GI Flashcards
(59 cards)
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
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
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
4
Q
how does venous drainage flow through GI tract?
A
GI venous drainage –> portal vein –> liver –> hepatic vein –> inferior vena cava
5
Q
how are esophageal varices treated?
A
- endoscopy banding or sclerosis of varices
- esophageal balloon tamponade (Sengstaken-Blakemore tube)
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
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)
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
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
10
Q
what causes pancreatitis?
A
alcoholism, gall stone obstruction, ab surgery, drugs, HLD, trauma, infection
11
Q
what are pulmonary complications of acute pancreatitis?
A
- atelectasis, LLL
- L pleural effusion
- B crackles
- ARDS
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
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
14
Q
what happens when beta cells are injury?
A
hyperglycemia, hyperglycemic hypertonic syndrome
15
Q
how is ARDS a complication of pancreatitis?
A
phospholipase A released –> kills Type II alveolar cells –> decreased surfactant
16
Q
how is left atelectasis or left pleural effusion a complication of pancreatitis?
A
left diaphragm is lifted
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
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
19
Q
what is the most common cause of acute and chronic liver failure?
A
APAP; EtOH abuse
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
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
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
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
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
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
26
what are signs of spleen rupture?
- sharp left shoulder pain - KEHR'S SIGN
| - ab distention with absent bowel sounds
27
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
28
what happens if pressure in abdominal cavity > pressure in capillaries that perfuse abdominal organs?
ischemia and infarction may result
29
what may result in reduced CO, increased SVR, reduced venous return, and decreased renal perfusion?
increased intra-abdominal pressure
30
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
31
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
32
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
33
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
34
the superior mesenteric artery provides arterial perfusion to where?
small intestine
35
what are some causes of bowel infarction?
- thrombosis
- hypercoagulability
- arteriosclerosis
- surgery
- vasopressors (endogenous/exogenous)
- intra-abdominal infection
36
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
37
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
38
what is the treatment for bowel infarction?
- ABCs
- fluids
- gastric decompression (NGT)
- treat pain
- bowel resection with debridement of necrotic tissue
- monitor for sepsis
39
what can cause a paralytic ileus?
- hypokalemia
- ab surgery
- peritonitis
- intestinal distention
- PNA
- pancreatitis
- opiates
- sepsis
40
what can cause small bowel obstruction?
- adhesions
- hernia
- volvulus
- neoplasm
41
what can cause large bowel obstruction?
- neoplasm
- stricture
- diverticulitis
- fecal or barium impaction
42
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
43
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
44
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)
45
what causes bowel perforations?
- peptic ulcer
- bowel obstruction
- appendicitis
- penetrating would
- ulcerative colitis
46
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
47
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
48
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
49
describe the S/S of gastritis? (pain location, quality and other symptoms)
- epigastric or slightly left
- indigestion
- n/v, hematemesis, ab tenderness
50
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)
51
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
52
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
53
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
54
- 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
55
- describe the S/S of ruptured spleen? (pain location, quality and other symptoms)
- L shoulder (Kehr's sign)
- sharp
- ab distention, no BS
56
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
57
when should a promotility agent be considered?
- if GRV >250mL after a second gastric residual check
| - GRV >500mL should result in holding feeding
58
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
59
T/F PN meets total nutritional needs but does not enhance anabolism as well we enteral nutrition
True
