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pipi&pi2 > Conditions > Flashcards

Conditions Flashcards

1
Q

What is PUD?

A
  • Erosion of the GIT (usually proximal duodenum and stomach)
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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)
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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
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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
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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
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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
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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
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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
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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
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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
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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)
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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
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13
Q

What are the 4 parts of the colon?

A

1) Ascending (right)
2) Transverse
3) Descending (left)
4) Sigmoid

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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

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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
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16
Q

What food should px on colostomy bag avoid?

A
  • Eggs, garlic, cabbage, onion
  • Beer, radishes, soy products
  • Chocolate, spicy food, alcohol
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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
Q

What is cholecystitis and what is it caused by?

A
  • 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
Q

What is in the biliary tree?

A
  • Liver
  • Gallbladder
  • Bile ducts
27
Q

Acute vs chronic cholecystitis?

A
  • Acute: Bile builds up in gallbladder and irritates mucosal lining, causing inflammation
  • Chronic: Ongoing inflammation causes fibrosis and calcification
28
Q

Symptoms of acute cholecystitis?

A
  • Pain on RUQ of epigastric region
  • Boas sign (pain in right shoulder)
  • Positive Murphy sign (pain when breathing in)
  • Intolerance for fatty food
29
Q

What is the definitive treatment for cholecystitis?

A
  • 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
Q

What are the major causes of cirrhosis?

A
  • Chronic Help B/C
  • Alcoholic liver disease
  • Nonalcoholic fatty liver disease
  • Hemochromatosis (too much iron in blood)
31
Q

What is cirrhosis and liver failure?

A
  • Irreversible end stage of hepatitic injuries
  • Characteristics:
    ~ Fibrosis surrounding liver nodules
    ~ Presence of regenerative nodules (distorted liver architecture)
    ~ No cell hyertrophy
32
Q

What is ascites?

A
  • Accumulation of water in the peritoneal cavity
  • Complication of liver cirrhosis
33
Q

What is the management strategy for ascites?

A
  • 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
Q

Are there alternative diuretics that can be used?

A
  • Eplerenone (same family as Spironolactone)
  • Amiloride (for px with tender gynecomastia)
  • Hydrochlorothiazide (may cause rapid hyponatremia if added to basic 2 drugs)
35
Q

What is the management for hepatic encephalopathy?

A
  • 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
Q

What are the s/s of cirrhosis?

A
  • Jaundice
  • Ascites
  • Anemia/Leukopenia/Thrombocytopenia
  • Collateral channgels/Caput medusae
  • Haemorroids
  • HE
37
Q

What are the mechanisms leading to ascites?

A
  • Increased hydrostatic pressure (from Pulmonary HTN)
  • Salt and water retention by kidneys
  • Decreased colloidal osmotic pressure due to impaired albumin synthesis
38
Q

Type of Hepatitis?

A

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
Q

How does liver cirrhosis lead to hepatic encephalopathy?

A
  • Liver unable to convert ammonia into ammonium
  • Ammonia buildup crsses the BBB and impair CNS funcitoning -> HE
40
Q

What does HbsAg, HbsAb, HbcAg and HbeAg mean?

A
  • 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
Q

Types of jaundice?

A

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
Q

What is the treatment for Hepatitis B?

A
  • 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

pipi&pi2 (16 decks)

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