GI Disorders Flashcards
(129 cards)
1
Q
What are 4 etiology/risk factors for diverticular disease?
A
Poor diet (low fibre), poor bowel habits (constipation), inactivity, and ageing.
2
Q
What is the patho for diverticular disease?
A
Normal weak points in gut for BV entry into gut & increased intraluminal pressure (from RF) results in mucosa herniating through muscularis externa causing a bowel protrusion (out pouch)
3
Q
Where abouts in the GIT is diverticulosis most common?
A
Sigmoid colon
4
Q
What is diverticulosis?
A
Formation of non-inflamed out pouchings.
5
Q
What is diverticulitis?
A
Inflamed out-pouching as a result from strangulation.
6
Q
Do manifestations occur in diverticulosis or litis? What are the 3 manifestations?
A
Diverticulitis. Dull pain, N and V, low grade fever.
7
Q
What are the four treatments for diverticular disease?
A
Addressing risk factors, anti-inflm, pain meds, Sx for complications (perforation or obstruction).
8
Q
IBS is a GI _____ disorder
A
Motility
9
Q
What is the etiology for IBS?
A
Unclear, but triggers are related to diet, stress, and smoking.
10
Q
What are the 5 manifestations of IBS?
A
Abdominal pain and discomfort, diarrhea/constipation, flatulence, nausea, and mucoid stools.
11
Q
What are the two theories for the patho of IBS?
A
1st theory - malabsorption of fermentable CHO and polyols leads to gut flora processing and flatulence.
2nd theory - alteration in CNS regulation of GI sensory/motor fx results in a molecular signalling defect of serotonin.
12
Q
What are the 4 functions of serotonin?
A
Pain, secretion, perfusion, motility.
13
Q
How is IBS diagnosed?
A
Exclusion of organic disease and sigmoidoscopy.
14
Q
What are the 5 treatments for IBS?
A
Eliminate triggers, reduce stress, antispasmodic drug (Modulon), antidiarrheal/laxative, abx with caution to reduce normal flora and reducing flatulence.
15
Q
What is peritonitis?
A
Inflammation of the peritoneum.
16
Q
What is the etiology of peritonitis?
A
Bacteria (E.coli) or chemical irritation (HCl, bile, pancreatic juice).
17
Q
In what two ways can the etiologic factor in peritonitis enter the abdominal cavity?
A
Perforated ulcer or ruptured appendix.
18
Q
What is the patho of peritonitis?
A
Etiologic agent impacts peritoneum leading to inflammation.
19
Q
The peritoneum is highly vascularized, why is this negative?
A
Quick absorption of bacteria toxins.
20
Q
The peritoneum is a large structure, what is negative about this?
A
The agent of injury spreads easily.
21
Q
What forms as a result of inflammation to the peritoneum? Is this beneficial?
A
Thick exudate. Beneficial because is localizes the inflammatory process, seals perforations and limits the spread of the agent of injury.
22
Q
How does the body compensate for peritonitis? What happens?
A
The SNS limits GI motility and an ileus forms.
23
Q
What are the 4 manifestations of severe peritonitis?
A
Dyspnea (due to pain of diaphragm pushing against abdominal cavity), mucoid stools, ileus, hyperemia (altered perfusion, blood shunting and vasodilation)
24
Q
What is the biggest concern with peritonitis? (Complication)
A
Hypovolemic shock due to massive fluid shift.
25
What are the 5 STAT treatments for peritonitis?
IV abx, anti-inflm, IV fluids, pain meds, surgery if necessary.
26
Appendicitis is acute inflammation of the _________
Appendix wall.
27
What is the etiology for appendicitis? 2 possibilities?
Idiopathic. Fecalith obstruction of cecum or twisting of bowel or appendix.
28
What is the patho for appendicitis?
Appendix lumen obstruction blocks drainage and blocks cecum which results in mucus being secreted into lumen and increases intraluminal pressure. Intraluminal pressure exceed venous and eventually arterial pressure. Then tissue becomes ischemic and eventually necrotic. Bacteria then enters wall from fecal matter and causes infection and inflammation.
29
How does pain progress throughout appendicitis?
Acute epigastric pain moves to periumbilical region, it increases and then becomes colicky over 12 hours and localizes to LRQ and becomes rebound pain.
30
What 4 manifestations are there for appendicitis?
Inc WBC, inc temp, N and V, severe pain.
31
How is appendicitis diagnosed?
US, CT, Px.
32
What are the 5 treatments for appendicitis?
IV abx, IV fluids, pain meds, anti inflm, and appendectomy (if necessary must be done within 24-48 hours)
33
What 2 conditions comprise IBD?
Chrons and ulcerative colitis
34
What are the 2 etiologic factors for IBD?
Genetic susceptibility + environmental trigger = complex trait, IR against normal gut flora (not autoimmunity).
35
What is the patho for IBD if the etiologic factor is an inappropriate IR toward normal gut flora?
IR targets bacteria on gut lining resulting in inflammation which also destructs gut lining.
36
Which disease is this? Terminal ileum most commonly affected, granulomatous skip lesions present, submucosa primarily affected.
Chron disease.
37
Which disease is this? Begins in rectum and spreads proximally. Primarily involves mucosa of colon and rectum. Continuous lesions.
Ulcerative colitis.
38
What happens to the inflamed tissue in ulcerative colitis?
It becomes thickened and hardened.
39
Development of cancer, and rectal bleeding/bloody diarrhea are common in UC or CD?
Ulcerative colitis.
40
Fistulas, strictures, and perianal abcesses are common in UC or CD?
Chrons disease.
41
What are 3 manifestations of Chron disease?
Weight loss (due to decrease absorptive area), intermittent abdominal pain, and diarrhea (increased peristalsis and exudate in lumen)
42
What are 3 manifestations of ulcerative colitis?
Bloody diarrhea, intermittent abdominal pain, weight loss (decreased appetite)
43
What 4 important diagnostics/diagnostic considerations are there for IBD?
Exclude viral/bacterial/parasitic/fungal GI infection, colonoscopy, sigmoidoscopy, biopsy.
44
If IBD is mild, what might a possible treatment be?
Diet modification.
45
If IBD is moderate-severe, what treatment will be done? What treatment will be done if pt is non-responsive to one of the previous treatment? What treatment might slow the progression of BD? What is a final treatment option if pt is not responsive to any drugs?
Sulfasalazine (anti-inflm). Steroids. Methotrexate. Surgery.
46
What two things must be in place for herniation to occur?
Weakened retaining structure (via injury, ageing, congenital defect) and increased intra abdominal pressure (via pregnancy or obesity).
47
Sliding hiatial hernia: what portion of stomach enters TC? Where is the GEJ? What are the 3 manifestations?
Upper part of stomach and GEJ enter TC. Pain (organ constriction), heart burn, reflux.
48
Rolling/paraesophageal hernia: what portion of stomach enters TC? Where is the GEJ? What are 2 manifestations?
Non-upper part of stomach in TC. GEJ is below diaphragm. Chest pain (impacting lung) and fullness after eating small meals.
49
What are 3 treatment options for symptomatic hernias?
Lifestyle modifications, behavioural modifications, diet modifications, drugs for reflux (antacid, PPI, H2RA), surgery.
50
What 2 things does fundoplication accomplish?
1. Increases the GEJ size so it cannot move upward and 2. wraps fundus around GEJ which fortifies cardiac sphincter.
51
What is an inguinal hernia?
Weakening of aperture in which vas deferens, BVs and others pass through.
52
Which organs protrude through the inguinal ring? What forms the hernia sac?
Intestine and omentum. The peritoneum forms the hernial sac.
53
By surgically reducing the hernia, what 2 things are accomplished?
1. Intestine and mesentery put back into normal place and 2. Tighten inguinal ring.
54
What is a direct hernia?
Herniation through a retaining structure ie. muscle.
55
What is an indirect hernia?
Herniation through an already existing aperture.
56
Which part of the GIT is most commonly affected by PUD? And which layer of the GIT is most commonly affected?
Duodenum. Mucosa.
57
What is the etiologic factor contributing to PUD? What two things does this etiologic factor do to remain in the GIT? What occurs once the etiologic factor has settled in the GIT?
Helicobacter pylori infection. Attaches to epithelial cells with adhesion proteins. Secretes urease to break down urea into HCO3 to neutralize stomach acid in area of niche. Hypergastrinemia - bacteria stimulate host cells to secrete gastrin... results in increase acid secretion.
58
What are 5 risk factors of PUD?
HCl and biliary acids, steroid and NSAID use, chronic gastritis, smoking ETOH and caffeine, stress.
59
What is the patho for PUD?
H. pylori infection results in inflammation and tissue damage to mucosa. Increase gastrin production results in an increased acid secretion which contributes to tissue damage.
60
What are 3 of our body's defensive mechanisms in the GIT?
Regulate acid secretion, regeneration of new epithelial lining, intact perfusion
61
What are 2 manifestations of PUD?
N and V, abdm burning or cramping pain.
62
What are 3 complications of PUD?
Perforation leading to peritonitis, hemorrhage, gastric obstruction due to edema, spasm, or scar tissue contraction.
63
What 5 ways is PUD diagnosed?
UBT, fecal Ags, endoscopy, rule out other diseases, Ab serology.
64
How is PUD treated?
Triple regimen. H2RA (Zantac) or PPI (Losec) + amoxil and biaxin.
65
What are the 3 etiologic factors for hepatitis? Which factor is most common?
Microbial infection (viral, bacterial, fungal, parasitic), hepatotoxic drugs, autoimmunity. Most commonly viral infection.
66
Which form of viral hepatitis(') is most common?
A B C
67
Hep A: MOT? Incubation period? Acute or chronic? Mild or severe? Carrier state?
Fecal-oral route. 15-50 days. Acute. Mild. No.
68
Hep B: MOT? Incubation period? Acute or chronic? Mild or severe? Carrier state?
Sexually, saliva. 28-160 days. Sometimes chronic form develops (not super common). More severe. Sometimes carrier state.
69
Hep C: MOT? Incubation period? Acute or chronic? Mild or severe? Carrier state? Often leads to?
Blood and blood product, sexually. 15-160 days. Most commonly chronic. Severe. Yes. Cirrhosis.
70
What are the 2 mechanisms of patho for all types of hepatitis? What is damaged? What is released by the hepatocytes upon damage? How long for complete recovery from acute forms?
1. Viral injury leads to necrosis of hepatocytes. 2. IR leads to inflammation and further necrosis of hepatocytes. Hepatocytes, BVs, ducts are all damaged. ALT/AST enzymes released. 4 months (16 wk).
71
What are the 3 phases of manifestations in hepatitis?
Prodromal, clinical, recovery.
72
What 6 manifestations occur during the prodromal phase in hepatitis?
Lethargy, myalgia, fever, abdominal pain (liver enlargement results in stretching of liver capsule), anorexia, N and V.
73
What 4 manifestations occur during the clinical phase of hepatitis?
Jaundice, pruitis (bile salt deposition in skin), hepatomegaly, tender liver on palpation.
74
What occurs during the recovery phase of hepatitis?
Acute manifestations subside in approx. 3 wk. Full recovery in 16 wk.
75
What 4 treatment methods are used for hepatitis?
Bed rest (reduce energy requirement), small meals with high calories and low fat (reduce need for bile production), no hepatotoxic substances, symptomatic treatment (pruitis, pain).
76
What are prophylactic measures for hep A/B? Hep C?
A/B: gamma globulins, vaccine. C: no vaccine available, antiviral drugs.
77
Is autoimmune hep a acute or chronic form? What is the etiology for it?
Chronic. Idiopathic, complex trait (HLA gene mutation chromosome 6 + enviro trigger - chemical/viral agent)
78
T1 autoimmune hep: common/not common? Who does it occur in more commonly? Which abs inflict damage?
More common of the two. Occurs in females under 40 more commonly. Anti-nuclear abs and anti-smooth muscle abs (target BV wall and duct wall)
79
T2 autoimmune hep: common/not common? Who does it occur in more commonly? Which abs inflict damage?
Not as common. 2 - 14 yr. Anti-cytosol abs and anti-microsomal abs.
80
How is autoimmune hepatitis diagnosed? What must be excluded?
Excessive increase in abs involved in either type. Viral hep and other diseases of the liver.
81
How is autoimmune hep treated? What must be done if the primary treatment doesn't work?
Immunosuppressant drugs. Liver transplant.
82
Cirrhosis is _____ liver failure
End stage.
83
What are the 6 etiologic factors for cirrhosis?
Alcohol abuse, hep, hepatotoxic drugs, biliary disease, metabolic disorder (hemochromatosis - ++ iron deposit in lvier), cryptogenic (idiopathic)
84
What is the patho for cirrhosis? What are three issues that arise from the patho?
Hepatocytes detr. and when cells regen. fibrous scar tissue forms around cells resulting in a "nodular liver". 1. vessels become constricted from scar tissue resulting in impeded perf. and portal HTN - increasing HP - fluid shifts into surrounding tissue and abdominal cavity - ascites. 2. duct constriction - bile flow impeded - bile stasis. 3. decreased metb waste clearance - toxicity
85
What are 4 manifestations of cirrhosis? What is another that does not always occur in each case?
Anorexia, weakness, wt loss, hepatomegaly. Jaundice doesn't always occur.
86
What are 5 complications of cirrhosis?
Portal HTN, ascites, varices, GI bleeds, splenomegaly.
87
What number reflects portal HTN? What is normal?
>12 mmHg. 5 - 10 mmHg.
88
What is the etiology for portal HTN? What are the three areas called to determine the area of etiologic factor causing portal HTN?
Cirrhosis. Pre - intra - and post- hepatic.
89
What is a major complication of portal HTN? Other 3 complications?
Rupture varix (dilated associated vein - esophageal vein). Ascites, portosystemic shunt, splenomegaly (from congestion, excess of heme).
90
What is ascites?
Accumulation of fluid in the abdominal cavity.
91
What are the 4 etiologic factors for ascites?
Cirrhosis and portal HTN, severe change in OP or HP, RS heart failure, H2O and Na retention.
92
What are 2 manifestations of ascites?
Abdominal organ distention and dyspnea (diaphragm pushes against pressure in abdominal cavity)
93
What is the treatment for small volume (5L) ascites?
Small vol: diuretic, fluids and electrolytes. Large vol: paracentesis and albumin simultaneously.
94
Liver failure: acute or chronic?
Can be both.
95
What is 1 etiologic factor for chronic liver failure and 2 etiologic factors for acute liver failure? What does fulminant mean?
Cirrhosis. Fulminant hepatitis and toxic liver damage. Fulminant = any condition that arises acutely and severely.
96
How does liver failure affect hematology? In what 4 ways?
Impaired clotting and anemia due to: 1. impaired protein synthesis (ie clotting factors and fibrinogen). 2. depressed bone marrow fx - thrombocytopenia and leukopenia (needs protein for resources - protein synth is impaired). 3. inadequate clearance of clotting factors. 4. GI bleeds (ruptured varices and no clotting)
97
In what 4 ways is metabolism affected in liver failure?
1. inadequate bilirubin clearance (jaundice). 2. hypoalbuminemia (leads to ascited and edema). 3. hyperammonemia (defective urea cycle). 4. hyperestrogenism (decreased estrogen catabolism)
98
How does hepatorenal syndrome come about in liver failure? What are two consequences of this?
Severe decrease in renal perf. due to portal HTN (engorged with blood) and other areas of body lack blood AND ascites results in a decreased circulating blood volume = kidneys underperfused. Oligura and azotemia.
99
What causes hepatic encephalopathy (three things)? What is this? Early manifestations? Late?
Azotemia (build up of nitrogenous waste product in blood), liver impairment, and portosystemic shunts. Neurologic manifestations of liver failure, ammonia converted to glutamate which alters neurotransmission and dehydrates brain tissue (d/t increased osmolarity [glutamate]). Early: hyperreflexia and asterixis. Late: confusion, coma, death.
100
What 5 treatment methods are used for liver failure?
Treating complications and manifestation. Reverse the cause. Purgative (remove all protein from GIT to reduce ammonia production). Non-absorptive abx (destroy all bacteria that breakdown compounds into toxins that would otherwise move into circulation). Liver transplant.
101
What are 4 etiologic factors for cholelithiasis?
Abnormal bile composition, bile stasis (time to precipitate out), inflammatory debris/nucleus (allows for bile components to attach to it - E.coli and Strep. falcalis). ? Genetics
102
What 3 types of gall stones are there? What are their compositions?
Cholesterol stones (bile + ++cholesterol), pigment stones (bilirubin + calcium salts), mixed stones
103
What are 2 manifestations of gall stones?
Colicky, severe, radiating pain and N and V.
104
How are gall stones diagnosed?
US and differential diagnosis (need to exclude many other causes).
105
What are 3 treatments for gall stones?
Pain meds, dissolving agents (contain bile acid), surgery.
106
What are 3 complications of gall stones?
Pancreatitis, perforation and cholecystitis.
107
Pancreatitis is? What is often the cause?
Inflammation of the pancreas. Autodigestion.
108
What are 5 etiologic factors contributing to pancreatitis? What is the most common?
Alcohol abuse, gall stones, idiopathic, pancreatic trauma, drugs. Alcohol abuse most common.
109
What do pancreatic enzymes need in order to be activated? Where does this activation occur in a person without disease?
Bile. Occurs in the duodenum.
110
What is the patho for two ways pancreatitis can occur? (Obstruction and alcohol)
1. Bile flow obstructed - premature activation of pancreatic enzymes - enzymes damage pancreas directly and damage occurs from inflammation too(autodigestion, hemorrhage, necrosis) 2. alcohol increases pancreatic secretion and constricts hepatopancreatic spincter opening into duodenum - bile and pancreatic juice accumulate and mix - congestion occurs - secretions enter pancreas and activate enzymes.
111
What two things does alcohol do that contributes to pancreatitis?
1. Increases pancreatic secretion and 2. constricts hepatopancreatic spincter allowing bile and pancreatic ducts to empty into duodenum.
112
When do pancreatitis manifestations appear? What often brings on the appearance of manifestations? Are the manifestations local or systemic? What are the 2 manifestations? What is a concern(s) that might develop if manifestations are not addressed quickly enough?
Very quickly. After a large meal or alcohol binge. Systemic manifestations affecting other organs. Severe abdominal pain in epigastric region that radiates into back/chest and ascites (massive third spacing due to inflammation). Hypovolemic shock and vasculature collapse are concerns.
113
How is pancreatitis diagnosed? Which measurement is more effective? Why?
Measurement of pancreatic enzymes in blood (released when cells necrose). Lipase is more effective as it is released only by the pancreas whereas amylase is also released by the salivary glands.
114
What are the 4 treatments for mild pancreatitis? How long is the recovery period?
NPO (stop enzyme production), fluid/lytes, pain meds, correct metabolic abnormality (insulin and glucagon). Approximately 1 week.
115
What are the 3 treatments for severe pancreatitis?
Renal, circulatory and hepatobiliary support. IV opiates. Surgery for gallstones.
116
Are primary or secondary malignancies more common in the liver? Why?
Secondary because the liver is a large organ and is highly vascularized. Also has portal drainage.
117
Hepatocellular carcinoma: primary or secondary tumor? How common is this tumor? Cell of origin? 2 etiologic factors? Manifestations? Prognosis? 2 treatment options?
Primary. 90% of primary liver CA. Hepatocytes. Chronic liver disease (hepatitis C - virus = genetic mutation) and environmental toxins. Manifestations often masked by those of liver failure. Poor prognosis as cancer is advanced by diagnosis. Partial hepatoectomy (early tx) or chemo and radiation (palliative).
118
Cholangeocarcinomas: primary or secondary? How common? Cell of origin? What is this cancer often associated with?
Primary. Not as common. Epithelial cells of bile ducts. Chronic inflammation of the epithelial tissue of ducts.
119
Metastatic (secondary) liver tumors: where does cancer often come from? Manifestations? Prognosis? Treatment?
Colon, breast, or lung CA. Those of liver failure: hepatomegaly, ascites, abdominal pain and anorexia, fever and weight loss. Poor prognosis, death in 3-6 months if intervention not successful. Supportive and palliative treatment.
120
Pancreatic cancer: what is the mortality rate in first year? Who is it more common in? What is the most common form of this CA?
90%. Males, smokers, black people. Adenocarcinoma (duct epithelium).
121
What is the etiologic factor for pancreatic cancer? What are some links?
Unclear. Linked to: smoking, alcohol, DM, pancreatitis, age >50, poor diet/lifestyle.
122
What are 3 manifestations of pancreatic cancer? What are the manifestations usually a result from?
Weight loss, jaundice, abdominal pain. Due to mass/size of tumor rather than decreased function of the pancreas.
123
How is pancreatic cancer diagnosed? Has it metastasized by diagnosis? What are 2 treatment options? Another option if first does not work? What treatment method is NOT useful for this type of CA?
US, CT. Yes. Pain control (IMPORTANT - cannot do much else). Surgery (first approach). If surgery doesn't work then palliative radiation. Chemo not useful.
124
What are 4 risk factors for colorectal cancer?
Chrons, UC, familial adenomatous polyposis, low fibre and high fat diet.
125
Why are vitamins ACE protective factors for colorectal cancer? Aspirin?
Oxygen free radial scavenger (decrease tissue damage). Inhibits synthesis of prostaglandins, prostaglandin involved in signal system that influences cell proliferation and or tumor growth.
126
What occurs in these stages of colorectal cancer? Stage 1, 2, 3, and 4.
Stage 1: tumor invades mucosa and submucosa. Stage 2: tumor infiltrates into (but not through) muscularis externa. Stage 3: tumor invades serosa and regional lymph nodes. Stage 4: tumor penetrates serosa and adjacent organs.
127
What is an early manifestation of colorectal cancer? Late manifestation?
Bleeding. Pain.
128
What are two treatment methods for colorectal cancer?
Surgery. Chemo and radiation (palliative).
129
What 5 diagnostics/exams can be used to diagnose colorectal cancer?
FOBT, sigmoidoscopy, colonoscopy, barium enema, and digital rectal exam.
