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CCRN > GI > Flashcards

GI Flashcards

1
Q

what are the two types of acute GI bleeds?

A
  • 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
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2
Q

how do you manage upper GI bleeds?

A
  • 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
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3
Q

what is the common cause of esophageal varices?

A

portal HTN secondary to liver disease; liver cirrhosis prevents normal drainage through liver; pressure backs up into esophageal vein

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4
Q

how does venous drainage flow through GI tract?

A

GI venous drainage –> portal vein –> liver –> hepatic vein –> inferior vena cava

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5
Q

how are esophageal varices treated?

A
  • endoscopy banding or sclerosis of varices

- esophageal balloon tamponade (Sengstaken-Blakemore tube)

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6
Q

how is the esophageal balloon tamponade managed?

A
  • 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
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7
Q

what are the exocrine functions of the pancreas?

A

secrete: bicarbonate to neutralize stomach acid, H2O, Na+, K+, digestive enzymes (trypsin, amylase, lipase)
secretion increases by: parasympathetic stimulation, food (secretin & cholecystokinin)

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8
Q

what are the endocrine functions of the pancreas?

A
  • alpha cells secrete glucagon
  • beta cells serene insulin
  • delta cells inhibit secretion of above
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9
Q

what happens in acute pancreatitis?

A
  • 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
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10
Q

what causes pancreatitis?

A

alcoholism, gall stone obstruction, ab surgery, drugs, HLD, trauma, infection

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11
Q

what are pulmonary complications of acute pancreatitis?

A
  • atelectasis, LLL
  • L pleural effusion
  • B crackles
  • ARDS
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12
Q

what are S/S of acute pancreatitis?

A
  • 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
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13
Q

why is calcium low in acute pancreatitis?

A
  • 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
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14
Q

what happens when beta cells are injury?

A

hyperglycemia, hyperglycemic hypertonic syndrome

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15
Q

how is ARDS a complication of pancreatitis?

A

phospholipase A released –> kills Type II alveolar cells –> decreased surfactant

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16
Q

how is left atelectasis or left pleural effusion a complication of pancreatitis?

A

left diaphragm is lifted

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17
Q

what are signs of hemorrhagic pancreatitis?

A
  • 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
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18
Q

how is acute pancreatitis treated?

A
  • 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
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19
Q

what is the most common cause of acute and chronic liver failure?

A

APAP; EtOH abuse

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20
Q

what lab abnormalities an be seen in liver failure?

A

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

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21
Q

what are some clinical findings of liver failure?

A
  • 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
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22
Q

what happens during the stages of hepatic encephalopathy?

A

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

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23
Q

what factors increase serum NH3? (worsens encephalopathy)

A
  • 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
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24
Q

how do you manage liver failure?

A
  • 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
25
Q

why is encephalopathy a complication of trans jugular intrahepatic porto-systemic shunt (TIPS) procedure

A
  • stent allows shunting of blood directly from hepatic veins into portal vein, BYPASSING LIVER (decreases portal HTN), but decreases detoxification of blood
26
Q

what are signs of spleen rupture?

A
  • sharp left shoulder pain - KEHR’S SIGN

- ab distention with absent bowel sounds

27
Q

what are some clinical signs of abdominal trauma?

A
  • 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
28
Q

what happens if pressure in abdominal cavity > pressure in capillaries that perfuse abdominal organs?

A

ischemia and infarction may result

29
Q

what may result in reduced CO, increased SVR, reduced venous return, and decreased renal perfusion?

A

increased intra-abdominal pressure

30
Q

what is intra-abdomainl HTN (IAH)? what is abdominal perfusion pressure (APP)? what is abdominal compartment syndrome (ACS)?

A 
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

31
Q

what most closely approximates intraperitoneal pressure?

A

bladder pressure; level transducer to symphysis pubis; compromise begins at 12-15mmHg; decompression laparotomy should be considered if pressure >20mmHg

32
Q

how would you treat an IAP of >12mmHg; IAP >20mmHg?

A
  • 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
33
Q

what are some complications of bariatric surgery?

A
  • 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
34
Q

the superior mesenteric artery provides arterial perfusion to where?

A

small intestine

35
Q

what are some causes of bowel infarction?

A
  • thrombosis
  • hypercoagulability
  • arteriosclerosis
  • surgery
  • vasopressors (endogenous/exogenous)
  • intra-abdominal infection
36
Q

what is the pathophysiology of a bowel infarction?

A

decreased blood flow to mesenteric vessels –> prolonged ischemia –> edema of intestinal wall –> full thickness necrosis –> perforate, peritonitis

37
Q

what are some S/S of bowl infarction?

A
  • ab pain (sever cramping - periumbilical or diffuse)
  • ab distention, vomiting
  • hypoactive or absent BS
  • fever, tachycardia, hypoTN
38
Q

what is the treatment for bowel infarction?

A
  • ABCs
  • fluids
  • gastric decompression (NGT)
  • treat pain
  • bowel resection with debridement of necrotic tissue
  • monitor for sepsis
39
Q

what can cause a paralytic ileus?

A
  • hypokalemia
  • ab surgery
  • peritonitis
  • intestinal distention
  • PNA
  • pancreatitis
  • opiates
  • sepsis
40
Q

what can cause small bowel obstruction?

A
  • adhesions
  • hernia
  • volvulus
  • neoplasm
41
Q

what can cause large bowel obstruction?

A
  • neoplasm
  • stricture
  • diverticulitis
  • fecal or barium impaction
42
Q

what are some S/S of small bowel obstruction?

A
  • sharp, episodic pain
  • vomiting EARLY; projectile or fecal
  • hypokalemia
  • high pitched BS (increased early; decreased late)
  • KUB, dilated loops of gas-filled bowel
43
Q

what are some S/S of large bowel obstruction?

A
  • dull pain
  • change in bowel habits
  • vomiting LATE
  • ab distention
  • low-pitched BS (increased early, decreased late)
  • KUB dilated loops of gas-filled bowel
44
Q

what is the treatment for bowel obstruction?

A
  • 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)
45
Q

what causes bowel perforations?

A
  • peptic ulcer
  • bowel obstruction
  • appendicitis
  • penetrating would
  • ulcerative colitis
46
Q

what are the S/S of bowel perforation?

A
  • 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
47
Q

what is the pathophysiology of bowel perforations?

A

leakage of GI content into peritoneal cavity –> leakage of bacteria causes infection, and chemical irritation causes inflammation of peritoneum –> peritonitis

48
Q

how is bowel perforation treated?

A
  • 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
49
Q

describe the S/S of gastritis? (pain location, quality and other symptoms)

A
  • epigastric or slightly left
  • indigestion
  • n/v, hematemesis, ab tenderness
50
Q

describe the S/S of peptic ulcer? (pain location, quality and other symptoms)

A
  • epigastric or RUQ
  • gnawing, buring
  • ab tenderness, hematemesis (gastric) or melena (duodenal)
51
Q

describe the S/S of pancreatitis? (pain location, quality and other symptoms)

A
  • epigastric or LUQ, may radiate to back, flanks, left shoulder
  • boring, worsened by lying down
  • n/v mild fever, ab tenderness
52
Q

describe the S/S of cholecystitis? (pain location, quality and other symptoms)

A
  • epigastric or RUQ, may be referred to below right scapula
  • cramping
  • n/v, ab tenderness in RUQ
53
Q

describe the S/S of appendicitis? (pain location, quality and other symptoms)

A
  • epigastric or periumbilical pain, later localizes to RUQ
  • dull to sharp
  • anorexia, n/v, fever, leukocytosis, diarrhea, rebound tenderness
54
Q
  • describe the S/S of small bowel obstruction? (pain location, quality and other symptoms)
A
  • across ab, in waves, tender to palpation
  • cramping, severe, sharp
  • distention, vomiting, hypokalemia, hyperactive to hypoactive BS
55
Q
  • describe the S/S of ruptured spleen? (pain location, quality and other symptoms)
A
  • L shoulder (Kehr’s sign)
  • sharp
  • ab distention, no BS
56
Q

describe the S/S of peritonitis “acute abdomen”? (pain location, quality and other symptoms)

A
  • generalized, may become localized later
  • dull initially, then intensifies and worse with movement
  • rigid abdomen, “board like” rebound tenderness, BS diminished/absent
57
Q

when should a promotility agent be considered?

A
  • if GRV >250mL after a second gastric residual check

- GRV >500mL should result in holding feeding

58
Q

when is parenteral nutrition indicated?

A
  • 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
59
Q

T/F PN meets total nutritional needs but does not enhance anabolism as well we enteral nutrition

A

True

CCRN (10 decks)

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