Conditions Flashcards
What is PUD?
- Erosion of the GIT (usually proximal duodenum and stomach)
What is the pathophysiology of PUD?
- Gastric lining is damaged when gastric juices overpower protective mechanisms (tightly joined epithelial cells which resist penetration and protective layer of mucus)
What are the signs and symptoms of PUD?
- Epigastric pain
- Gastric ulcers: Pain 15-30 mins after meals
- Duodenal ulcers: Pain 2-3 hours after meal
- Bloating, fullness, nausea
- Hematemesis or melena if erosion reaches muscularis
- Fatigue, pallor or SOB from anemia
How does PUD progress to peritonitis?
- Ulcer perforates through all 4 layers of gastric lining and into peritoneal cavity
- Free air and gastric contents entering peritoneum cause infection
How do risk factors contribute to PUD?
- H. pylori infection
~ Inflammatory response disrupts protective mechanisms in the gastric mucosa - NSAIDs
~ Inhibits prostalglandin synthesis, which is used in gastric mucosa protection - Smoking/alcohol
~ Reduces blood flow to mucosa and result sin cell death and poor healing
~ Increases cell permeability - (Rare) Zollinger-Ellison syndrome
~ Increases gastric acid secretion
Diagnosis of PUD?
- History and PA
- Biopsy or urea breath test to detect H, pylori
- Fecal occult blood to test for bleeding/anemia
Treatment for PUD?
- Discontinue use of NSAIDs
- PPI/H2RA to decrease production of stomach acid
- Avoid caffeine, alcohol and fatty, processed food
- Triple therapy if H. pylori detected
How is H. Pylori infection transmitted?
- Fecal-contaminated food
- Intrafamilial clustering of infection
- Bacteria survives from pH 4-8 but grows best in pH 6-8
What is the 2-pronged approach to treating H. Pylori infection? (IMPT)
- 2 antibiotics (Clarithromycin + Amoxicillin)
~ 500mg Clarithromycin 2x/day
~ 1000mg Amoxicillin 2x/day
~ Monitor I/O (due to diarrhea/vomiting)
~ Check for rash (first signs of allergy) or anaphylaxis
~ Check ECG (first QTC prolongation)
~ Taken after food - 1 Acid suppressing agent (Esomeprazole)
~ Esomeprazole is a PPI
~ 20-40mg 2x/day
~ Makes gastric juice more alkaline and promotes ulcer healing
~ Monitor for rash, anaphylaxis, dry mouth
~ Taken on an empty stomach/30 mins-1 hr before food
~ Pills cannot be crushed
Why do antibiotics and esomeprazole have to be taken together when treating H. pylori infection?
- H. Pylori grows better in increased pH (whichc occurs when PPI is used)
- Antibiotics work better when H. Pylori is multiplying
How long does the 3-pronged approach usually take?
- Duodenal ulcers: 4-8 weeks
- Gastric ulcers: 8-12 weeks
- Need to discontinue therapy 2 weeks before tests done to confirm eradication (Urea Breath Test)
Why is H. Pylori infection hard to treat?
- Breaks down urea into ammonia which is toxic to the membrane/lining
- Corkscrew shape allows bacteria to burrow in the wall, making it hard to get rid of
What are the 4 parts of the colon?
1) Ascending (right)
2) Transverse
3) Descending (left)
4) Sigmoid
What is the analgesic/pain relief ladder?
Step 1:
- NSAIDs or paracetamol
~ NSAIDs not to be given for px with PUD
Step 2:
- Mild opioids
~ Codeine, tramadol
Step 3:
- Strong opioids
~ Morphine, fentanyl
~ Can be administered continuously or by PCA
What are signs and symptoms of colon cancer?
- Obstruction
- Decreased calibre/narrowing of stool
- Constipation/diarrhea
- Colicky pains
- Blood in stool
- IDA
- Vomiting
- Barium enema (test) showing apple core sign in intestines
What food should px on colostomy bag avoid?
- Eggs, garlic, cabbage, onion
- Beer, radishes, soy products
- Chocolate, spicy food, alcohol
What tests can be used to diagnose colon cancer?
- Colonoscopy or sigmoidoscopy with biopsy
- Oesophagogastroduodenoscopy (OGD)
- Hb, HCT and WBC on blood tests
- C-urea breath test (Urea broken down into ammonium and bicarbonate, which goes to the lungs and is exhaled out as CO2)
What are the layers of the GIT?
1) Mucosa (innermost)
- Epithelial lining
- Enables nutrient and fluid absorption
2) Submucosa
- Blood vessels, lymphatics and nerves
- Dense tissue
3) Muscular
- Aids in peristalsis
4) Serosa/adventitia (outermost)
- Faces peritoneal cavity
- A bit of serous fluid
What are the causes of intestinal obstruction?
1) Mechanical
- Actual blockage
- Either partial or complete
- Simple (blood supply maintained) or strangulated (compromised)
2) Functional
- Disrupts peristalsis
- Even without blockage, food will still not move through
What can lead to mechanical obstruction?
- Postoperative adhesions/fibrous tissue during healing
- Hernia
- Intussusception
- Volvulus (tied and kinked off)
- Tumors
- Fecal impaction
- Foreign body
What can lead to functional obstruction of the intestine?
- Any condition that reduces smooth muscle contractility
- Transient paralysis of SM in intestines (due to trauma from thrombus)
- Electrolyte abnormalities
- IBS
- Crohn’s disease
What is the pathology of intestinal obstruction?
- Stool and gas start to accumulate, causing bowel to dilate and abdomen to expand
- Increased pressure from accumulation causes intestinal contents to push against wall and compress the mucosal blood and lymphatic vessels.
- Pressure forces water in vessels into surrounding tissues -> edema, inflammation and damage
- Further compression can lead to ischemia
What are the clinical manifestations of intestinal blockage?
- Abdominal pain
- Vomiting (Projectile, bile may present)
- Diarrhea/constipation
- Distal small bowel block has ^ of vomiting which may contain feces
- Proximal small bowel block has more abdominal distention
- Large bowel obstruction will have no or late onset vomiting w/ significant abdominal distention
What food to avoid when px has constipation?
- Broccoli, brussel sprouts, cabbage, sodas
- White bread, rice, red meat
What is cholecystitis and what is it caused by?
- Inflammation of the gallbladder
- Caused by biliary stasis, so bile flow is impaired
1) Calculous type
- Most common
- Usually from cholelithiasis (gallstone)
2) Acalculous type
- Gallbladder dysfunction leading to impaired emptying
- Usually due to ischemia of gallbladder
What is in the biliary tree?
- Liver
- Gallbladder
- Bile ducts
Acute vs chronic cholecystitis?
- Acute: Bile builds up in gallbladder and irritates mucosal lining, causing inflammation
- Chronic: Ongoing inflammation causes fibrosis and calcification
Symptoms of acute cholecystitis?
- Pain on RUQ of epigastric region
- Boas sign (pain in right shoulder)
- Positive Murphy sign (pain when breathing in)
- Intolerance for fatty food
What is the definitive treatment for cholecystitis?
- Cholecystectomy (removal of gallbladder)
- Gallbladder drainage
- Sims position (lying on side with leg stretched out) to move CO2 away from the nerve and make breathing easier
- Consume high fibre foods
What are the major causes of cirrhosis?
- Chronic Help B/C
- Alcoholic liver disease
- Nonalcoholic fatty liver disease
- Hemochromatosis (too much iron in blood)
What is cirrhosis and liver failure?
- Irreversible end stage of hepatitic injuries
- Characteristics:
~ Fibrosis surrounding liver nodules
~ Presence of regenerative nodules (distorted liver architecture)
~ No cell hyertrophy
What is ascites?
- Accumulation of water in the peritoneal cavity
- Complication of liver cirrhosis
What is the management strategy for ascites?
- Diuretics (Spironolactone + Furosemide)
~ Spironolactone (K-sparing) 50-400mg once/day
~ Furosemide (Loop) 20-360mg in divided doses
~ Need to be taken together as 1 removes K+, one spares them
~ Relieves symptoms and congestion as they remove water from the body~ Need to monitor K+ levels, I/O, weight, abdominal girth, BP and gynecomastia - Sodium restriction
~ Max 2g/day (low salt diet)
Are there alternative diuretics that can be used?
- Eplerenone (same family as Spironolactone)
- Amiloride (for px with tender gynecomastia)
- Hydrochlorothiazide (may cause rapid hyponatremia if added to basic 2 drugs)
What is the management for hepatic encephalopathy?
- Lactulose as 1st choice
~ 30 ml 3-6x/day
~ Ensure >2x BO
~ To convert ammonia to ammonium and has a prebiotic effect - Rifaximin as add-on antibiotic
~ 550mg 2x/day
~ To modulate gut flora overgrowth - Both to treat and prevent HE
What are the s/s of cirrhosis?
- Jaundice
- Ascites
- Anemia/Leukopenia/Thrombocytopenia
- Collateral channgels/Caput medusae
- Haemorroids
- HE
What are the mechanisms leading to ascites?
- Increased hydrostatic pressure (from Pulmonary HTN)
- Salt and water retention by kidneys
- Decreased colloidal osmotic pressure due to impaired albumin synthesis
Type of Hepatitis?
1) Viral
- Hep A (fecal-oral, person-to-person/sexual)
- Hep B,C,D (person-person/sexual/body fluids)
- Hep B (mother to baby)
- Hep D (in the presence of Hep B)
- Hep E (fecal-oral)
2) Non-viral
- Alcohol, medications
- Autoimmunity
3) Acute
- Quick and severe damage to the liver
- < 6 months
4) Chronic
- Progressive damage to the liver
- > 6 months
- Can manifest as hepatic cytolysis (liver cells destroyed and leak out enzymes)
How does liver cirrhosis lead to hepatic encephalopathy?
- Liver unable to convert ammonia into ammonium
- Ammonia buildup crsses the BBB and impair CNS funcitoning -> HE
What does HbsAg, HbsAb, HbcAg and HbeAg mean?
- HbsAg (surface antigen): Current infection, usually acute
- HbsAb (Antibody): Develops when px recovers from infection or shows vaccination
- HbcAg (core antigen): Shows previous infection
- HbeAg (envelope protein): Usually in newly infected px, with high infectiousness and viral load
Types of jaundice?
1) Hemolytic
- By hemolysis of RBC
- Hemolytic anemia, sicle cell anemia, G6PD, blood transfusion rxn, reabsorption of large hematomas
2) Hepatocellular
- Conditions that damage the liver
- Hepatitis, cirrhosis, liver failure
- Medications that causes hepatotoxicity (acetaminophen, rifampin)
3) Obstructive
- By blocked ducts
- Gallstones, pancreatitis, pregnancy
What is the treatment for Hepatitis B?
- Entecavir (Antiviral)
~ 0.5-1mg once/day
~ Given on an empty stomach before or after a meal
~ To reduce viral DNA synthesis
~ Usually given indefinitely
