TEST 5: GI Flashcards

1
Q

Functions of GI tract
(Lecture, p.1285)

A
  1. Food ingestion
  2. Propulsion of food/waste from mouth to anus
  3. Secretion of mucous, water, enzymes
  4. Mechanical/ chemical digestion of food
  5. Absorption of digested food
  6. Elimination of waste
  7. Immune and microbial protection against infection
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2
Q

What controls the GI tract?
(Lecture)

A
  1. Muscle control (chewing, swallowing; defecation)
  2. Hormonal control through the autonomic nervous system (GI motility, secretion of substances that aid in digestion)
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3
Q

GI anatomy overview
(Lecture)

A

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

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4
Q

GI blood flow
(Lecture)

A

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

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5
Q

Hepatic circulation
(Lecture, p. 1304)

A

-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

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6
Q

Countercurrent blood flow in villi
(Lecture)

A

-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)

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7
Q

Motility disorders- Constipation
(Lecture, p.1319)

A

-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

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8
Q

Motility disorders- Diarrhea
(Lecture, p. 1320)

A

-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

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9
Q

GI bleeding
(Lecture, p. 1322)

A

-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

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10
Q

Ulceration
(Lecture, p.1331)

A

-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

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11
Q

Gastric ulcers
(Lecture, p. 1333)

A

-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

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12
Q

Duodenal ulcers
(Lecture, p. 1331)

A

-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

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13
Q

Inflammatory bowel disease
(Lecture, p. 1336)

A

-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

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14
Q

Ulcerative colitis
(Lecture, p. 1336)

A

-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)

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15
Q

Crohn’s Disease
(Lecture, p.1338)

A

-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

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16
Q

Irritable bowel syndrome
(Lecture, p. 1340)

A

-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)

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17
Q

Diverticular disease of the colon
(Lecture, p. 1340)

A

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

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18
Q

Bowel obstructions
(Lecture)

A

-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

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19
Q

Bowel obstruction— large vs small intestine
(Lecture, p. 1326)

A

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

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20
Q

Appendicitis
(Lecture, p. 1341)

A

-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

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21
Q

Cholelithiasis (gallstones)
(Lecture, p. 1353)

A

-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

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22
Q

Acute Pancreatitis
(Lecture, p. 1355)

A

-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

23
Q

Chronic pancreatitis
(Lecture)

A

-Pancreatic tissue is replaced by fibrotic and/ or calcified tissue
-Forms cysts, structures and obstructions
-Chronic pain
-Increased risk for pancreatic CA

24
Q

Pyloric stenosis
(Lecture, p. 1377)

A

-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

25
Q

Anorexia of aging
(Lecture)

A

-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

26
Q

Acute liver injury vs acute liver failure
(Lecture)

A

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

27
Q

Chronic liver failure (cirrhosis)
(Lecture, p. 1348)

A

-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

28
Q

Chronic liver failure manifestations
(Lecture)

A
  1. Jaundice
  2. Portal hypertension
  3. Ascites
  4. Hepatic encephalopathy
29
Q

Jaundice
(Lecture, p. 1345)

A

-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

30
Q

Portal hypertension
(Lecture, p. 1342)

A

-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)

31
Q

Ascites
(Lecture, p. 1344)

A

-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

32
Q

Hepatic encephalopathy
(Lecture, p.1345)

A

-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

33
Q

Alcoholic liver disease
(Lecture, p. 1348)

A

-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

34
Q

Hepatitis A
(Lecture, p. 1351)

A

-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

35
Q

Hepatitis B
(Lecture)

A

-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

36
Q

Hepatitis C
(Lecture)

A

-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)

37
Q

Hepatitis phases
(Lecture)

A

-Usually presents with an elevated ALT and AST

  1. Prodromal phase:
    -Starts within 2 weeks of expose
    -Have flu like illness
    -Ends with presence of jaundice
  2. Icteric phase
    -Lasts 2-3 weeks
    -Liver enlarges
    -Other non abdominal symptoms improve
  3. Recovery phase
    -6-8 weeks post exposure
    -Begins with resolution of jaundice
    -LFT’s normal by 12 weeks
  4. Chronic phase
    -HBV, HCV carrier
    -Persistent manifestations of liver inflammation
    -Predisposition to cirrhosis and liver carcinoma
38
Q

Neonatal Jaundice
(Lecture)

A
  • 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

39
Q

Upper GI tract structures
(AO)

A

-Mouth
-Pharynx
-Esophagus
-Stomach
-Duodenum

40
Q

Lower GI tract structures
(AO)

A

-Jejunum and Ileum
-Cecum
-Colon
-Rectum
-Anus

41
Q

Hepatoportal circulation anatomy
(AO)

A

-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)

42
Q

Effects of aging on the GI tract
(AO)

A

-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

43
Q

Small intestine disorders
(AO)

A

-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

44
Q

Large intestine disorders
(AO)

A

-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

45
Q

Clinical manifestations of liver injury
(AO)

A

-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

46
Q

Viral hepatitis
(AO)

A

-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

47
Q

Transmission of different Hepatitis versions
(AO)

A

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)

48
Q

Hepatitis Labs
(AO)

A

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

49
Q

Cholecystitis
(AO)

A

-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

50
Q

Esophageal cancer
(AO)

A

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

51
Q

Colon cancer
(AO)

A

-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

52
Q

Pancreatic CA
(AO)

A

-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

53
Q

Intussception
(AO, p. 1382)

A

-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

54
Q

Hirschsprung’s disease
(AO, p.1379)

A

-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