Pass Ccrn Gastrointestinal: Conditions

Front 1

Mallory-Weiss tear

Back 1

acute longitudinal tear of the esophagus caused by forceful retching

Front 2

what bacteria causes ulcer disease

Back 2

helicobacter pylori

Front 3

common causes of upper GI hemorrhage

Back 3

peptic ulcer disease, cirrhosis (portal htn), mallory-weiss tear, gastritis

Front 4

meds for upper GIB (IV gtts)

Back 4

vasopressin (constricts arterial bed, decreases portal venous pressure), octreotide (reduces splanich blood flow, gastric acid sxrn and motility)

Front 5

sclerotherapy

Back 5

agent is injected into varices, causing inflammation and later scar tissue

Front 6

balloon tamponade for varices, management

Back 6

HOB 45', pt can't swallow with tube in so frequent suctioning, scissors ready if balloon moves into pharynx and obstructs breathing,

Front 7

types of gastrectomy

Back 7

partial (Billroth I or II) or total

Front 8

Billroth I

Back 8

partial gastrectomy. antrectomy, vagotomy(resection vagus nerve) and gastroduodenostomy

Front 9

Billroth II

Back 9

partial gastrectomy. antrectomy, vagotomy (resectio vagus nerve) and gastrojejunostomy (stomach connects to jejunum)

Front 10

total gastrectomy

Back 10

gastrectomy with esophagus anastomosed to duodenum or jejunum

Front 11

early dumping syndrome

Back 11

common complicatino of gastrectomy. Problem is hyperosmolar dump of food into duodenum (absence pyloric valve), clammy & dizzy, tachycardia. 30 minutes post meal.

Front 12

late dumping syndrome

Back 12

hyperinsulinism effect r/t an increase in insulin production by the pancreas in response to a large bolus of food causing an increase in blood glucose, 2 hrs post meal, dizzy, clammy tachycardia

Front 13

TIPS procedure

Back 13

invasive angiographic method, connection made between hepatic and portal veins and a stent is paced in the tract. This decrease portal HTN (cause of esophageal varice bleed)

Front 14

Types of viral hepatitis (letters)

Back 14

A, B, C, D, E, F and G (very little known)

Front 15

Hepatitis A

Back 15

fecal/oral. Acute onset (never chronic). 99% resolves, supportive treatment.

Front 16

Hepatitis B

Back 16

parenteral/sexual/perinatal. Chronicity rare. Treatment: interferon, antivirals. Cancer in 20%.

Front 17

Hepatitis C

Back 17

parenteral/sexual/perinatal. Chronicity 50-60%. 40-50% develop cirrhosis, 20% liver failure. Treatment: interferon, corticosteroids.

Front 18

Hepatitis D

Back 18

superinfection in patient with chronic hepatitis B, same treatment as for Hep B.

Front 19

viruses that can cause acute liver failure

Back 19

fulminant hepatitis (all types), herpes simplex & zoster, Epstein-Barr, Adenovirus, cytomegalovirus

Front 20

hepatotoxic drugs that can cause liver failure

Back 20

acetaminophen, halothane, methyldopa, isoniazid, ectasy, toxins (mushrooms, sea anemone sting)

Front 21

Budd Chiari syndrome

Back 21

hepatic vein obstruction

Front 22

causes of acute exacerbation in chronic liver failure

Back 22

primary/metastatic tumors of liver, cirrhosis, Wilson's disease

Front 23

Wilson's disease

Back 23

genetic disorder where copper accumulates in tissues (causes liver disease and neuro stuff)

Front 24

cirrhosis

Back 24

liver parenchymal cells are destroyed progressively and are replaced with fibrotic tissue

Front 25

what % of liver can be destroyed (in cirrhosis) before symptoms appear?

Back 25

3/4

Front 26

How does cirrhosis cause portal HTN?

Back 26

distortion, twisting and constrictino of central sections cause impedance of portal blood flow

Front 27

fulminant hepatitis

Back 27

liver cells fail to regenerate and necrosis occurs

Front 28

If portal HTN causes splenomegaly, what problems can occur?

Back 28

thrombocytopenia (low platelets) and vitamin K deficiency

Front 29

When liver is unable to produce adequate amounts of bile and is impaired in protein, carb and fat metabolism (d/t portal HTN), what issues arise?

Back 29

1) serum bili is elevated because liver can't conjugate it and make bile. 2) deficiency of fat soluble vitamins may occur since bile salts aren't available. 3) hypoglycemia if liver can't produce fxn of glycogenolysis (carbs to simple sugars) and gluconeogenesis (fats/proteins to simple sugars)

Front 30

If liver is unable to manufacture plasma proteins and inactive hormones (aldosterone, estrogen) what problems arise?

Back 30

decreases proteins cause fluid shifts and edema can occur (pleural effusions, ascites). Increased circulating levels of aldosterone cause sodium and water retention thus hypoK, Hypocalcemia and hypomag.

Front 31

Babinski's reflex

Back 31

sole of foot is hit, foot extends (not flexes). Can be sign of neuro damage (encephalopathy)

Front 32

steatorrhea

Back 32

excessive fat in stool (liver disease)

Front 33

Stage I encephalopathy

Back 33

mild confusion, decreased attention span, forgetful, irritabel, personality changes, EEG normal

Front 34

Stage II encephalopathy

Back 34

lethargy, confusion, apathy, tremor (liver flap), slowing of EEG,

Front 35

Stage III encephalopathy

Back 35

severe confusion, incomprehensible speech, hyperactive deep tendon reflexes, EEG abnormal (intubation usually required)

Front 36

Stage IV encephalopathy

Back 36

posturing/no response to stimuli, + Babinski's reflex, EEG abnormal

Front 37

drug for acetaminophen toxicity

Back 37

Mucomyst, administred within 24 hrs of acetaminophen

Front 38

LeVeen shunt

Back 38

uses positive abdominal pressure caused by the diaphragm descent during inspiration to open a intraperitoneal valve and shunt fluid from the peritoneum to the superior vena cava (for ascites)

Front 39

Denver shunt

Back 39

adds a SQ pump that can be compressed manually to irrigate the intraperitoneal tubing (relief of ascites)

Front 40

hyperammonemia and respirations

Back 40

causes respiratory alkalosis. At this point patient on ventilator d/t encephalopathy so make sure you control their respirations (paralysis)

Front 41

Why avoid LR in liver failure?

Back 41

liver converts lactate to bicarbonate, extra work for liver

Front 42

clinical indications of hepatorenal syndrome

Back 42

(renal failure d/t blood flow changes caused by liver failure) oliguria, low urine sodium, elevated BUN & creatinine

Front 43

azotemia

Back 43

a medical condition characterized by abnormally high levels of nitrogen-containing compounds, such as urea, creatinine, various body waste compounds, and other nitrogen-rich compounds in the blood. It is largely related to insufficient filtering of blood by the kidneys

Front 44

neomycin

Back 44

(aminoglycoside) kills the bacteria that convert nitrogenous wastes to ammonia

Front 45

lactulose in liver disease

Back 45

bonds with ammonia by changing gut pH, which results in ammonia excretion. Changes gut flora to foster growth of non-ammonia forming bacteria.

Front 46

When do you allow/restrict dietary protein in liver failure?

Back 46

increase it in cirrhosis and liver failure, restrict it in hepatic encephalopathy

Front 47

mild acute pancreatitis

Back 47

edematous pancreas with little necrosis damage, hypovolemia may occur as a result of fluid leak into peritoneal cavity.

Front 48

severe acute pancreatitis

Back 48

extensive necrosis or pancreas and peripancreatic tissue and fat: erosion into blood vessels; hemorrhage occurs; SIRS usually too

Front 49

common causes of pancreatitis

Back 49

obstruction of common bile duct (gallstone = cholelesthiasis MOST common, post ERP), ETOH, drugs, 20% idiopathic

Front 50

how do we decrease release of and destruction by pancreatic enzymes during pancreatitis?

Back 50

NPO during acute phase, NGT suction decompress stomach if ileum, drugs that decrease this Octreotide SQ & histamine receptor antagonists, keep environment free of food odors

Front 51

System for grading pancreatitis from CT findings

Back 51

Grade A = normal
Grade B = focal/diffuse enlargement
Grade C = Mild peripancreatic inflammatory changes
Grade D = fluid collection in a single location
Grade E = multiple fluid collections or gas within pancreas or peripancreatic inflammation

Front 52

What causes hypocalcemia in pancreatitis?

Back 52

inflammatory process causes necrosis of fat in pancreas and exudates with high albumin content leading to hypoalbuminemia and ascites: fat necrosis results in precipitation of calcium, leading to hypocalcemia

Front 53

pancreatic fistula

Back 53

caused by pancreatitis pancreas communicating with skin

Front 54

intestinal infarction

Back 54

necrosis of the intestinal wall resulting from ischemia

Front 55

intestinal obstruction (2 types)

Back 55

failure of the intestinal contents to progress forward through bowel lumen. Function (loss of peristalsis aka paralytic ileus) or structural (mechanical obstruction)

Front 56

2 types of structural intestinal obstructions (mechanical)

Back 56

simple = luminal obstruction without compromise of blood supply.
strangulated = luminal obstruction with compromise of blood supply.

Front 57

intestinal performation

Back 57

penetration of the lumen of intestine with resultant spillage of intestinal contents into peritoneal cavity

Front 58

causes of intestinal infarction

Back 58

emboli, hypercoagulability, vascular disease, surgical procedures involving aortic clamping, vasopressors, strangulated intestinal obstruction, infection, cirrhosis

Front 59

most common type of intestinal obstruction and which type is it?

Back 59

paralytic ileus (functional obstruction)

Front 60

what things can cause functional intestinal obstruction?

Back 60

(this is loss of peristalsis). abdominal surgery, hypoK, pancreatitis, peritonitis, severe trauma, PNM, spinal cord injury, narcotics, sepsis etc......

Front 61

What can cause peritonitis in bowel infarction?

Back 61

prolonged ischemia increases the permeability of the bowel and edema of the intestinal wall. Normal bowel flora (e coli) may penetrate the bowel wall, causing peritonitis

Front 62

obstruction specific to small intestine (unique problems)

Back 62

increased intraabdominal pressure puts pressure on diaphragm, causing atelectatic changes and possibly PNM. Reverse peristalsis occurs N&V early

Front 63

obstruction specifict to large intestines (unique problems)

Back 63

distention of bowel eventually causes perforation with leakage of intestinal bacteria into peritoneal cavity (peritonitis and sepsis). Vomiting is late symptom.

Front 64

flat plate of abdomen xray shows what in obstruction

Back 64

dilated loops of gas filled bowels

Front 65

bed rest activity to encourage obstruction/infarction/perforation patients to do

Back 65

knee flexion to relax abdominal muscles

Front 66

Biggest concern if bowel obstruction is present

Back 66

preventing perforation of bowel!

Front 67

drugs that enhance GI motility in partial intestinal obstruction

Back 67

erythromicin, Reglan, Octreotide

Front 68

Purpose of nasointestinal tube

Back 68

decompresses bowel, ONLY use if obstruction is reversible or patient can't have surgery (so NOT in paralytic ileus or complete intestinal obstruction). This tube moves through the GI tract by peristalsis. Once tube at final position (confirmed on X-ray) tape in place. Irrigate tube as required.

Front 69

how to prevent bowel performation in intestinal obstruction

Back 69

NPO, NGT low suction, drugs, maybe nasointestinal tube, rectal tube (reduce trapped air), therapeutic colonoscopy

Front 70

When is surgery indicated in intestinal performation/obstruction/infarction?

Back 70

vascular obstruction, complete bowel obstruction or bowel performation

Front 71

surgical procedure for infarction of bowel

Back 71

exploratory lap and embolectomy and/or arterial reconstruction with resection of irreparably damaged bowel

Front 72

surgical procedure for obstruction of bowel (when indicated)

Back 72

correction of cause:if adhesion, laparoscopic adhesiolysis, herniorrhaphy for hernia reduction, bowel resection for tumors/malignant lesions

Front 73

brachytherapy in colon cancer

Back 73

the placement of radioactive seeds in the area where the tumor was removed

Front 74

abdominal trauma

Back 74

trauma that occurs between the nipple line and mid thigh

Front 75

What abdominal organ is most often affected by penetrating trauma?

Back 75

liver

Front 76

what abdominal organ(s) is most often affected by blunt trauma? (crushing)

Back 76

spleen and then pancreas as well

Front 77

Kehr's sign

Back 77

left shoulder pain indicative of splenic rupture caused by blood below diaphragm that irritates the phrenic nerve

Front 78

Rovsing sign

Back 78

pain in RLQ with plapation of LLQ indicates peritoneal irritation

Front 79

Coopernail's sign

Back 79

ecchymosis of scrotum or labia indicative of fractured pelvis

Front 80

Ballance's sign

Back 80

resonance over right flank with patient on left side indicates ruptured spleen

Front 81

explain the FAST (focused abdominal sonography for trauma) study

Back 81

detects fluid or blood in the pericardium, abdomen, or pelvis and allows visualization of the spleen and liver (although test can't reliably identify injury to the intraabdominal organs, need CT for this, it can accurately predict the need for laparotomy in trauma patients)
BEDSIDE ULTRASOUND

Front 82

laparotomy

Back 82

large incision made through abdominal wall to gain access to abdominal cavity

Front 83

DPL (diagnostic peritoneal lavage). Explain study.

Back 83

can assess for intraabdominal bleeding, though FAST ultrasound is usually the preferred method. Put 1L NS into peritoneal catheter over 15 minutes (if peritoneal catheter fills with blood once inserted, go straight to ex. lap). Move patient side to side, drain fluid. Send for analysis. Considered positive if newsprint can't be read through lavage.

Front 84

What are the limitations of DPL study in terms of assessing for abdominal injuries

Back 84

does not detect diaphragmatic or retroperitoneal injuries

Front 85

Whipple procedure

Back 85

removal of lower stomach and duodenum w/ anastomosis of the remaining stomach to the jejunum with partial/total pancreatectomy and possible splenectomy
(done in cancer of pancreas or post necrotic tissues of pancreatitis)

Front 86

esophagogastrostomy

Back 86

removal of all or a portion of esophagus possibly with a portion of stomach, with anastomosis to the remaining portion of stomach

Front 87

esophagoenterostomy

Back 87

removal of all or a portion of the esophagus along with replacement with a segment of the colon

Front 88

total colectomy and ileostomy

Back 88

removal of the entire large intestine and the formation of a stoma at the end of the ileum

Front 89

abdominoperineal resection

Back 89

removal of the anus, rectum and sigmoid colon with creation of a permanent colostomy

Front 90

2 restrictive procedures

Back 90

2 restrictive = vertical banded gastroplasty and gastric banding

Front 91

2 malabsorptive procedures for morbid obesity

Back 91

intestinal bypass and Roux-Y gastric bypass

Front 92

vertical banded gastroplasty

Back 92

stomach "stapled" smaller, eat less food. Dangerous operation, done less now.
(restrictive procedure for obesity)

Front 93

gastric banding

Back 93

placement of a prosthetic device around the gastric cardia to limit oral intake
(restrictive procedure for obesity)

Front 94

intestinal bypass

Back 94

(malabsorptive procedure) formation of an anastomosis between the upper small intestine and the lower small intestine or large intestine. High complication rate.

Front 95

Roux-Y gastric bypass

Back 95

combines gastric restriction and malabsorption; in addition to creating a gastric pouch the small bowel is resected so that upper jejunum is connected to pouch and lower jejunum is anastomosed to the biliopancreatic limb (digestive juices do not come into small bowel until the lower jejunum so absoroption is decreased).
Laparoscopic

Front 96

Post GI surgery, what can you expect as fluid mobilizes 2nd/3rd day post op

Back 96

increased u/o

Front 97

Why don't you want to use wound packing soaked in betadine?

Back 97

toxic to fibroblasts, decreases epitheliazation, increases risk infection, iodine may be absorbed and cause nephrotoxicity

Front 98

drainage from ileostomy is _______

Back 98

watery, excoriating and continuous

Front 99

drainage from ascending colostomy is _______

Back 99

watery or semi solid, excoriating and continuous

Front 100

drainage from transverse colostomy is ________

Back 100

pastelike or semisolid and occurs at unpredictable intervals (maybe 3-5 days post op before any drainage)

Front 101

drainage from descending or sigmoid colonscopy is _____

Back 101

formed stools that may be at predictable intervals (i.e. after breakfast), may be 3-5 days post op until stool.

Front 102

what color should stoma be?

Back 102

same color as oral mucosa