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500 vocabulary flashcards covering gastrointestinal, urinary, respiratory, endocrine, neurological, musculoskeletal, and cardiovascular system disorders based on lecture notes.
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Peptic Ulcer Disease (PUD)
Ulceration of GI mucosa and underlying tissues caused by gastric secretions that have a low pH (acidic).
Most common location of Peptic Ulcer Disease
Duodenum (98−99%) or the stomach (ratio of 4:1).
Chronic peptic ulcer definition
Gastritis.
Commonest cause of Peptic Ulcer Disease
H. pylori infection.
Zollinger Ellison syndrome
Tumor secreting gastrin which increases HCl secretion, causing peptic ulcer disease.
Medication causes of PUD
NSAIDs, aspirin, steroids, and Indomethacin.
Blood type associated with PUD
Blood type O.
Duodenal Ulcer incidence
4 times more common than Gastric Ulcer.
Duodenal Ulcer common age group
20−50yr.
Duodenal Ulcer primary location
First part (2cm) of the duodenum.
Duodenal Ulcer pain pattern
Food-relief pattern (reduced by food or antacids).
Duodenal Ulcer pain timing
Burning epigastric pain that occurs 2−4hours after eating; night pain is common.
Duodenal Ulcer stool manifestation
Melena is more common.
Duodenal Ulcer palpation finding
Deep tenderness in right hypochondrium.
Gastric Ulcer common age group
>60yr.
Gastric Ulcer primary etiology
Disruption of the mucosal barrier.
Gastric Ulcer primary location
Lesser curvature and pyloric antrum.
Gastric Ulcer pain pattern
Food-pain pattern (no night pain).
Gastric Ulcer pain timing
Burning epigastric pain that occurs 1−2hours after eating.
Gastric Ulcer common clinical features
Vomiting, hematemesis, significant loss of weight, and deep tenderness in the epigastric region.
Pyrosis
Heartburn.
Bismuth administration in PUD
2tab 1hour AC (stools will be stained black).
Sucralfate dosing rule
2mg BD; do not use antacids half an hour before or after the dose as it reduces effectiveness.
Triple therapy duration for H. pylori
6weeks (one drug from each specified column).
Triple therapy Column A drug options
Clarithromycin 500mg BD, Amoxicillin 500mg BD, or Tetracycline.
Triple therapy Column B drug options
Metronidazole 400mg TDS or Tinidazole.
Triple therapy Column C drug options
Omeprazole 20mg BD, Pantoprazole 40mg BD, or Lansoprazole.
Quadruple treatment duration for H. pylori
14days.
Quadruple treatment regimen for H. pylori
PPI standard dose (or ranitidine 150mg PO BD) + Bismuth 525mg PO QID + Metronidazole 500mg PO QID + Tetracycline 500mg PO QID.
Preferred positioning for PUD nursing management
Semi-Fowler's position.
Billroth I
Gastroduodenostomy; removal of the lower part of the stomach and attachment to the duodenum.
Billroth II
Gastrojejunostomy; removal of the antrum and distal portion of the stomach with anastomosis of the remaining section to the jejunum.
Antrectomy
Removal of the antrum portion of the stomach.
Gastrectomy
Removal of 60%−80% of the stomach.
Complications of PUD
Pyloric or duodenal obstruction, hemorrhage, ulcer perforation, and iron deficiency.
Complications of PUD Surgery
Dumping Syndrome, hemorrhage, pneumonia, and pernicious anemia.
Dumping Syndrome (DS)
Rapid gastric emptying; rapid passage of food (especially carbohydrates/sugar) from the stomach to the jejunum/duodenum.
Most common condition following Bariatric surgery
Dumping Syndrome.
Early Dumping Syndrome timing
GI and vasomotor symptoms occur 10−30minutes after a meal.
Early Dumping Syndrome GI symptoms
Abdominal pain, bloating, borborygmi, diarrhea, nausea, and vomiting.
Early Dumping Syndrome Vasomotor symptoms
Diaphoresis, flushing, headache, hypotension, palpitations, syncope, and tachycardia.
Late Dumping Syndrome timing
Adrenergic and neuroglycopenic symptoms occur 2−3hours after eating.
Late Dumping Syndrome Adrenergic symptoms
Palpitations, perspiration, and tremors.
Late Dumping Syndrome Neuroglycopenic symptoms
Difficulty concentrating, fatigue, hunger, and syncope.
Liver Cirrhosis
Irreversible fibrosis and degeneration of the liver where normal functioning parenchyma is replaced with scar tissue and regenerative nodules.
Alcoholic cirrhosis
Cirrhosis related to alcohol abuse; alcoholism is the main cause of liver cirrhosis.
Post necrotic macro-nodular cirrhosis
Most common type of cirrhosis, related to hepatitis B and hepatitis C.
Biliary cirrhosis
Cirrhosis related to biliary stasis in the hepatic duct; may be an autoimmune response.
Cardiac cirrhosis
Cirrhosis related to long-term right-sided heart failure (associated with peripheral edema).
Fetor hepaticus
Musty, sweetish odor of the breath seen in liver cirrhosis.
Cause of Esophageal Varices in cirrhosis
Portal hypertension.
Delirium in liver failure cause
Increased blood ammonia level.
Best diagnostic method for Liver Cirrhosis
Liver biopsy.
Serum enzyme changes in liver cirrhosis
Increased AST, ALT, ALP, and GGT due to release from damaged hepatic cells into the bloodstream.
Albumin levels in liver cirrhosis
Decreased serum albumin due to dilution from fluid retention (ascites).
Prothrombin Time in liver cirrhosis
Prolonged Prothrombin Time due to failure of the liver to produce sufficient clotting factors.
Medications to decrease blood ammonia in cirrhosis
Neomycin and Lactulose.
Abdominal paracentesis
Also known as abdominal tapping; procedure to remove excess abdominal fluid.
Cirrhosis dietary protein and sodium guidelines
Protein restricted to 80−100g/day and sodium restricted to 500−1000mg/day.
Hepatic Encephalopathy (Hepatic Coma)
Gradual or sudden onset of altered level of consciousness as a result of liver failure.
Hepatic Encephalopathy dietary restrictions
Protein reduced to 15−30g, high calorie diet (1500−2000kcal), and minimized fluid intake.
Vasopressin mechanism in esophageal varices
Decreases portal pressure in portal hypertension.
Sengstaken-Blakemore Tube
Balloon tamponade device used to control bleeding from esophageal varices by applying direct pressure.
Octreotide mechanism in esophageal varices
Constricts splanchnic arterioles, decreasing blood inflow to the portal system and significantly reducing intra-variceal pressure.
Appendicitis
Compromised circulation and inflammation of the vermiform appendix; more common in males (>30yrs).
Fecalith (appendicolith)
Calcified mass formed by hardened fecal matter causing obstruction in the appendix.
Parasite associated with appendicitis
Enterobius vermicularis (worm).
McBurney's point pain location
Right lower quadrant pain characteristic of appendicitis.
Rovsing's sign
Pain elicited in the right lower quadrant when palpation pressure is applied to the left lower quadrant.
Psoas sign
Right lower quadrant pain elicited with extension of the right hip or flexion of the right hip against resistance.
Obturator sign
Right lower quadrant pain on passive internal rotation of the hip when the right knee is flexed.
Bloomberg's sign
Rebound tenderness observed in appendicitis.
Intestinal Obstruction
Interference with peristaltic movement of intestinal contents; obstruction in the forward movement of fecal contents.
Volvulus
Twisting of the intestine; the commonest cause of intestinal obstruction in Nepal.
Intussusception
Telescoping of the bowel into itself.
Mesenteric infarction
Occlusion of arterial blood supply to the bowel leading to necrosis.
Peritonitis
Inflammation of the peritoneal cavity.
Commonest causative organism of peritonitis
E. coli.
Cholelithiasis
Stone formation in the gallbladder.
5F risk factors for Cholelithiasis
Female, fertile, fatty, forty, and fair.
Cholecystitis
Inflammation of the gallbladder, enlarged lymph nodes, or tumor of the gallbladder; main cause is a gallstone blocking the cystic duct.
Murphy sign
Rebound tenderness in abdomen that increases on inspiration; classic sign of cholecystitis.
Steatorrhea
Presence of excess fat in the stool.
Oral dissolution therapy drugs for small gallstones
Chenodiol (Chenodeoxycholic acid; CDCA) or Ursodiol (UDCA) given for 6−12months.
Antispasmodic given in cholecystitis
Baralgan 5mL IV.
Expected T-tube bile drainage post-cholecystectomy
300−500mL of bile-colored drainage for the first 24hours, decreasing to 200mL/24hours for 3−4days.
Pancreatitis
Inflammation of the pancreas characterized by escape of pancreatic juice into surrounding tissue leading to fat necrosis.
Acute pancreatitis mechanism
Auto-digestion of the pancreas by pancreatic enzymes (Trypsin).
Most common cause of pancreatitis
Gallstones.
Cullen sign
Peri-umbilical bruising seen in severe necrotizing pancreatitis.
Grey Turner's sign
Flank bruising seen in severe necrotizing pancreatitis.
Glasgow Criteria for Acute Pancreatitis (PANCREAS)
PaO2 <8kPa (60mmHg), Age >55years, Neutrophils WBC >15×109/L, Calcium <2mmol/L, Renal Urea >16mmol/L, Enzymes LDH >600IU/L or AST/ALT >200IU/L, Albumin <32g/L, Sugar glucose >10mmol/L (3 or more denotes severity).
Haemorrhoids
Collection of dilated, tortuous plexuses of veins covered by mucous membrane at the anorectal junction.
Grade I Haemorrhoid
No prolapse; prominent blood vessels that only bleed.
Grade II Haemorrhoid
Prolapse upon bearing down, but reduces spontaneously.
Grade III Haemorrhoid
Prolapse upon bearing down that requires manual reduction.
Grade IV Haemorrhoid
Permanent prolapse that cannot be manually reduced.
Positions of the three prominent hemorrhoidal cushions
Left lateral (3o’clock), Right posterior (7o’clock), and Right anterior (11o’clock).
Sclerotherapy for 2nd degree hemorrhoids
Submucosal injection of 5% phenol in arachis oil or almond oil above the pectinate line.
Reducible Hernia
Protruding organ or structure that can be manipulated back into place.