GI Flashcards
what are the two types of acute GI bleeds?
- upper - 80%, HIGHER MORTALITY peptic ulcer disease, esophageal, stress ulcers, Mallory-Weiss tear, cancer
- lower - 20%; diverticulosis, angiodysplasia, tumor, radiation, colitis, Crohn’s, C. diff, E. coli
how do you manage upper GI bleeds?
- TREAT CAUSE
- isotonic fluids for hypovolemic shock
- PRBCs
- replace clotting factors (FFP, plt)
- vaso constricts splanchnic arteriolar bed, decreases portal venous pressure, watch for CP, ST elevation
- octreotide (sandostatin) reduces splanchnic blood flow, gastric acid secretion, GI mobility
- osmotic laxatives (sorbitol) removes nitrogenous materials (blood) out of gut to prevent ammonia conversion; important in presence of liver disease
- BB constrict mesenteric arterioles reducing portal venous flow
what is the common cause of esophageal varices?
portal HTN secondary to liver disease; liver cirrhosis prevents normal drainage through liver; pressure backs up into esophageal vein
how does venous drainage flow through GI tract?
GI venous drainage –> portal vein –> liver –> hepatic vein –> inferior vena cava
how are esophageal varices treated?
- endoscopy banding or sclerosis of varices
- esophageal balloon tamponade (Sengstaken-Blakemore tube)
how is the esophageal balloon tamponade managed?
- gastric balloon - 200-500mL, attached to suction, empty stomach
- esophageal balloon, 20mmHg or up to 40mmHg to control bleeding
- if esophageal balloon displaced up, the inflated balloon ma occlude the airway –> CUT ESOPHAGEAL BALLOON IF RESPIRATORY DISTRESS
what are the exocrine functions of the pancreas?
secrete: bicarbonate to neutralize stomach acid, H2O, Na+, K+, digestive enzymes (trypsin, amylase, lipase)
secretion increases by: parasympathetic stimulation, food (secretin & cholecystokinin)
what are the endocrine functions of the pancreas?
- alpha cells secrete glucagon
- beta cells serene insulin
- delta cells inhibit secretion of above
what happens in acute pancreatitis?
- diffuse inflammation, destruction, and auto-digestionof the pancreas from premature activation of exocrine enzymes
- activation of inflammatory mediatory (cytokines, kinins, histamine, clotting factors)
- systemic inflammatory response syndrome (SIRS) increased vascular permeability, vasodilation, vascular stasis, micro thrombosis
what causes pancreatitis?
alcoholism, gall stone obstruction, ab surgery, drugs, HLD, trauma, infection
what are pulmonary complications of acute pancreatitis?
- atelectasis, LLL
- L pleural effusion
- B crackles
- ARDS
what are S/S of acute pancreatitis?
- ab pain that radiates to all quadrants and lumbar area
- N/V, rigid ab
- decreased/absent BS
- low grade fever
- Increased: WBC, lipase, glucose, amylase (peaks in 4-24hrs, normal in 4 days)
- decreased: calcium
why is calcium low in acute pancreatitis?
- it is used up for auto digestion, precipitates hypocalcemia –> Trousseau’s sign, prolonged QT, sz
- Trousseau’s - during inflation of BP cuff, brachial artery is occluded –> SPASM OF MUSCLES OF HAND AND FOREARM
what happens when beta cells are injury?
hyperglycemia, hyperglycemic hypertonic syndrome
how is ARDS a complication of pancreatitis?
phospholipase A released –> kills Type II alveolar cells –> decreased surfactant
how is left atelectasis or left pleural effusion a complication of pancreatitis?
left diaphragm is lifted
what are signs of hemorrhagic pancreatitis?
- Cullen’s sign - bluish discoloration and ecchymosis of periumbilical area; METHEMALBUMIN forms from digested blood and tracks around abdomen from the inflamed pancreas
- Grey Turner’s sign - bluish discoloration of flanks
how is acute pancreatitis treated?
- replace fluids, Ca, K, Mg
- H2 blockers or PPIs to decrease gastric pH
- NG suction to decrease gastric secretion
- manage pain
- control glucose
- enteral feeding below duodenum
- MONITOR FOR PULMONARY COMPLICATIONS
what is the most common cause of acute and chronic liver failure?
APAP; EtOH abuse
what lab abnormalities an be seen in liver failure?
decreased: serum protein, albumin, glucose; pancytopenia (WBC, RBC, plt)
increased: PT/PTT, AST, ALT, GGT, alkaline phosphatase, bilirubin, NH3, BUN/creatinine (late), hyperventilation, respiratory alkalosis –> increase lactate –> metabolic acidosis
what are some clinical findings of liver failure?
- mental status change r/t hepatic encephalopathy secondary to elevated NH3
- ASTERIXIS - flappy hand tremor r/t elevated NH3
- ascites r/t low albumin and protein
- jaundice r/t elevated bilirubin
- renal failure
- sepsis r/t decreased immune function
- hepatomegaly during acute inflammatory response…necrosis
what happens during the stages of hepatic encephalopathy?
I - mild confusion, forgetfulness, irritability, change in sleep patterns, EEG normal
II - lethargy, confusion, apathy, aberrant behavior, asterisks, EEG normal
III - severe confusion, semi-stupor to stupor, hyperactive deep tendon reflexes, hyperventilation, EEG abnormal
IV - no response to stimuli, posturing, positive Babinski, areflexia except for pathologic reflexes, EEG abnormal
what factors increase serum NH3? (worsens encephalopathy)
- hypokalemia - triggers ammonia genesis in kidneys
- increased BUN, protein - breakdown nitrogen
- increased lactic acidosis - r/t to LR administration; liver failure can’t convert to bicarb
how do you manage liver failure?
- prevent anything that will increase NH3
- restrict protein ONLY if hepatic encephalopathy is present
- administer clotting factors
- lactulose
- neomycin - kills bacteria in gut that produce NH3 (Vit K deficiency)
- monitor glucose
- administer acetylcysteine (Mucomyst) or Acetadote for ALL suspected APAP OD
- neuro checks
- trans jugular intrahepatic porto-systemic shunt (TIPS) to relieve esophageal varices or ascites
why is encephalopathy a complication of trans jugular intrahepatic porto-systemic shunt (TIPS) procedure
- stent allows shunting of blood directly from hepatic veins into portal vein, BYPASSING LIVER (decreases portal HTN), but decreases detoxification of blood
what are signs of spleen rupture?
- sharp left shoulder pain - KEHR’S SIGN
- ab distention with absent bowel sounds
what are some clinical signs of abdominal trauma?
- CULLEN’S - ecchymosis around umbilicus; intraperitoneal bleeding
- GREY TURNER’S - ecchymosis of flank; retroperitoneal bleeding
- KEHR’S SIGN - L shoulder pain; ruptured spleen (referred pain r/t to diaphragmatic irritation)
- ecchymosis over ULQ; soft tissue trauma or splenic injury
- no BS with ab distention and guarding; visceral injury
- BS in chest; diaphragmatic rupture
- free air in ab by X-ray; disruption of GI tract
- diagnostic peritoneal lavage positive for bleed –> intra-abdominal bleeding
what happens if pressure in abdominal cavity > pressure in capillaries that perfuse abdominal organs?
ischemia and infarction may result
what may result in reduced CO, increased SVR, reduced venous return, and decreased renal perfusion?
increased intra-abdominal pressure
what is intra-abdomainl HTN (IAH)? what is abdominal perfusion pressure (APP)? what is abdominal compartment syndrome (ACS)?
IAH = intra-ab pressure (IAP) >12-15mmHg APP = MAP-IAP; >60 improved survival; <50 increased mortality
ACS = sustained IAP of >20mmHg with or without APP of 60mmHg, associated with new organ dysfunction or failure
what most closely approximates intraperitoneal pressure?
bladder pressure; level transducer to symphysis pubis; compromise begins at 12-15mmHg; decompression laparotomy should be considered if pressure >20mmHg
how would you treat an IAP of >12mmHg; IAP >20mmHg?
- place in reverse Trendelenburg, HOB <20 degrees
- loosen constrictive clothing, dressings, binders
- manage pain, agitation
- prevent overhydration
- NGT to LIS to decompress ab
- optimize stool management
gastro/colo prokinetics? - abdominal compartment syndrome
- decompression surgery
what are some complications of bariatric surgery?
- malabsorption - vitamin deficiencies: protein, Ca, Fe, B12, folate; vomiting, HA, diplopia, memory loss
- wounds
- enteric leakage from anastomosis
- gallstones - 52% within a year
- bowel obstruction secondary to scar tissue or kink
the superior mesenteric artery provides arterial perfusion to where?
small intestine
what are some causes of bowel infarction?
- thrombosis
- hypercoagulability
- arteriosclerosis
- surgery
- vasopressors (endogenous/exogenous)
- intra-abdominal infection
what is the pathophysiology of a bowel infarction?
decreased blood flow to mesenteric vessels –> prolonged ischemia –> edema of intestinal wall –> full thickness necrosis –> perforate, peritonitis
what are some S/S of bowl infarction?
- ab pain (sever cramping - periumbilical or diffuse)
- ab distention, vomiting
- hypoactive or absent BS
- fever, tachycardia, hypoTN
what is the treatment for bowel infarction?
- ABCs
- fluids
- gastric decompression (NGT)
- treat pain
- bowel resection with debridement of necrotic tissue
- monitor for sepsis
what can cause a paralytic ileus?
- hypokalemia
- ab surgery
- peritonitis
- intestinal distention
- PNA
- pancreatitis
- opiates
- sepsis
what can cause small bowel obstruction?
- adhesions
- hernia
- volvulus
- neoplasm
what can cause large bowel obstruction?
- neoplasm
- stricture
- diverticulitis
- fecal or barium impaction
what are some S/S of small bowel obstruction?
- sharp, episodic pain
- vomiting EARLY; projectile or fecal
- hypokalemia
- high pitched BS (increased early; decreased late)
- KUB, dilated loops of gas-filled bowel
what are some S/S of large bowel obstruction?
- dull pain
- change in bowel habits
- vomiting LATE
- ab distention
- low-pitched BS (increased early, decreased late)
- KUB dilated loops of gas-filled bowel
what is the treatment for bowel obstruction?
- ABCs
- prevent perforation (NGT)
- fluids, lytes
- treat pain
- monitor for infection, complications
- nutritional support; might feed distal to obstruction
- surgery or complete or strangulated SBO; if perforation occurred (lysis of adhesion, reduction of volvulus, bowel resection with debridement of necrotic tissue)
what causes bowel perforations?
- peptic ulcer
- bowel obstruction
- appendicitis
- penetrating would
- ulcerative colitis
what are the S/S of bowel perforation?
- n/v
- fever, tachypnea, tachycardia
- ab pain, tenderness that increases with coughing or hip flexion
- rigid ab, “boardlike”
- rebound tenderness
- BS diminished, absent
- KUB free air in peritoneum
what is the pathophysiology of bowel perforations?
leakage of GI content into peritoneal cavity –> leakage of bacteria causes infection, and chemical irritation causes inflammation of peritoneum –> peritonitis
how is bowel perforation treated?
- ABCs
- gastric decompression (NGT)
- fluids, lytes
- treat pain
- abx, blood cx
- monitor for infection, complications
- nutrition
SURGERY - repair perforation, possible temporary bowel diversion to allow anastomosis to heal; abx lavage during surgery
describe the S/S of gastritis? (pain location, quality and other symptoms)
- epigastric or slightly left
- indigestion
- n/v, hematemesis, ab tenderness
describe the S/S of peptic ulcer? (pain location, quality and other symptoms)
- epigastric or RUQ
- gnawing, buring
- ab tenderness, hematemesis (gastric) or melena (duodenal)
describe the S/S of pancreatitis? (pain location, quality and other symptoms)
- epigastric or LUQ, may radiate to back, flanks, left shoulder
- boring, worsened by lying down
- n/v mild fever, ab tenderness
describe the S/S of cholecystitis? (pain location, quality and other symptoms)
- epigastric or RUQ, may be referred to below right scapula
- cramping
- n/v, ab tenderness in RUQ
describe the S/S of appendicitis? (pain location, quality and other symptoms)
- epigastric or periumbilical pain, later localizes to RUQ
- dull to sharp
- anorexia, n/v, fever, leukocytosis, diarrhea, rebound tenderness
- describe the S/S of small bowel obstruction? (pain location, quality and other symptoms)
- across ab, in waves, tender to palpation
- cramping, severe, sharp
- distention, vomiting, hypokalemia, hyperactive to hypoactive BS
- describe the S/S of ruptured spleen? (pain location, quality and other symptoms)
- L shoulder (Kehr’s sign)
- sharp
- ab distention, no BS
describe the S/S of peritonitis “acute abdomen”? (pain location, quality and other symptoms)
- generalized, may become localized later
- dull initially, then intensifies and worse with movement
- rigid abdomen, “board like” rebound tenderness, BS diminished/absent
when should a promotility agent be considered?
- if GRV >250mL after a second gastric residual check
- GRV >500mL should result in holding feeding
when is parenteral nutrition indicated?
- if EN isn’t feasible/available over first 7 days following admission to ICU
- in the pt who was previously healthy before critical illness with no evidence of protein-calorie malnutrition, use of PN should be reserved and initiated only after the first 7 days
- if there is protein-calorie malnutrition at admission and EN is not feasible, initiate PN ASAP after resuscitation
T/F PN meets total nutritional needs but does not enhance anabolism as well we enteral nutrition
True
