GI Disorders Flashcards
1
Q
Diverticulosis…
A
entry to out pouch is patent, asymptomatic
2
Q
Why would a fever occur without the presence of exogenous pyrogens?
A
Injured or abnormal cells induce production of endogenous pyrogens
3
Q
Tx for diverticular disease
A
address etiologic/risk factors, if complications occur tx, inflammation, sx. for obstruction or perforation
4
Q
Irritable Bowel Syndrome (IBS) is what kind of GI disorder
A
MOTILITY
5
Q
Are there abnormal structural or functional components in IBS?
A
None obvious.
6
Q
What layers are involved in diverticular disease?
A
Mucosa herniates through muscular externa
7
Q
Etiologic factors for IBS
A
Usually triggers (diet, stress, smoking, lactose, etc)
8
Q
1st Patho theory for IBS (re: malabsorption)
A
Malabsorption of fermentable CHO & polyols. These are processed by gut flora, and the by product is gas, which leads to flatulence experienced by those w IBS
9
Q
2nd Patho theory for IBS (re: serotonin)
A
- Altered CNS regulation of GI sensory & motor fx
- Molecular signalling defect for serotonin (in its synthesis, binding, transmission, etc) which leads to effects linked to serotonins functions (pain on peristalsis, etc)
10
Q
Serotonin’s fx within the GIT
A
facilitates motility, secretion, perfusion, and pain
11
Q
What must be excluded when diagnosing IBS?
A
Organic disease.
12
Q
What 2 factors contribute to an out pouching to occur?
A
Increased intraluminal pressure & a weakened entry point
14
Q
Etiology/Risk factors for diverticular disease
A
Poor diet (low fibre), inactivity, poor bowel habits (constipation, aging
15
Q
Pharma Tx for IBS
A
antispasmodic drugs (to address peristalsis problem) EG. MODULON
antidiarrheals/laxatives
Abx (to lower normal gut flora causing flatulence)
16
Q
Where can outpuchings occur in Diverticular Disease? Usually where?
A
Anywhere in the GIT. Sigmoid colon
17
Q
How do the etiologic factors work within the peritoneum?
A
Must enter the peritoneal cavity via
- PERFORATED ULCER
- RUPTURED APPENDIX
18
Q
Peritoneum is highly vascularized. This leads to…
A
Rapid absorption of bacterial toxins
19
Q
What causes ileus in peritonitis?
A
SNS compensation to limit GI motility
20
Q
Mnfts of diverticulitis
A
dull pain, nausea, vomiting, low grade fever
21
Q
Diverticulitis…
A
entry to out pouch is strangulated. Inflammation and mnfts
22
Q
Fluid shift from peritoneal cavity into bowels leads to…
A
Mucoid stools and increased intraluminal pressure
23
Q
What leads to hyperemia in peritonitis?
A
Altered perfusion, vasodilation, and blood shunting d/t serious inflammation
24
Q
What mainly leads to fluid shifts and the potential for hypovolemia in peritonitis?
A
Fluid shifting into the bowels and the peritoneal cavity (as exudate)
25
Q
Tx for peritonitis
A
IV Abx
fluids and electrolytes
pain management
sx if indicated
26
Appendicitis is...
inflammation of the appendix WALL
27
Etiologic factors of appendicitis
Entry to appendix obstructed by:
- fecalith
- twisted appendix/bowel
28
Non Pharma Tx for IBS
Eliminate trigger, decrease stress.
28
Ethology of Peritonitis
Bacterial (E.Coli)
| Chemical (HCl, bile, pancreatic juice)
29
When drainage of cecum is blocked in appendicitis, this leads immediately to...
Mucous secretion, which increases intraluminal pressure
30
Increased intraluminal pressure by blocked cecum/mucous secretion leads to...
Venous pressure is overcome by IL pressure, cutting off venous supply, then arterial supply. This leads to ischemia and necrosis
31
Once necrosis of the appendix wall occurs...
Bacteria within the appendix enter the wall, causing inflammation and infection
32
How does the course of pain look in appendicitis
```
PERIUMBILICAL PAIN ~12 hrs (pain increases, colicky, dull pain)
LRQ PAIN (rebound pain)
```
33
Tx for appendicitis
IV fluids, Abx, analgesics, appendectomy (w/i 24-48 hrs, or perforation and sub sequential peritonitis can occur)
34
Thick exudate formed in peritonitis is good because..
Limits Spread
| Seals up perforation
35
Inflammatory Bowel Disease (IBD) includes which 2 diseases?
Crohn's Disease & Ulcerative Colitis
36
Ethology for IBD
environmental trigger (bacterial infection) & genetic susceptibility
37
Which area of the GIT is most affected in Crohns?
Ileum of small intestine
38
Which area of the GIT is most affected in UC?
Colon & rectum
39
manifestations of IBS
abdominal discomfort, pain, diarrhea/constipation, flatulence, nausea, mucoid stool
41
Which layer of the GIT is affected in UC?
mucosa
42
Granulomatous skip lesions are characteristic of...
Crohn's disease
43
Which kinds of lesions are present in UC?
Continuous ulcerative lesions
44
Diarrhea is present in both UC and C? T/F?
T
45
Bleeding occurs in UC/C?
UC
46
Are those with Crohns or UC more likely to develop strictures/fistulas?
Crohns
47
Development of CA is most common in which IBD?
Ulcerative Colitis
48
What happens to the ulcerations in UC?
They harden and thicken.
49
Inflammation in UC leads to what in the lumen?
Exudate moving into the bowel, leading to edema/congestion.
50
What direction of spread do the lesions in UC follow?
Proximal to distal (anus to gut)
51
Why does dyspnea occur in peritonitis?
Pt is in ++ pain, will not want to irritate abdomen further by breathing
52
Why does weight loss occur in UC?
There is an impediment in the bowel
53
First line tx for IBD
SULFASALAZINE (antiinflammatory) & ABX
54
What other pharmacologic interventions are given if IBD not responsive to first line tx?
```
Steroids
Immunomodulatory drugs (METHOTREXATE)
```
55
What 2 factors must be in place for a hernia to occur? Some examples of each?
Increased intraluminal pressure (pregnancy, obesity) and a weakened retaining structure (trauma, aging, congenital defects)
56
Sliding Haitial Hernia
- What enters the thoracic cavity?
- mnfts?
- GEJ & upper part of stomach
| - pain, heartburn, reflux
57
Rolling Haitial Hernia
- What enters the thoracic cavity?
- Where is the GEJ?
- mnfts?
- non-upper part of stomach
- below the diaphragm
- dyspnea (lung impacted), fullness after meals (lowered volume of stomach)
58
Fundoplication
- for what disorder?
- what 2 benefits?
- Haitial hernias
| - increases GEJ size (lowers chance of moving) and fortifies cardiac sphincter (to decrease reflux)
59
Inguinal Hernia
- organs protrude through what?
- usually contains...
- what forms hernial sac?
- Inguinal ring into scrotum
- intestines & momentum
- peritoneum
60
What other mnfs besides pain accompany appendicitis?
Nausea, vomiting, increased WBCs
61
What happens at the cellular level in IBD?
IR targets normal gut flora, as well as the lining of the GIT the flora is attached to. There is a loss of tolerance towards the normal gut flora, causing inflammatory damage
62
Indirect Hernia...
Herniation through existing aperture
63
Peptic ulcer disease usually affects which area and layer ...
Duodenum & Stomach, mucosa layer
64
Etiology of PUD
Helicobacter pylori infection.
- attach via adhesion proteins, release urease = bicarbonate = neutralizing acid to live
- mechanism to create ulcer unclear, but bacterial infection = inflammation, and increased acid secretion = tissue damage
- HP stimulates host cell to secrete gastrin = increase HCl sec = hypergastrinemia
65
Risk factors for PUD
Stress, HCl/biliary acids, NSAIDS, smoking, chronic gastritis
66
What defences does the body have against gastric secretion?
- regulates HCl sec
- perfusions takes away toxins and brings defence
- epithelial lining regenerates itself
67
Why will there be nutritional deficiency and weight loss in Crohns?
Loss of absorptive area d/t inflammatory damage (S.I.) = decreased absorption.
68
Manifestations of PUD?
abd pain, nausea/vomiting
69
Potential complications of PUD
perforation = peritonitis
damaged BVs = hemorrhaging
gut obstruction from scar tissue/edema/spasm
70
3 unique tests for PUD
Serology (for Abs against HP)
UBT
Fecal Ag (surface markers on HP)
71
Etiology for hepatitis
Microbial infection (usually virus)
Hepatotoxins
Autoimmunity
72
Which layer of the GIT is affected in Crohns?
submucosa
73
Tx for PUD
| Why these drugs
Triple regimen
- PPI/H2RA + 2 Abx
PPIs block H sec
H2RA block histamine, needed for HCl sec
74
HEPATITIS B
- severity
- MOT
- incubation period
- carrier state?
- more severe, some chronic cases
- saliva/serum
- 28- 160 days
- carrier state possible
75
3 Main Patho points for Viral Hepatitis
IR & viral damage = damage/necrosis = decreased hepatocyte fx
Vasculature & ducts = inflammatory damage
Healing in ~4 months for acute forms (for complete hepatocyte regeneration)
76
Etiologic factors for cirrhosis
```
chemicals (ETOH abuse)
viral damage (Hep C)
drugs (Methotrexate)
Biliary disease
Metabolic disorders (hemochromatosis = overload of Fe, deposit in liver = toxicity)
cryptogenic (=idiopathic)
```
77
Examples of drugs used for PUD
PPI: Losec
H2RA: Zantac
Abx: Amoxil & Biaxin
78
Why is there no reflux in a rolling hiatial hernia?
Content is going and staying within stomach
79
Mnfts during Prodromal Stage of Viral Hepatitis
| WHY ABD PAIN?
Lethargy, myalgia, fever, anorexia, nausea, vominting, abd pain.
Liver swells = liver capsule stretched = pain
80
Direct Hernia...
Herniation through retaining structure
81
Tx for viral hepatitis?
rest, eliminate hepatotoxic drugs, diet changes, pain/pruritis relief, post exposure prophylaxis
82
Prophylaxis for Hep A/B
gamma globulins/vaccine
83
HEPATITIS C
- severity
- MOT
- incubation period
- carrier state?
- worst, most severe, almost all cases become chronic
- blood & sexually transmitted
- 15-160 days
- frequent carrier states
84
Prophylaxis for Hep C
no vaccine, antiviral drugs
85
Etiology for Autoimmune Hepatitis
complex trait, gene mutations of HLA on Chr 6, environmental trigger (viral infection/chemicals)
86
Type 1 Autoimmune Hepatitis
affects women
Antinuclear Abs (target nuclear cell components)
Anti-smooth-muscle Abs (target SM of ducts and vessels)
87
Stage 4 CR CA
metastatic tumors penetrate serosa and adjacent organs
88
HEPATITIS A
- severity
- MOT
- incubation period
- carrier state?
- mild, self limiting, acute
- oral fecal
- 15-50 days
- NO
89
Type 2 Autoimmune Hepatitis
```
young kids (2-14)
Anticytosol and Antimicrosome Abs
```
90
Dx for Autoimmune Hepatitis
exclude viral hep and other liver disease
| there will be increased serum gamma globulins
91
Colorectal Cancer
Etiology
Risk Factors
Idiopathic
| increased age, family hx, IBD, high dietary fat and refined sugars, and inadequate intake of protective macronutrients
92
High levels of dietary fat contribute to colorectal CA how?
High fat = high synth bile
| Bile is converted by bacterial flora into potential carcinogens
93
Aspirins role in protecting against colorectal CA?
Decreases synthesis of prostaglandin, which can influence cell proliferation and tutor growth
94
When do manifestations subside? What is this stage called in viral hepatitis?
~3 weeks. Recovery stage
95
Stage 1 CR CA
tutor limited to invasion of mucosal and submucosal layers
96
Stage 2 CR CA
tutors goes into but not through muscular externa
97
When do mnfts occur in CR CA?
CA present for long time before any presentations. Early = bleeding
98
MNFTS of CR CA
changes in bowel habits, urgency, incomplete emptying.
99
Tx of CR CA
sx removal
preoperative radiation
postoperative chemotherapy
100
Cirrhosis is..
end stage liver disease
101
In a nutshell, what happens that leads to cirrhosis. What primary problems do we encounter?
hepatocytes = necrosis = formation of scar tissue (fibrosis) = nodular liver
decreased liver fx and portal HTN
102
3 Main points for Patho of Cirrhosis
- hepatocytes destroyed and are replaced w non fx fibrinous scar tissue = puts pressure on vessels and become constricted = impeded perfusion
- duct constrictions = impeded bile flow = bile stasis
- decreased metabolic waste clearance = toxicity
103
Complications of cirrhosis
| What is their chance of occurring?
portal HTN, ascites, varices, GI bleeds, splenomegaly
They will always occur
104
Tx for cirrhosis
maximize hepatocyte regeneration by...
- modifying diet (decrease fat)
- eliminating hepatotoxins
- managing comps as they arise
105
Portal HTN = ? in mmHg?
> 12 mmHg
106
Complications of portal HTN
```
Ruptured varix (eg. esophageal vein)
ascites, portosystemic shunts, splenomegaly
```
107
Ascites is...
ACCUMULATION of fluid in the abdominal cavity
108
Stage 3 CR CA
tumor invades serosal layer, regional lymph node involvement
109
Why dyspnea in ascites?
Fluid opposes movement of diaphragm
110
Protective macronutrients against colorectal CA
Vit A, C, E.
| Free radical scavengers
110
Dx of CR CA
digital rectal exam, FOBT, barium enema, sigmoidoscopy, colonoscopy
111
Tx for small volume ascites (
```
Diuretics
Dec. BV = Dec HP
HP in cavity > HP in vessel
fluid -> vessel
Can be excreted
```
112
Tx for large volume ascites (>5L)
paracentesis and volume expander (eg. albumin)
113
Is liver failure acute or chronic?
Can be both
114
Etiologic factors leading to acute liver failure
toxic liver damage, fulmiant hepatitis
115
Etiologic factor leading to chronic liver failure
cirrhosis
116
How is hematology impacted in liver failure?
impaired protein synth = impaired haemostats & anemia
depressed marrow fx (liver cannot supply resources) = leukopenia and thrombocytopenia
inadequate clearance of activated CFs = disseminated intravascular coagulation DIC (liver isn't removing CFs = remain active = clotting w/i BVs)
GI Bleeds
117
How is metabolism affected in liver failure?
inadequate bilirubin clearance = JAUNDICE
hypoalbuminemia = EDEMA/ASCITES
defective urea cycle = HYPERAMMONEMIA
decreased estrogen catabolism = HYPERESTROGENSIM
118
What is hepatorenal syndrome? In which disease does it occur?
Severe decrease in renal perfusion. Portal HTN = blood shunting = decreased perfusion to kidneys = low renal perfusion.
Leads to OLIGURIA (low urine volume) and AZOTEMIA (build up of nitrogenous products in blood)
Liver failure
119
Why does hepatic encephalopathy occur in liver failure?
Toxic compounds are not detoxified by liver d/t liver failure and portosystemic shunts. This leads to a build up of these toxins and their entrance into the systemic circuit out of the hepatic venous circuit.
120
Mnfts during Clinical Stage of Viral Hepatitis
| WHY PRURITIS?
manifestations during prodromal persist and worsen, jaundice, hepatomegaly, tender liver, pruritus
bile salts deposit in skin
121
What does hepatic encephalopathy present with?
ASTERIXIS (hand tremors)
HYPERREFLEXIA
confusion, coma, death
122
Walk me through ammonia conversion in hepatic encephalopathy
ammonia converted to glutamate
increased levels of glutamate = increased solute concentration/altered osmolarity = cellular dehydration/death of brain
increased glutamate also alters neurotransmission (why those with HE present with hyperreflexia, etc)
123
Why are purgatives used in liver failure?
potent laxatives = clearance of gut of proteins
| no protein = no protein catabolism = no ammonia = aversion of azotemia
124
Why are non absorbable Abx used in liver failure?
move through gut and are not absorbed, kill bacteria involved in protein breakdown
125
Etiologic factors contributing to cholelithiasis
abnormal bile composition ( eg. inc cholesterol and dec bile salts)
bile stasis (gives rise to precipitation)
inflammatory debris (nuclei for stone formation)
genetics
126
What bacteria contribute to cholelithiasis?
E. Coli and Strep Faecalis
| Alter composition of bile and give rise to inflammatory debris for stone formation
127
Cholesterol Stones
bile components + cholesterol
128
Pigment Stones
bilirubin + Ca salts
129
Mixed Stones
made of many different components
130
What complications can occur in cholelithiasis
cholecystitis, pancreatitis, perforation
131
Et for portal HTN
pre-hepatic, intra-hepatic, or post-hepatic issue that increases resistance to blood flow in portal system. Mostly d/t cirrhosis
132
Is pancreatitis self limiting?
Yes
133
What is the main problem in pancreatitis?
INflm of pancreas and auto digestion of structural components of it
134
Etiologic factors pancreatitis
ETOH, gall stones, idiopathic, pancreatic trauma, drugs that inflict injury on the panc
135
Patho pancreatitis
bile flow obstructed = pre mature activation of pancreatic enzymes = enzymes damage pancreas via autodigestion
136
When do the mnfts present in pancreatitis
following alcohol binge or a large meal
137
Where does the pain occur in pancreatitis
epigastric => back and chest
138
Et/patho of ascites
R sided HF, portal HTN, severe changes in OP/HP, cirrhosis, Na/H20 retention
139
What tx for mild pancreatitis
NPO, correct metabolic props (insulin/glucagon)
140
Why does hyperammonemia occur in liver failure?
Usually, liver combined ammonia with CO2 to form urea to be excreted as waste. Since the liver is non functional, ammonia cannot be combined into urea, so there is a build up of it in the blood
141
What is the best diagnostic test to determine pancreatitis?
measure pancreatic lipase in blood
142
What tx for cholelithiasis
```
pain management
dissolving agents (contain bile acid. e.g.. ACTIGALL. only if NO obstruction/complications)
sx (retrograde endoscopy)
```
143
How does alcohol contribute to pancreatitis?
It increases pancreatic secretion and constricts the sphincter in pancreatic duct = bile and pancreas secretions accumulate in the ducts = Es activated = congestion = secretions into pancreas = auto digestion and inflam = hemorrhage and necrosis
144
What are the risks for Diverticular disease?
ageing, poor diet, inactivity, constipation
145
What layers herniate in diverticular disease?
mucosa herniates through muscular external
