Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

NRSG 331 > GI > Flashcards

GI Flashcards

1
Q

functions of GI tract

A
  • major role: convert ingested nutrients into simpler forms that can be transported from the tract’s lumen to the portal circulation and then used in metabolic processes
  • plays vital role in detoxification and elimination of bacteria, viruses, chemical toxins, and rugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

ligament of treitz

A

anatomic division between upper and lower GI tracts (proximal to the ligament is the upper GI, distal to it is lower)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

causes of upper GIB

A 
SPEM 
-PUD
-Stress related erosive syndrome
-esophageal varices
-mallory-weiss tear 
those are the important ones. others are:
-esophagitis
-neoplasm
-aortoenteric fistula
-angiodysplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

lower GIB causes

A
  • diverticulosis
  • angiodysplasia hemorrhoids
  • inflammatory bowel disease
  • trauma
  • infectious colitis
  • radiation colitis
  • ischemia
  • aortoenteric fistula
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

patho of PUD

A
  • PUD occurs after protective mechanisms cease to function (glycoprotein mucous barrier, adequate blood flow, bicarbonate secretion, prostaglandins and nitric oxide) and the gastroduodenal mucosa breaks down
  • once the mucosa is penetrated, gastric secretions autodigest the layers of the stomach or duodenum, leading to injury of the mucosal and submucosal layers, leading to damaged blood vessels and hemorrhage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

causes of PUD

A
  • increase acid production and decreased mucosal blood flow causing ischemia and degeneration of the mucosal lining
  • 2 main causes: H pylori and NSAIDs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

PUD tx; surgical and post op care

A 
surgical:
-vagotomy
-pyloroplasty
-stress ulcer prophylaxis
-gastric resection
-bilroth I
-bilroth II
-patch hole
-excise ulcer
post op:
-fluid/electrolytes for imbalances
-adequate nutrition, TPN for ileus
-tx wound infection
-tx/monitor for peritonitis if anastamosis rupture
-pain
-lung infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is a mallory weiss tear

A

it is an UGIB. an acute, arterial tear in gastroesophageal mucosa, accounting for 10-15% of UGIBs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

causes of mallory weiss

A
  • excessive ETOH
  • long term NSAID/ASA
  • forceful retching
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

portal vein pressures (normal, when do varices develop, when do they rupture)

A
  • norm:2-6 mm Hg
  • varices: 10
  • varices rupture: 12
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

tx of esophagago varices rupture

A
  • establish airway and patient stabilization!
  • gastric lavage
  • pharm:
  • somatostatin and octreotide
  • vasopressin
  • endoscopics
  • endoscopic injection sclerotherapy
  • endoscopic band ligation
  • TIPS
  • mechanical tamponade (sengstaken-blakemore, minnesoate, linton)
  • portocaval shunt (surgical, last resort)
  • mesocaval shunt (surgical, last resort)
  • fluids for hemodynamic stability (crystalloids, colloids, blood and blood products)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

possible complications of varice rupture

A
  • hypovolemic shock

- gastric perforation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

s/s of UGIB

A
  • hypovolemic shock (hypotn, tachycardia, cool clammy skin, change in LOC, decreased UO, decreased gastric motility)
  • hematemesis
  • hematochezia
  • melena
  • abd discomfort
  • hyperactive bowel sounds
  • ST segment depression
  • flattening of t wave
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is a consideration when assessing H/H for GIB pts?

A

H/H levels are poor indicators of the severity of blood loss if the bleeding is acute. it may take 24-72h for the redistribution of plasma from the extravascular place.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

labs/tests for UGIB

A
  • over/occult blood (guaiac testing)
  • Hgb normal then down
  • hct normal then down
  • wbc up
  • platelets up then down
  • K down then up
  • sodium down
  • calcium normal or down
  • bun/cr up
  • ammonia possibly up
  • glucose up
  • lactate up
  • PT/PTT up
  • respiratory alkalosis
  • metabolic alkalosis
  • gastric aspirate possibly acidotic
  • endoscopy
  • barium study
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

endoscopy for UGIB

A

this is the choice for diagnosis, treatment, and prevention of UGIB.
-PT MUST BE HEMODYNAMICALLY STABLE FOR ENDOSCOPY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

tx of UGIB

A
  • gastric lavage (before endoscopy)
  • colloids, crystalloids, blood, blood products (priority is restore adequate circulating volume to tx or prevent shock)
  • antacids
  • H2 blockers
  • PPIs
  • mucosal barrier enhancers
  • sclerotherapy (morrhuate sodium)
  • thermal therapy
  • endoclipping
  • o2 therapy
  • large NG may be inserted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

nurse role in UGIB surgery

A
  • assist MD
  • watch for complications: respiratory complications, fever, oozing
  • position pt in L. lateral reverse trendelenburg to prevent respiratory complications
  • monitor pt at all times
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

antacids for UGIB: how do they work and examples

A
  • direct alkaline buffer to control the pH of the gastric mucosa
    ex: aluminum hydroxide, calcium carbonate, magnesium hydroxide, and magnesium oxide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

histamine antagonists (h2 blockers): how do they work and examples

A
  • block parietal cells secretion of Hcl

ex: cimetidine, famotidine, nizatidine, ranitidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

PPIs: how do they work and examples

A
  • inhibit gastric acid secretion by specific inhibition of the hydrogen-potassium-adenosine-triphosphatase enzyme system
    ex: esomeprazole, lansoprazole, omeprazole, pantoprazole
22
Q

mucosal protectors: how they work and examples

A
  • reduce effect of acid secretion, promote healing

ex: sucralfate, colloidal bismuth

23
Q

tx of h pylori?

A

first line is triple agent therapy: usually 2 ABX (amoxicillin and clarithromycin) with a PPI (omeprazole) for 14 days.

second line therapy is quadruple therapy: it’s implemented when 1st line fail or infection is resistant to clarithromycin: PPI OR h2 receptor antagonist + bismuth, metronidazole, and tetracycline.

Levofloxacin 10 day course can be used alternatively to second line therapy.

24
Q

acute gastric perforation s/s

A
  • abrupt onset of severe ABD pain
  • board like abd
  • usually absent bowel sounds
  • leukocytosis
  • presence of free air on radiography
  • peritonitis occurs shortly after
25
Q

tx of acute gastric perforation

A
  • emergent surgery
  • IV fluid resuscitation
  • NGT for decompression
  • broad spectrum ABX
  • antacid or histamine blockers
26
Q

causes of acute pancreatitis

A

-gallstone migration biliary dysfunction (cholelithiasis, CBD obstruction)
-alcoholism
less common causes:
-surgical trauma, hypercalcemia, various toxins, ischemia, infections, use of certain meds (lasix, thiazides, estrogen, procainamide)

27
Q

what is acute pancreatitis?

A

the inflammation of the pancreas/injury or disruption of pancreatic acinar cells associated with premature activity of its digestive enzymes that are essential for CHO, fat, protein metabolism (trypsin, chymotrypsin, elastase).
leads to damaged cells, impaired exocrine/endocrine function, and systemic damage

28
Q

how does acute pancreatitis have systemic effects?

A

cellular destruction in pancreatic injury results in the release of toxic enzymes and inflammatory mediators into the systemic circulation and causes injury to vessels and other organs distant from the pancreas; this may result in SIRS, MODS, and death.
there is release of prostaglandins, kinins, and histamine causing vasodilation, increased vascular permeability

29
Q

s/s acute pancreatitis

A

-n/v
-acute onset ABD pain
-fever
-grey turner sign (may indicate hemorrhage)
-cullens sign (may indicate hemorrhage)
other s/s:
-abd guarding/distention
-hypoactive or absent bowel sounds
-signs of hypovolemic shock
-severe disease
-peritoneal signs
-ascites
-jaundice
-palpable abd mass (indicating pseudocyst or abscess)
-dehydration

30
Q

what is used to classify mortality and severity of acute pancreatitis?

A
  • ranson criteria (one of the most commonly used scoring systems for severity of acute pancreatitis)
  • atlanta classification (defines severe as 3 or more on the ranson criteria or as a score of 8 and up on the Acute Physiologic and Chronic Health Eval aka APACHE II)
  • SOFA (sepsis related organ failure assessment)
31
Q

diagnostic tests/labs for acute pancreatitis

A
  • serum amylase/lipase are most specific: they’re released as pancreatic cells are destroyed
  • trypsin is late pancreatitis i think
  • CRP increases within 24 hrs and is a marker of the severity
  • ABD US for presence of stones
  • CT is GOLD STANDARD for diagnosing pancreatitis and ascertaining the overall degree of pancreatic inflammation and necrosis (more accurate than US and can determine complications like pseudocyst, abscess, biliary obstruction, etc)
  • endoscopy
  • leukocytosis
  • hyperglycemia
  • K decreased with GI loss, might increase if AKI develops
  • Ca decreased in severe pancreatitis, associated with fat necrosis
  • triglyceride elevation, possibly causative
  • hyperbilirubinemia
  • hypoalbuminemia
32
Q

tx for acute pancreatitis

A
  • pain is priority (PCA, morphine but meperidine/demerol is actually better, fentanyl, hdromorphone, knee-chest position)
  • decrease gastric release and prevent gastric content entry to duodenum
  • intra-abd pressure monitoring if intra-abd HTN suspected
  • closely monitor for pancreas infection (increased ABD pain, tenderness, fever, increased WBC)
  • educate on alc cessation
  • fluids: colloids, LR, FFP, albumin immediately to prevent hypovolemic shock (aggressive 5-10 ml/kg/hr and vigorous 20 ml/kg/hr for 8-12 hrs)
  • closely monitor and correct hypocalcemia (<8.5 associated with high mortality), hypokalemia, hypomagnesemia, hyperglycemia
  • early initiation of enteral (preferred over TPN)
  • anticholinergics
  • glucagon
  • somatostatin
  • cimetidine
  • calcitonin
  • ABX in cases of pseudocyst/abscesses to prevent sepsis
  • pancreatic resection through laparoscopy for failed conventional tx or peritonitis
  • for pseudocyst, external/internal drainage, needle aspiration, acute surgical intervention if infected/perf
  • cholecystectomy if gallstones are the cause of pancreatitis
  • surgical procedure of choice (i dont know if for all pancreatitis or just necrotizing): minimally invasive necrosectomy
33
Q

causes of ALF

A

viral hepatitis and common hepatotoxic drugs

34
Q

viral hep types and sources

A

-Hep A: fecal oral, parenteral, sexual
-Hep B: parenteral, sexual
-Hep C: parenteral
-Hep D: parenteral, sexual, fecal oral
-Hep E: fecal oral
Hep G: parenteral, sexual

35
Q

common hepatotoxic drugs

A
  • analgesics
  • anesthetics
  • anticonvulsants
  • antidepressants
  • antimicrobial agents
  • antipsychotic drugs
  • cardiovascular drugs
  • hormonal drugs
  • sedatives
36
Q

patho of ALF

A
  • lack of perfusion (shock) or inflammation (hepatitis) causes massive necrosis of hepatocytes and liver can longer perform functions
  • can also be caused by prolonged liver disease when healthy tissue is replaced by fibrotic tissue (cirrhosis)
  • if normal cells are replaced by fat cells/tissue it is fatty liver disease
37
Q

what is ALF characterized by

A

development over 1-3 wks with encephalopathy within 8 weeks in a patient with a previously healthy liver

38
Q

s/s of ALF

A
  • initial symptoms are vague: weakness, fatigue, loss of appetite, weight loss, n/v, change in bowel habits, abd discomfort.
  • progression: portal HTN, impaired liver metabolic processes, impaired bile formation
  • hyperexcitability
  • HA
  • palmar erythema
  • spider nevi
  • bruises, edema
  • insomnia
  • irritability
  • lethargy
  • decreased LOC
  • coma
  • convulsions
  • sudden onset high fever
  • N/V
  • chills
  • jaundice
  • asterixis
39
Q

labs for ALF

A
  • increased: ammonia, total bilirubin >3mg/dl, direct/conjugated bilirubin, cholesterol, PT/PTT, APT, AST, ALT, urine bilirubin, urobilinogen
  • decreased alb
40
Q

tx of ascites in ALF

A
  • may require intubation
  • semi fowlers
  • daily weights
  • diuretics
  • low Na diet
  • fluid restriction
  • paracentesis
  • LeVeen or Denver shunt
41
Q

tx of portal systemic encephalopathy (hepatic encephalopathy) in ALF

A
  • limit protein
  • lactulose is first line tx: causes acidic pH in bowel resulting in ammonia flowing out of serum into bowel and has laxative effect to secrete more ammonia
  • second line tx are neomycin and metronidazole: destroy normal bowel flora which reduces ammonia production from protein breakdown (but neomycin is nephrotoxic so monitor renal and monitor hearing)
42
Q

tx for hepatorenal syndrome in ALF

A

poor prognosis. palliative care

43
Q

tx for hepatopulmonary syndrome in ALF

A

oxygen, TIPS, transplant

44
Q

tx of bleeding in ALF

A

-vit K, ffp, platelet transfusions

45
Q

tx to prevent complications or tx of complications for ALF

A
  • prophlyactic ABX
  • ICP monitoring if cerebral edema
  • CRRT if renal failure develops
  • fluid administration and vasoactive meds to prevent prolonged episodes of hypotension
  • transplant if ALF continues and no signs of immediate improvement
  • monitor glucose: hypoglycemia common
46
Q

when is liver transplant contraindicated

A
  • hiv
  • malignancy
  • severe heart/lung/renal disease
47
Q

alternatives to liver transplant

A
  • bio artificial liver devices as a bridge to transplant

- molecular adsorbents recirculating system (MARS)

48
Q

types of cirrhosis

A
  • Laennecs: alcoholic
  • Biliary: decreased bile flow from obstructed ducts
  • Cardiac: prolonged R sided HF causing decreased oxygenation of liver cells
  • Post necrotic: exposure to chemical toxins causing massive death of liver cells
49
Q

causes of nonalcoholic fatty liver

A

obesity, dm, starvation, TPN, hepatic resection

50
Q

s/s of portal HTN / effects of it

A
  • s/s are similar to R sided HF

- esophageal and gastric varices: massive GI bleed, splenomegaly

51
Q

s/s of hepatic encephalopathy

A
  • early: asterixis
  • ALOC, confusion, coma in severe cases, impaired motor ability

Stage 1: tremors, slurred speech, impaired decision making

Stage 2: drowsiness, loss of sphincter control, asterixis

Stage 3: dramatic confusion and somnolence

Stage 4: profound coma, unresponsiveness to pain, GI alterations

NRSG 331 (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions