GI Disorders Flashcards
Diverticulosis…
entry to out pouch is patent, asymptomatic
Why would a fever occur without the presence of exogenous pyrogens?
Injured or abnormal cells induce production of endogenous pyrogens
Tx for diverticular disease
address etiologic/risk factors, if complications occur tx, inflammation, sx. for obstruction or perforation
Irritable Bowel Syndrome (IBS) is what kind of GI disorder
MOTILITY
Are there abnormal structural or functional components in IBS?
None obvious.
What layers are involved in diverticular disease?
Mucosa herniates through muscular externa
Etiologic factors for IBS
Usually triggers (diet, stress, smoking, lactose, etc)
1st Patho theory for IBS (re: malabsorption)
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
2nd Patho theory for IBS (re: serotonin)
- 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)
Serotonin’s fx within the GIT
facilitates motility, secretion, perfusion, and pain
What must be excluded when diagnosing IBS?
Organic disease.
What 2 factors contribute to an out pouching to occur?
Increased intraluminal pressure & a weakened entry point
Etiology/Risk factors for diverticular disease
Poor diet (low fibre), inactivity, poor bowel habits (constipation, aging
Pharma Tx for IBS
antispasmodic drugs (to address peristalsis problem) EG. MODULON
antidiarrheals/laxatives
Abx (to lower normal gut flora causing flatulence)
Where can outpuchings occur in Diverticular Disease? Usually where?
Anywhere in the GIT. Sigmoid colon
How do the etiologic factors work within the peritoneum?
Must enter the peritoneal cavity via
- PERFORATED ULCER
- RUPTURED APPENDIX
Peritoneum is highly vascularized. This leads to…
Rapid absorption of bacterial toxins
What causes ileus in peritonitis?
SNS compensation to limit GI motility
Mnfts of diverticulitis
dull pain, nausea, vomiting, low grade fever
Diverticulitis…
entry to out pouch is strangulated. Inflammation and mnfts
Fluid shift from peritoneal cavity into bowels leads to…
Mucoid stools and increased intraluminal pressure
What leads to hyperemia in peritonitis?
Altered perfusion, vasodilation, and blood shunting d/t serious inflammation
What mainly leads to fluid shifts and the potential for hypovolemia in peritonitis?
Fluid shifting into the bowels and the peritoneal cavity (as exudate)
Tx for peritonitis
IV Abx
fluids and electrolytes
pain management
sx if indicated
Appendicitis is…
inflammation of the appendix WALL
Etiologic factors of appendicitis
Entry to appendix obstructed by:
- fecalith
- twisted appendix/bowel
Non Pharma Tx for IBS
Eliminate trigger, decrease stress.
Ethology of Peritonitis
Bacterial (E.Coli)
Chemical (HCl, bile, pancreatic juice)
When drainage of cecum is blocked in appendicitis, this leads immediately to…
Mucous secretion, which increases intraluminal pressure
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
Once necrosis of the appendix wall occurs…
Bacteria within the appendix enter the wall, causing inflammation and infection
How does the course of pain look in appendicitis
PERIUMBILICAL PAIN ~12 hrs (pain increases, colicky, dull pain) LRQ PAIN (rebound pain)
Tx for appendicitis
IV fluids, Abx, analgesics, appendectomy (w/i 24-48 hrs, or perforation and sub sequential peritonitis can occur)
Thick exudate formed in peritonitis is good because..
Limits Spread
Seals up perforation
Inflammatory Bowel Disease (IBD) includes which 2 diseases?
Crohn’s Disease & Ulcerative Colitis
Ethology for IBD
environmental trigger (bacterial infection) & genetic susceptibility
Which area of the GIT is most affected in Crohns?
Ileum of small intestine
Which area of the GIT is most affected in UC?
Colon & rectum
manifestations of IBS
abdominal discomfort, pain, diarrhea/constipation, flatulence, nausea, mucoid stool
Which layer of the GIT is affected in UC?
mucosa
Granulomatous skip lesions are characteristic of…
Crohn’s disease
Which kinds of lesions are present in UC?
Continuous ulcerative lesions
Diarrhea is present in both UC and C? T/F?
T
Bleeding occurs in UC/C?
UC
Are those with Crohns or UC more likely to develop strictures/fistulas?
Crohns
Development of CA is most common in which IBD?
Ulcerative Colitis
What happens to the ulcerations in UC?
They harden and thicken.
Inflammation in UC leads to what in the lumen?
Exudate moving into the bowel, leading to edema/congestion.
What direction of spread do the lesions in UC follow?
Proximal to distal (anus to gut)
Why does dyspnea occur in peritonitis?
Pt is in ++ pain, will not want to irritate abdomen further by breathing
Why does weight loss occur in UC?
There is an impediment in the bowel
First line tx for IBD
SULFASALAZINE (antiinflammatory) & ABX
What other pharmacologic interventions are given if IBD not responsive to first line tx?
Steroids Immunomodulatory drugs (METHOTREXATE)
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)
Sliding Haitial Hernia
- What enters the thoracic cavity?
- mnfts?
- GEJ & upper part of stomach
- pain, heartburn, reflux
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)
Fundoplication
- for what disorder?
- what 2 benefits?
- Haitial hernias
- increases GEJ size (lowers chance of moving) and fortifies cardiac sphincter (to decrease reflux)
Inguinal Hernia
- organs protrude through what?
- usually contains…
- what forms hernial sac?
- Inguinal ring into scrotum
- intestines & momentum
- peritoneum
What other mnfs besides pain accompany appendicitis?
Nausea, vomiting, increased WBCs
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
Indirect Hernia…
Herniation through existing aperture
Peptic ulcer disease usually affects which area and layer …
Duodenum & Stomach, mucosa layer
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
Risk factors for PUD
Stress, HCl/biliary acids, NSAIDS, smoking, chronic gastritis
What defences does the body have against gastric secretion?
- regulates HCl sec
- perfusions takes away toxins and brings defence
- epithelial lining regenerates itself
Why will there be nutritional deficiency and weight loss in Crohns?
Loss of absorptive area d/t inflammatory damage (S.I.) = decreased absorption.
Manifestations of PUD?
abd pain, nausea/vomiting
Potential complications of PUD
perforation = peritonitis
damaged BVs = hemorrhaging
gut obstruction from scar tissue/edema/spasm
3 unique tests for PUD
Serology (for Abs against HP)
UBT
Fecal Ag (surface markers on HP)
Etiology for hepatitis
Microbial infection (usually virus)
Hepatotoxins
Autoimmunity
Which layer of the GIT is affected in Crohns?
submucosa
Tx for PUD
Why these drugs
Triple regimen
- PPI/H2RA + 2 Abx
PPIs block H sec
H2RA block histamine, needed for HCl sec
HEPATITIS B
- severity
- MOT
- incubation period
- carrier state?
- more severe, some chronic cases
- saliva/serum
- 28- 160 days
- carrier state possible
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)
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)
Examples of drugs used for PUD
PPI: Losec
H2RA: Zantac
Abx: Amoxil & Biaxin
Why is there no reflux in a rolling hiatial hernia?
Content is going and staying within stomach
Mnfts during Prodromal Stage of Viral Hepatitis
WHY ABD PAIN?
Lethargy, myalgia, fever, anorexia, nausea, vominting, abd pain.
Liver swells = liver capsule stretched = pain
Direct Hernia…
Herniation through retaining structure
Tx for viral hepatitis?
rest, eliminate hepatotoxic drugs, diet changes, pain/pruritis relief, post exposure prophylaxis
Prophylaxis for Hep A/B
gamma globulins/vaccine
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
Prophylaxis for Hep C
no vaccine, antiviral drugs
Etiology for Autoimmune Hepatitis
complex trait, gene mutations of HLA on Chr 6, environmental trigger (viral infection/chemicals)
Type 1 Autoimmune Hepatitis
affects women
Antinuclear Abs (target nuclear cell components)
Anti-smooth-muscle Abs (target SM of ducts and vessels)
Stage 4 CR CA
metastatic tumors penetrate serosa and adjacent organs
HEPATITIS A
- severity
- MOT
- incubation period
- carrier state?
- mild, self limiting, acute
- oral fecal
- 15-50 days
- NO
Type 2 Autoimmune Hepatitis
young kids (2-14) Anticytosol and Antimicrosome Abs
Dx for Autoimmune Hepatitis
exclude viral hep and other liver disease
there will be increased serum gamma globulins
Colorectal Cancer
Etiology
Risk Factors
Idiopathic
increased age, family hx, IBD, high dietary fat and refined sugars, and inadequate intake of protective macronutrients
High levels of dietary fat contribute to colorectal CA how?
High fat = high synth bile
Bile is converted by bacterial flora into potential carcinogens
Aspirins role in protecting against colorectal CA?
Decreases synthesis of prostaglandin, which can influence cell proliferation and tutor growth
When do manifestations subside? What is this stage called in viral hepatitis?
~3 weeks. Recovery stage
Stage 1 CR CA
tutor limited to invasion of mucosal and submucosal layers
Stage 2 CR CA
tutors goes into but not through muscular externa
When do mnfts occur in CR CA?
CA present for long time before any presentations. Early = bleeding
MNFTS of CR CA
changes in bowel habits, urgency, incomplete emptying.
Tx of CR CA
sx removal
preoperative radiation
postoperative chemotherapy
Cirrhosis is..
end stage liver disease
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
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
Complications of cirrhosis
What is their chance of occurring?
portal HTN, ascites, varices, GI bleeds, splenomegaly
They will always occur
Tx for cirrhosis
maximize hepatocyte regeneration by…
- modifying diet (decrease fat)
- eliminating hepatotoxins
- managing comps as they arise
Portal HTN = ? in mmHg?
> 12 mmHg
Complications of portal HTN
Ruptured varix (eg. esophageal vein) ascites, portosystemic shunts, splenomegaly
Ascites is…
ACCUMULATION of fluid in the abdominal cavity
Stage 3 CR CA
tumor invades serosal layer, regional lymph node involvement
Why dyspnea in ascites?
Fluid opposes movement of diaphragm
Protective macronutrients against colorectal CA
Vit A, C, E.
Free radical scavengers
Dx of CR CA
digital rectal exam, FOBT, barium enema, sigmoidoscopy, colonoscopy
Tx for small volume ascites (
Diuretics Dec. BV = Dec HP HP in cavity > HP in vessel fluid -> vessel Can be excreted
Tx for large volume ascites (>5L)
paracentesis and volume expander (eg. albumin)
Is liver failure acute or chronic?
Can be both
Etiologic factors leading to acute liver failure
toxic liver damage, fulmiant hepatitis
Etiologic factor leading to chronic liver failure
cirrhosis
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
How is metabolism affected in liver failure?
inadequate bilirubin clearance = JAUNDICE
hypoalbuminemia = EDEMA/ASCITES
defective urea cycle = HYPERAMMONEMIA
decreased estrogen catabolism = HYPERESTROGENSIM
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
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.
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
What does hepatic encephalopathy present with?
ASTERIXIS (hand tremors)
HYPERREFLEXIA
confusion, coma, death
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)
Why are purgatives used in liver failure?
potent laxatives = clearance of gut of proteins
no protein = no protein catabolism = no ammonia = aversion of azotemia
Why are non absorbable Abx used in liver failure?
move through gut and are not absorbed, kill bacteria involved in protein breakdown
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
What bacteria contribute to cholelithiasis?
E. Coli and Strep Faecalis
Alter composition of bile and give rise to inflammatory debris for stone formation
Cholesterol Stones
bile components + cholesterol
Pigment Stones
bilirubin + Ca salts
Mixed Stones
made of many different components
What complications can occur in cholelithiasis
cholecystitis, pancreatitis, perforation
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
Is pancreatitis self limiting?
Yes
What is the main problem in pancreatitis?
INflm of pancreas and auto digestion of structural components of it
Etiologic factors pancreatitis
ETOH, gall stones, idiopathic, pancreatic trauma, drugs that inflict injury on the panc
Patho pancreatitis
bile flow obstructed = pre mature activation of pancreatic enzymes = enzymes damage pancreas via autodigestion
When do the mnfts present in pancreatitis
following alcohol binge or a large meal
Where does the pain occur in pancreatitis
epigastric => back and chest
Et/patho of ascites
R sided HF, portal HTN, severe changes in OP/HP, cirrhosis, Na/H20 retention
What tx for mild pancreatitis
NPO, correct metabolic props (insulin/glucagon)
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
What is the best diagnostic test to determine pancreatitis?
measure pancreatic lipase in blood
What tx for cholelithiasis
pain management dissolving agents (contain bile acid. e.g.. ACTIGALL. only if NO obstruction/complications) sx (retrograde endoscopy)
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
What are the risks for Diverticular disease?
ageing, poor diet, inactivity, constipation
What layers herniate in diverticular disease?
mucosa herniates through muscular external
