glucose in the blood (normal blood glucose level 3.5-6.0 mmol/l)

90 mg/100ml

Type 1 ( insulin-dependent DM, IDDM) destruction of insulin-secreting pancreatic β

cells (autoimmune response) juvenile diabetes-tends to begin in early

childhood patient always needs insulin

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Type 2 (non-insulin dependent DM, NIDDM) insulin resistance Β cell dysfunction, ↓insulin secretion

Causes of insulin resistance: metabolic syndrome (central obesity,

hyperglycaemia, hypertension, ↓HDL cholesterol, ↑triglycerides)

renal failure pregnancy cystic fibrosis polycystic ovarian syndrome

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Glucose in urine- Because when insulin is not present, glucose is not taken up out of the blood at the target cells.

So blood glucose is very highly increased → increased glucose filtered and excreted in the urine (exceeds transport maximum)

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Mechanisms of insulin resistance:

post-receptor defects in insulin action

gene mutation circulating

autoantibodies

Page 30: Mrs. Ashley Medical Assistant Science. PANCREAS ANATOMY stomach esophagus ductus choledocus duodenum duct of Santorini duct of Wirsung pancreas.
Page 31: Mrs. Ashley Medical Assistant Science. PANCREAS ANATOMY stomach esophagus ductus choledocus duodenum duct of Santorini duct of Wirsung pancreas.

Diagnosis

blood glucose level urine sample HbA1c test

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Treatment:

diet oral

hypoglycaemics

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Control dietCarbohydrates should make up about

55-60% of patient’s total caloriesFats should make up <30% of patient’s

total caloriesProteins should make up about 15-20%

of patient’s total calories

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Monitor exerciseRemember: muscles are a target tissue of

insulin, and metabolize much glucose for energy

Sometimes exercise →irregular blood glucose levels So diabetic patients should be monitored when they are exercising

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insulin injections (long-acting, short-acting, rapid-acting)

insulin pen insulin pump therapy

Page 36: Mrs. Ashley Medical Assistant Science. PANCREAS ANATOMY stomach esophagus ductus choledocus duodenum duct of Santorini duct of Wirsung pancreas.

Complications

Page 37: Mrs. Ashley Medical Assistant Science. PANCREAS ANATOMY stomach esophagus ductus choledocus duodenum duct of Santorini duct of Wirsung pancreas.

diabetec ketoacidosis hypoglycaemia diabetic retinopathy

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atherosclerosis (heart disease and stroke) neuropathy (diabetic foot care)

Page 39: Mrs. Ashley Medical Assistant Science. PANCREAS ANATOMY stomach esophagus ductus choledocus duodenum duct of Santorini duct of Wirsung pancreas.

Age over 40 years Diabetes during a previous pregnancy Excess body weight Family history of diabetes Dyslipidaemia (large amount of lipids in

body) Hypertension Low activity level Metabolic syndrome Polycystic ovarian syndrome Acanthosis nigricans- darkening and

thickening of skin