Lecture 9b: GI disorders Flashcards
Acute Abdomen
a condition that demands urgent surgical attention; may be caused by infection, inflammation, vascular occlusion, obstruction or perforation.
Abdominal X-ray
Rules out free air
CT
Gold standard for everything else
GI Disorders (5)
- ACUTE UPPER GI-BLEEDING
- LOWER GI BLEEDING
- Small Bowel Obstruction
- Pancreatitis
- Hepatitis
Upper gastrointestinal bleeding: Peptic ulcer disease (4)
Primary factor:
- H. pylori
- ingestion of ASA
- NSAIDs
- smoking
Upper gastrointestinal bleeding: Stress-related erosive syndrome (2)
Decreased perfusion of stomach mucosa
related to physiological stress
Upper gastrointestinal bleeding: Esophageal varices (1)
Collateral circulation as a result of portal hypertension, rising pressure causes tortuous distended veins or varices
Upper gastrointestinal bleeding: Mallory-Weiss tears (2)
1) Laceration of the distal esophagus, gastroesophageal junction, and cardia of the stomach
2) Heavy alcohol use, binge drinking, forceful vomiting/retching, or violent coughing
Upper gastrointestinal bleeding: Dieulafoy’s lesions (2)
- Vascular malformations, usually in the proximal stomach’
- Occurs more in men with HTN
UG: Clinical Presentation (4)
what is the hallmark of lower GIB/upper GIB
Presentation depends on the amount of blood loss.
Orthostatic changes imply volume depletion of 15% or more.
Upper GIB—hematemesis, “coffee ground,” melena
Hallmark of Lower GIB is hematochezia*, sometimes melena
TIP:
s1-4 with hypovolemic blood loss.
500- not so sick
150—2000
Hematochezia- bright red blood- ominous sign from the small bowel.
Bright red blood in stool
UG: ASSESSMENT
1) history (2)
2) PE: (7)
History:
- History of PUD, dyspepsia, alcohol, smoking, vomiting/retching, NSAIDs or ASA,
- blood thinners
Physical examination:
- Hemodynamic stability?
- VS
- orthostatic
- tissue perfusion
- LOC
- Abdominal exam
- rectal exam
tip:
What values would drop? – CVP, (Watch the MAP if CVP isn’t available). ——-SVR would increase.
Auscultation before palpation
-Rectal exam- not within the scope of the RN, necessary to do- can immediately diagnose cause of bleeding.
-Patient at DRH who had vaginal bleeding and
UG: LABS (7)
Low H & H (Hemoglobin and Hematocrit)
Mild leukocytosis and hyperglycemia
High BUN
Hypernatremia, hypokalemia
Prolonged PT/PTT
Thrombocytopenia
Lactic Acid
- Loss of tissue perfusion
- Arterial clot –-> ischemic bowel
tip:
Na becomes conetrated, we lose K+ with Blood.
-Protein from digested blood turns to BUN-
UG: Management (6)
1) Volume resuscitation with IVF or blood products, vasopressors – Central or large bore
2) Oxygen, central line
3) NPO (Complete), NGT
4) Electrolyte repletion
5) Acid-suppressive therapy—PPI or H2
- Protonix IV
6) Pharmacotherapy for decreasing portal hypertension
- Vasopressin, octreotide, somatostatin
tip:
Protonix, dose dependent acid-inhibition- 20mg/hr, for 24 hours.
Vasopressin- dilates the venous vasculature.
Ocreotide- reduces portal vein htn, reduces peristalsis.
Somatostatin- reduces peristalsis.
Central line- allows 3 point access, limits hemolysis.
UG: Definitive Diagnostics (3)
1) Endoscopy within 12 to 24 hours to identify the site
- Can be done at bedside
2) Angiography—locates the site or abnormal vasculature, insensitive in venous bleeding
3) Barium studies are often inconclusive, and risk of retained barium.
Angio- contrast via fem artery-
UG: Interventions (5)
1) Endoscopy—
hemostasis 90% of cases
2) Angiography
Embolization
3) Balloon tamponade—
with esophageal varices
4) Transjugular intrahepatic portosystemic shunt (TIPS)
For severe portal htn
5) Surgery
Rarely indicated; severe hemorrhage unresponsive to initial resuscitation, unavailable/failed endoscopy, perforation, obstruction, malignancy
tip:
Endo- epinephrine or electrocautery.
Minnesota or Blakemore tubes
Beezor at the pyloric sphincter – pain, nausea, vomiting,
-Chemicals and electricity
Transjugular intrahepatic portosystemic shunt (TIPS)
a procedure that creates new connections between two blood vessels in your liver.
- Cleaning blood with kupfer cells and hepatocytes
UG: Pharm mgmt (5)
- Eradication of H. pylori, stop NSAIDs.
- PPI or H2 blockers and COX-2 inhibitor (if ASA or NSAIDs are unavoidable)
- Beta-blockade reduces portal pressure.
- Prophylactic antibiotics
- Alcohol cessation
tip:
Breaht test for Gas.
ABX for perf or surgery
LOWER GI BLEEDING: Diverticulosis (what, RF (4))
1) Sac-like protrusions in the colon; arteries are prone to injury.
2) Risk factors:
- diet low in fiber
- ASA/NSAIDs
- advanced age
- constipation
LOWER GI BLEEDING: Angiodysplasia/AV malformation (2)
- Dilated, tortuous submucosal veins, small AV communications, or enlarged arteries
- Occurs anywhere in the colon and can be venous or arterial bleed
LG: Clinical presentation (5)
Hemodynamic instability and hematochezia
Diverticular bleeding is often painless, may complain of cramping.
Angiodysplasia presents with painless hematochezia.
Chronic LGIB presents with iron deficiency anemia.
Hemorrhoids can present with massive bleeding from rectal varices from portal hypertension.
tip:
- cramping gets worse with accumulation of blood
- chronic: low hemoglobin with stability and anemia
LG: Assessment
1) history (3)
2) PE: (3)
History:
- PUD, inflammatory bowel disease, renal/liver disease
- Medication, color and consistency of stool, abdominal pain, fever, rectal urgency, weight loss
- Change in bowel habits
Physical examination:
- VS, palpable mass, rectal exam
tip:
NSAIDS, ASA- wont cause lower GI bleeding, but ASA may exacerbate- older folks are aso on coumadin, Eliquis, etc
- abdominal pain, fever
- look for rigid and board like hardness
LG: LABS (5)
CBC
Electrolytes
BUN and creatinine
PT/PTT
Type and cross-match
tip:
colony stimulating factors, IV iron. When refusing blood
- cbc emphasis on h-h
- bun/cr increase (consuming nitrogenous waste while absorbing blood)
- give O- if don’t have type and cross
LG: MANAGEMENT (6)
what is the gold standard?
Fluid resuscitation, NGT to LIS
Colonoscopy for diagnosis and treatment
Upper endoscopy distinguishes the source.
Radionucleotide imaging—locates the site of bleed
Angiography—for diagnosis and embolization
gold standard
Surgical intervention
- Exploratory lap, segmental bowel resection, total colectomy
tip:
RBCs taken from the patient, tagged with nuclear isotope- then re-introduced into the body. Then put under films.
- colonoscopy vs esophagoscopy
- angiography (gold standard)
- surgery: rarely indicated unless said otherwise (can take out just the bowel or the entire colon)
- total colectomy:
GI obstruction - Pathophysiology (4)
Gut is unable to decompress the accumulation of fluid/gas (if issues is in duodenum)
Normal colonic flora continues to produce methane and ammonia, which add to distention.
Fluid and gas accumulate, increasing intraluminal pressure.
- Colonic wall becomes ischemic and risks perforation
Changes in normal flora and translocation of bacteria (to sterile peritoneum) can cause septic complications.
GI: Small Bowel Obstruction (3 types + pathophysiology (3))
1) Adhesions (Abnormal union between adjacent tissue)
- most common cause of SBO, occurring after laparotomy, radiation, ischemia, infection, or foreign body.
- usually occurs with previous surgery
2) Hernias—strangulated
3) Tumors—uncommon in the small bowel
4) Pathophysiology:
- Fluid and air accumulate proximal to obstruction causing distention.
- Bowel wall becomes edematous and distended.
- Peristalsis decreases and normal function halts.
SBO GI upper clinical presentation (7)
Severity of symptoms is proportionate to?
Acute onset of what?
what relieves the pai?
In ________ SBO, the pain is?
3 symptoms?
Hemodynamic _________
________- diarrhea leaking around the stool mass.
Severity of symptoms is proportionate to severity of ischemia.
Acute onset of intermittent, crampy, periumbilical pain
Vomiting often relieves the pain.
In strangulated SBO, the pain is localized, steady, severe.
Fever, constipation, obstipation
Hemodynamic instability
Encoparesis- diarrhea leaking around the stool mass.
SBO GI Assessment
1) history: 6)
2) PE: (3)
- s/sx (3)
1) History of abdominal surgery/trauma, inflammatory bowel disease, diverticulitis, radiation, PUD, pancreatitis
- Medication history
2) Physical examination:
- Visible peristalsis and distention, epigastric/periumbilical/diffuse abdominal tenderness, hyperactive BS early then high-pitched tinkling
- S & S of dehydration, palpable mass; palpate for inguinal hernia.
SBO GI Diagnostics (4)
1) Labs for differential
2) Radiography
- Dx of obstruction, perforation, barium
3) Computed tomography
- Obstructive lesions, neoplasms, hernias, and ischemia
4) Endoscopy
- Direct visualization of obstruction in colon or proximal SB (not common)
SBO GI management
1) medical mgmt: (7), montior (5)
2) surgical mgmt:
- what requires immediate surgery (4)
- what can be done?
Medical management:
- NPO, NGT, IVF, electrolyte repletion, I & Os, TPN, central line
- Monitor for S & S of sepsis, perforation, ischemia, necrosis, gangrene
Surgical management:
- Strangulated bowel, volvulus, incarceration, or closed loop obstructions need immediate surgery.
- Lysis of adhesions, resection, ostomy, bowel decompression
Large Bowel Obstruction: Clinical presentation (7)
- Abdominal pain, distention, progressive obstipation
- Colicky pain in peritonitis, severe constant pain in gangrenous bowel
- Vomiting may occur late.
- Changes in bowel habits
- Dehydration
- Diarrhea may be present if stool is leaking past an obstruction.
- Dyspnea from abdominal distention
Large Bowel Obstruction: assessment
1) history: 7
2) PE: 3
- s/sx of (4)
- ______ exam
1) History of altered bowel movements, bloody stool, iron deficiency anemia, weight loss, anorexia, fever, pain
2) Physical examination
- Abdominal distention, tympany, ascites
- S & S of dehydration, hyperactive then hypoactive BS, mass, diffuse abdominal tenderness with guarding or rebound
- Rectal exam
The 6 F’s:
Fluid
Flatus
Feces
Fetus
Fat
Fatal tumor
Large Bowel Obstruction: labs (labs (2), imaging (2))
1) Iron deficiency, leukocytosis
2) Imaging:
- Abdominal films identify site of obstruction.
- CT distinguishes anatomic and pseudo-obstruction
Large Bowel Obstruction: Management (3)
Fluid and electrolytes, NPO, NGT, rectal tube
Surgical management:
- Excision and re-anastomosis or ostomy
Endoscopic therapy:
- Stents as a palliative measure until surgery
- Used to de-bulk obstructing tumors
Ileus
1) when could this occur? (6)
2) pathophysiology (2)
Post-op, metabolic abnormalities, medications, local/systemic inflammation, spinal cord injury, blood-borne toxins
Pathophysiology:
- Poorly understood
- Peristalsis decreased or ceases; distention occurs as gas/fluid/electrolytes accumulate.
ileus: Clinical Presentation (5)
2) history of (4)
3) PE: 6
4) labs
5) imaging (2)
1) Diffuse abdominal pain, nausea/vomiting, constipation, hiccups, bloating
2) History of thyroid/parathyroid disease, heavy metal exposure, diabetes, scleroderma
3) Physical examination:
- Abdominal distention
- decreased/absent BS
- resonant to percussion
- tachycardia
- orthostatic
- S & S of dehydration
4) Labs—electrolyte abnormalities
5) Abdominal radiography shows colonic dilation; CT/abdominal Xray
ileus: Mgmt (6)
Treat the underlying cause.
NPO, IVF, electrolyte repletion, NGT
Hold medications that affect motility (narcotics).
‘Entereg’
Neostigmine, prokinetic medications
Colonoscopy
Surgery for perforation
perforations
1) what
2) requires
3) treatment
1) Open abdomen in severe cases
2) Require lots of fluids to correct hypovolemia
- Implications for hemodynamic monitoring
3) Broad spectrum abx
Pancreatitis
1) _______ and ______ ______ ______ in 70-80%
2) what are things to consider?
3) pathophysiology?
1) Gallstones and excessive alcohol abuse in 70% to 80%
2) Hypercalcemia and hypertriglyceridemia, medications, infectious processes
3) Pathophysiology:
- Pancreatic enzymes become prematurely activated.
- Results in autodigestion of the pancreas and peripancreatic tissue
- Substances released from injured pancreas cause a cascade of events that lead to systemic sequelae.
pancreatitis: Clinical presentation (2)
history (7)
PE (3)
- Deep, boring midepigastric or periumbilical pain
- Nausea/vomiting without pain relief, tachycardia, hypotension, abdominal distention, low-grade fever
History of biliary disease, alcohol use, diabetes, medications, location of pain, weight loss, N/V
Physical examination:
- Diffuse abdominal tenderness and guarding, tympanic to percussion
- Hypoactive BS, jaundice, ascites, S & S of dehydrations or hypovolemic shock
- Grey Turner’s or Cullen’s sign
tip:
Jaundice- Inability to conjugate red blood cells.
Grey- flank (side) bruising, pancreas
Cullens- umbilicus, organ rupture (edward cullen sucking on my belly button)
- both grey and cullen’s sign are indications of peritoneal rupture
pancreatitis: diagnostics
1) labs (5)
2) imaging studies (3)
Labs:
- Elevated serum amylase and lipase
- electrolyte imbalance
- hyperglycemia
- LFTs elevated with concurrent liver disease
- elevated ALT and alkaline phosphatase with biliary disease
Imaging studies:
- Radiographs exclude other causes.
- CT is the preferred test.
- MRCP for bile duct stones, ERCP locates and removes stones.
tip:
Amylase stays elevated longer
Hypertriglyceridemiapa
pancreatits: complications
local (3)
pulmonary (3)
cardiovascular (1)
renal (1)
hematological (1)
metabolic (4)
GI (1)
Local—pancreatic necrosis, pseudocyst, abscess
Pulmonary—atelectasis, ARDS, pleural effusion
Cardiovascular—shock states
Renal—ARF
Hematological—DIC
Metabolic—hyperglycemia, hypertriglyceridemia, hypocalcemia, metabolic acidosis
Gastrointestinal—GIB
pancreatitis: management (3)
1) IVF, electrolyte repletion, pain management, rest pancreas with NGT to suction
2) NPO, TPN, bed rest
3) Surgical management:
- With massive necrosis, pancreatic resection is done.
- Broad-spectrum antibiotics
Hepatitis (8)
Noninfectious hepatitis:
- Excessive alcohol use
- Autoimmune disorders
- Biliary obstruction
- Medications (Tylenol)
- Right-sided heart failure
- sarcoidosis
- lupus
- RA
Infectious Hepatitis
1) ________ contagious
2) classified according to?
3) presents with?
4) symtoms more severe in _____?
1) Highly contagious
2) Classified according to specific infecting agent and corresponding serology markers
- Hepatitis A, B, C, D, E, F, and G
3) Present with nonspecific flu-like symptoms
4) Symptoms more severe in hepatitis B
Hepatitis Pathophysiology (4)
1) Hepatocytes, blood vessels, and Kupffer cells are responsible for uptake and degradation of foreign and potentially harmful substances in the body.
2) In mild disease, hepatocytes may regenerate.
3) In severe disease, regeneration is incomplete and fibrosis leads to cirrhosis and impediment of blood flow through the liver.
4) Fulminant liver failure can progress to cerebral edema, coma, and death
Ammonia based product from blood into urea nitrogen- ammonia will cause confusion- we give lactulose for that.
hepatitis Assessment
1) history of (7)
2) PE: 12
1) History of alcohol use, drug use, medications, herbal supplements, surgery and transfusion history, occupational and travel history, sexual history
2) Physical examination:
Jaundice, hepatomegaly, splenomegaly
Muscle wasting, ascites, peripheral edema
Vitamin deficiencies, bruising, telangiectasis, spider nevi
Abdominal wall vein dilation, bruit over the liver
hepatits: Laboratory Studies
test for (3)
- what examples for each?
1) Tests for evaluating hepatocellular injury
- AST (Aspartate Aminotransferase), ALT (Alanince Aminotransferase)
2) Tests for evaluating liver synthetic function
- Albumin, total protein, and PT
3) Tests for evaluating cholestasis (excretory function)
- Serum bilirubin
- Alkaline phosphatase and GGT
tip:
GGT- gamma glutamyltransferase
(Alkaline phosphatase -ALP)
AST- Aspartate Aminotransferase
ALT – Alanine Aminotransferase
hepatitis mgmt (9)
Treatment is supportive.
Rest, hold harmful medications.
Monitor hemodynamic status.
Monitor hepatic enzymes, electrolytes.
Strict I & O, daily weight, abdominal girth
High-calorie, low-protein diet
Monitor for bleeding.
Avoid alcohol, narcotics, barbiturates.
Treat encephalopathy by lowering ammonia levels
tip:
Binds to ammonia and excretes it via the bowel. Lactulose—
Cirrhosis
1) what?
2) caused by?
3) pathophysiology
4) results in (4)
5) inability to?
1) Complication of liver disease
2) Caused by:
chronic Hepatitis infection, alcohol abuse, nonalcoholic steatohepatitis, hereditary hemochromatosis, Wilson’s disease, and alpha1-antitrypsin deficiency
3) Inflammation, fibrotic changes, and increased intrahepatic vascular resistance cause compression of the liver lobule
- increased resistance or obstruction of normal blood flow through the liver, (which is normally a low-pressure system)
4) Results in splenomegaly, varices, hemorrhoids, cardiac dysfunction
5) Inability to perform normal function of liver
cirrhosis: Assessment (5)
H & P reveals altered liver function.
Altered glucose, carbohydrate, fat, and protein metabolism
Decreased synthesis of albumin leads to interstitial edema and decreased plasma volume.
Clotting dysfunction
Ascites, lower extremity edema, hypotension
cirrhosis mgmt (4)
Monitor nutrition, fluid balance, urine output, electrolytes, PT/PTT, platelet function, hematocrit.
Monitor LOC, abdominal girth.
Manage ascites—paracentesis or VP shunt.
TIPS (trans-hepatic portal vein stent) procedure to decompress portal venous system
tip:
7Liters - - - we can give albumin pre and post paracentesis.
complications of hepatitis
1) _________ ________
- caused by?
- limit (2)
- treat with?
2) _______ ________
- often? -> treatment is supportive
3) ________ _______ ________
- infected _______ fluid
- treat with?
1) Hepatic encephalopathy:
- Caused by accumulation of toxic agents absorbed in intestinal tract
- Limit protein intake,
- lactulose, neomycin, or metronidazole (Abx to kill NH3 producing bacteria)
2) Hepatorenal syndrome
- Often fatal: treatment is supportive.
- advanced liver disease causes low production of albumin, leading to third spacing and hypoperfusion to the kidneys, causing kidney damage
3) Spontaneous bacterial peritonitis
- Infected ascitic fluid
- treat with broad-spectrum antibiotics
