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Advance Pathophysiology > Lecture 8 Gastrointestinal diseases > Flashcards

Lecture 8 Gastrointestinal diseases Flashcards

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1
Q

ESOPHAGEAL

A

Normal Function
Transport food from mouth to stomach, peristalsis, prevent backflow
Interfered by obstruction, dysfunction, punching, reflux/regurg

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2
Q

ESOPHAGEAL

A

Obstruction
Foreign objects, nodes, cancers, etc.
S/Sx:
Dysphagia (w/ solids, liquids as it progresses)
Chest pain/angina like
Regurgitation of undigested food
Has not reached the stomach yet!

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3
Q

Muscle/Innervation Dysfunction PNS -> rest/digest

A

PNS input compromise -> disruption of sensory or motor pathway

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4
Q

Muscle/Innervation Dysfunction Failure to contract

A

Dilation d/t collagen structure damage (scleroderma, connective tissue dx., Chagas dx)

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5
Q

Muscle/Innervation Dysfunction Failure to Relax

A

Diffuse spasms
Can present as chest pain/angina

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6
Q

Achalasia (Contract & Relaxation Issue)

A

Triad of S/Sx
Incomplete LES (lower esoph sphincter) relaxation
Increased LES tone
Aperistalsis of lower ⅔ of esophagus
Barium swallow test -> bird beak; dilated, tortuous esophagus

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7
Q

Diverticula

A

Outpouching of esophagus
Obstruction increases contractions (where its closest to the obstruction)
Leads to wall weakness
Congenital or lymph node related
Pulsion Diverticulum
Proximal to obstruction
Zenker Diverticulum
Behind upper esophageal sphincter

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8
Q

Reflux general

A

Backwash of acid through LES
Burning of esophageal mucosa -> esophagitis

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9
Q

Reflux etiology

A

Incompetent sphincter
Hernial distortion
Excess pressure from impaired stomach emptying

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10
Q

reflux s/s

A

Worse when bending over or lying down after eating
Heartburn
Epigastric pain
Chest pain
Sour, bitter taste in mouth d/t stomach contents
Complications
Barrett’s Esophagus -> metaplasia of epithelium d/t damage -> esophageal adenocarcinoma

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11
Q

Esophagitis

A

Etiology
Medications (chemo)
Radiation
Crohn/s Dx
Infection

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12
Q

Esophageal Varices

A

Varix: abnormal dilation of artery, vein, lymphatic vessel
Increased risk for rupture causing esophageal bleeding

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13
Q

Esophageal Varices etiology

A

Liver disease, portal HTN

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14
Q

Esophageal Varices s/s

A

Asymptomatic until there is rupture
Hematemesis
HypoTN Sx
Tachy
Abdominal bloating
Severe -> hypovolemic shock

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15
Q

Esophageal Cancer histology/etiology

A

Adenocarcinoma
GERD-induced Barrett’s esophagus is precursor
Squamous Cell Carcinoma
Smoking and alcohol is precursor

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16
Q

Esophageal Cancer s/s

A

Dysphagia
Indigestion
Reduced appetite, regurgitation
Chronic cough, hoarseness
Respiratory sx if trach becomes compressed

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17
Q

STOMACH General

A

Normal -> produce acid to break down food, produce intrinsic factor for Vitamin B12 absorption, digested food through pyloric sphincter to duodenum

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18
Q

Stomach parietal cells

A

Pump H+ into stomach in exchange for K+
Stimulated by gastrin, histamine, acetylcholine
Inhibited by somatostatin, prostaglandin, secretin, VIP
Makes sure not too acidic when entering the small intestine

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19
Q

stomach mucus cells

A

protective layer, regulated by prostaglandin

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20
Q

Acute Gastritis etiology

A

NSAIDS, alcohol, bile
Uremia, decreased O2 delivery, ingestion of harsh chemicals

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21
Q

Acute Gastritis s/s

A

Epigastric pain
N/V
Severe -> mucosal erosion, ulceration, hemorrhage

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22
Q

Peptic Ulcer Disease (PUD) etiology

A

Decreased Mucosal Protection
Prolonged NSAID use (decreases prostaglandin fxn)
Cox-2 inhibitors
Tobacco/alcohol
Stress Related Mucosal Disease -> physiological (ischemia, shock from sepsis, burns and hemorrhage)
Many inpatients get anti-ulcer prophylaxis
Decrease in perfusion
Increased Acid Secretion
Zollinger Ellison Syndrome
Increased gastrin (increases acid pdxn and ulceration multi-site)

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23
Q

Peptic Ulcer Disease (PUD) Dx

A

secretin injection -> if pancreas is normal, no change to gastrin secretion (if not normal, see a paradoxical increase in gastric acid)

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24
Q

Peptic Ulcer Disease (PUD) sx

A

Pain IMMEDIATELY after eating -> gastric ulcer
Relief with vomiting + antacids (acidity going down)
Pain HOURS after meal -> duodenal ulcer
Relief with eating
Epigastric pain
N/V
Melena (black stool)
Appetite changes
Severe/perforation of duodenal or gastric wall
Acute abd pain, air under diaphragm, visible on radiograph

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25
Peptic Ulcer Disease (PUD) Tx
Neutralize acids PPI (omeprazole) to inhibit parietal cells Decrease parietal cell stimulation by H2 blockers (histamine stimulates acid release) Vagotomy to sever vagus nerve PNS input to acid secretion Increase mucosal defense Sucralfate viscous gel barrier Prostaglandins decrease stomach acid Antibiotics for H.Pylori
26
Peptic Ulcer Disease (PUD)
Bleeding -> may be first indication of ulcer Perforation -> rarely first indication of ulcer Obstruction Secondary to edema or scarring, mostly in chronic ulcers Duodenal ulcers more likely to obstruct food vs gastric D/t less area for food to move!
27
Chronic Gastritis etiology
Autoimmune Radiation Mechanical injury (NG tube) Crohns Reflux of bile or pancreatic secretion
28
Chronic Gastritis complications
Mucosal atrophy Intestinal metaplasia Dysplasia Gastritis cystica
29
Loss of Intrinsic Factor general
Normally If is produced from parietal cells Type II Hypersensitivity Pernicious anemia Autoimmune gastritis -> antibodies form against parietal cells
30
Loss of Intrinsic Factor s/s
Megaloblastic anemia Atrophic glossitis (smooth beefy red tongue) Malabsorptive diarrhea CNS changes Marrow deficiency
31
Obstruction etiology
Foreign body Gastric polyp Gastric cancer External -> pancreatic tumor
32
obstructions s/s
Vomiting Early satiety Abdominal distention
33
Congenital Pyloric Stenosis
Projectile vomiting after feeding, frequent refeeding demand Palpable olive like mass Visible waves of peristalsis (stomach tries to overpower stenosis but fails)
34
Gastroparesis general
Paralysis of the stomach
35
Gastroparesis etiology
Nerve damage (ex. Diabetic neuropathy) Acetylcholine blockers Since PNS nerves release Ach at the synapse Drugs that decrease gastric motility (opioids)
36
Gastroparesis s/s
Indigestion Bloating Early satiety; prolonged; loss appetite Upper abdominal pain N/V Regurgitation of partially undigested food Acid reflux and heartburn Blood glucose fluctuations d/t malabsorption Constipation
37
Gastric Cancer etiology
Etiologies of gastritis predispose someone to gastric cancer development
38
Gastric Cancer s/s
N/V Early satiety GI bleed Usually occur in late stage of dx/ prognosis is poorer
39
SMALL INTESTINE (normal fx & interference)
Normal function -> absorption Interferences -> obstruction, tumor, bleeding, malabsorption
40
Malabsorption
Digestion Problem Gastroparesis Failure of enzyme secretion into gut lumen Pancreatic insufficiency or failure Decreased digestive enzymes Liver disease or gallbladder obstruction Resulting decreased bile acids
41
absorption problems etiology
Reduced surface area Damage to absorbing mucosa Biochemical/metabolic Obstruction of lymphatics and lacteals by tumors
42
absorption problems s/s
Abdominal pain + distention Bloating N/V Diarrhea Steatorrhea
43
Small Bowel Tumor (benign)
Adenoma, lipoma, leiomyoma
44
Small Bowel Tumor (malignant)
Adenocarcinoma (gland lining organ), lymphoma, carcinoids, GIST, sarcoma
45
Small Bowel Tumor s/s
Bleeding Obstruction N/V Abdominal pain Weight Loss Fatigue
46
bowel obstruction etiology
Hernia, adhesion, intussusception Tumors Nearby tumors from other organs Gallstones Inflammatory (Crohn’s)
47
bowel obstruction s/s
Abdominal pain N/V Lacking appetite Malaise Diarrhea Dehydration (tachy + low urine output) Severe constipation Complete small bowel obstruction -> medical emergency! All others can be medically or interventionally managed
48
LARGE INTESTINE (normal fx & interference)
Normal Fxn -> Water and Na+ reabsorption, delivery of stool to outside Interference -> Diarrhea, constipation, (muscle fxn, obstruction), tumors, inflammation, bleeding
49
Hirschsprung's Disease (Aganglionic Megacolon)
Functional obstruction of the colon Problem of chronic constipation in children Massive nerve malformation -> dilation
50
Colonic Diverticula (general)
Low fiber -> excess work on large intestines to squeeze stool -> weakened -> diverticulum forms (irregular pouch usually in descending colon)
51
Colonic Diverticula s/s
Intermittent cramping Lower abdominal discomfort Abdominal distention Diverticulosis -> GI bleeding, LLQ pain Severe -> rupture, adherence to bladder, or air/feces in urine
52
Enterocolitis (definition)
Inflammation of colon secondary to infection, ischemia, drugs, injury, IBD
53
Enterocolitis
Changes in bowel pattern Diarrhea Abdominal pain Urgency Incontinence, Lower GI bleed
54
Colon Cancer (etiology)
Common -> colon adenocarcinoma Genetic, regular screening after age 50 with fecal occult blood testing
55
Colon Cancer s/s
Abdominal pain Lower GI bleed Intestinal obstruction
56
IBS Dx
Abdominal pain at least 3 days per month over 3 months Following defecation and change in stool frequency/form
57
IBS S/s
Chronic relapsing abdominal pain Bloating Changes in bowel habits Diarrhea. Constipation, mixed subtypes predominance
58
IBD (general)
Chronic condition from inappropriate mucosal immune activation In combination with host-microbe interactions and epithelial barrier issues Comprised of Ulcerative Colitis Crohn Disease
59
H pylori - Mechanism of gastric injury and protection
Increases gastric secretion, initiating inflammation and susceptibility to acid damage
60
NSAIDs - Mechanism of gastric injury and protection
Inhibit COX 1 & 2, reducing prostaglandin production and mucosal protection
61
Tobacco - Mechanism of gastric injury and protection
Inhibits prostaglandin synthesis Promotes oxidative stress and reduces bicarb -> inhibits neutralization of gastric acid Result -> weakened mucosal barrier
62
alcohol - Mechanism of gastric injury and protection
Increases membrane permeability leading to cell death Impairs mucosal blood flow and suppresses prostaglandin synthesis
63
Gastric Hyperacidity - Mechanism of gastric injury and protection
Overwhelms and degrades mucosal defenses Ex. Zollinger-Ellison syndrome and continuous acid secretion
64
Duodenal-Gastric Reflux - Mechanism of gastric injury and protection
Reflux of bile acids, pancreatic enzymes, etc disrupt mucosal barrier Toxic to gastric epithelial cells
65
What factors increase risk for peptic ulcer formation/disease?
H. Pylori infection Long term NSAID use Smoking Excessive alcohol consumption Corticosteroid use Family/Past Medical history Stress related -> shocks (burns, sepsis, hemorrhage)
66
gastric ulcer vs duodenal ulcer
GU- Worse with eating Occur shortly after meals DU-Relieved by eating but… Worsens 1-3 hours after meal or at night Associated with increased acid secretion
67
What are the results of a secretin test to determine if there is normal pancreatic function vs. a pancreatic tumor (gastrinoma)?
Normal Secretin stimulates bicarbonate production -> increased pancreatic juice pH Gastrinoma (pancreatic tumor) Secretin paradoxically increases gastrin levels (more acidic) Key differentiator is a higher vs lower pH
68
What are complications from chronic gastritis?
Mucosal atrophy (significant loss of parietal cell mass) Intestinal metaplasia Normal stomach cells adapt to become more like intestinal cells after prolonged irritation Precancerous! Dysplasia (abnormal growth and development) Gastritis Cystica Cyst formation in the stomach
69
What are the types of intestinal obstructions? (mechanical)
Adhesions, hernias, tumor formation
70
What are the types of intestinal obstructions? (functional)
Paralytic ileus Muscle dysfunction or nerve dysfunction
71
What are the types of intestinal obstructions? (complete vs partial)
Partial can be managed by NPO, NG tube, decompression, IV fluid Complete is surgical emergency
72
Irritable Bowel Syndrome (IBS) vs Irritable Bowel Disease (IBD)
IBS: Functional disorder, no structural abnormalities Dx: abdominal pain 3 days per month for 3+ months with improvement after defecating With change in stool frequency or form Diarrhea/Constipation predominant or both IBD: Chronic condition Involves inflammation with potential structural changes Comprised of Crohn’s and Ulcerative Colitis
73
Liver failure s/s - metabolic
Hypoglycemia Hypoalbuminemia (edema) Hepatic encephalopathy
74
Liver Fx
Stores glycogen Glucose access Hormone metabolism (from vitamin) Substance detoxification (by making things water soluble for excretion) Produces bile Conjugates bilirubin for excretion
75
Liver failure s/s - impaired detoxification
Jaundice Bleeding and bruising (d/t low synthesis of clotting factors)
76
Liver failure s/s - portal HTN
Esophageal varices Ascites Splenomegaly
77
Liver failure s/s - overall
Reduced immune fxn Decreased bile production Signs/Symptoms by System Skin: Jaundice, spider angiomas, palmar erythema, bruising. Abdomen: Ascites, hepatomegaly (if not shrunken in cirrhosis), caput medusae (dilated abdominal veins). Neurological: Confusion, lethargy, asterixis, coma (hepatic encephalopathy). Gastrointestinal: Nausea, vomiting, esophageal varices (hematemesis), anorexia. Cardiovascular: Hypotension (reduced albumin and vascular tone).
78
Explain how ascites occurs in liver cirrhosis
Portal HTN and hypoalbuminemia increase capillary oncotic pressure Fluid now pushed out and leaks into the peritoneal cavity
79
Know location and causes of portal hypertension
pic on doc
80
Etiology: Pre-hepatic
Portal vein thrombosis/ increased pressure in portal venous system External compression by tumors or cysts Structural abnormalities
81
etiology: Intrahepatic
Cirrhosis, hepatitis, fibrosis, liver tumors Anything disrupting normal liver blood flow inside the liver NASH (nonalcoholic steatohepatitis)
82
etiology: post hepatic
Right HF IVC thrombosis/obstruction Pericarditis Thickened pericardium impeding venous return from liver
83
etiology: general
Alcohol abuse with high risk cirrhosis Chronic viral hepatitis Autoimmune liver disease Obesity and infection
84
Understand bile metabolism and general causes for jaundice
Bilirubin is a byproduct/component of bile, helps digest fats Stored in gallbladder Secreted into duodenum Impaired liver function, bile duct obstruction, or excessive RBC breakdown -> bilirubin accumulation Accumulation in bloodstream (unconjugated) -> yellow discolorations
85
AST/ALT
Elevated indicate hepatocyte injury
86
Alk Phos
Elevated indicates cholestasis (slowing/stalling of bile flow)
87
Bilirubin
High levels indicate impaired excretion/metabolism
88
Albumin
Low levels suggest chronic disease Albumin synthesized in liver to maintain capillary oncotic pressure
89
Prothrombin Time (PT)
Prolonged PT indicates poor synthesis of clotting factors
90
How are amylase and lipase levels affected in acute pancreatitis?
Amylase/Lipase levels increased d/t damage and inflammation in pancreatic tissue -> released into bloodstream
91
hepatities
transmission, vaccines, tx, prevention
92
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Advance Pathophysiology (8 decks)

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