GI Flashcards

1
Q

Celiac Disease: What is it? Which 3 proteins? What is the toxin called? Patho?

A

Gluten intolerance

Wheat, barley and rye gluten proteins elicit an immune response in genetically predisposed individuals

In Celiac disease
-Leaky junctions= Gluten can reach lamina propria

-Genetic predisposition = Abnormally heightened immune response

-Protected transport of toxic gliadins = Transcytosis of IgA/gliadin immune complexes to lamina propria without degradation- Immune complexes present to
APC and trigger activation of local T-cells
Cytokine production – intestinal tissue damage
§ Villous atrophy
§ Crypt hyperplasia

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2
Q

Celiac Disease: Symptoms and Complications

A
Symptoms
§ Diarrhea
§ Abdominal pain
§ Malabsorption
§ Cramping
§ Bloating
§ Dermatitis herpetiformis

Complications
§ T-cell lymphomas
§ GI carcinomas

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3
Q

Celiac Disease: Diagnosis

A

Diagnosis:
Biopsy of duodenal specimen
§ Mucosal damage
§ Villous atrophy

Serology testing
§ IgA transglutaminase (tTG) antibodies and IgA endomysial antibodies

Positive response to gluten free diet

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4
Q

Celiac Disease: Treatment

A
  • Strict, lifelong avoidance of gluten

- Treatment of nutritional deficiencies

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5
Q

Diverticular disease: What is it? Where is it? Patho?

A

Diverticula = “colonic pouches”
§ Acquired deformity- Consumption of refined foods with little fiber
§ Occur in the colon- Descending and sigmoid
§ Mucosa and submucosa herniate through the muscularis externa
§ Increased intraluminal pressure causes outpouching through weakened areas of colon
§ These pouches can become inflamed and infected from passing fecal matter (diverticulitis)

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6
Q

Diverticular disease: Symptoms and Complications

A
Symptoms
-Inactive disease (Diverticulosis)
§ Chronic constipation
§ Straining during defecation
§ Otherwise patients asymptomatic
-Active disease (Diverticulitis)
§ Intense lower abdominal pain
§ Fever
§ Elevated WBC
-Complications
§ Perforation
§ Diverticular Bleeding
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7
Q

Diverticular Disease: Diagnosis

A

Diverticulosis
§ Routine colonoscopy

Diverticulitis
§ Clinical symptoms
§ CT findings

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8
Q

Diverticular disease: Treatment

A
Diverticulosis
§ High fiber and increased liquids
Diverticulitis
§ Antibiotics
§ Bowel rest (IV fluids)
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9
Q

Ischemic Bowel: What is it? Patho?

A

Insufficient blood flow to intestines = Causing ischemia

Likelihood of ischemia based on
§ Collateral adequacy
§ # and size of splanchnic vessels affected
§ Duration of insult

Occlusive or non-occlusive
§ Occlusive: Arterial or venous, SMA most common, Embolic disease = Dislodged from L side of the heart
Thrombotic disease = Atherosclerotic plaque rupture
§ Non-occlusive: Splanchnic vasoconstriction- Low cardiac output, Hypotension

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10
Q

Ischemic Bowel: Symptoms and Risk factors

A

Symptoms
§ Acute, severe abdominal pain
§ N/V, diarrhea, bloody stools

Risk factors
§ Atrial fibrillation
§ Recent MI
§ Valvular heart disease: Particularly a recent valve replacement

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11
Q

Ischemic Bowel: Diagnosis & Treatement

A

Clinical suspicion
§ Risk factors present
§ Labs: Cardiac enzymes, Lactic acid
§ Imaging: Abdominal x-ray, CT scan
§ IV and PO contrast
§ Laparotomy (Surgery): Also the treatment
-Vascular bypass, Endovascular stenting, Resection of areas of necrosis

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12
Q

CHOLELITHIASIS: Risk factors

A
Risk factors
§ Female
§ Obese
§ Middle age
§ Pregnancy
§ High dietary fat consumption
§ Oral contraceptive use
§ Rapid weight loss
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13
Q

CHOLELITHIASIS: What is it? Patho?

A

Gall Bladder stones

-Increased biliary secretion of cholesterol
§ Cholesterol solubility in bile exceeded
§ large, small, sludge all possible
§ Sludge is a precursor

-Gall bladder motility/contraction also plays a role

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14
Q

CHOLELITHIASIS: Diagnosis

A

§ Abdominal ultrasound
§ CT
§ ERCP
§ HIDA scan

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15
Q

CHOLELITHIASIS: Symptoms and Complications

A

Symptoms:
-Stones in gallbladder
§ Asymptomatic
§ Can be found on routine imaging
-Migration into cystic duct or CBD (choledocholithiasis)
§ Biliary colic
§ Severe, steady ache in RUQ or epigastric region
§ Can radiate into the scapula and shoulder

Complications:
§ Choledocholithiasis
§ Cholecystitis
§ Cholangitis

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16
Q

Cholelithiasis : Treatment

A
  • Cholecystectomy (Laparoscopic)

- ERCP

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17
Q

CHOLECYSTITIS: What is it? Patho? Acute, Acalculous vs Chronic

A

Inflammation of the gallbladder

Acute
§ Usually the result of obstruction from a stone
§ Increased pressure within the gallbladder - distention and ischemia within the gallbladder mucosa and wall
§ Release of local inflammatory tissue factors
§ Bacterial inflammation

Acalculous cholecystitis
§ >50% no cause is found
§ Biliary sludge may be responsible
§ More common in
-Burn or trauma
-Postpartum after prolonged labor
-Prolonged TPN use

Chronic inflammation of gallbladder

  • Almost always associated with gallstones
  • Repeated acute cholecystitis episodes
  • Bacteria may be present in the bile
  • Can be asymptomatic for years
  • Can present with acute cholecystitis after being chronic
  • Can present with a complication
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18
Q

Cholecystitis: Symptoms & Complications (Acute vs Chronic)

A
Symptoms:
¡ Typically starts with biliary colic that doesn’t remit
and progressively gets worse
¡ N/V
¡ Not eating
¡ +/-Fever
Complications:
§ Empyema
§ Hydrops
§ Gangrene
§ Jaundice
§ Perforation
§ Fistula formation
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19
Q

Diagnosis: Cholecystitis

A

¡ Clinically

  • Physical Exam findings: RUQ tender to palpation
  • Labs: White blood cell count, Bilirubin and alkaline phosphatase
  • Vitals: Fever

Same as cholelithiasis
¡ Ultrasound
¡ ERCP
¡ HIDA

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20
Q

Cholecystitis: Treatment

A

§ Bowel rest- IV fluids
§ Antibiotics (If indicated)
§ Pain medications
§ Cholecystectomy

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21
Q

Jaundice: Conjugated vs Unconjugated

A

Unconjugated
§ Increased bili production (increased RBC breakdown)
§ Impaired bili transport into hepatocytes preventing conjugation
§ Defective conjugation within the hepatocyte

Conjugated
§ Impaired transport from hepatocyte to biliary duct
§ Extrahepatic obstruction resulting in buildup of bili in hepatocytes causing backward leakage into the blood

22
Q

Cholangitis: What is it? Patho?

A

Acute infection in the biliary tract

¡ Usually from biliary stasis/obstruction
¡ Bacteria migrate upwards from the duodenum
¡ Normal defense mechanisms disrupted: Sweeping action of bile, Sphincter of Oddi, Biliary duct permeability

23
Q

Cholangitis: Symptoms and Complications

A
Symptoms
§ Charcot’s triad
§ Fever
§ Abdominal pain
§ Jaundice
Complications
§ Sepsis
§ Bacteremia
§ Septic shock
§ Death
24
Q

Cholangitis: Diagnosis

A
Diagnosis
§ Clinical picture (Charcot’s triad)
§ Elevated WBC
§ Neutrophils
§ Elevated ALP, GGT and bilirubin
§ Ultrasound
§ Evaluate for dilatation or stones
25
Q

Cholangitis: Treatment

A
Treatment
§ ERCP: Stone removal, Stenting of bile duct (To allow for biliary drainage)
§ Infection: Antibiotics
§ Sepsis (+/- shock): Fluids, Pressors
§ Cholecystectomy: To prevent recurrence
26
Q

Pancreatitis: Endocrine Function: cells and hormones

A

-secrete product (hormone) directly into the bloodstream
-The islets of Langerhans are small collections of cells in the pancreas that secrete hormones
¤ α - glucagon - ↑ glycogenolysis –> ↑ glucose
¤ β - insulin - Shift glucose intracellularly
¤ δ – somatostatin - ↓ glucagon ↓ insulin

27
Q

Pancreatitis: Exocrine Function: cells and hormones

A

Exocrine = secrete product through a duct directly onto epithelium

Acinar cells (acini) secrete pancreatic enzymes into the duodenum to aid with digestion
¤ Amylase – starches
¤ Lipase – triglycerides
¤ Protease – proteins

Ductal cells secrete water and bicarbonate in response to food intake and secretin release from the small intestine
¤ The pancreatic duct and common bile duct join together to form the hepatopancreatic duct or ampulla
of vater

28
Q

Pancreatitis: Patho/ causes

A

Acinar cell injury –> Chemo-attraction of
leukocytes & macrophages in the pancreas =
inflammation –> Cytokine and proteolytic enzyme
release = breakdown of pancreatic tissue and edema
-Cycle repeats

Causes:
Acute
¤ Gall-stone associated
¤ Alcoholic
¤ Hypertriglyceridemia
¤ Drug-Induced
¤ Post-endoscopic retrograde cholangiopancreatography (ERCP)

Chronic
¤ M-ANNHEIM

29
Q

Gall stone induced pancreatitis

A

Gallstones that lodge in the hepatopancreatic
duct can prevent the normal flow of enzymes
into the small intestine
¤ This can lead to breakdown and inflammation of the
pancreatic tissue

30
Q

Alcoholic pancreatitis: Patho

A

Associated with large consumption of alcohol for an
extended period of time
¨ Exact mechanism unknown
¨ Proposed mechanism multifactorial:
¤ Alcohol ingestion stimulates pancreatic enzyme production
¤ Formation of reactive oxygen species (ROS) can damage pancreatic tissue and cause inflammation

31
Q

Hypertriglyceridemia-induced pancreatitis: patho

A

Free fatty acid production via the breakdown of lipids by pancreatic lipase causes pancreatic inflammation

32
Q

Acute Pancreatitis vs Chronic: Clinical Presentation

A
Acute:
Abdominal
pain/distention
Nausea/Vomiting
Fever
Leukocytosis
Jaundice
Chronic:
Abdominal pain
Steatorrhea
Weight loss
Jaundice
Hyperglycemia
33
Q

Diagnosis: Acute pancreatitis vs chronic pancreatitis

A

Acute:
¨ Physical findings consistent with pancreatitis:
abdominal pain
¨ Lipase or amylase > 3x ULN
¤ Lipase is the most sensitive
¨ Imaging-CT
¤ Not routinely done for uncomplicated cases

Chronic:
Amylase and lipase may be normal
¤ Damage to exocrine pancreatic cells may prevent
adequate production of pancreatic enzymes
¨ Imaging may reveal atrophic pancreas and
complications of chronic pancreatitis
¤ Calcifications, dilations of pancreatic duct, pseudocysts
¨ Secretin stimulation test
¤ Measures the ability of the pancreas to respond to
secretin

34
Q

Pancreatitis (acute vs chronic): Complications

A
Acute:
Necrosis
Hemorrhage
Pseudocyst
Infection
¤ Abscess
¤ Systemic infection --> shock 
Chronic:
¨ Loss of endocrine and exocrine function
¤ Diabetes
¤ Nutritional deficiencies
¨ Pseudocyst
¨ Ascites
¨ Biliary stricture
¨ Pancreatic cancer
35
Q

Treatment: Acute vs Chronic pancreatitis

A
Acute
Goal: supportive
Remove/avoid cause
¤ Medication, triglycerides, alcohol
Re-hydration
Avoid oral intake
Treat complications
¤ Pain management
¤ Antiemetics
¤ Antibiotics?
Chronic:
Goal: symptom management
¤ Pain management
¤ Antiemetics
¨ Optimize nutrition
¤ Low-fat meals
¤ Frequent small meals
¤ Fat-soluble vitamin supplementation
¨ Avoid cause
¤ Alcohol
¨ Pancreatic enzyme replacement
36
Q

Cirrhosis vs Liver Disease: What are they

A

Liver Disease
§ Any disease or disorder that causes the liver to function improperly
§ Can be acute or chronic

Cirrhosis
§ Final phase of chronic liver disease
§ Fibrosis and scarring present
§ Poor liver function
§ Not to be confused with elevated LFTs
37
Q

CAUSES OF CHRONIC LIVER DISEASE/

CIRRHOSIS

A

Alcohol

Hepatitis B & C

Primary biliary cirrhosis, primary sclerosing cholangitis

Nonalcoholic fatty liver disease (NAFLD)

Genetic/Metabolic: Hemochromatosis, alpha 1 antitrypsin deficiency, Wilson’s Disease

Drugs: More commonly acute liver injury

38
Q

Cirrhosis: SIGNS AND SYMPTOMS

A
¡ Hepatomegaly
¡ Pruritus, jaundice
¡ Palmar erythema, spider angiomata
¡ Ascites, edema,
¡ Painful, tense abdomen
¡ Confusion-if encephalopathic
¡ Asterixis
39
Q

ASCITES: Patho

A

It all starts with increased sinusoidal pressure
§ Hepatocytes fibrose and scar over, impeding blood flow through the sinusoids
§ Forcing blood to run through other still functioning areas of the liver

¡ The pressure in the sinusoids of the remaining functional lobules increases
¡ Eventually the pressure is so high that the blood can no longer overcome that pressure and the blood will back up in the portal vein all the way into the small splanchnic vessels.

¡ The pressure in the splanchnic vessels increases due to increased blood flow

¡ The body releases vasodilatory nitric oxide to dilate the splanchnic vessels to compensate

¡ At the same time, there is now more blood in the splanchnic vessels and less blood coming through the liver because of the impedance to flow

¡ Therefore, less blood ultimately returns to the heart through the hepatic vein then through the
heart and into arterial circulation resulting in decreased effective circulating volume and
reduced blood pressure.

¡ Baroreceptors sense this reduction in effective circulating volume and activate a neurohormonal
response.

¡ The sympathetic nervous system, Renin-angiotensin-aldosterone-system (RAAS) and anti-diuretic
hormone (ADH) all become activated in response to the detected decreased effective circulating
volume and hypotension signaling the retention in the kidney causing fluid overload.

¡ Splanchnic vessel permeability is increased due to loss of oncotic pressure between intravascular
and extravascular space due to decreased albumin

¡ Increased vasodilation of the splanchnic vessels causes increased lymph production
¡ Increased lymph production coupled with increased vessel permeability results in fluid and lymph leakage into the peritoneal cavity

¡ Effective circulating volume continues to remain low as fluid continues to move into the peritoneum

¡ The body continues neurohormonal activation to attempt to increase effective circulating volume
resulting in more fluid accumulation…the cycle continues….

40
Q

ASCITES: DIAGNOSIS

A

¡ Physical examination
§ Full, tense, bulging abdomen
§ Abdominal ultrasound

Abdominal paracentesis
§ Removal of ascitic fluid from the peritoneum
§ Ascitic fluid analysis
§ SAAG= Serum-ascites albumin gradient
§ Use same day values
§ SAAG ≥ 1.1 g/dL = portal hypertension
41
Q

ASCITES: TREATMENT

A

Na+ restriction
§ 2 grams/day

Aldosterone antagonists

+/- Loop diuretics

Diuretic refractory ascites
§ Large volume paracentesis (4-8 L)
§ Rapidly removes fluid
§ Does nothing to correct the underlying problem though
§ Needs to be in combination with Na+ restriction and diuretics

42
Q

PORTAL HYPERTENSION: DEFINITION

A

Hepatic venous pressure gradient (HVPG)
§ Difference between the portal vein and inferior vena cava
§ Portal hypertension = HVPG > 5 mmHg
§ SAAG ≥ 1.1 g/dL also used for diagnosis

43
Q

PORTAL HYPERTENSION: COMPLICATIONS

A

Ascites

Variceal bleeding

44
Q

Varices: What are they? Why do they form?

What are collaterals?

A

Gastric and esophageal varices form as a result of shunting of blood away from the liver into splanchnic collaterals
§ Collaterals = growth of or several blood vessels to provide blood to an organ or vascular bed
§ Varices = abnormally dilated vessels

§ 1/3 of cirrhotic related deaths
§ Risk factor for SBP
§ Complication of portal hypertension

45
Q

Portal Hypertension: Treatment

A

Goal: Prevent variceal bleeding
§ How?
§ Treat the portal hypertension
¡ Non-selective beta blockers (Propanolol, nadolol)

-Transjugular intrahepatic portosystemic shunt (TIPS): Shunt bypasses the liver providing immediate relief for the high pressure portal vein
§ Side effect: Hepatic encephalopathy
¡ Used for refractory acute variceal bleeding or
¡ Refractory ascites patients intolerant of large-volume
paracentesis

46
Q

Spontaneous bacterial peritonis: What is it? Patho?

A

Bacterial infection of the ascitic fluid
¡ Often caused by enteric gram negatives found in the GI tract

¡ Pathogenesis
§ Not completely known
§ Bacterial translocation from gut to lymph
§ Reduced host defense

47
Q

Spontaneous Bacterial Peritonis: Diagnosis

A

Elevated ascitic fluid white blood cell count

Positive ascitic fluid bacterial culture

48
Q

Spontaneous Bacterial Peritonitis: Treatment

A

¡ Antibiotic therapy
§ 3rd generation cephalosporin
§ Ciprofloxacin would be alternative therapy

49
Q

HEPATIC ENCEPHALOPATHY (HE): What is it? Patho?

A
Accumulation of toxins from
§ Declining hepatic function
§ Portal-systemic blood flow shunting
¡ Toxins
§ Ammonia
¡ Results in altered mental status
¡ Ammonia levels are not correlated with HE severity
50
Q

Hepatic encephalopathy: Treatment

A

¡ Decrease ammonia production by increasing ammonia excretion through the GI tract
§ Lactulose

¡ Dietary protein
§ Balance between protein restriction and correcting malnutrition