Conditions Flashcards
1
Q
What is PUD?
A
- Erosion of the GIT (usually proximal duodenum and stomach)
2
Q
What is the pathophysiology of PUD?
A
- Gastric lining is damaged when gastric juices overpower protective mechanisms (tightly joined epithelial cells which resist penetration and protective layer of mucus)
3
Q
What are the signs and symptoms of PUD?
A
- 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
4
Q
How does PUD progress to peritonitis?
A
- Ulcer perforates through all 4 layers of gastric lining and into peritoneal cavity
- Free air and gastric contents entering peritoneum cause infection
5
Q
How do risk factors contribute to PUD?
A
- 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
6
Q
Diagnosis of PUD?
A
- History and PA
- Biopsy or urea breath test to detect H, pylori
- Fecal occult blood to test for bleeding/anemia
7
Q
Treatment for PUD?
A
- 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
8
Q
How is H. Pylori infection transmitted?
A
- Fecal-contaminated food
- Intrafamilial clustering of infection
- Bacteria survives from pH 4-8 but grows best in pH 6-8
9
Q
What is the 2-pronged approach to treating H. Pylori infection? (IMPT)
A
- 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
10
Q
Why do antibiotics and esomeprazole have to be taken together when treating H. pylori infection?
A
- H. Pylori grows better in increased pH (whichc occurs when PPI is used)
- Antibiotics work better when H. Pylori is multiplying
11
Q
How long does the 3-pronged approach usually take?
A
- 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)
12
Q
Why is H. Pylori infection hard to treat?
A
- 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
13
Q
What are the 4 parts of the colon?
A
1) Ascending (right)
2) Transverse
3) Descending (left)
4) Sigmoid
14
Q
What is the analgesic/pain relief ladder?
A
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
15
Q
What are signs and symptoms of colon cancer?
A
- Obstruction
- Decreased calibre/narrowing of stool
- Constipation/diarrhea
- Colicky pains
- Blood in stool
- IDA
- Vomiting
- Barium enema (test) showing apple core sign in intestines
16
Q
What food should px on colostomy bag avoid?
A
- Eggs, garlic, cabbage, onion
- Beer, radishes, soy products
- Chocolate, spicy food, alcohol
17
Q
What tests can be used to diagnose colon cancer?
A
- 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)
18
Q
What are the layers of the GIT?
A
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
19
Q
What are the causes of intestinal obstruction?
A
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
20
Q
What can lead to mechanical obstruction?
A
- Postoperative adhesions/fibrous tissue during healing
- Hernia
- Intussusception
- Volvulus (tied and kinked off)
- Tumors
- Fecal impaction
- Foreign body
21
Q
What can lead to functional obstruction of the intestine?
A
- Any condition that reduces smooth muscle contractility
- Transient paralysis of SM in intestines (due to trauma from thrombus)
- Electrolyte abnormalities
- IBS
- Crohn’s disease
22
Q
What is the pathology of intestinal obstruction?
A
- 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
23
Q
What are the clinical manifestations of intestinal blockage?
A
- 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
24
Q
What food to avoid when px has constipation?
A
- Broccoli, brussel sprouts, cabbage, sodas
- White bread, rice, red meat
25
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
26
What is in the biliary tree?
- Liver
- Gallbladder
- Bile ducts
27
Acute vs chronic cholecystitis?
- Acute: Bile builds up in gallbladder and irritates mucosal lining, causing inflammation
- Chronic: Ongoing inflammation causes fibrosis and calcification
28
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
29
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
30
What are the major causes of cirrhosis?
- Chronic Help B/C
- Alcoholic liver disease
- Nonalcoholic fatty liver disease
- Hemochromatosis (too much iron in blood)
31
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
32
What is ascites?
- Accumulation of water in the peritoneal cavity
- Complication of liver cirrhosis
33
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)
34
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)
35
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
36
What are the s/s of cirrhosis?
- Jaundice
- Ascites
- Anemia/Leukopenia/Thrombocytopenia
- Collateral channgels/Caput medusae
- Haemorroids
- HE
37
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
38
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)
39
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
40
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
41
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
42
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
