TEST 5: GI Flashcards
Functions of GI tract
(Lecture, p.1285)
- Food ingestion
- Propulsion of food/waste from mouth to anus
- Secretion of mucous, water, enzymes
- Mechanical/ chemical digestion of food
- Absorption of digested food
- Elimination of waste
- Immune and microbial protection against infection
What controls the GI tract?
(Lecture)
- Muscle control (chewing, swallowing; defecation)
- Hormonal control through the autonomic nervous system (GI motility, secretion of substances that aid in digestion)
GI anatomy overview
(Lecture)
Upper GI: mouth, stomach, esophagus, duodenum
Lower GI: small and large intestine, colon
Sphincters: between organs that assist in gut compartmentalization
Gut wall: organized into well defined layers that contribute to functions of certain regions
GI blood flow
(Lecture)
Arterial blood supply:
-Celiac artery
-Mesenteric artery
Venous blood supply:
-Flows through the gut to hepatic circulation via portal vein
-Liver blood flow
-From liver via hepatic vein to IVC after detoxification
Hepatic circulation
(Lecture, p. 1304)
-Blood flows through liver sinusoids where reticuloendothelial cells (Kupffer cells) remove toxins, bacteria, and metabolic waste products
In addition to detox:
-Water soluble nutrients are absorbed by gut and hepatic circulation
-Reticuloendothelial cells and reproduces absorb and store the nutrients
-Intermediate chemical processing of nutrients occurs in liver
Countercurrent blood flow in villi
(Lecture)
-Arterial and venous blood vessels are close to each other but with opposite directionality
-O2 diffuses out of arterial blood into venules (shunting) before perfusing villi tips
-With normal blood flow this isn’t a problem but in states of low perfusion villi tips become oxygen decisive and cells die—> decrease absorptive capacity + gut bacterial flora translocate into blood stream (increased infection risk)
Motility disorders- Constipation
(Lecture, p.1319)
-Difficult/ infrequent stooling
-Individualized definitions based on a persons stool patterns (2-3 day- weekly)
Primary:
-Functional: normal motility but difficult to pass stool
-Slow transit: slow colon transit and accumulation of stool in sigmoid colon
-Pelvic floor dysfunction: failure of pelvic floor or anal sphincter muscle relaxation
Secondary:
-Opioid induced, stroke, Parkinson’s, hirschsprung disease
-Manifestations that last 3+ months:
-Straining with stooling, lumpy/hard stools, sensation of incomplete emptying, and/or use of manual maneuvers to facilitate stooling >25% of the time, <3 stools per week
Motility disorders- Diarrhea
(Lecture, p. 1320)
-Less than or equal to 3 loose, watery stools per day
-Categorized as acute, persistent, chronic
-Osmotic: ingestion of high solar substances that pull water in and increase stool weight and volume
-Ions (mag, phosphate)
-sugars (sorbitol)
-lactose
-tube feeding formulas
-Treatment revolves around dietary changes to avoid offending substances
Secretory: increased secretion of chloride or bicarb rich fluids or decreased sodium reabsorption
-infection (e coli, c diff, rotavirus)
-inflammatory bowel disease (UC, crohns)
-Treatment revolves around addressing infectious or hormonal agent
GI bleeding
(Lecture, p. 1322)
-Classified as either upper or lower based on origin of bleed
-Upper: esophageal or gastric varices, Mallory Weiss tear, cancers peptic ulcer, medications
-Lower: polyps, IBD, diverticular disease, cancer, hemorrhoids
Manifestations:
-Increased peristalsis (emesis or diarrhea)
Upper:
-Hematemesis: bloody (fresh bright red), coffee ground (dark, grainy, digested)
Lower:
-Melena: black, tarry, foul smelling stool
-Hematochezia: fresh, bright blood via rectum
-Occult blood: trace amounts in normals appearing stool or gastric secretions
Ulceration
(Lecture, p.1331)
-Peptic ulcer disease: a break in the lining of the esophagus, stomach, or duodenum
-Risks: H. Pylori, ASA and NSAID use, alcohol, smoking, pancreatitis, COPD, obesity, 65+, low socioeconomic status
Gastric ulcers
(Lecture, p. 1333)
-50-70 years old
-Stress increases risk
-Increases risk for cancer
-60-80% are H. Pylori, associated with increased gastric and gastritis
-Pain: intermittent, with food, relieved with antacids
Duodenal ulcers
(Lecture, p. 1331)
-25-50 year olds, family history
-Ulcerogenic drug use increases risk
-H. Pylori 95-100%, increased parietal cell mass and acid production, NOT associated with gastritis
-Pain: intermittent, nocturnal, remission and exacerbation of pain
Inflammatory bowel disease
(Lecture, p. 1336)
-Relapsing, chronic disease
-Prevalent in white and Ashkenazi Jews
-Causes: genes, environment, alteration in epithelial cells, altered immune response to intestinal microflora (T cell mediated)
-Increases risk for developing colon cancers
Ulcerative colitis
(Lecture, p. 1336)
-Risk factors: 10-40 years old, NO family
History, idiopathic
-Patho:
-Continuous lesions common in colon and rectum
-Affects the mucosal layer ONLY
-Manifestations:
-Diarrhea with bloody stools and presence of antineutrophil cytoplasmic antibodies (hallmark of diagnosis)
Crohn’s Disease
(Lecture, p.1338)
-Risk factors: 10-30 year olds, WITH family history
-Patho:
-“Skip” lesion common in ileocecal region, small intestine, and colon
-Affect ENTIRE intestinal wall
-Common to have fistulae, strictures, obstruction
-Manifestations:
-Abdominal pain, mucous diarrhea, abdominal mass, Malabsorption
Irritable bowel syndrome
(Lecture, p. 1340)
-Brain gut interaction with abdominal pain and altered bowel habits
-Risks: youth and middle age, women, also with anxiety and depression
-NO structural or biochemical causes known
-Possible causes: Visceral hypersensitivity, abnormal Motility, post inflammatory, changes in gut microbiome, food allergy, epigenetic
-Manifestations: spectrum of severity of symptoms (pain and bloating, fecal urgency and incomplete emptying but does not impact sleep)
Diverticular disease of the colon
(Lecture, p. 1340)
Diverticulosis: saclike outpouching (hernias) of the mucosal layer of colon through the muscle wall
Diverticulitis: inflammation of diverticula
Risks: older age, genetics, obesity, smoking, lack of activity, NSAIDS, lack of dietary fiber
Manifestations: cramping, diarrhea, constipation, distention, flatulence
-Fever, leukocytosis, LLQ tenderness associated with common location for diverticula to develop
-Treatment: increase dietary fiber, antibiotics if inflamed
Bowel obstructions
(Lecture)
-Anything that blocks normal flow or motility of intestines
Can be:
-Acute or chronic
-Partial or complete
-Intrinsic or extrinsic
-Mechanical (needs surgical intervention) or functional
Common causes:
-Herniation, constriction from adhesion, volvulus, intusseption
Bowel obstruction— large vs small intestine
(Lecture, p. 1326)
Small intestine:
-Leads to distention and decreased absorption with increased fluid accumulation (proximal to obstruction) which causes emesis, dehydration and electrolyte abnormalities
-Presents as colicky pain associated with peristaltic waves
-Once ischemia occurs, pain increases and is more constant
Large intestine:
-Less common, often related to cancer
-Presents with hypogastric pain and distention, bowel sounds usually still present
-Vomiting is considered a LATE sign
Risk with bowel obstruction: Perforation= results from distention and abdominal wall tension that decreases arterial blood flow—> ischemia
Appendicitis
(Lecture, p. 1341)
-Inflammation of the appendix (projection at the apex of the cecum)
-Pathophysiology is unclear
-Manifestations: epigastric or periumbilical pain (increases in intensity over time)
-MAY subside and then RLQ pain with rebound tenderness
-N/ V/ fever
-Treatment : surgery or antibiotics
Cholelithiasis (gallstones)
(Lecture, p. 1353)
-Causes obstruction and inflammation of the gallbladder
-If the obstruction is in the cystic duct = cholecystitis
-Risks: female, obesity, age over 40, on oral contraception, white
-Patho: stones result from impaired metabolism of cholesterol, unconjugated bilirubin, fatty acids, calcium carbonates and phosphates (hepatocytes secrete bile that is super saturated in cholesterol)
Manifestations: asymptomatic until blocking duct, then;
-epigastric pain (30 mins to hours after eating), intolerance of fatty foods
-Vague: heartburn, epigastric discomfort, jaundice
-Obstruction: fever, jaundice
Acute Pancreatitis
(Lecture, p. 1355)
-Inflammation of the pancreas (that is acute or chronic), from mild to severe
-Autodigestion of pancreatic cells that triggers Inflammation
-Risks: obstructive biliary disease, alcoholism, hyperlipidemia, genetics
-Manifestations:
-Pain: constant epigastric pain or mid abdominal
-Fever and leukocytosis
-N/V and abdominal distention
-Jaundice from obstruction of bile duct
-Diagnosis: Elevated amylase and LIPASE, elevated CRP
Chronic pancreatitis
(Lecture)
-Pancreatic tissue is replaced by fibrotic and/ or calcified tissue
-Forms cysts, structures and obstructions
-Chronic pain
-Increased risk for pancreatic CA
Pyloric stenosis
(Lecture, p. 1377)
-Developmental disease in kids (males)
-Hypertrophy and hyperplasia of the pyloric sphincter between the stomach and duodenum; obstruction prevents gastric emptying, leading to symptoms
-Thought to be related to increased gastrin release in 3rd trimester of pregnancy (also with family history)
-Presents first week of life to 6 months old
Manifestations:
-Present with projectile vomiting with any food
-Weight loss/ failure to thrive
-Dehydration
-Palpable “olive” mass in right upper quadrant of abdomen
-Repair it with surgery
Anorexia of aging
(Lecture)
-Decrease in appetite/ food intake in older adults with adequate food supply
-Risks: functional impairment, depression, grief, meds
-Patho: decreased energy needs, decrease smell and taste, poor production of saliva, high levels of Ghrelin all decrease food intake—>
Malnutrition, frailty, mitochondrial dysfunction, increase oxidative stress, hormone Imbalance
Acute liver injury vs acute liver failure
(Lecture)
Acute liver injury: severe acute hepatocyte necrosis without hepatic encephalopathy without previous liver disease or cirrhosis
Acute liver failure: acute liver injury + coagulopathy and hepatic encephalopathy
-INR >2x
-ALT > 10 times normal
-Bili > 3
Other considerations: elevated ammonia, Tylenol level, renal failure
Common causes of acute liver failure: Tylenol OD, acute on chronic liver failure (Hep B&C, metabolic liver disease)
Manifestations: anorexia, vomiting, abdominal pain, progressive jaundice—> ascites and GI bleeding
Chronic liver failure (cirrhosis)
(Lecture, p. 1348)
-Irreversible, inflammatory, fibrotic liver disease
-Kupffer cells activate—> release inflammatory mediators—> ROS—> activate fibrotic hepatic stellate cells
-Fibrosis results in destruction of biliary channels and blood flow
-Develops over a parried of years (severity and progression depend on underlying cause)
-Etiology: Viral, autoimmune, genetic, alcohol, NAFLD
Chronic liver failure manifestations
(Lecture)
- Jaundice
- Portal hypertension
- Ascites
- Hepatic encephalopathy
Jaundice
(Lecture, p. 1345)
-Yellow/ green pigmentation of the skin caused by hyperbilirubinemia
-Causes:
-Extrahepatic obstruction of bile (gallstones)
-Intrahepatic obstruction (liver disease- bile canaliculi)
-Prehepatic excessive production (RBC hemolysis)
-Manifestations are a result of bili in systemic circulation:
-conjugated bili is excreted in urine
-stools light in color d/t lack of bile pigment
-extrahepatic— increased risk for bacterial translocation and sepsis
-skin discoloration (sclera FIRST) —> skin xanthoma and pruritis
Portal hypertension
(Lecture, p. 1342)
-High blood pressure in the portal venous system
Prehepatic: thrombosis and narrowing of portal vein
Intrahepatic: vascular remodeling (associated with cirrhosis, hepatitis, parasitic infections)
Posthepatic: hepatic vein thrombosis or right sided heart failure
Long term complications:
-Varices
-Splenomegaly
-Hepatopulmonary syndrome (asymptomatic hypoxia related to intrapulmonary vasodilation and shunting)
Ascites
(Lecture, p. 1344)
-Accumulation of fluid in the peritoneal cavity (complication of portal hypertension)
-Fluid builds up in peritoneal cavity with no way to get out (decreases intricacies fluid volumes)
-Caused by: cirrhosis, right heart, nephrotic syndrome, malnutrition
-Splanchic vasodilation—> decrease SVR—> triggers RAAS to increase ADH—> fluid retention and shifting
-Increased risk for: peritonitis with translocation of gut bacteria
Hepatic encephalopathy
(Lecture, p.1345)
-Impaired behavior, cognition, or motor function associated with advanced liver disease
-Results from: alteration in neurotransmitters and increased neurotoxins in circulation
-Ammonia is typically worst offending agent due to mechanism of cerebral metabolism (results in cytotoxic edema, changes to BBB, increased GABA—> reduced LOC)
-Manifestations: change in LOC, hand tremor (asterixis), slow speech, bradykinesia, stupid, seizure, coma
Alcoholic liver disease
(Lecture, p. 1348)
-Relates to amount and duration of alcohol ingested and acetyldehyde
-Spectrum steatosis—> alcoholic hepatitis—> alcoholic cirrhosis
-Malnutrition from alcohol abuse increases severity risk
-Patho:
-increased fat deposition in hepatocytes—> oxidative stress with lipid peroxidation and permanent hepatocyte injury
-Acetyldehyde inhibits liver metabolism + auto antibodies to hepatic cells + increased bacterial translocation—> inflammation and cell injury
Hepatitis A
(Lecture, p. 1351)
-Fecal/ oral transmission
-4-6 week incubation
-Anti-HAV IgM antibodies develop within 4 weeks—> IgG antibodies stay elevated for years
-LEAST SEVERE, chronic form
Hepatitis B
(Lecture)
-Serum + sexual transmission
-6-8 week incubation
-Vaccine preventable
-Can be transmitted from mother to baby
-Hep B surface antigen indicates positive for active infection
Hepatitis C
(Lecture)
-Serum + sexual transmission
-6-8 week incubation
-Anti-HCV IgG elevated
-HCV PCR positive indicates active infection
-High rates of undiagnosed infection, leads to cirrhosis (leading cause after ETOH)
Hepatitis phases
(Lecture)
-Usually presents with an elevated ALT and AST
- Prodromal phase:
-Starts within 2 weeks of expose
-Have flu like illness
-Ends with presence of jaundice - Icteric phase
-Lasts 2-3 weeks
-Liver enlarges
-Other non abdominal symptoms improve - Recovery phase
-6-8 weeks post exposure
-Begins with resolution of jaundice
-LFT’s normal by 12 weeks - Chronic phase
-HBV, HCV carrier
-Persistent manifestations of liver inflammation
-Predisposition to cirrhosis and liver carcinoma
Neonatal Jaundice
(Lecture)
- Transient and benign first week of life
(Determined based upon serum level per hours of age)
-Risks: ABO and Rh incompatibility, prematurity, breastfeeding, maternal age, male, delayed meconium passage, birth trauma
-Patho:
-Increased bili production (hemolysis)
-Impaired hepatic uptake or excretion of unconjugated bili
-Delayed maturation of liver conjugation mechanisms
-Risk of NOT treated:
Kernicterus (toxic deposition in brain cells)
-Treatment: phototherapy
Upper GI tract structures
(AO)
-Mouth
-Pharynx
-Esophagus
-Stomach
-Duodenum
Lower GI tract structures
(AO)
-Jejunum and Ileum
-Cecum
-Colon
-Rectum
-Anus
Hepatoportal circulation anatomy
(AO)
-Main vessel is the portal vein (which carries nutrient rich blood from the digestive organs and spleen directly
To the liver)
-Liver receives 75% of blood supply from portal vein and 25% from hepatic artery
-Hepatic veins: after being processed in the liver, blood leaves thru the hepatic veins (they then drain into inferior vena cava)
Effects of aging on the GI tract
(AO)
-Oral cavity: tooth enamel thins, gums recede, taste buds decrease, dry mouth
-Esophagus: reduced motility, weakening of sphincter (gerd)
-Stomach: decreased stomach acid production, delayed gastric emptying
-Small intestine: decreased absorption of nutrients, deceased lactase production
-Large intestine (colon): constipation, diverticulosis
-Rectum and anus: decreased sensation, pelvic floor changes
-Liver and pancreas: metabolism changes, decreased pancreatic enzymes
Small intestine disorders
(AO)
-Celiac: immune reaction to gluten
-Crohns: often affects terminal ileum
-Infections: Giardia (cause malabsorption)
-Small intestinal bacterial overgrowth (SIBO): excess bacterial growth interfering with nutrient absorption
Manifestations: malabsorption and steatorrhea, diarrhea, pain, weight loss
-Patho: damage to intestinal mucosa reduces effective digestion, chronic inflammation, autoimmune damage
Large intestine disorders
(AO)
-Ulcerative colitis: chronic inflammatory condition limited to colon and rectum
-Diverticulosis/ litis: formation of diverticula
-Colorectal cancer: malignant changes In colonic epithelium
Manifestations:
-Pain, diarrhea, rectal bleeding, constipation, altered bowel habits
Patho:
-Ulcers and strictures that cause inflammation, altered motility and pressure, neoplastic changes
Clinical manifestations of liver injury
(AO)
-Spider angiomas and palmar erythema: due to increased estrogen levels
-Gynecomastia in males: hormonal imbalances
-Coagulopathy: due to reduced synthesis of clotting factors
-Muscle wasting and edema: result of altered protein synthesis and metabolism
Viral hepatitis
(AO)
-Refers to liver inflammation caused by distinct hepatitis viruses, primarily A, B, C,D, E
Manifestations: start with nonspecific symptoms, move to jaundice, dark urine, pale stools
Patho: acute inflammation attack of hepatocytes, viral replication
M
Transmission of different Hepatitis versions
(AO)
A: fecal- oral (often contaminated food or water)
B: infectious body fluids (blood, semen, saliva)
C: blood to blood contact
D: requires the presence of HBV to propagate (satellite virus)
E: similar to HAV, transmitted fecal oral (in areas of poor sanitation)
Hepatitis Labs
(AO)
Hep A:
-Anti-HAV IgM= recent infection
-Anti-HAV IgG= indicates past infection/ vaccination or immunity
Hepatitis B:
-HBsAG= active infection
-Anti- HBs= indicates immunity or recovery
-Anti-HBc= previous ongoing infection
-HBV DNA= indicates viral replication and infectivity
Hep C:
-Anti-HCV= indicates exposure
-HCV RNA= active viral replication and infection
Hep D:
-Anti-HDV= recent infection
-HDV RNA= active replication
Hep E:
-Anti- HEV IgM= active or recent infection
-Anti HEV IgG= past infection or immunity
Cholecystitis
(AO)
-Gallbladder inflammation
-Risk factors: gallstones, female, infection
-Etiology: most often caused hby gallstone obstruction leading to inflammation
-Chronic: results from repeated episodes of biliary colic or inflammation due to gallstones
-Manifestations: severe RIGHT upper quadrant pain (can radiate to right shoulder or back)
-Patho: obstruction and inflammation, ischemia, infection, edema
Esophageal cancer
(AO)
Risk factors: tobacco, ETOH, Barrett’s esophagus, obesity, diet, men over 60
-Etiology: 2 main types
Adenocarcinoma: Barrett’s esophagus
Squamous cell: smoking and ETOH (occurs higher in esophagus)
-Manifestations: dysphagia, weight loss, chest pain, hoarseness, cough
-Patho: chronic irritation from reflux, normal squamous cell change to columnar epithelium, tumor growth and invasion
Colon cancer
(AO)
-Risks: >50, family history, genetics, diet, lifestyle factors, inflammatory bowel disease
-Etiology: originates from adenomatous polyps (benign precursors), genetics
-Manifestations: changes in bowel habits, blood in stool, abdominal pain,
Weakness, fatigue, unexplained weight loss
-Patho: begins with genetic mutations in epithelial cells lining the colon, then adenomatous polyps to tumors
Pancreatic CA
(AO)
-Risks: smoking, chronic pancreatitis, diabetes, obesity and diet, family history and genetics
-Etiology: adenocarcinomas arising from ducts epithelial cells, genetic mutations (KRAS, p16)
-Manifestations: Jaundice, abdominal pain, weight loss and anorexia. New onset diabetes, steatorrhea
-Patho: genetic mutations leading to uncontrolled cell growth, tumors invade locally and metastasize early (usually to liver), fibrotic reactions surround tumors which complicates treatment
Intussception
(AO, p. 1382)
-The telescoping of a proximal segment of intestine into a distal segment, causing an obstruction
-Risks: 6mo-3 years old, post viral infections, congenital conditions like Meckels diverticulum
-Etiology: often idiopathic, but can be triggers by a polyp or diverticulum
-Manifestations: sudden onset abdominal pain, vomiting, “currant jelly”
Stools (blood and mucous), sausage shaped abdominal mass in right upper quadrant
Hirschsprung’s disease
(AO, p.1379)
-Congenital aganglionic megacolon (functional obstruction of the colon)
-Risks: mutations like RET proto-oncogene, males, family history
-Etiology: absence of ganglion cells I the distal colon that leads to a lack of peristalsis in that segment
-Manifestations: delay in meconium passage, chronic constipation, enterocolitis
-Patho: absence of ganglion cells leads to a function obstruction because effected bowel cannot relax and move stool forward
-Results in dilation of proximal colon (megacolon) and potential complications like enterocolitis
