Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
144 Cards in this Set
- Front
- Back
|
Define a peptic ulcer.
|
It is a break in the protective mucosal lining of the lower esophagus, stomach or duodenum
|
|
|
The breaks from peptic uclers expose the submucosa to what products? What occurs?
|
Gastric secretions and autodigestion occurs
|
|
|
What is the major player in the development of ulcers?
|
Gastic acid
|
|
|
If a peptic ulcer occurs in the stomach, what location is it most commonly in?
|
The antrum: it has the most acid
|
|
|
Where do peptic ulcers most common occur?
|
In the duodenum
|
|
|
Define erosion. When does it occur?
|
Penetration of only the superficial layer. They occur when you have a minimal amout of submucosa expose and just a wearing away. Not true ulcers
|
|
|
What is an acute ulcer?
|
Penetration into the muscle layer
|
|
|
Why are acute ulcers usually painful?
|
They are extended into the nervous tissue and cause damage to blood vessels.
|
|
|
Why can acute ulcers cause a person to be chronically anemic?
|
Because of the damage to blood vessels bleeding is very common and is usually persistent
|
|
|
What is the worst case ulcer?
|
Perforating ulcer: penetration of the wall.
|
|
|
What can occur with a perforating ulcer?
|
Periotonitits and sepsis
|
|
|
List the risk factors for peptic ulcer disease.
|
1. Smoking
2. H. Pylori 3. Habitual use of NSAIDs or alcohol 4. high psychological stress |
|
|
Why do NSAIDs commonly cause ulcers?
|
They are prostaglandin inhibitors and we need prostaglandins for mucus production by the gastric mucosa. The stomach is not protected from acid
|
|
|
Describe how stress can cause ulcers.
|
It reduces intestinal blood flow and thus your ability to produce mucus
|
|
|
What % of peptic ulcers have H.pylori involvement?
|
80-90%
|
|
|
What is H. pylori?
|
an incredible prevalent bacteria found in the GI tract in 50% of people, especially in developed countries. Usually does not produce problems, but can trigger an infection and thus a peptic ulcer
|
|
|
Describe the correlation between antibiotic use and obesity.
|
When antibiotics are taken, they kill off the bacteria that is able to derive calories from food. Leaving behind the fat promoting bacteria to run rampant and thus gain weight.
|
|
|
Why are duodenal ulcers the most commonly seen ulcer?
|
They receive the acid contents from the stomach, but they lack the alkaline mucus that naturally protectss the mucosal lining of the stomach
|
|
|
What is responsible for giving the alkaline mucus to the duodenum? What can an interference in this cause?
|
The pancreas will realease sodium bicarb.
An interference in this can cause a duodenal ulcer |
|
|
What are the common causes of DUODENAL uclers?
|
1. Hypersection of gastric acid and pepsin
2. Elevated plasma gastrin levels 3. Inadequate secretion of pancreatic sodium bicarb 4. Excessively rapid gastric emptying 5. Immune reaction to H. Pylori |
|
|
Which cells of the pancreas are responsible for Na bicarb?
|
The duct cells
|
|
|
Describe the characteristic manifestation of duodenal ulcers.
|
Chronic, intermittent pain in the epigastric region
Food-pain relief pattern |
|
|
What are some common treatments for duodenal ulcers?
|
1. Use of antacids
2. Proton pump inhibitors 3. antibiotic Tx for H. Pylori 4. Anticholinergics to inhibit secretion, suppress gastric motility and delay gastric emptying |
|
|
Describe the pain associated with GASTRIC ulcers.
|
Pain is persitent and requires treatement to heal (30 mins to 1 hour after you eat)
-When food is present there is no pain, but as soon as the food passes there is a lot of pain. |
|
|
Define a Stress ulcer.
|
An acute form of peptic ulcer that tend to accompany severe illness, systemic trauma or neural injury
|
|
|
Where do stress ulcers often occur and what are they essentially?
|
They often occur at multiple sites distributed throughout the stomach and duodenum. They are essentially ischemic ulcers
|
|
|
State the progression of stress ulcer development from the slide,
|
Sympathetic stimulation --> Decreased mucosal blood flow --> Mucosal metabolism declines -->Decreases mucous production -->Exposes mucosa to gastric acid --> Autodigestion and ulcer formation
|
|
|
What are cushing's ulcers?
|
They are a severe form of stress ulcer that is caused by ischemia as well as a head trauma that causes stimulation of the cells in the brain where the vagus nerve originates. This causes even more acid production and results in wide spread ulceration
|
|
|
What are trauma patients given prophylactically and why?
|
PPIs to prevent stress ulcers
|
|
|
What are curling ulcers?
|
Ulcers that occur because of significant burns over the body.
|
|
|
What is maldigestion?
|
Interferes with the process of digestion
|
|
|
The term for an interference in the absorption of food products?
|
Malabsorption
|
|
|
Why do cancer patients often suffer from malabsorption?
|
They lose mitotically active cells and get a dying off of the mucosal lining and thus absorption problems
|
|
|
What is celiac disease? What occurs with nutrition?
|
Gluten allergy. Immune attack against mucosal cells and they die and slough off. These individuals have a muscle wasting beceause they are not absorbing calories
|
|
|
What is a severe version of maldigestive disorder?
|
Pancreatic insufficiency
|
|
|
Describe pancreatic insufficiency.
|
poor production or release of pancreatic enzymes: all of the ones needed in the breakdown of all food categories. Cannot breakdown food
|
|
|
What causes pancreatic insufficiency?
|
pancreatic disease of cystic fibrosis
|
|
|
People with pancreatic insufficiency have the most problem with what food product? Why is this a big problem?
|
Fat. We derive most of our calories from fat and these people have a hard time maintaining weight.
|
|
|
What are the hallmark signs of pancreatic insufficiency?
|
Weight loss and Steatorrhea: large amounts of fat in the stool (foul in odor and light in color due to fat content)
|
|
|
What is lactase?
|
Brush border Enzyme on the lumen side of the small intestine necessary to breakdown lactose (disaccharide in all dairy products)
|
|
|
Why are mammals different from other organisms on the planent in terms of food consumption?
|
We continue to eat milk products after weaning
|
|
|
What type of trait allows for the continued production of lactase?
|
A recessive and beneficial one
|
|
|
What happens when individuals who cannot produce lactase ingest dairy products?
|
The lactose moves to the LI where it encouters the natural flora and is broken down in the LI through fermentation where the byproduct is GAS. Creates painful gas cramping and raises the osmolarity of the contents of the colon
|
|
|
What dairy product is considered the easiet to breakdown? Why?
|
Yorgurt because it already has bacteria in it to breakdown the dairy product.
|
|
|
What is the funciton of bile?
|
to emulsify fat. Turns large droplets into smaller droplets that cannot recombine and increases the surface are that lipase has access to breakdown the fats
|
|
|
What are some causes of bile salt dificiency?
|
Advanced liver disease (cirrhosis of the liver) and obstructions of the bile ducts
|
|
|
List the clinical manifestations of bile salt dificiencies.
|
1. Will have fat in the stool (not as much as pancreatic insufficiency)
2. Clay colored stool 3. poor absorption of fat soluble vitamins |
|
|
What does bile do to stool?
|
It gives stool its brown color
|
|
|
A deficiency of Vitamin A can lead to what?
|
Night blindness
|
|
|
Vitamin D deficiencies will lead to what disorders?
|
Decreased Ca absorption leading to osteoporosis and fractures
|
|
|
What can Vitamin K deficincy cause?
|
Associated with prolonged Prothrombin time, leads to bleeding and spontaneous bruising
|
|
|
Neurological effects in children have been associated with a deficiency in what vitamin?
|
Vitamin E
|
|
|
What 2 conditions are describe as inflammatory bowel disease?
|
Ulcerative Colitis and Crohn's Disease
|
|
|
Where do ulcers occur in ulcerative colitis?
|
Limited to the COLON!! Only!
|
|
|
Where do ulcers occur in crohn's disease?
|
They can occur anywhere along the GI tract (mouth to anus)
|
|
|
Describe the depth of ulcers in UC
|
Ulcerative colitis ulcers are usually shallow (in the mucosa)
|
|
|
Describe the depth of ulcers in Crohn's disease.
|
They are usually deep, starting in the submusocal later and often become perforating
|
|
|
What is the pattern of ulcers in UC?
|
They start in the colon and spread in a continuous pattern and occupy a greater area of the colon
|
|
|
Which inflammatory bowel disease has ulcers with a patchy pattern ?
|
Crohn's disease
|
|
|
What are some of the factors leading to ulcerative colitis?
|
1. Sensitivity to foods: can triger onset or flare ups
2. H. pylori 3. Genetic predisposition 4. autoimmune factors: anticolonic antibodies. Found circulating Tcells that attack the colon |
|
|
Where does the inflammation of UC usually start?
|
In the crypts of Lieberkhan
|
|
|
what are the crypts of leiberkhan?
|
Folds of the mucosa where in the valley of them are the stem cells that replenish the mucosa
|
|
|
What does inflammation in the crypts create as far as pain and sensation/
|
Cause cramping pain, the urge to deficate often leading to diarrhea and bleeding
|
|
|
Acute ulcerative colitis is characterized by?
|
Colitis with extensive mucosal ulceration involving the entire colon and is usually irrepairable
|
|
|
What is the definition of uclerative colitis?
|
A chronic inflammatory disease that causes ulcerations of the colonic mucosa: usually the rectum and sigmoid colon
|
|
|
Describe mild UC.
|
Confined to the rectum or rectosigmoid. Intermittent rectal bleeding, mild diarrhea, mild cramping, some periods of constipation. No significant problems with hydration or nutrition
|
|
|
What is moderate UC?
|
Involves more of the colon. Frequent loose, bloody stools (up to 10 a day).
Mild anemia, low grade fever, abd pain: not severe, adequate nutrition is maintained |
|
|
Which form of UC involves rapid weight loss with more than 10 bloody stools a day?
|
Severe UC
|
|
|
What must occur in response to the bleeding of severe UC?
|
Transfusion
|
|
|
What are the Tx for ulcerative colitis?
|
1. First line: anti-inflammatory drugs: NSAIDs and steroids
2. antibiotics 3. Treat hydration or nutritional deficiencies 4. Removal or resection of the colon and usually colonostomy |
|
|
What is the most common area of the GI tract to see ulcers in Crohn's disease?
|
Ileocecal region
|
|
|
What amount of individuals with Crohn's disease have perianal disease?
|
1 in 3
|
|
|
What occurs when you have Crohn's disease that manifests in the small intestine?
|
Skip lesions of the haustra
|
|
|
What is a skip lesion?
|
Manifestation of crohn's disease where you have a lesion in one haustra and then it skips to another down the line
|
|
|
How do ulcers of crohn's disease manifest when they are in the colon?
|
Exactly like UC: bloody stool, cramping, anemia
|
|
|
What is Crohn's disease?
|
An idiopathic inflammatory disorder that effects any part of the GI tract
|
|
|
What deficiency can occur if ulcers from Crohn disease are located in the ileum?
|
B12 deficiency
|
|
|
If a person with crohn's disease has a mineral deficiency, where might they have an ulcer?
|
In the duodenum
|
|
|
What is a common complication of ulcers from Crohn's disease?
|
Fistulas
|
|
|
What is a fistula?
|
Any channel that is formed between 2 hollow structures. Can have one loop of intestine that lies next to another loop; the ulcer begins in one, perforates that loop and then goes on to the neighboring one
|
|
|
What is the Tx for Crohn's disease?
|
Anti-inflammatories, hydration, antibiotics. 80% of patients need some kine of surgery
|
|
|
What is diverticular disease?
|
Common age related disease that is characterized by small pouches along the LI wall
|
|
|
What is the cause of diverticular disease?
|
Increased intracolonic pressure brought about by age (narrowing of the colon with age) and a diet low in fiber and high in refine foods
|
|
|
What does increase pressure from diverticular disease lead to>
|
Herniation of the colon mucosa at weak points along the colon wall. M
|
|
|
What is diverticulitis?
|
When the herneation pouches of diverticular disease become inflamed and infected
|
|
|
What are common symptoms of diverticular disease
|
Cramping, diarrhea, constipation, low grade fever if they are inflamed or rupture
|
|
|
What is the % of individuals that have diverticular disease by age 60? By 80?
|
60: 30%
80: 65% |
|
|
What is the best advice to give pts who may have diverticular disease?
|
Avoid seeds, corn etc: things that pass through the colon undigested and tend to get trapped.
|
|
|
What are the clinical manifestations of liver disease?>
|
1. Portal HTN
2. Ascites 3. Hepatic Encephalopathy 4. Jaundice |
|
|
What is portal HTN?
|
Abnormally high BP in the portal circulation caused by any disease that obstructs or impedes blood flow through any component of the portal venous system or the vena cava
|
|
|
What can long term portal HTN lead to?
|
1. Varices
2. Ascities 3. splenomegaly 4. heptic encephalopathy |
|
|
What are the 2 sources that the liver gets its blood from?
|
1. Hepatic artery (profuses the liver with O2)
2. Portal vein: send blood to the liver from the GI tract |
|
|
What is the blood metabolized for in the liver?
|
toxic substances, infectious agents pass through immune cells of the liver
|
|
|
The pressure in the portal vein is usually what?
|
Very low
|
|
|
Describe varices?
|
Sistended and tortuous collateral veins: varicose veins seen in the lower esophagus and the stomach
|
|
|
What is heptic encephalopathy?
|
nuerological manifestations when you have bypassing of blood away from the liver and the blood goes straight into general circulation.
|
|
|
How does varices occur as a result of portal HTN?
|
The drainage of blood from the mesentaric veins and spelic veins becomes impaired, which makes it so that blood stays in the vessels, increasing the pressure and they expand
|
|
|
What are some clinical complications of varices>
|
Rupture: catasprophic
-can leat to vomiting up large volumes of blood, blood in stool, anemia and hemorrhagic shock |
|
|
What is the mortality rate for a variceal rupture?
|
30-60%
|
|
|
What is ascites?
|
condition of pathologic fluid accumulation within the abdominal cavity. Traps fluid in a "third space" from which it cannot escape
|
|
|
What is a common cause of ascites?
|
Cirrhosis of the liver
|
|
|
What are the contributing factors to ascites?
|
Portal HTN, Hypoalbunemia, impaired liver breakdown of ADH and aldosterone
|
|
|
What are individual with ascites at major risk for? Why?
|
A BP crash. They are hemodynamically unstable and the hydrostatic pressure against the capillaries increase the risk for fluid rushing out of the vessels!
|
|
|
What are the symptoms of heptic encephalopathy?
|
Impaired cerebral function, flapping tremors, EEG changes, personality changes and intellecutal impairement
-depressed LOC |
|
|
What is an important prerequisite to hepatic encephalopathy?
|
Diversion of portal blood into the systemic ciruclation through portosystemic collateral vessels
|
|
|
Describe the ammonia hypothesis for hepatic encephalopathy?
|
Ammonia is produced through normal digestion and normally digested by the liver. When it gets bypassed,"", the levels in the blood stream rise and cause HE.
|
|
|
How does GABA levels cause Hepatic encephalopathy
|
The liver usually neutralizes GABA, but when the liver doesn't function GABA builds up and gains access to the brain and cuases inhibitory effects. Increases the permeability of the BBB
|
|
|
Describe Grade 0 and 1 of HE.
|
Only those close to the patien would notice a change. Would have normal mental status, but changes in memory or concentration. May feel mild confusion, euphoria or depression. Hard time maintaining attention.
|
|
|
Which grade of HE will cause inappropriate behavior? What are the other symptoms of this grade?
|
Grade 2: also include drowsiness, lethargy, time disorientation, gross deficits in the ability to perfom mental tasks
|
|
|
What describes grade 3 of HE?
|
Difficult to arouse, very confused, fits of rage, amnesia, present but incomprehensible speech
|
|
|
What is the stage related to coma with HE?
|
Grade 4
|
|
|
Describe Juandice.
|
Discoloration of the skin or sclera to a yellow/orange tint. Cause by deposition of bilirubin in peripheral tissue. HALLMARK sign of hepatocellular death
|
|
|
Where is bilirubin initially produced?
|
By the spleen
|
|
|
What are the 2 functions of the spleen?
|
1. Lymphatic tissue
2. Red pulp: major area where old RBC are trapped and eliminated |
|
|
Which parts of the RBCs get recycled? What gets removed normally?
|
Recycled: protein and iron
Heme is converted into bilirubin |
|
|
What is bilirubin in its initial form?
|
uncojugated: highly lipid soluble
|
|
|
What is the pathway of bilirubin?
|
Leaves the spleen unconjugated through the spleinic vein --> binds to albumin to travel through the blood --> travels to the liver and enters portal vein and portal circulation --> in liver it is conjugated (sugar groups attaches) --> leaves liver through bile ducts (gives bile yellow color) --> enters gallbladder for storage --> released when fat is eaten
|
|
|
What enzyme is responsible for the conjugation of bilirubin?
|
glucoronyl transferase
|
|
|
What metabolized conjugated bilirubin? What does it become?
|
Enzyme: beta glucoronidase and become sterobilinogen SBG: which gives feces the brown color
|
|
|
Why does liver disease lead to bilirubin in circulation without conjugation?
|
1. Liver disease = less albumin and less unconjugated bilirubin can get to the liver to be conjugated
2. as liver function goes down the conjugation of bilirubin goes down. You also have more portal HTN and less blood flow to the live, so less unconjugated bilirubin can even make it to the liver |
|
|
What is hepatitis?
|
inflammation of the liver
|
|
|
What can cause hepatitis?
|
Exposure to environmental polluatant ie alcohol or a viral infection
|
|
|
What is the most reliable way to test for hepatitis?
|
Biopsy
|
|
|
What is the composition of the hepatic tetrad?
|
The center is a branch of the portal vein, you have a branch of the hepatic artery and some bile ducts
|
|
|
What direction does the bile move through the liver>
|
In the opposite direction of blood. Starts towards the hepatic vein and moves towards the portal veins and hepatic areteries
|
|
|
Where is inflammation of the liver often seen?
|
At the site that the injury gained access to the liver. If the injury is in the blood then you will see inflammation around the tetrad where blood enters.
|
|
|
What is the widening of the connective tissue around a tetrad in heptatis refer to?
|
Scar tissue that has formed.
|
|
|
Which 2 forms of Hep are transmitted through fecal/oral?
|
Hep A and E
|
|
|
Which forms of hepatitis are acute and can make a full recovery?
|
Hep A and E
|
|
|
Which formes of hepatitis are transmitted peranterally?
|
Hep B and C
|
|
|
How is Hep D transmitted?
|
Must already have Hep B to get it. Is transmitted peranterally. It requires B to replicate. Can cause fulminant hepatitis and is a form of chronic liver failure
|
|
|
What do all forms of Hep have in common? Why is this dangerous?
|
Incubation period. You can be contagious without any SxS that you are infected
|
|
|
What is the prodromal phase?
|
first appearance of SxS. Non-specific symptoms of general viral infections. Are very contagious
|
|
|
What is the hallmark sign of the acute phase of hep has been reached?
|
Jaundice
|
|
|
What will blood work look like in the acute phase of Hep?
|
rise in bilirubin, serum aminotransferase values rise, ASTs and ALTs ( enzymes present when hepatocytes die)
|
|
|
What happens after the acute phase of Hep B,C or D?
|
you enter the chronic phase where the immune system will reduce the viral count, but cannot get rid of it completely. Damage contiues which causes ongoing inflammation and suffer consequences
|
|
|
When does the prodromal phase of Hep begin?
|
2 weeks after exposure.
|
|
|
When does the icteric phase of Hep begin?
|
1-2 weeks after prodromal phase and lasts 2-6 weeks
|
|
|
What is liver cirrhosis? What characterizes it?
|
Irreversible condition, liver failure. Characterized by extensive bands of scar tissue that are separated by nodules of regenerated liver tissue
|
|
|
What is a consequence of the scar tissue of cirrhosis?
|
Drastic reduction in functional liver tissue. Also leads to portal HTN because the scar tissue increases the pressure around the tetrads which leads to blood bypassing the liver and toxins building up in the body (GABA and Ammonia)
|
|
|
Why is the presence of heptic carcinoma so detrimental?
|
Disqualifies an individual for transplant
|
|
|
List the examples of Cirrhosis?
|
1. Alcoholic (includes reversible fatty liver phase)
2. Postnecrotic cirrhosis (post viral Hep B, C, or D 3. Fulminant Hep (acute liver failure) |
|
|
What are some Tx for Hep B and C? why are they not used often?
|
Interferon therapy: tries to erradicate the virus but they are hard drugs to take.
|
|
|
What can cause fulminant Hep?
|
Tylenol overdose, environmental expsoure or Hep D from Hep B
|
