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CMT > GI Accessory Organ Pathophys > Flashcards

GI Accessory Organ Pathophys Flashcards

1
Q

Liver Disorders/Enzymes

Liver structure/function

A
  • largest structure in the body
  • dual blood supply (hepatic artery is 20% of supply w/ oxygenated blood; portal vein is 80% of blood & is nutrient rich)
  • 2 lobes divided by the coronary ligament
  • contains R & L hepatic duct which join to form the common hepatic duct which joins with the cystic duct (GB) to form the common bile duct
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2
Q

Liver Disorders/Enzymes

role/function of hepatocytes

A
  • remove and excrete waste/hormones/drugs/toxins (alter them to help urinary excretion) & processes nutrients
  • synthesize plasma proteins (clotting factors)
  • produces immune factors (phagocytes in liver produce acute reactants)
  • produce bile acids for fat absorption
  • excrete bilirubin
  • stores vitamins, minerals, sugars
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3
Q

Liver Disorders/Enzymes

pathophys of bilirubin

A
  • catabolism of hgb –> heme –> biliverdin –> unconjugated bilirubin –> bound to albumin or unbound
  • unconjugated bili: lipid souble, not excreted by renal system
  • unbound bili: taken up by hepatocytes –> conjugated bili/water soluble –> becomes part of bile
  • normal total serum bili: 0.2-1.2 mg/dL
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4
Q

Liver Disorders/Enzymes

flow of bile

A
  • R or L hepatic duct –> common hepatic duct
  • 50% into cystic duct for storage in GB
  • 50% into common bile duct –> emptying into duodenum via sphincter of Oddi
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5
Q

Liver Disorders/Enzymes

pathophys of biliary obstruction

A
  • blockage of bile flow into SI (inability of bilirubin to reach intestinal tract giving stool a pale color)
  • can occur anywhere along path from liver to intestines (most common = gallstones)
  • can lead to jaundice (consequence of bile stasis and buildup on conjugated bili in blood; total serum bili > 3 mg/dL)
  • can lead to bili excretion in urine (normally none in urine)
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6
Q

Liver Disorders/Enzymes

jaundice classifications

A
  • prehepatic: overproduction or impaired uptake by liver leading to unconjugated hyperbilirubinemia
  • hepatic: reduced conjugation (unconjugated hyperbilirubinemia)
  • posthepatic: reducted excretion (conjugated hyperbilirubinemia)
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7
Q

Liver Disorders/Enzymes

Hyperbilirubinemia evaluation

A
  • determine if it is conjugated (direct) or unconjugated (indirect)
  • unconjugated: results from overproduction, impairment of uptake, or impaired conjugation, evaluate for hemolytic anemia
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8
Q

Liver Disorders/Enzymes

describe 4 liver enzymes

A
  • alanine aminotransaminase (ALT): liver specific (40 IU/mL)
  • aspartate aminotransaminase (AST): found in liver, cardiac, and muscle tissue (40 IU/mL)
  • Alkaline Phosphatase (ALK): found in liver, bone, and intestinal tissue (120 IU/mL)
  • Gamma-Glutamyl transpeptidase (GGTP): found in liver (50 IU/mL)
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9
Q

Liver Disorders/Enzymes

how to use liver enzymes to differentiate hepatocellular injury and cholestasis

A
  • hepatocellular injury: elevated AST/ALT
  • Cholestasis: elevated ALK +/- high total bili
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10
Q

Hepatitis

4 phases of classic presentations

A
  1. viral replication (pt is asx but pos serology and enzyme markers)
  2. prodromal (anorexia, n/v/d, malaise, urticaria, pruritis, altered taste, arthralgia, fatigue, cigarette smoke aversion)
  3. icteric (dark urine, pale stools, GI sx persist, malaise, RUQ pain, hepatomegaly)
  4. convalescent (sx and incterus resolve, normal LFTs)
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11
Q

Hepatitis

potential clinical outcomes of HBV

A
  1. resolution (90%)
  2. fulminant (< 1%)
  3. HBsurfaceAg > 6 mo (9%); can lead to resolution, asx carrier, chronic persistent hepatitis, chronic active hepatitis
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12
Q

Hepatitis

what do each of these mean for HBV infection?
* HBsAg
* HBeAg
* Anti-HBc
* Anti-HBe/Anti-HBc

A
  • HBsAg: HBV surface antigen indicating active infection
  • HBeAg: HBV envelope antigen indicating infection is transmissible
  • Anti-HBc: anti-core, indicates infection
  • Anti-HBe/Anti-HBc: immunity
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13
Q

Hepatitis

clinical outcomes of HCV

A
  • recovery (15-20%)
  • chronic infection (80-85%); leading to cirrhosis (can have end stage liver disease and/or hepatocellular carcinoma)
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14
Q

Liver Diseases

progression from normal liver function to cirrhosis

non-alcoholic

A
  • normal liver
  • non-alcoholic fatty liver disease (effects: dyslipidemia, insulin resistance, obesity, metabolic syndrome, T2 DM); caused by lipogenesis
  • non-alcoholic steatohepatitis caused by further inflammation (effects: lipi peroxidation, mitochondrial dysfunction, oxidative stress, apoptosis, pro-inflammatory cytokine activation)
  • cirrhosis: fibrosis of liver (effects: scarring, advanced cell damage)
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15
Q

Liver Diseases

describe caput medusae

A
  • cardinal feature of portal HTN
  • occurs due to cutaneous portosystemic collateral formation between distended and engorged paraumbilical veins which radiate from umbilicus
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16
Q

Liver Diseases

pathophys of cirrhosis

A
  • hepatocyte dysfunction: inability of hepatocytes to perform normal tasks
  • portosystemic shunting: portal vein blood flow not flowing through liver; blood not presented to hepatocytes for filtering
  • portal HTN: obstructed liver blood flow increases pressure and results in blood back up
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17
Q

Liver Diseases

describe use of lactulose as tx of hepatic encephalopathy

A
  • non-absorbable disaccharide syrup
  • digested by colonic bacteria (favors formation of non-absorbable ammonium ion NH4+
  • favors change in bowel flora to reduce ammonia forming organisms
  • can reduce recurrences
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18
Q

Liver Diseases

pathophys of cirrhosis causing ascites

A
  • late stage liver disease
  • extensive liver fibrosis blocks blood flow from portal vein
  • blood then backs up in portal vein leading to portal HTN
  • fluid leaks out of portal vein and into abd
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19
Q

Liver Disease

albumin levels indicating portal HTN in presence of ascites?

A

if serum albumin minus ascitis fluid albumin > 1.1

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20
Q

Liver Diseases

describe use of liver transplant for cirrhosis

A
  • consider transplant when cirrhosis has caused ascites, hepatic encephalopathy, variceal hemorrhage, or hepatocellular dysfunction
  • perform comprehensive PMHx (cardiac, pulm, dental, cancer screening)
  • prioritize based on model of end stage liver disease score (MELD-Na)
  • exclusion criteria: severe pulmonary PTN, extrahepatic malignancies, severe CV/pulm/PV disease, substance abuse, poorly controlled psych illness, no social support
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21
Q

Liver Diseases

describe components of Child-Pugh scoring for cirrhosis

A

Bilirubin (total
* < 2 mg/dL: 1 pt
* 2-3 mg/dL: 2 pts
* > 3mg/dL: 3 pts

Albumin
* > 3.5 g/dL: 1pt
* 2.8-3.5 g/dL: 2 pts
* < 2.8 g/dL: 3 pts

INR
* < 1.7: 1 pt
* 1.7-2.3: 2 pts
* > 2.3: 3 pts

Ascites
* absent: 1 pt
* slight: 2 pts
* moderate: 3 pts

Encephalopathy
* absent: 1 pt
* grade 1/2: 2 pts
* grade 3/4: 3 pts

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22
Q

Liver Diseases

describe scoring of Child-Pugh assessment

A
  • class A: 5-6 pts, 100% survival
  • class B: 7-9 pts, 80% survival
  • class C: 10-15 pts, 45% survival
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23
Q

Gallbladder

anatomy of gallbladder

A
  • small GI accessory organ in RUQ in posterior aspect of R lobe of liver
  • part of biliary system
  • regions: fundus (widest), body, neck
  • cystic duct: carries bile to the common bile duct
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24
Q

Gallbladder

describe bile

A
  • yellow brown/green alkaline fluid formed by the liver (~1 L daily)
  • drains into gallbladder for storage
  • composed of cholesterol, bilirubin, water, bile salts, phospholipids, proteins, electro, bicarb
  • essential for: digesting/emulsifying fats, excreting cholesterol, anti-microbial activity
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25
Q

Gallbladder

describe biliary tree

A
  • series of ducts w/in liver, GB, and pancreas that empty into small intesting
  • components: intrahepatic and extrahepatic
  • flow: Liver –> common hepatic duct –> GB –> cystic duct –> common bil duct –> addition of pancreatic duct to common bile duct –> sphincter of Oddi –> ampulla of Vater –> duodenum
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26
Q

Gallbladder

physiology of GB

A
  • store, concentrate, and releases bile into duodenum via common bile duct
  • signaled by CCK which is relseased by fatty foods/proteins entering the duodenum
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27
Q

Gallbladder

physiology of CCK

A
  • cholecystokinin
  • peptide hormone released by I cells in duodenum and jejunum
  • stimulates smooth muscle of GB to contract and release bile into biliary tree
  • signals sphincter of Oddi to relax
28
Q

Cholelithiasis

why should pts increase vit C?

A

ascorbic acid effects the rate limiting step in the catabolism of cholesterol

29
Q

Pancreas

anatomy

A
  • oblong, glandular GI accessory organ approx 6in long
  • performs exocrine and endocrine functions
  • lies transversely in the retroperitoneum behind the stomach
  • regions: head, neck, body, tail
30
Q

Pancreas

regions/functions of each of the pancreas

A
  • Head: widest part of pancreas, found nestled into curve of duodenum, head proper/uncinate process
  • Neck: thin section of gland between head/body of pancreas
  • Body: middle part of pancreas between neck/tail; SMA/V run behind
  • Tail: thin tip of pancreas in L abd; close to hilum of spleen
31
Q

Pancreas

exocrine and endocrine functions

A
  • Exocrine: acinar cells (secrete pancreatic juice into ducts; cells in clusters located at terminal end of pancreatic ducts)
  • ducts: pancreatic duct joins CBD just before duodenum (amp of Vater) and accessory duct (duct of Santorini) runs from pancreas directly into the duodenum superior to pancreatic duct
  • Endocrine: islets of langerhans which produced insulin, glucoagon, pancreatic polypeptide, and somatostatin
32
Q

Pancreatitis

describe pseudocyst in pancreatitis

A

collection of leaked pancreatic fluids that form next to pancreas

33
Q

Pancreatitis

describe hemorrhagic pancreatitis

A
  • 1% of cases
  • indicator of poor prognosis
  • Gray Turner Sign: ecchymosis of flanks due to blood in retroperitoneum
  • Cullen: ecchymosis of umbilical region due to blood in peritoneum
34
Q

Chronic Pancreatitis

consequences of fat malabsorption due to pancreatitis

A
  • Vitamin ADEK deficiencies
  • A: night blindness
  • D: osteomalacia, hypocalcemia
  • E: neuropathy, hemolytic anemia
  • K: coagulopathy
35
Q

Chronic Pancreatitis

direct vs indirect pancreatic function tests

A
  • Direct: inject exogenous secretin & CCK to stimulate pancreas –> duodenal/pancreatic aspirated measured for bicarb, protease, amylase, lipase
  • Indirect: measure chymotrypsin/elastase in fecal samples to look for exocrine insufficiency
36
Q

Review Questions

most common cause of acute pancreatitis?

A

gallstones

37
Q

Review Questions

high pitched peristalsis/boyborygmi in a pt w/ acute abd pain and distention suggests what?

A

bowel obstruction

38
Q

Review Questions

which elevated labs correlates most closely w/ increased mortality in acute pancreatitis?

A

BUN

39
Q

Pancreatic Cancer

categories

A
  • Endocrine pancreatic cancer (develops from cells in endocrine gland of pancreas)
  • Exocrine pancreatic cancer (develops from ductal or acinar cells of pancreas)
  • cystic neoplasms (can be mistaken for benign cysts)
40
Q

Pancreatic Cancer

what influences risk of pancreatic cancer in pt’s w/ T2 DM?

A
  • Increased risk: insulin use + GLP-1 therapies
  • Reduced risk: metformin + ASA use
41
Q

Pancreatic Cancer

which hereditary conditions can increase risk of pancreatic cancer?

A
  • MEN-1
  • BRCA-1 and BRCA-2 (breast/ovarian cancer syndrome)
  • Familial pancreatic carcinoma
  • Hereditary pancreatitis (PSS1 mutation)
  • Peutz-Jeghers syndrome
  • Lynch Syndrome
42
Q

Pancreatic Cancer

define:
* Courvoisier sign
* Sister Mary Joseph’s sign
* Trousseau Syndrome

A
  • Cour: enlarged, non-tender gallbladder
  • SMJ: hard, palpable nodule bulging into umbilicus
  • Trousseau: recurring, migratory thrombophlebitis; red/tender extremities
43
Q

Pancreatic Cancer

describe Whipple procedure

A
  • procedure of choice when possible
  • resection of pancreatic head, distal stomach, duodenum, GB, and CBD
  • indicated for cancers limited to head ot pancreas, periampullary area, and duodenum
  • after surgery: bile duct attached to SI; remaining pancreas attached to SI; stomach attached to SI
44
Q

Fluid Replacement in Children

why are kids particularly vulnerable to developing dehydration

A
  • higher % of TBW
  • higher insensible water loss
  • elevated metabolic rates requiring more fluid
  • can’t communicate their needs
45
Q

Fluid Replacement in Children

define dehydration

A
  • defined as decrease in TBW
  • includes intracellular and extracellular water loss
46
Q

Fluid Replacement in Children

etiology of fluid loss

A

Excessive Loss
* GI: diarrhea (norovirus, rotavirus), vomiting
* Urinary (hyperosmolar state like DM)
* Increased insensitive loss from evaporation (febrile illnesses, burns, increased resp loss w/ resp loss)

Reduced intake
* anorexia from illness
* lack of access to (clean) H2O
* neglect

47
Q

Fluid Replacement in Children

how does phototherapy (jaundice tx) lead to insensible water loss

A
  • used to prevent neurotoxic effects of high serum unconjugated bilirubin
  • amount of phototherapy needed depends on level of hyperbilirubinemia
  • mechanism: lowers serum bilirubin level by transforming bilirubin into water soluble isomers which can be eliminated in urine w/out conjugation in live
  • Increases insensible water loss by 25-50% due to warming effect; monitor body temp & wet diapers
48
Q

Fluid Replacement in Children

clinical presentation of minimal fluid loss (< 3%)

A
  • normal: mental status, HR, mucous membranes, cap refill, turgor
  • warm extremities
  • reduced urine output
49
Q

Fluid Replacement in Children

clinical presentation in moderate fluid loss (3-9%)

A
  • fatigued/irritable
  • elevated HR
  • dry mucuous membranes
  • cap refill 3-4s
  • normal turgor
  • cool extremities
  • decreased urine output
50
Q

Fluid Replacement in Children

clinical presentation of severe fluid loss (>10%)

A
  • lethargic
  • very high HR
  • parched mucous membranes
  • cap refill >4s
  • tenting turgor
  • mottled extremities
  • very decreased urine output
51
Q

Fluid Replacement in Children

3 most sensitive exam findings for determining severe dehydration

A
  • prolonged cap refiill
  • abnormal resp pattern
  • abnormal skin turgor
52
Q

Fluid Replacement in Children

components of dx

A
  • HPI (number wet diapers/urination daily, increased thirst/water intake, recent illnesses, behavioral changes) & PE are sufficient to dx dehydration
  • lab testing if severe & for monitoring rehydration
53
Q

Fluid Replacement in Children

BMP results in:
* mild dehydration
* moderate dehydration

A
  • mild: slightly elevated BUN, reduced glucose
  • mod: increased Na, Cl, BUN; reduced bicarb, glucose
54
Q

Fluid Replacement in Children

BMP in severe disease- results

A
  • glucose: low
  • BUN: high
  • Na/Cl: high
  • Bicarb: low
  • Creatinine: high
55
Q

Fluid Replacement in Children

define lethargy

A
  • pathologic state of sleepiness or deep unresponsiveness and inactivity (difficult to wake and will fall right back asleep if you do wake)
  • symptoms of disease w/ varied levels of medical seriousness
  • true lethargy is a seconds to minutes emergency and could be due to: sepsis, meningitis, severe dehydration, med/drug OD
56
Q

Fluid Replacement in Children

define irritability

A
  • inconsolability; fussiness or whining despite attempts to comfort and console
  • pts appear well (not ill)
  • true irritability can be due to: fracture, head trauma, intussusception, meningitis, hair tourniquet
57
Q

Fluid Replacement in Children

management in mild to mod disease

A
  • oral rehydration therapy (ORT): give solutions w/ similar electrolyte contents to fluid lost (high sugar drinks can worsen diarrhea)- if fail this, can do IV hydration
  • provide 50-100 cc/kg of fluids of 2-4 hrs (syringe, spoon feed, NG tube)
  • Zofran PRN (if vomiting)
58
Q

Fluid Replacement in Children

medical management in severe dehydration

A
  • medical emergency due to hypoperfusion of brain/vital organs

Acute Resuscitation phase (goal is to prevent/correct hypovolemic shock)
* rapid volume expansion (bolus): 10-20 cc/kg over 20 min (repeated up to 3x, max of 1L) with isotonic fluids ONLY (lactated ringers or 0.9% NS)
* Glucose monitoring: POC for hypoglycemia; IV glucose PRN (5-10 mL/kg of D10 NS or 2-4 mL/kg of D25 NS)

Resuscitation Phase
* slower replacement of lost fluids of 24 hrs
* total fluid of resuscitation phase = maintence fluids + (rehydration - bolus given)
* rehydration is divided in 2 phases: 50% over first 8 hrs, 50% over next 16 hrs

59
Q

Fluid Replacement in Children

standard bolus calculation for rehydration

A
  • 10-20 mL/kg Q20 minutes
  • up to 3x w/ a max of 1L of fluid
  • continual monitoring of VS with each bolus
60
Q

Fluid Replacement in Children

maintenance calculations for rehydration

A

4-2-1 Rule
* 1st 10 kg: 4mL/kg/hr
* 2nd 10gk: 2mL/kg/hr
* further kg: 1mL/kg/hr
* preferred fluid for IV maintenance: 0.9% NS w/ 5% glucose

61
Q

Fluid Replacement in Children

example calculation for 37kg pt

A
  • 1st 10 kg: 4x10= 40mL
  • 2nd 10kg: 2x10= 20mL
  • remaining: 1x17= 17mL
  • total fluids: 77mL/hr
62
Q

Fluid Replacement in Children

volume replacement calculations

A

calculated by wt and severeity of dehydration

Less than 10kg
* mild: 50cc/kg/day
* mod: 100cc/kg/day
* severe: 150cc/kg/day

More than 10kg
* mild: 30cc/kg/day
* moderate: 60cc/kg/day
* severe: 90cc/kg/day

63
Q

Fluid Replacement in Children

complete management example (calaculate both acute resuscitation phase and maintence):

child weighs 25kg w/ severe dehydration

A

Acute Resuscitation:
* 25 kg x 20mL/kg = 500mL bolus Q20 min PRN
* can do up to 1L, so 2 bolus max

Resuscitation Phase (use eqn
* maintenance fluid (using 4-2-1 rule to get hrly and multiply by 24 for daily needs): 1,560 mL/day
* rehydration fluid (based on wt and dehydration status): 2,250 mL/day
* BUT 1000mL bolus already given, so 1,250 mL/day is still needed
* 1560 + 1250 = 2810 mL/day needed
* first 8 hrs: 1,405 mL; next 16 hrs 1,405 mL

64
Q

Fluid Replacement in Children

monitoring response to fluids

A
  • urine output: optimal is > 1 cc/kg/hr
  • clinical signs: improved turgor, pulse, cap refll, mental status; can cry tears
65
Q

A 2-year-old boy presents with a refusal to drink liquids. He has a heart rate of 130 bpm with otherwise normal vitals. He weighs 12 kg. Initial observation shows a tired appearing crying child who is producing tears. HEENT exam shows moist mucosa with erythematous papulovesicular eruptions on the buccal mucosa. What is the most appropriate rehydration strategy for this patient?

A. D5 normal saline 120 mL IV over 30 minutes
B. Water 500 mL over 2 hours
C. Commercial drink with low carbohydrates and no sodium 750 mL over 2-4 hours
D. Compounded oral solution with 1:1 glucose/sodium content 600 mL over 4

A
  • mild dehydration
  • oral intake prefered
  • Compounded oral solution with 1:1 glucose/sodium content 600 mL over 4
66
Q

Hepatitis

overall pathophys

A

cytotoxic killing of hepatocytes by CD8 T cells leading to cellular apoptosis and liver damage

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