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Digestive Musculoskeletal Nervous diseases

Gastroscopy The use of a gastroscope (fiber optic camera) to view the stomach and esophagus.
Colonoscopy The use of an endoscope to view the large intestine, sigmoid colon and rectal canal
Barium Swallow contrast X-ray to view the esophagus and stomach. Looking for reflux. Also called upper GI
Barium enema Contrast X-ray to view the large intestine. Also called lower GI.
Laporoscopy The use of an endoscope that is introduced through a small incision in the abdominal wall, to view the outside of the organs of the abdominal and pelvic cavities.
What scope is used to view the small intestine? none - M2A is a camera capsule that is swallowed and takes pictures. It is the only way to view the small intestine.
Ulcer lesion of the skin or mucusol lining.
Peptic Ulcer an ulcer caused by pepsin and aggravated by HCL
Duodenal Ulcer -peptic ulcers caused by stomach secretions(pepsin & HCL)- usually occures due to pancreatic problems - Pancreatitis, cyctic fibrosis and gall stones can cause.-Cause a blockage which blocks bicarbonates from pancreas which neutralize stomach acids.
Gastric ulcer Peptic ulcer of the stomach. Not caused by stomach secretions, but they will prevent the ulcer from healing. Gastric secretions can aggrevate and cause ulcer to get worse.
Esophageal Ulcer Peptic ulcer of the esophagus caused by stomach secretions. Conditions like GERD and Bolemia increase the risk.
Pepsin and HCL usually do not cause a gastric ulcer but will keep the ulcer from healing.Contribute to a gastric ulcer but do not cause.
Etiology of Gastric Ulcers -Over 95% are caused by chronic infections of the mucosa in the stomach-Helicobacter Pylori is the bacteria that causes stomach ulcers - Infection leads to Inflammation and necrosis - if necrosis goes through mucosa you have an ulcer.
What conditions make a person more at risk of stomach ulcers? Most of the rest(5%)are caused by medications such as aspirin and NSAID's taken for arthritis. Long term Cortizone treatment also weakens the immune system making you at higher risk.
What things keep a gastric ulcer from healing? pepsin, HCL, and spicy foods
S/S of gastric ulcer Burning pain in LUQ or epigastric region. Pain is not constant. Pain is more severe at mealtime.
Diagnosis of Gastric ulcers. Gastroscope, Upper GI or UBT (Urea Breath Test). UBT tests for infection.
Treatment for Gastric Ulcer -If still infected (Helicobacter Pylori) give antibiotics - Avoid foods that make it burn- H2 blockers and Proton Pump Inhibitors-Time, one to two months it will heal
What are H2 blockers and Proton Pump Inhibitors? Decrease production and secretions of stomach acids. Pepsin is only active with HCL (pepsinogen).
Name three H2 Blockers Tagamet, Pepsin and Zantac
Name three Proton Pump Inhibitors Prylosec, Nexium, and Protonix
Prognosis for gastric ulcers. Treatable - but people die every year because they ignor the ulcer.
Crohn's disease Inflammatory Bowel Disorder - Causes skip lessions and patches at various places - Affects all layers of the intestine. - occures most often in the small intestine
Colitis and Ileitis Inflammatory Bowel Disorders affecting only the inner lining of the intestine.
Etiology of Crohn's Disease Ideopathic
S/S of Crohn's Disease -Chronic disorders in small intestine- Severe diarrhea - Fluid loss - weight loss - abdominal pain and cramping - dehydration - usually starts in the Ileum - RLQ pain
Diagnosis of Crohn's Disease Biopsy obtained by a Laporoscopy. Diagnosed by ruling out other disorders, but not always confirmed.
Treatment for Crohn's Disease - antiinflamatory and anti-diarrhea medications during flar ups - Hospitalization during flar ups due to dehydration - Removal of section of small intestine in severe cases
Prognosis of Crohn's Disease Life changing disease sometimes life threatening. Can lead to obstruction and perforation.
Diverticulum Sac or pouch that developes off of a tubular structure like the intestine. Most common in the later part of the decending or in the sigmoid colon. Because of high pressure.
Diverticulosis Condition where you have diverticulum present in the intestine.
Diverticulitis Inflamation of pouch or sac (diverticulum)
Etiology of Diverticulosis very common in older people - Frequent constipation over many years - Lack of fiber, fluid, and activity.
S/S of Diverticulosis none
Diagnosis of Diverticulosis Colonoscopy
Treatment of Diverticulosis - increase fiber, fluids and activity - Avoid seeds and nuts - Keep from getting worse
Prognosis of Diverticulosis Good - Rarely causes a problem
Eitology of Diverticulitis Lack of fiber, fluids, and activity - Irritation or infection - seeds or nuts - E coli gets trapped causing infection.
S/S of Diverticulitis Pain, cramping, diarrhea - LLQ pain
Diagnosis of Diverticulitis Colonoscopy
Treatment of Diverticulitis Antibiotics - could lead to surgery
Prognosis of Diverticulitis Can be life threatening in elderly because it can cause perforation.
Steatorrhea The liver produces bile salts, which are needed for the digestion and absorption of lipids. A damaged liver produces less, so lipids remain in the stool, resulting in FATTY DIARRHEA.
Ascites The liver produces albumin, which maintains osmotic balance in blood. A damaged liver produces less, resulting in ABDOMINAL EDEMA
Clotting problems/bleeding The liver produces most of the clotting factors. A damaged liver produces less of them, resulting in slow clotting - Vitamin K is needed for the production of many clotting factors.Vitamin K is a lipid, and is poorly absorbed due to a lack of bile salts.
Malnutrition lack of bile salts leads to lack of lipid digestion and absorption
Weakened Immune System Malnutrition (due to lack of bile salts) weakens the immune system.
Gynecomastia The liver helps to process steroids such as estrogen. Liver damage leads to a build up of estrogen in men, which can lead to BREAST DEVELOPMENT IN MEN
Hypoglycemia The liver converts glucose to glycogen. The glycogen is what supplies your body with glucose between meals. A damaged liver makes and stores less glycogen and hypoglycemia will occure between meals. LOW BLOOD SUGAR
Elevated Liver Markers ALT,AST, Alkaline Phosphatase - These are enzymes found in liver cells. When inflammation of the liver occurs, the cells are damaged and levels of these enzymes will rise in the blood.
Elevated Bilirubin, Hepatic Jaundice The liver and spleen break down heme and convert it to bilirubin. The liver adds the bilirubin to the bile, so that it can be excreted as waste into the intestines. A damaged liver produces less bile, so bilirubin levels rise in the body.
S/S of all Liver Disease's Steatorrhea, Ascites, Clotting problems/bleeding, Malnutrition, Weakened immune system, Gynecomastia, Hypoglycemia, Elevated liver markers, Elevated bilirubin, Hepatic jaundice
Jaundice A rise in bilirubin levels to the point that is causes visible discoloration of the Sclera, Skin, or Hair
Prehepatic Jaundice HEMOLYTIC - RBC's are being destroyed faster than the liver can remove bilirubin from the body. Occures commonly in newborns and occures in people with sickle cell anemia.
Hepatic Jaundice HEPATOCELLULAR - The liver and spleen break down heme and convert it to bilirubin. The liver adds the bilirubin to the bile so that it can be excreted as waste into the intestine. A damaged liver produces less bile, so bilirubin levels rise in the body.
Hepatic Jaundice occures in which conditions? People with Thalassemia, hepatitis, alcohol abuse or any other condition that can cause liver damage.
Posthepatic Jaundice OBSTRUCTIVE - To eliminate bilirubin from the body, bile has to flow from the liver/gall bladder through ducts and into the duodenum. Anything that obstructs these ducts can cause.Occurs in people with gallstones, cystic fibrosis and pancreatitis
Cirrhosis of the Liver Necrosis and scarring of the liver due to chronic inflammation of about 10 - 15 years. The liver usually recovers well from damage. Number 1 cause is alcohol abuse.
Hepatitis A Hepatitis A virus - AKA Infectious Hepatitis
Hepatitis B Hepatitis B virus - AKA Serum Hepatitis
Hepatitis C Hepatitis C virus
Transmission for Hep A sewage-contaminated water. Affects over 90% of people in some countries. In US is mostly caused from flooding.
Transmission for Hep B Blood, semen or vaginal secretions
Transmission for Hep C Blood, semen or vaginal secretions
Incubation for Hep A 1 month
Incubation for Hep B 2 - 3 months
Incubation for Hep C 2 - 3 months
Diagnosis for Hep A Test for antibodies
Diagnosis for Hep B Test for virus (Australia Antigen)
Diagnosis for Hep C Test for antibodies
Prognosis for Hepatitis A mild S/S - rarely any treatment needed
Prognosis for Hepatitis B Unpredictable/most cases are mild initially and recover with no further problems/ few cases are mild initially but develop into chronic hepatitis, leading to liver failure or cancer - A few cases are severe initially and require hospitilazation(1/2 fatal)
Prognosis for Hepatitis C mild initially, but 85% develop chronic hepatitis. Is the most likely to cause chronic hepatitis.
treatment for Hepatitis A Palliative
Treatment for Hepatitis B HBIG are the antibodies for Hep B. Hematovax is to prevent Hep B.
The more severe the liver problems The more likely to have several S/S
What is Cholelithiasis gall stones
S/S of Cholelithiasis #1 = Abdonimal pain - RUQ, Not a constant pain. More at mealtimes especially fatty meals.
Eitology of cholelithiasis Idopathic, increased risk with high fat diet.
Treatment for cholelithiasis Surgical removal of gall bladder, so now you have to limit Fat intake. Lithotripsy
What is lithotripsy? The application of sound waves, chemicals, or lazar to crush the gall stones. not done very often anymore.
Osteoporosis Less minerals in your bones than you would expect so bones are weak and brittle. Porous bones.
Risk factors for Osteoporosis #1 = Menopause, menopausal women, #2 = Lack of calcium in diet, Inactivity, smoking, excess of alcohol or caffine
Diagnosis of Osteoporosis Bone Density Scan
Treatment of Osteoporosis Calcium Suppliments, Exercise( weight bearing), Fosamax, Boniva (help post menopausal women store calcium, can reverse osteoporosis)
Prognosis of Osteoporosis Most are managable. If not managed you are at an increased risk of breaking bones. Not fatal but leads to decreased life expectancy due to life style capacity.
Osteoarthritis Normal wearing of joints leads to arthritis. Osteoarthritis is a disease, arthritis is a symptom. Caused by normal wear and tear.
Risk factors for Osteoarthritis Living to be old, Being active, Repeatative use of a joint, weight ( increased weight = increased strain on joints)
Diagnosis for Osteoarthritis Based of S/S, Physical exam, Range of motion testing
Treatment of Osteoarthritis Based on how often symptoms occur.-Weekend warrior = anti-inflamatory, rest, massage Aleve: PRN - Bothered more days than not = same only done on a daily basis (take NSAID's with food)-Starts affecting lifestyle = possible surgery
What are the surgical options for Osteoarthritis? Arthroscope- to clean up joint, remove fragments, smooth surfaces Replacemant of joint - more serious cases.
Prognosis for Osteoarthritis Lifelong managable for most; life changing for some. Can decrease life expectancy because it affects lifestyle (Activity)
Why is Osteoarthritis more common today? We live longer and we weigh more than past generations.
Muscular Dystrophy Not a disease but a family of diseases. Cause a wasting away of muscle tissue. Most are fairly slow at how fast the muscles waste away. All of them are life-long.
What are the two types of Muscular Dystrophy? Neuropathies and Myopathies
Muscular Dystrophy Neuropathies Problems with in the nervous tissue that stimulate muscles. No stimulation leads to atrophy.
Most common neuropathic Muscular Dystrophy? Charcotte-Marie-Tooth Syndrome (CMT) very gradual form of disease. Starts in lower extremities and causes problems with the feet. Contracture leads to Hammer toes lead to surgery.
Muscular Dystrophy Myopathies Problems with muscle itself leads to contracture. Muscles contain more connective tissue than muscle tissue. Most common form of MD.
Most common myopathic Muscular Dystrophy? Duchenne's Dystrophy. A Genetic, sex linked disease most common in males. Linked to X chromosome.
Diagnosis for Muscular Dystrophy EMG to determine if it is a neuropathy or a myopathy. Stimulate nerve = no response = Myopathy. Stimulate nerve = response = Neuropathy.
Prognosis of Muscular Dystrophy Depends of how fast it developes.Duchenne's = Fatal because it developes fast (eventually affects respiratory muscles). Slower developing = not fatal (affects skeletal muscles)
Multiple Sclerosis Inflammation of the Myelin sheath in the CNS. Oligodendrocytes are the cells that are inflammed. This inflammataion blocks the Nodes of Ranvier so the neuron can no longer carry impulses.
Nodes of Raviner Space between myelan sheeths of an axon. Axon must be exposed to enable the impulse to travel because it allows the movement of ions in and out of the axon.
Etiology of Multiple Sclerosis Ideopathic. But increased risk for young females (20-30) and more common in northern climates.(suggests there is some sort of trigger that lives in northern climates. Suspect it is a virus)
S/S of Multiple Sclerosis Depends on neurons being affected. Possible = changes in vision(optic nerve) or weakness or paralysis (nerves going to muscles) or ability to think or behavior changes (nerves in brain)
Diagnosis of Multiple Sclerosis Angiogram to rule out vascular = normal results - X-ray, CAT scan looking for tumors = normal results -MRI, PET scan = can find areas of inflammation
Treatment for Multiple Sclerosis Treat inflammation with Steroid Anti- Inflammatory drugs. When inflammation goes away S/S go away.
Prognosis for Multiple Sclerosis Shortens your life but prognosis's have a huge range of differences. Comes and Goes but leads to scaring of myelin sheath which leads to S/S don't go away.
Prognosis for Relapse/Remit MS -S/S come and go over a period of years - S/S become permanent - S/S get progressively worse - Fatal
Prognosis for Progressive MS -S/S do not go away - S/S get progressively worse - fatal
Prognosis for Stable MS S/S reach a certain point then stop progressing - not fatal
Parkinson's Disease Dopaminergic neurons in Basal Ganglia are being destroyed which leads to less dopamine in Basal Ganglia which leads to increased muscle tone everywhere in your body.
Dopamine Removes some impulses and helps adjust muscle tone. All neurons pass through a bath of dopamine in the Basal Ganglia.
Muscle tone Always present impulses going to all muscles of the body.
Etiology of Parkinson's Disease Ideopathic - More common in men in the late middle age (50 - 60). Can occure in younger people and women too.
S/S of Parkinson's Disease -Tremors (head to toe due to increased muscle tone in opposing muscles)-Rigid(opposing muscles fighting each other)-Flex(Flexors dominate extendors)-Slow deliberagte movements(jerky)-Blank facial expression-Pill rolling with fingers-NONE MENTAL
Diagnosis for Parkinson's Disease Physical exam. In early stages = no definitave test. Rate on scale of 1-5 a list of symptoms. If you get enough points = Parkinson's DX
Treatment for Parkinson's Disease -Dopaminergic Drugs = Sinemet(raise the level of dopamine in Basal Ganglia, contains Levodopa and Carbidopa) - Anticolinergics(block the aceytocholine neurotransmitters, works at muscle level)
What are the problems with Dopaminergic drugs? Leads to an increased level of dopamine from other sources because we can not control where the drug goes in the body. Too high levels of dopamine lead to Schizophrenia.
What are the problems with Anticolinergic drugs? They slow down digestion secretions and contractions because we can't control where the drugs will go in the body.
Prognosis of Parkinson's Disease Slow but progressive disorder. Managable in early years. As it progresses S/S eventually return and get worse. S/S return when you reach the maximun level of medications. A decreased life expectancy but not by much.
Alzheimer's Disease A gradual destruction of the Cerebral Cortex.
The two changes in the cerebral cortex that are observable in an autopsy -Tau Tangles = Collapse of framework of cells in the cerebral cortex (don't know why) - Amyloid Plaques = Amyloid starts to form plaque, hard deposits, in the brain(don't know why)
Etiology of Alzheimer's Disease Ideopathic - increase risk with age
Pathogenesis of Alzheimer's Disease Early and Late stages. Changes in level of dementia and behavior
S/S of early stage Alzheimers Disease Dementia- mostly short term memory is lost Behavior - Fustration, repetative obscessive behavior, restless, depression
S/S of late stage Alzheimer's Disease -Dementia- starts to affect long term memory as well -Behavior-all the early stage behaviors become more exagerated but also there is a lot of anger. - Will eventually start to affect basis body functions like chewing and swallowing.
Diagnosis for Alzheimer's Disease S/S of dsease - Do Imaging(angiogram, X-ray, CAT scan, MRI,Pet scan) with normal results. -Eventually you will see changes but at a very well advanced stage.
Treatment for Alzheimer's Disease Try to keep safe and independent(early stage). Help with medications, food and finances. Aricept and Namenda help in early stages with memory problems.(affect aceytocholine) Later stages require round the clock care. Professional care.
Prognosis for Alzheimer's Disease Fatal- average about 10 years from diagnosis to death
Created by: owossopatho