Pathophysiology Final - Gi

Front 1

Gastroesophageal reflux: 3 mechanisms involving the LES (lower esophageal sphincter)

Back 1

1) Weak basal LES pressure
2) Inadequate LES response to increased abdominal pressure
3) Transient relaxation of the LES without peristalsis

Front 2

Antireflux barrier: Anatomy

Back 2

-lower esophageal sphincter
-crural diaphragm
-phrenoesophageal ligament

Front 3

Reflux esophagitis

Back 3

esophageal injury that is due to reflux of acidic gastric contents into the esophagus

Front 4

Pill-induced esophagitis

Back 4

Caustic injury from lingering in the esophagus

Examples
-KCl
-FeSO4
-quinidine
-NSAIDS
-tetracycline

Front 5

Infectious esophagitis (causes, host factors)

Back 5

Causes
-Candida
-HSV
-CMV

Host factor: Immunocompromised

Front 6

Barrett's Esophagus

Back 6

-patch or patches of metaplastic columnar epithelium (specialized intestinal metaplasia) in the lower esophagus, often due to severe reflux esophagitis
-increased prevalence of adenocarcinoma

Front 7

GERD: External factors

Back 7

-Diet (eg high fat foods)
-Smoking
-Medication

Front 8

GERD: Mucosal pathophysiology

Back 8

Impaired esophageal mucosal resistance

Front 9

GERD: Reasons for diminished esophageal clearance

Back 9

-Peristalsis
-Body position
-Saliva

Front 10

GERD: Gastric factors

Back 10

-Acid
-Bile acids
-Gastric emptying
-Gastric distention

Front 11

Heartburn: Indications of severe disease

Back 11

-Age > 40
-Symptoms > 3 years
-Alarming symptoms
--Dysphagia
--Weight loss
--Anemia

Front 12

Heartburn: differential diagnosis

Back 12

-Esophagitis
-Stricture
-Barrett's esophagus

Front 13

Approach to patient with dysphagia

Back 13

Algorithm image

Front 14

Spastic esophageal motility disorders: Syndromes

Back 14

-DES (Diffuse esophageal spasm)
-Nutcracker esophagus
-Hypertensive LES (lower esophageal sphincter_
-Nonspecific

Front 15

Spastic esophageal motility disorders: Symptoms

Back 15

-Chest pain
-Dysphagia

Front 16

Spastic esophageal motility disorders: Manometric features

Back 16

-Some normal peristalsis
-Contractions (simultaneous/spontaneous/repetitive/high-amplitude)
-High LES pressure

Front 17

Achalasia manometry

Back 17

-Incomplete relaxation
-Aperistalsis
-Lower esophageal sphincter hypertension

Front 18

Scleroderma manometry

Back 18

-Weak contractions
-LES hypotension

Front 19

Parietal cell function

Back 19

In: Ca, ACh, Gastrin.
Out: HCl

Front 20

Evidence for H. Pylori's role in gastric ulcer

Back 20

1. Colonization precedes ulcer
2. Eradication of H. Pylori ends cycle of recurrent ulcers

Front 21

How are peptic ulcers named?

Back 21

By location:
-Gastric
-Duodenal
-Esophageal

Front 22

Percentage of ulcers caused by H. Pylori

Back 22

Duodenal: 70% (if not used NSAIDs to excess)
Gastric: 65-95% (45% if NSAID related)

Front 23

Testing for H. Pylori

Back 23

Noninvasive
-serology (rare)
-Urease breath test

Invasive (biopsy)
-rapid urease test
–special stains

Front 24

Difference between ulcers in NSAID related disease and H. Pylori related disease

Back 24

NSAIDS: less surrounding inflammation

Front 25

NSAID related injury: Preventive factors in normals

Back 25

i. mucus
ii. superoxide scavengers in mucosa (e.g. glutathione)
iii. bicarbonate
iv. high blood supply of stomach (promoting repair and cellular metabolic functions)

Front 26

Risk factors for NSAID-induced damage

Back 26

-history of ulcer disease, dyspepsia, gastritis
-age (lower gastric perfusion)
-high/prolonged NSAID dose
-corticosteroids
-anticoagulants

Front 27

Typical location of gastrinoma

Back 27

Pancreas

Front 28

Causes of diarrhea

Back 28

-Osmotic-lactose intolerance (High fecal osmotic gap: > 125)
-Malabsorption/fatty
-Inflammatory
-Secretory (Low fecal osmotic gap: <50)
-Altered motility

Front 29

Fecal osmotic gap: calculation

Back 29

290 - 2(Na + K)

Front 30

Causes of diarrhea by location

Back 30

Picture

Front 31

Celiac Sprue: antibodies

Back 31

-Tissue transglutaminase
-Anti-gliadin
-Anti-endomysial

Front 32

Celiac Sprue: MHC

Back 32

HLA-DQ2 associated

Front 33

Celiac Sprue: Triggers and manifestations

Back 33

Trigger: gluten

Manifestations:
-Abdominal symptoms
-Malnutrition
-Low nutrients (Iron, Vit. D, Vit. K)

Front 34

Ulcerative Colitis: Major features

Back 34

Symptoms: Bloody diarrhea

Inflammation
-continuous (no skip lesions)
-Rectum involved

Front 35

Crohns Disease: Major features

Back 35

Symptoms:
-Diarrhea (not necessarily bloody)
-RLQ pain
-Fever
-Weight loss

Inflammation:
-Transmural
-Large ulcers
-Skip lesions

Fistulae and Strictures

Front 36

IBD: Medical Treatment

Back 36

Induce and maintain remission

Drugs:
1) 5-amino-salicylates (inhibit COX and 5-Lipox --> anti-inflammatory)
2) Corticosteroids
3) Antibiotics
4) Immune modulators (6-MP, azathoprine)

Front 37

IBD: Surgical therapy

Back 37

Ulcerative colitis: Total colectomy: curative

Crohn's Disease: Usually recurs after surgery

Front 38

Ulcerative Colitis: Complications

Back 38

Massive hemorrhage
Fulminant colitis
Colonic stricture (rare)
Colon cancer

Front 39

Crohn's Disease: Complications

Back 39

Bile acid malabsorption
-Secretory diarrhea: bile acids on colon
-Gallstones: bile more lithogenic
-Steatorrhea: vitamins ADEK malabsorption
-Nephrolithiasis: steatorrhea causes more oxalate absorption leading to calcium oxalate stones --- NOT uric acid stones

Malignancy:
-colon cancer
-small bowel cancer (lymphoma or adenocarcinoma – very rare)

Front 40

Benign colon disorders: Differential

Back 40

-Constipation
-Diverticula
-Hemorrhoids
-Anorectal fistula
-Anal fissure

Front 41

Gallstones: Epidemiology

Back 41

-women
-people over age 60
-Native Americans
-Mexican Americans
-overweight men and women
-people who fast or lose a lot of weight quickly
-hormonal women

Front 42

Gallstones: Types

Back 42

-Cholesterol stones (90% of US gallstones)
-Pigment stones

Front 43

Gallstones: Cholesterol stone causes

Back 43

-Hypersecretion of cholesterol into bile (Obesity, OCPs, estrogen, rapid weight loss)
-Hyposecretion of bile acids (Impaired synthesis, intestinal loss (t.i.resection), progesterone)
-Gallbladder stasis (Progesterone, pregnancy, total parenteral nutrition)

Front 44

Gallstones: Pigment stones

Back 44

Black pigment
–cirrhosis
-hemolytic anemia --hemoglobinopathy
--red cell disorders

Brown pigment
-Asian patients (infection)

Front 45

Gallstones: Diagnosis

Back 45

ultrasound

Front 46

Gallstones: Treatment

Back 46

Laparoscopic cholecystectomy

Front 47

Gallstones: Symptoms/Manifestations

Back 47

-Asymptomatic (in gallbladder) (75%)
-Intermittent biliary colic (floating in and out of cystic duct) (20%)
-Acute pain/cholecystitis (impacted in cystic duct) (10%)
-Jaundice/biliary colic (impacted in distal common bile duct) (5%)

Front 48

Pancreatitis: Most common etiologies

Back 48

Image

Front 49

Pancreatitis: Local effects of enzymes

Back 49

-Inflammation
-Third space losses
-Fat necrosis
-Pancreatic/peripancreatic necrosis

Front 50

Pancreatitis: Signs and Symptoms

Back 50

-Abdominal pain/tenderness
-Nausea/vomiting
-Fever
-Tachycardia

Front 51

Pancreatitis: Lab tests

Back 51

-Increased WBC
-Increased serum amylase
-Increased serum lipase

Front 52

Pancreatitis: Differential diagnosis

Back 52

-Choledocholithiasis (gallstone in common bile duct)
-Perforated ulcer
-Mesenteric ischemia
-Intestinal obstruction
-Salpingitis
-Ectopic pregnancy

Front 53

Chronic Pancreatitis: Most common etiologies

Back 53

Alcohol: 70%
Idiopathic: 12.5%

Front 54

ALT levels: Vary with?

Back 54

-BMI
-Elevated lipids
-Glucose

Front 55

High AST/ALT ratio

Back 55

Alcoholic liver disease

Front 56

Level for AST for 95% chance of hepatocellular liver disease

Back 56

>300 IU

Front 57

Elevated alkaline phosphatase indicates:

Back 57

1. Liver disease – overproduction of alkaline phosphatase by liver and regurgitation into blood. Highest values in bile duct obstruction and some drug toxicities.
2. Bone disease – overproduction by bone

Front 58

Difference between direct and indirect bilirubin

Back 58

Direct: conjugated with glucouronides. water soluble. excreted in urine

Indirect: unconjugated bilirubin, insoluble in water and not excreted in urine

Front 59

Direct bilirubin: normal
Indirect bilirubin: elevated
Bilirubinuria: none

Back 59

Increased production: Hemolysis, PA, Thal

Decreased conjugation: Gilbert's syndrome, Crigler-Najjar Syndrome

Front 60

Direct bilirubin: elevated
Indirect bilirubin: elevated
Bilirubinuria: positive

Back 60

Decreased excretion: All types of liver disease

Front 61

Normal albumin levels + liver symptoms = ?

Back 61

Possibly acute liver disease

Front 62

Low albumin levels + liver symptoms = ?

Back 62

Possibly chronic liver diseasse

Front 63

Prolonged PT (prothrombin time)

Back 63

Vitamin K deficiency: Administer vitamin K and recheck --> if PT normalizes, it's Vit K deficiency

Front 64

Which coagulation factor is not made in the liver?

Back 64

Factor VIII – made vascular endothelium and R-E cells

Front 65

Hep A IgM antibody

Back 65

acute infection

Front 66

Hep A IgG antibody

Back 66

prior infection

Front 67

Hep B surface Ag: +
Hep B surface Ab: -
Hep B core IgM Ab: +
Hep B core IgG Ab: -
Hep B e Ag: +
Hep B e Ab: -
HBV-DNA: +

Back 67

Acute

(only time Hep B core IgM Ab is positive)

Front 68

Hep B surface Ag: -
Hep B surface Ab: +
Hep B core IgM Ab: -
Hep B core IgG Ab: +
Hep B e Ag: -
Hep B e Ab: +
HBV-DNA: -

Back 68

Resolved acute infection

(Hep B core IgM is negative --> Hep B surface Ab is positive -->
Hep B e Ab is positive --> Resolved Acute infection)

Front 69

Hep B surface Ag: -
Hep B surface Ab: +
Hep B core IgM Ab: -
Hep B core IgG Ab: -
Hep B e Ag: -
Hep B e Ab: -
HBV-DNA: -

Back 69

Vaccinated

(Hep B core IgM is negative --> Hep B surface Ab is positive --> Hep B e Ab is negative OR nothing else is positive --> Vaccinated)

Front 70

Hep B surface Ag: +
Hep B surface Ab: -
Hep B core IgM Ab: -
Hep B core IgG Ab: +/-
Hep B e Ag: -
Hep B e Ab: +
HBV-DNA: -

Back 70

Chronic carrier state

(Hep B core IgM is negative --> Hep B surface Ab is negative --> Hep B e Ab is positive -->
HBV DNA is negative --> Chronic carrier state)

Front 71

Hep B surface Ag: +
Hep B surface Ab: -
Hep B core IgM Ab: -
Hep B core IgG Ab: +/-
Hep B e Ag: +
Hep B e Ab: -
HBV-DNA: +

Back 71

Chronic active hepatitis

(Hep B core IgM is negative --> Hep B surface Ab is negative --> Hep B e Ab is negative --> Chronic active hepatitis)

Front 72

Hep B surface Ag: +
Hep B surface Ab: -
Hep B core IgM Ab: -
Hep B core IgG Ab: +/-
Hep B e Ag: -
Hep B e Ab: +
HBV-DNA: -

Back 72

Chronic active hepatitis pre-core mutant

(Hep B core IgM is negative --> Hep B surface Ab is negative --> Hep B e Ab is positive -->
HBV DNA is positive --> Chronic active hepatitis pre-core mutant)

Front 73

HVPG < 12

Back 73

Normal

Front 74

HVPG > 12

Back 74

Portal hypertension - Intrahepatic. Due to sinusoidal arteries (due to cirrhosis)

Front 75

Portal hypertension, Pre-hepatic

Back 75

Portal or splenic vein thrombosis

AV fistulas in the splanchnic bed or spleen

Front 76

Portal hypertension, Intrahepatic, normal HVPG

Back 76

Pre-sinusoidal --> Normal HVPG
Sarcoid, Schistosomiasis

Post-sinusoidal --> Budd Chiari – can’t get into hepatic veins (clot in veins)

Front 77

Portal hypertension, Post hepatic

Back 77

Webs in IVC

Cardiac disease --> constrictive pericarditis, right heart failure

Front 78

Complications of cirrhosis

Back 78

Varices

Ascites

Hepatic encephalopathy

Hepatorenal syndrome

Front 79

Prokinetic Agents - Subbclasses

Back 79

-Cholinergic agents
-Serotonin receptor modulators
-Dopamine receptor blockers
-Motilin-like agents

Front 80

Drugs for constipation - subclasses

Back 80

-Bulk forming agents
-Softeners/surfactants
-Osmotic agents
-Stimulants
-Miscellaneous

Front 81

Prokinetic agents - Cholinergic agents

Back 81

Bethanechol

Front 82

Prokinetic agents - Serotonin receptor modulators

Back 82

-Metoclopramide
-Cisapride
-Tegaserod

Front 83

Prokinetic agents - Dopamine receptor blockers

Back 83

-Domperidone
-Metoclopramide

Front 84

Constipation drugs - Bulk-forming agents - Toxicities and examples

Back 84

Toxicity
-Bloating

Natural
-Psyllium (Metamucil)

Semi-synthetic
-Methylcellulose
-Polycarbophil

Front 85

Constipation drugs - Softeners/Surfactants - Mechanism, toxicities and examples

Back 85

Mechanism: Lowers surface tension of stool

Toxicities:
-Impaired absorption of fat soluble agents
-Oil leakage
-Lipid pneumonitis

Examples
-Docusate
-Mineral oil

Front 86

Constipation drugs - Osmotic agents - Mechanism, toxicities and examples

Back 86

Mechanism
-Osmotically-mediated water retention stimulates peristalsis

Toxicities
-Abdominal distention, flatulence
-Saline: caution if renal/cardiovascular disease or electrolyte disorder. Monitor electrolytes.

Examples
-Saline-based
-Sugar/alcohol-alcohol based
-Other (PEG solutions)

Front 87

Constipation drugs - Stimulant Laxatives - Mechanism, toxicities and examples

Back 87

Mechanism: Migrating colonic contractions

Concern: Overuse

Examples:
-Diphenylmethanes
-Anthraquinones
-Castor oil

Front 88

Constipation drugs - Lubiprostone - Mechanism, toxicities

Back 88

Mechanism: Activates Cl channels within GI tract --> increasing intestinal fluid secretion

Toxicities:
Nausea
Abdominal distention and pain
Diarrhea and flatulence
Headache
Avoid in pregnancy

Front 89

Anti-diarrheals - Bulk-forming & binding agents - Examples

Back 89

Natural
-Psyllium
Semi-synthetic
-Methylcellulose
-Polycarbophil
Other agents
-Cholestyramine
-Bismuth subsalicylate

Front 90

Anti-diarrheals - classes

Back 90

-Bulk-forming/binding agents
-Antimotility agents
-Antisecretory agents
-Miscellaneous