1
Q
What does GERD stand for?
A
gastroesophageal reflux disease
2
Q
describe the development of GERD and the most frequent clinical manifestation
A
development:
- chyme in the stomach breaches the lower esophageal sphincter due to relaxation of the lower esophageal sphincter
- can occur spontaneously and contents are usually neutralized and cleared within minutes
- if the occurrence is above frequent = esophagitis
- gastroparesis = slowing of the movement of food from the stomach can also add to factors causing GERD (increase gastric volume and pressure)
most frequent clinical manifestation:
- heartburn= burning sensation under the sternum
- dyspepsia = upset stomach
3
Q
for GERD, long-term inflammation increases the risk of developing what conditions?
A
- fibrosis
- precancerous lesions
4
Q
what is dyspepsia?
A
upset stomach
5
Q
what is gastroparesis?
A
slowing of movement of food from the stomach
6
Q
Describe some factors that increase the likelihood of GERD
A
- common in infancy - sphincter may not have proper muscle tone
- may be major reason of colic (constantly crying)
- increased intra-abdominal pressure (anything that puts extra pressure on the stomach)
- obesity
- pregnancy
- smoking- relaxes esophageal sphincters
- certain foods relax the LES
- fats
- coffee
- alcohol
- people with lupus have more problems with GERD due to connective tissue problems
7
Q
What is a peptic ulcer?
A
a break in the protective mucosal lining of the lower esophagus, stomach, or duodenum = acid connects to tissues and causes ulcerations
8
Q
Define melena and hematemesis (know that these can be complications of peptic ulcer disease)
A
- melena = black foul-smelling stools from the digestion of blood
- hematemesis = vomiting of blood when there is ulcer in upper digestional tract
- either bright red or “coffee ground” appearing (slightly digested blood)
**both caused by hemorrhage = a complication of peptic ulcer disease
9
Q
Describe three other complications of peptic ulcer disease (other than melena and hematemesis)
A
- perforation = ulcer erodes through wall and contents enter peritoneum
- penetration = same, but erosion is into another organ (ex: liver)
- gastric/duodenal outlet obstruction = from edema or scarring
10
Q
what are two high-risk factors for the development of peptic ulcers?
A
- helicobacter pylori pass through the mucous layer that protects the stomach
- NSAIDs interfere with prostaglandin synthesis
11
Q
describe the pathophysiology behind the effects of helicobacter pylori for the development of peptic ulcers
A
- survives pH of 2
- stomach acid normally keeps the mucin lining in the epithelial cell layer a spongey gel-like state = barrier
- helicobacter pylori create urease (enzyme) to neutralize stomach acid = mucin layer liquefies and bacteria can swim through it
12
Q
describe the pathophysiology behind the effects of NSAIDs for the development of peptic ulcers
A
- inhibits prostaglandin production (mucous and bicarbonate) and increases acid production = stomach vulnerable to injury from acid and enzymes
- less mucous and bicarbonate = easier risk for ulceration
13
Q
What are two similarities between duodenal ulcers and gastric ulcers?
A
- mainly caused by Helicobacter pylori and chronic use of NSAIDs
- clinical manifestations are similar (intermittent pain in upper abdomen)
14
Q
Describe three differences between duodenal ulcers and gastric ulcers (include the pattern of pain).
A
- duodenal:
- occur with greater frequency than other types of peptic ulcers
- tend to develop in younger people (more common in males)
- pain relieved rapidly by ingestion of food or antacids
- pain begins 2-3 hours after eating because it takes a bit longer from digestion
- gastric:
- about ¼ as common as duodenal ulcers
- tend to develop in older adults (55-65)
- tend to be more chronic and the duration of treatment is longer
- pain frequently occurs immediately after eating because food coming into stomach = secretion of gastric juices for digestion = initiates ulcers from acidity
15
Q
What are the main treatments for peptic ulcers?
A
- eradicate H. pylori with antibiotics
- reduce acidity
- antacids (ex: calcium carbonate)
- proton pump inhibitors (stops secretion of hydrogen ions from parietal cells)
- h2 receptor antagonists (blocks action of histamine which causes HCI secretion)
- minimally invasive surgical resection if ulcers are bleeding or have perforated the GI wall
16
Q
What are the two diseases that make up inflammatory bowel disease?
A
- ulcerative colitis
- crohn’s disease
17
Q
what is the typical age range affected for ulcerative colitis?
A
20-40 years old
18
Q
what are the regions of the bowel affected and the nature of the inflammatory process for ulcerative colitis?
A
- regions affected:
- colonic mucosa
- most commonly in the rectum and sigmoid colon
- beginning in the rectum, the ulceration spreads in a continuous manner
- colonic mucosa
- process:
- inflammation of mucosa = edema, and thickening of the wall of the tract
- destruction of mucosa = bleeding, pain, and an urge to defecate (poop), even if the colon is empty (tenesmus)
- frequent bloody diarrhea is a common symptom
- fluid loss, bleeding and inflammation produce dehydration, weight loss, anemia, and fever
- high risk for development of cancer in the colon
19
Q
what is the appearance of inflamed tissues for ulcerative collitis?
A
usually beginning in the rectum, the ulceration spreads in a continuous manner
20
Q
what are the risk factors of ulcerative colitis?
A
- age (20-40 y/o)
- family history
- the normal state of bacterial tolerance has been disrupted = unregulated immunological response
21
Q
what are the clinical manifestations of ulcerative colitis?
A
- edema and thickening of the wall of the tract
- bleeding, pain, and an urge to defecate, even if the colon is empty (tenesmus)
- frequent bloody diarrhea
- dehydration
- weight loss
- anemia
- fever
- toxic megacolon = abrupt increase in diameter of colon in a few days that could rupture (extreme case)
22
Q
what are the possible complications of ulcerative colitis?
A
toxic megacolon
23
Q
what is the typical age range affected for Crohn’s disease?
A
20-30, slightly more common in women
24
Q
what are the regions of the bowel affected and the nature of the inflammatory process for Crohn’s disease?
A
- begins in submucosa
- lesions have a “cobblestone” appearance
- affects both large and small intestine
- inflammation of the entire width of the intestinal wall
- sometimes occurs in patches (skip lesions)
25
what is the appearance of the inflamed tissues for Crohn's disease?
* cobblestone appearance
* inflammation of the entire width of the intestinal wall
* sometimes occurs in patches (skip lesions)
26
describe the risk factors of Crohn's disease
family history
27
what are the clinical manifestations of Crohn's disease?
* electrolyte imbalances
* anemia
* diarrhea
* weight loss
* abdominal pain
* toxic megacolon may also occur
28
what are the possible complications of Crohn's disease?
* fistulas
* abscesses
* obstruction
29
Define tenesmus
an urge to defecate (poop), even if the colon is empty
30
What is toxic megacolon?
an abrupt increase in diameter of colon (within one to a few days) that could rupture
31
what is celiac disease?
a malabsorptive disease where the mucosa fails to absorb digested nutrients
32
describe the development of celiac disease
* T-cell mediated immune disorder (causes an inflammatory response)
* intense immune reaction to gluten (gliadin) = the protein component of cereal grain
* inflammation brought on by immune reaction damages **small intestinal villous epithelium** = interfering with the absorption of macro and micronutrients
33
Describe the clinical manifestations of celiac disease and the consequences of malabsorption of nutrients in childhood and as an adult
* in childhood, failure to thrive
* abdominal pain
* diarrhea with fatty stools
* malabsorption of nutrients leading to:
* osteoporosis, seizures/tetany from lack of calcium
* anemia from lack of iron
* short stature, when it develops in childhood, from general malnutrition
* in pregnancy = miscarriage, neural tube defects (due to lack of folic acid, and other nutrients)
34
Define portal hypertension and its cause.
* abnormally high blood pressure in the portal venous system
* movement of blood from the digestive system to the liver
* cause:
* disorders that obstruct blood flow through the portal venous system/vena cava
* thrombosis of hepatic veins
* severe right-sided heart failure
* alcoholic
* cirrhosis
35
Define ascites and describe two causes for ascites
* accumulation of fluid in the peritoneal cavity
* can add pressure to diaphragm = SOB
* causes:
* portal hypertension
* decrease in serum protein production in the liver = lower osmotic pressure in capillaries = fluid retention that sees in the peritoneal cavity
* liver not making albumin
36
How can ascites be treated? What could happen if fluid is removed too quickly?
treatment:
* paracentesis to remove fluid and relieve breathing
* draining of abdominal cavity using a needle
* done with caution to avoid hypotension and shock
37
Describe the development of varices associated with the portal system
* veins that drain from the esophagus into the hepatic portal vein and inferior vena cava
* pressure increase too much in the portal system = increase resistance for blood flow from esophagus into the portal system
* collateral veins start to develop between the two sets of veins in the esophagus = back up of blood into inferior vena cava
* blood going to inferior vena cava = blood bypassing the liver
* collateral veins can't handle the pressure of the blood coming through the portal system= swelling and distennd (caricose veins = “varices”)
38
name the most common clinical manifestation of varices
* vomiting (bright red blood) of blood from hemorrhaging esophageal varices
* melena (dark bloody poop) may also occur if varices burst
39
Where are two other places where collateral shunts can occur due to portal hypertension? Name the varices that result
* between the veins on the abdominal wall (caput medusae)
* veins from the rectum (hemorrhoids)
40
Describe the development of hepatic encephalopathy
* liver dysfunctions and callateral vessels that shunt blood past the liver = toxins remain in the bloodstream and reaches the brain
* most hazardous is ammonia (liver normally converts to urea)
41
what is hepatic encephalopathy?
problem in the head because of the liver
42
what are the clinical manifestations of hepatic encephalopathy?
* neurotransmission is affected
* personality chnages
* loss of memory
* confusion
* flapping of hands (asterixis) possibly worsening to coma
43
Define asterixis
flapping of hands
44
what is icterus?
jaundince
* the green/yellow tinge to skin caused by hyperbilirubinemia
45
describe two causes of icterus that are related to diseases of gastrointestinal organs
1. too many RBC beinf broken down = interference/damage within the liver = alters the process of biliruben
2. obstructions of the common bile ducts = liver cannot excrete processed biliruben into the bile
46
Why may the feces be light in colour (“clay coloured”) and the urine dark in colour with jaundice?
* light colour “clay” feces = biliruben is not being excreted
* dark urine = bilireubin is everywhere else since not leaving/building up in bloodstream
47
Where does jaundice often occur first?
sclera of the eye, and then the skin
48
Describe why splenomegaly may occur with liver disorders
* due to portal hypertension
* causes shunting of blood into the spleninc vein
49
how are blood cell numbers affected with splenomeagaly from liver disorders
* as you get shunts, blood goes though spleen = longer to go through = easier to breakdown rbc = fewer RBC/WBC in blood stream
* formed elements take longer to filter through the enlarged spleed = ncreased rate of removal
50
what is acute viral hapatitis?
acute inflammation of the liver caused by infection with one of the five hepatitis viruses
51
outline some common causes and diagnostic features of acute hepatitis
* abnormal liver function test results
* 3 stages of the progression:
* **prodromal phase (typial viral infection)** = viral inflammatory effects
* begins **2 weeks** after exposure and ends with jaundince
* **icetric phase** = effects of liver damage
* begins after prodromal, **lasts 2-6 weeks**
* jaundice, dark urine, clay coloured stools, liver enlarged and tender
* **convalescent phase** = healing and repair
* begins with resolution of jaundice and most symptoms, about **6-8 weeks after exposure**
* liver remains large and tender
* liver returns to normal function 2-12 weeks after onset of jaundice
52
Name the viral strains involved in hepatitis and describe the differences between routes of infection
viral strains:
* A (infectious hepatitis)- from gastrointestincal route
* cause acute viral hepatitis… no worry transferring multiple viruses at same time
* B, C, D, E/I = route of transmission is the same (body fluids) = more rapid prrogression of liver disease
routes:
* all can cause actute hepatitis
* HBV/HCV can also cause chronic liver disease and liver cancer
53
Describe the damage to the liver caused by acute hepatitis.
* acute hepatitis causes destruction of hepatocytes (cells of liver), scarrinf and hyperplasia of hepatic macrophases
* if intrahepatic ducts are damages, obstruction and jaundice can occur due to damage of cells and internal lining of ducts
54
Name and describe the stages of disease of a typical acute viral hepatitis infection
1. prodromal phase = viral inflammatory effects
1. begins 2 weeks after exposure and ends with jaundice
2. fatigue, vomiting, headache, cough, low-grade fever
2. iceteric phase = effecs of liver damage
1. begins after prodromal, laster 2-6 weeks
2. jaundice, dark urine, clay-coloured stools, liver is enlarged and tender
3. convalescent phase = healing and reair
1. begins with resoluton of jaundice and most symptoms, about 6-8 weeks
2. liver remains large and tender
3. liver returns to nromal function 2-12 weeks after onset of jaundice
55
what is chronic viral hepatitis?
persistence of clinical manifestations and liver inflammation after acute stages of HBV and HCV infection
* liver function tests remain abnormal for longer than 6 months
56
name causative organisms, and possible resulting diseases from chronic hepatitis
* HBV/HCV surface antigen
* resulting diseases = cirrhosis and liver cancer
57
Define cirrhosis, describe its cause
an irreversible inflammatory, fibrotic liver disease
* caused by direct damage and inflammation from many disorders
* HBV/HCV infection
* excessive alcohol consumption
* prolonged exposure to drugs or toxins
* hepatoxin
58
what 3 disorders can lead to cirrhosis?
1. changes resulting from intial injury and resultant inflammation
1. fibrosis caused by release of inflammatory mediators by leukocytes, and activation of fibroblasts
2. liver metabolism is altered
3. liver structure is altered
59
Define hepatotoxin
a toxin that can harm the liver
60
What disorders can result from cirrhosis?
* Portal hypertension. The portal vein carries blood from your intestines and spleen to your liver. ...
* Enlarged blood vessels. ...
* Ascites. ...
* Kidney disease or failure.
* Easy bruising and severe bleeding. ...
* Type 2 diabetes. ...
* Liver cancer
61
Describe two types of alterations that occur in the liver during the development of cirrhosis.
1. liver metabolism and structure is altered by blockage of channels necessary for liver function
62
What is the “treatment” for cirrhosis? (Why is treatment in quotation marks?)
* treatment in quotes because there is no specific treatment
* rest
* vitamin supplements
* goof nutrition
* management of complications
* possible liver transplant
63
Define liver failure
the inability of the liver to perform its normal synthetic and metaboliv function as part of normal physilogy
* most severe clinical consequence of liver disease
64
Name and describe the clinical manifestations of liver failure
1. factor hepaticus - chronic musty odor of breath due to toxin build up goign to respiratory system
2. anemia, thrombocytopenia, leukopenia
3. loss of clotting factors and other plasma proteins leading to purpura, petechiae, spider angioma, epistaxis
4. hamolysis - caused by changed in RBC membrane lipids
5. hepatorenal syndrome - kidney failure generally due to decreased blood volume brought about throufh bleeding, loss of fluid, vasodilation resulting from liver failure
6. hapatic encephalopathy
65
what is fector hepaticus?
chronic must odor of the breath
66
what is purpura?
purple discolouration (3-10mm)
67
what is petechiae?
purple discolouration (\<3mm)
68
what is spider angioma?
appearance of radiating blood vessels on skin surface
69
what is epistaxis?
nose bleeds
70
Define cholelithiasis
the formation of gallstones
71
what is cholecystitis?
inflamation of the gallbladder
72
From what are most gallstones formed, and what conditions lead to their formation?
* most formed from cholesterol
* conditions:
* abnormalities in the composition of bile (more cholesterol excreted into bile)
* stasis (sitting of fluid) of bile
* inflammation of gallbladder (causes excessive absorption of water and bile salts)
73
What causes the pain associated with gallstones?
* pain occurs 30 mins to several hours after eating a fatty meal, caused by lodging of one or more gallstones in the cystic or common duct
74
What is the significance of the presence of jaundice in the diagnosis of cholelithiasis?
* jaundice indicates that the stone is lodged in the common bile duct since bile backs up into the liver
* lodging of a stone in the cytic duct will cause cholecystitis
75
Define acute pancreatitis
reversible inflammatory process caused by premature activation of pancreatic enzymes
76
describe the characteristic manifestations of acute pancreatitis
ongoing abdominal pain
77
describe the underlying pathophysiology and the diseases acute pancreatitis can lead to
* outflow of pancreatic digestive enzymes is obstructed, causing:
* accumulation of pancreatic secretions
* pathologic activation of enzymes within the pancreas
* results to autodigestion = vascular damage, necrosis, edema, and inflammation
* can deelop into “sever-acute” form = so much damage from digesting pancrease = systemic manifestations
78
Define chronic pancreatitis and describe some characteristic manifestations
prolonged, progressive and irreversible destruction of the exocrine and then endocrine pancreas
* characteristic manifestations:
* loss of pancreatic function
* the outcomes of chronic inflammatory processes
* malabsorption, weight loss, TSDM
* release of inflammatory cytokines into the bloodstream = systemic effects, anorexia, nausea
79
Identify the most common cause and for what condition chronic pancreatitis is a risk factor
* common cause = chronic alcohol abuse
* what condition chronic pancreatitis is a risk factor = pancreatic cancer
BIOL 2200
flashcards
Decks in class (12)
# Cards
-
module 1 Adaption, Inflammation, & Healing120
-
module 2: Immune System Disorders75
-
module 3: neoplasms102
-
module 4: blood disorders78
-
module 5: cardiovascular disorders164
-
module 6: respiratory disorders94
-
module 7: digestive disorders79
-
module 8: endocrine system disorders60
-
module 9: neurological disorders105
-
module 10: excretory system disorders109
-
module 11: Musculoskeletal and Reproductive Disorders69
-
definitions193
