Brainscape's Knowledge GenomeTM

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


See full index

CHEST SEEK Library > Gastrointestinal Disorders > Flashcards

Gastrointestinal Disorders Flashcards

1
Q

what diagnostic test can be done to check if a patient is on apixaban/edoxaban/rivaroxaban, if the AC is therapeutic or supratherapeutic?

A

direct measurement of factor Xa levels

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

since factor Xa level measurement is not readily available what other lab test might be helpful?

A

PT and INR might be elevated; but they might still be normal in a therapeutic or supratherapeutic patient

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

what diagnostic test can be done to check if a patient is anticoagulated w/ dabigatran?

A

thrombin time

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

what test is highly sensitive in excluding clinically therapeutic dabigatran therapy and eliminates it as a contributor to clinically relevant bleeding?

A

a normal thrombin time

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

if a thrombin time is elevated does that point to one specific DOAC as the culprit?

A

no, it can be any of the DOACs; a normal thrombin time only eliminates dabigatran as the culprit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

in a patient who p/w bleeding while taking a DOAC, evaluation should be made as to whether or not it is a major bleed; what are the 2 main determining factors?

A
  • site of bleed
  • volume of bleed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what site of bleeding are considered critical?

A
  • intracranial
  • intraocular
  • intra or extra-axial spinal hemorrhage
  • pericardial tamponade
  • posterior epistaxis
  • intrathoracic
  • intraabdominal
  • retroperitoneal
  • intramuscular
  • intraarticular
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

intraluminal GI bleeding is not considered a critical bleeding site; what might make a GIB considered to be major?

A

the volume of bleed leading to hemodynamic instability

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

what is the reversal antidote for factor X (abiXABAN, edoXABAN, rivoroXABAN) agents?

A

andeXanet alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the 2 major concerns regarding administration of andexanet alpha?

A
  • cost of medication (stupid expensive)
  • rebound thrombophilia w/ subsequent high rates of thrombotic events
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what can be used to reverse anti-Xa DOACs if andexanet alpha is not available?

A

4-factor prothrombin complex concentrate (4F-PCC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

4-factor prothrombin complex concentrate (4F-PCC) contains what?

A

factors II, IX, X, and VII

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

what must be given in conjunction w/ 4F-PCC and why?

A
  • vitamin K 10 mg ivp
  • factors II, IX, X, and VII are vitamin K-dependent coagulation factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the reversal antidote for dabigatran?

A

idarucizumab

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

what treatment measures are NOT helpful in reversing factor-Xa DOACs?

A
  • FFP; contains very little factor X
  • cryoprecipitate; does contain any factor X
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the mechanism of hepatotoxicity from acetaminophen overdose?

A

depletion of glutathione which overwhelms glucuronidation pathway, leading to a shift in metabolism toward NAPQI production which is a hepatotoxic metabolite

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

how does N-acetylcysteine (NAC) help in acetaminophen overdose?

A

replenishes glutathione activity and restores glucuronidation pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

treatment decisions for acetaminophen overdose are based on what?

A

serum acetaminophen concentration measured at least 4 hours after a single overdose when absorption is complete

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

the Rumack-Matthew nomogram for acetaminophen toxicity should NOT be used under what scenario?

A
  • if the h/o overdose time is NOT reliable
  • patient has been taking acetaminophen chronically
  • chronic alcohol use
  • preexisting liver disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are a couple of reasons why the Rumack-Matthew nomogram cannot be used for acetaminophen toxicity in a patient w/ chronic alcohol use?

A
  • chronic alcohol ingestion also depletes glutathione and upregulates CYP2E1, leading to decreased glucuronidation and increased NAPQI production
  • alcoholism may lead to inordinate delays in seeking medical attention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

in patients whom the Rumack-Matthew nomogram cannot be used to assess hepatotoxicity risk, what is the best next step?

A

treat w/ NAC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

treatment for presumed esophageal variceal bleed

A

octreotide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

treatment for variceal bleed

A

EGD w/ banding followed by emergent transjugular intrahepatic portosystemic shunting (TIPS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

EGD w/ banding followed by TIPS has what benefits?

A
  • reduces recurrent esophageal bleeding
  • reduces 3-month mortality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what additional treatment has been shown to reduce mortality in variceal bleeding?

A

abx, especially ceftriaxone or fluoroquinolones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

hb transfusion thresholds are well studied in critically ill patients, and in general, a hb threshold of 7 g/dL has been found to be similar or better in outcomes compared w/ higher transfusion thresholds; what patient subset was excluded from these studies?

A

active GI bleeding, but a later study directly addressed this question

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

one RCT specifically compared outcomes of patients p/w UGIB w/ both shock and variceal bleeding, and were randomized to receive transfusion of prbc if their hb was < 7 g/dL vs < 9 g/dL; what were the results?

A

the patients in the lower hb transfusion threshold had improved survival

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

why might there be a survival benefit in UGIB patients w/ variceal bleeding and shock when they receive prbc transfusions at a lower threshold of < 7 g/dL?

A

patients w/ esophageal varices developed higher portal pressure and more bleeding when they were transfused to a higher hb threshold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is the Child-Pugh score?

A

estimates cirrhosis severity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

how is the Child-Pugh score determined?

A
  • total bilirubin
  • albumin
  • INR
  • ascites
  • encephalopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what are the Child-Pugh scores and their associated 1-year survival rates?

A
  • 5-6 points; class A; 100% survival
  • 7-9 points; class B; 80% survival
  • 10-15 points; class C; 45% survival
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

hepatic encephalopathy grading

A
  • grade 0 = normal
  • grade 1 = restless, sleep disturbance, agitated, tremor
  • grade 2 = lethargic, disoriented, inappropriate, asterixis, ataxia
  • grade 3 = somnolent, stuporous, hyperactive reflexes, rigidity
  • grade 4 = unrousable coma, decerebrate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

emergency orthotopic liver transplantation (OLT) has been shown to improve outcomes in which patients?

A

acute or decompensated hepatic failure from alcoholic hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

numerous large randomized studies have shown what clinical outcomes when comparing transfusing the freshest units of prbcs and the oldest units?

A

no difference

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

clinical syndrome of acute liver decompensation and portal hypertension in individuals w/ chronic and active alcohol abuse

A

alcoholic hepatitis (AH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

alcoholic hepatitis is more common in what patient populations?

A
  • younger patients
  • females
  • binge drinkers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

patients w/ alcoholic hepatitis typically p/w subacute and nonspecific c/o

A
  • fatigue
  • jaundice
  • other common symptoms attributable to liver failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

physical exam of alcoholic hepatitis

A
  • fever
  • tachycardia
  • tachypnea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

common laboratory abnormalities seen in alcoholic hepatitis

A
  • leukocytosis w/ left shift
  • elevated AST and ALT w/ AST/ALT ratio > 1.5
  • elevated total bilirubin
  • coagulopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

alcoholic hepatitis can both contribute to and be confused w/ what conditions?

A
  • nonalcoholic steatohepatitis (NASH)
  • viral hepatitis
  • drug toxicity including acetaminophen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

in obese patients w/ an unreliable alcohol history, what can be helpful in differentiating AH from NASH?

A

alcohol-nonalcohol index

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what is a common and significant cause of morbidity and mortality in patients w/ alcoholic hepatitis and should be excluded?

A
  • infection
  • septic w/u including paracentesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what is the alcohol-nonalcohol index, aka alcoholic liver disease/nonalcoholic fatty liver disease index (ANI)?

A

scoring system that is highly accurate in distinguishing ALD from NAFLD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what is the alcohol-nonalcohol index, aka alcoholic liver disease/nonalcoholic fatty liver disease index (ANI) score based on?

A
  • AST
  • ALT
  • MCV
  • weight
  • height
  • gender
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what is the best next step in patients w/ severe, refractory alcoholic hepatitis who are being treated w/ corticosteroids?

A

d/c corticosteroids d/t risk of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what percentage of patients w/ alcoholic hepatitis do not respond to corticosteroids?

A

50-60%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

score that predicts mortality in patients w/ alcoholic hepatitis not responding to corticosteroids after 1 week of therapy

A

Lille score > 0.45

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Model for End-Stage Liver Disease (MELD-UNOS) score of what defines severe AH w/ an estimated 20% mortality?

A

≥ 20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

although controversial, current guidelines recommend what therapy in the setting of severe AH w/ a Maddrey discriminant function ≥ 32 or MELD-UNOS score ≥ 20?

A
  • prednisone 40 mg po daily
  • methylprednisolone 32 mg iv daily (if unable to take po)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

a recent high-quality systematic review showed what regarding the use of corticosteroids in patients w/ severe AH?

A

no benefit in all-cause mortality, health-related quality of life, or serious adverse events in either mild or severe AH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

the use of what medication had generated interest, but randomized studies have failed to demonstrate efficacy in severe AH or as salvage therapy for steroid nonresponders?

A

pentoxifylline (phosphodiesterase inhibitor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

a recent RCT showed what regarding the combination of prednisolone and NAC regarding survival benefit in patients w/ severe AH?

A
  • survival benefit at 28 days, but not 3 and 6 months
  • higher than expected mortality in the prednisolone arm
  • NAC is still not recommended for routine use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q
  • chronic nausea and vomiting
  • s/s of hypovolemia
  • relief of symptoms w/ hot shower
A

cannabinoid hyperemesis syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

complete resolution of cannabinoid hyperemesis syndrome requires what?

A

months of abstinence, and relapses are common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what diagnosis can resemble cannabinoid hyperemesis syndrome?

A

cyclic vomiting syndrome (CVS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

cyclic vomiting syndrome (CVS) clinical features

A
  • severe recurrent vomiting that lasts for hours or days followed by symptom-free periods
  • episodes tend to recur at FIXED intervals
  • most often begins in childhood
  • usually a/w mitochondrial DNA mutations
  • females > males
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q
  • bloating
  • abdominal pain
  • occasionally nausea/vomiting
  • primarily a diarrheal illness a/w greasy stools and flatulence
A

giardiasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

how is giardiasis contracted?

A

when Giardia duodenalis cysts w/i feces of infected cats, rodents, or other mammals contaminate food/water that then eaten/drunk

59
Q

who is at highest risk of contracting giardiasis?

A

people who drink untreated surface water from ponds, lakes, and streams

60
Q

how else can giardiasis be contracted?

A

eating undercooked pork

61
Q

in patients w/ newly diagnosed spontaneous bacterial peritonitis (SBP), it’s recommended that they be given what?

A
  • albumin 20% or 25% 1.5 g/kg be given w/i 6 hours of diagnosis
  • then albumin 20% or 25% 1 g/kg repeated on day 3
62
Q

why should patients w/ newly diagnosed SBP be given albumin w/i 6 hours of diagnosis and again on day 3?

A
  • decreased incidence of renal failure
  • improved survival
63
Q

patients w/ newly diagnosed SBP who have shown benefit from receiving albumin are the highest risk patients which are defined as what?

A
  • Cr > 1 mg/dL
  • BUN > 30 mg/dL, or
  • bilirubin > 4 mg/dL
64
Q

what is not recommended for cirrhotic patients undergoing paracentesis in the absence of evidence of peritonitis when a volume of < 5 liters is removed?

A

colloid replacement

65
Q

what are the guidelines regarding colloid replacement in the setting of large volume paracentesis?

A

6-8 g of albumin 25% for each liter removed after the 5th liter

66
Q

recent evidence-based guidelines suggest that ppx for stress ulcer ppx (SUP) should be limited to patients at high risk of clinically important bleeding; which patients are considered high-risk?

A
  • MV > 48 hours
  • coagulopathy (platelets < 50,000/µL, INR > 1.5, or PTT > 2x normal
  • TBI
  • h/o GIB or ulceration in the preceding year
67
Q

what conditions w/ weaker evidence for increased bleeding may benefit from SUP?

A
  • patients w/ sepsis
  • high-dose glucocorticoid therapy
  • sustained occult bleeding > 1 week
68
Q

is there a difference in effectiveness between PPI and H2 receptor antagonists in reducing risk of clinically important bleeding?

A

no

69
Q

is there a difference in effectiveness between iv and enteral PPI in reducing risk of clinically important bleeding?

A

hasn’t been studied in direct comparison, but both reduce bleeding risk

70
Q

risk of thrombocytopenia in patients receiving PPI vs H2 receptor antagonist for SUP?

A
  • both can cause
  • exceedingly rare adverse event
  • critically ill patients so have many other possible causes
71
Q

is there benefit of SUP in patients receiving enteral nutrition?

A

no, most studies have failed to show benefit

72
Q

risk of CDI in patients receiving PPI for SUP

A
  • evidence is mixed if PPI use is a/w w/ CDI
  • very high heterogeneity among studies
  • abx use has been a confounder in most studies (obviously…)
73
Q

risk of CDI in patients receiving H2 receptor antagonists for SUP

A

has not been a/w CDI

74
Q

bleeding is considered clinically significant based on what criteria?

A
  • if it causes orthostatic hypotension (> 20 mm Hg reduction in SBP, or > 20/min increase in pulse), or
  • 2 g/dL drop in hb w/o an appropriate response to prbc transfusion
75
Q

SUP in appropriately selected patients reduces clinically important bleeding, but what about overall mortality?

A

has not been shown to reduce overall mortality

76
Q

what are the potential etiologies for isolated gastric varices, aka gastric varices w/o esophageal varices?

A
  • liver dysfunction and subsequent portal hypertension
  • splenic vein thrombosis w/ left-sided portal hypertension
77
Q

splenic vein thrombosis w/ left-sided portal hypertension often occurs d/t what?

A
  • pancreatitis
  • pancreatic masses (pseudocysts, malignancies, cystic adenomas, etc)
  • left gastric artery pseudoaneurysm compressing the splenic vein
78
Q

when the splenic vein is thrombosed, venous blood from both the splenic and short gastric veins must drain back to the portal vein via collaterals, causing increased pressure in the short gastric vein, creating left-sided or sinistral portal hypertension, w/o right-sided portal hypertension; what is the treatment for this condition?

A

splenectomy, which can be curative

79
Q

in a patient w/ isolated gastric varices and suspected splenic vein thrombosis, what is the next best diagnostic step?

A

CT a/p w/ and w/o iv contrast

80
Q

what artery supplies blood flow to the gastric pylorus and proximal part of the duodenum, and is often embolized to stop bleeding from duodenal ulcers on the posterior wall which can erode into that same artery?

A

gastroduodenal artery

81
Q

what procedure can be lifesaving for patients w/ refractory variceal bleeds from classic portal hypertension?

A

transjugular intrahepatic portosystemic shunt (TIPS)

82
Q

transjugular intrahepatic portosystemic shunt (TIPS) is unlikely to help in which situation?

A

patient w/ sinistral portal hypertension w/ normal portal vein pressures d/t elevated pressures in the short gastric veins from splenic vein thrombosis

83
Q

treatment for decreasing mesenteric and portal pressures that prevents or delays rebleeding in patients w/ varices from portal hypertension 2/2 cirrhosis

A

nonselective β-blocking agent such as propranolol

84
Q
  • protracted vomiting
  • cxr showing pneumomediastinum
A

esophageal rupture (Boerhaave’s syndrome)

85
Q

next best step for assessment of possible esophageal leak

A

fluoroscopic esophageal swallow study

86
Q

treatment for esophageal rupture (Boerhaave’s syndrome)

A

emergent surgical repair

87
Q

what is Mackler’s triad in the setting of spontaneous esophageal rupture?

A
  • vomiting
  • chest pain
  • spontaneous emphysema
88
Q

spontaneous esophageal rupture can occur under what circumstances?

A
  • forceful retching
  • barotrauma in the chest
89
Q

in the majority of cases of esophageal rupture (Boerhaave’s syndrome), the rupture is described as what, and where is the tear?

A
  • linear
  • located in the distal esophagus just above the gastroesophageal junction
  • in a posterolateral position
90
Q

given the location of esophageal rupture (Boerhaave’s syndrome) is typically located in the distal esophagus just above the gastroesophageal junction and in a posterolateral position, what complications may occur?

A
  • left pneumothorax
  • contaminated mediastinal and pleural spaces w/ infection
  • left pleural effusion is common
91
Q

if thoracentesis is performed in the setting of esophageal rupture (Boerhaave’s syndrome), what are the expected results?

A
  • exudative pleural fluid
  • low pH
  • extremely high amylase level (related to saliva spillage)
92
Q

early diagnosis and repair for esophageal rupture (Boerhaave’s syndrome) is imperative; in most cases, definitive repair is done by thoracotomy, but another option is

A

stenting via endoscopy

93
Q

the MELD score was initially developed to predict outcome after TIPS, then was adopted to predict outcome in outcome in patients w/ chronic liver disease and acute hepatic failure, then by UNOS to determine eligibility for liver transplantation; what is the score based on?

A
  • serum bilirubin
  • serum Cr
  • PT/INR
  • serum Na+
94
Q

critically ill patients have delayed gastric emptying; 2 trials showed what regarding stopping feedings if nursing staff observed gastric residuals above a threshold level?

A

no benefit and it resulted in diminished nutrition

95
Q

the Gastric Residual Volume during Enteral Nutrition in ICU patients (REGANE) trial (great name…) showed that gastric residuals up to what volume could be tolerated w/o measurable adverse effects?

A

500 mL

96
Q

the Effect of Not Monitoring Residual Gastric VOlume on the Risk of Ventilator-Associated Pneumonia in Adults Receiving Mechanical Ventilation and Early Enteral Feeding (NUTRIREA 1) trial (seriously???) demonstrated what?

A

equivalent rates of aspiration and PNA, whether residual volumes were measured or not

97
Q

the Scottish Intensive Care Glutamine or Selenium Evaluative Trial (SIGNET) showed what?

A

no benefit to glutamine supplementation

98
Q

the Reducing Deaths Due to Oxidative Stress (REDOXS) trial showed what?

A

showed a 6.5% increase in mortality at 6 months in patients who received early high-dose parenteral feeding and enteral glutamine supplementation

99
Q

in the Impact of Early Parenteral Nutrition Completing Enteral Nutrition in Adult Critically Ill Patients (EPaNIC) trial, patients were randomized to enteral nutrition alone vs the addition of parenteral nutrition to achieve caloric needs; what did the study show?

A
  • enteral nutrition only supplied ~ 20% of estimated caloric need in the first week, BUT
  • patients receiving hypocaloric nutrition (no parenteral nutrition) had an earlier d/c from the ICU and hospital, less infections, and less ICU-acquired weakness
100
Q

in the Trophic vs Full-Energy Enteral Nutrition in Mechanically Ventilated Patients w/ Acute Lung Injury trial (EDEN), relatively young and well-nourished patients w/ acute respiratory failure were randomized to received small volumes of trophic feeding vs full enteral feeding in the first week of critical illness; what did the study show?

A

although patients randomized to more aggressive feeding received more calories and other nutrients, there was no difference in either acute or chronic outcomes

101
Q

in the Early Parenteral Nutrition, patients w/ a relative contraindication to enteral feeding were randomized to enteral or early parenteral nutrition; what did the study show?

A

no significant difference between the groups in 60-day mortality, but the duration of MV was shorter in the parenteral nutrition group (overall, studies do not support the use of early supplemental parenteral nutrition)

102
Q

what have numerous studies demonstrated regarding feeding patients w/ severe pancreatitis?

A

they can be fed enterally w/o increasing complications or worsening outcomes

103
Q

in patients w/ alcohol use d/o, when starting feedings what should be taken into consideration?

A

refeeding syndrome

104
Q

in patients at risk of refeeding syndrome, what management strategies should be taken into consideration?

A
  • start enteral nutrition at a lower rate
  • close monitoring of serum electrolytes (K+, PO4, Mg++)
105
Q

initiating enteral nutrition in patients w/ pancreatitis w/i what timeline may improve outcomes?

A

w/i 48 hours

106
Q

in a patient w/ advanced cirrhosis and portal hypertension c/b massive variceal hemorrhage, what might be an initial intervention to stabilize the patient?

A

orogastric tamponade device

107
Q

what is one of the most serious complications of using a orogastric tamponade device?

A

esophageal necrosis and rupture

108
Q

what is one part of the strategy to minimize the complication of esophageal necrosis and rupture when using a orogastric tamponade device?

A

deflating the balloon q12h, and if bleeding has stopped, leave the balloon deflate but in place

109
Q

typically, when indicated, esophageal tamponade has been achieved w/ placement of a orogastric tamponade device; what else can be used?

A

expandable metal stents placed endoscopically

110
Q

what might be needed when using a orogastric tamponade device to avoid dislodgement?

A

generous sedation +/- paralysis

111
Q

what are the 3 types of orogastric tamponade devices?

A
  • Linton-Nachlas tube
  • Sengstaken-Blakemore tube
  • Minnesota tube
112
Q

the Linton-Nachlas tube has how many ports?

A
  • 2 ports
  • 1 port for inflating the gastric balloon
  • 1 port for a gastric suction channel to monitor for bleeding below the balloon
113
Q

since the Linton-Nachlas tube only has a gastric suction channel, what else needs to be placed and why?

A
  • an additional nasogastric tube above the balloon
  • to avoid pooling of secretions and aspiration
114
Q

the Sengstaken-Blakemore tube has how many ports?

A
  • 3 ports
  • 1 port for inflating the gastric balloon
  • 1 port for a gastric suction channel to monitor for bleeding below the balloon
  • 1 port for inflating the esophageal balloon
115
Q

since the Sengstaken-Blakemore tube only has a gastric suction channel, what else needs to be placed and why?

A
  • an additional nasogastric tube
  • to avoid pooling of secretions and aspiration
116
Q

the Minnesota tube has how many ports?

A
  • 4 ports
  • 1 port for inflating the gastric balloon
  • 1 port for a gastric suction channel to monitor for bleeding below the balloon
  • 1 port for inflating the esophageal balloon
  • 1 port for an esophageal suction channel
117
Q

meticulous attention to the steps of inflation of a orogastric tamponade device will help avoid what disastrous outcome?

A

inflation of a gastric balloon in the esophagus

118
Q

esophageal tamponade is a

A

temporizing measure

119
Q

a orogastric tamponade device should be left in place for how long?

A

only 24-48 hours while other treatment options are arranged/implemented

120
Q

management of a orogastric tamponade device involves what steps to avoid esophageal necrosis and rupture?

A
  • deflating the balloon q12h
  • monitor the tamponading balloon pressure q1h
  • maintain tamponading pressure at 30-45 mm Hg (just enough to tamponade venous bleeding w/o eliminating critical perfusion to maintain viability of esophageal mucosa)
121
Q

what factors contribute to enteral feeding intolerance in patients who are critically ill?

A
  • gastric dysmotility
  • ileus
  • medications
122
Q

holding enteral feeding because of gastric intolerance and planned procedures is common in the ICU and can lead to

A

a potentially detrimental calorie deficit

123
Q

the current (2016) ASPEN guidelines make what recommendation regarding routine gastric residual volume (GRV) monitoring?

A

recommend against checking GRV

124
Q

what other signs of GI intolerance should be checked before deciding to withhold enteral feeding instead of checking GRV?

A
  • abdominal distention
  • vomiting
  • regurgitation
  • diarrhea
  • reduced passage of flatus or stool
  • abnormal abdominal radiographic findings
125
Q

does GRV correlate w/ the incidence of PNA, regurgitation, or aspiration?

A

no

126
Q

should GRV be measured in patients who are critically ill and have undergone abdominal surgery or have other intraabdominal abnormalities?

A

unclear

127
Q

what should be considered for patients receiving enteral nutrition meeting < 60% of their protein and energy needs by day 7-10?

A

supplemental parenteral nutrition

128
Q

instead of an hourly rate target, what has been shown to increase the proportion of prescribed protein and energy delivered by enteral nutrition?

A

volume-based feeding protocols that have a daily volume target

129
Q

hepatic venous outflow obstruction not d/t passive causes such as cardiac disease

A

Budd-Chiari syndrome

130
Q

primary Budd-Chiari syndrome (BCS) is defined as

A

venous obstruction d/t occlusion of any of the 3 major hepatic veins or IVC, usually d/t thrombosis

131
Q

secondary Budd-Chiari syndrome is d/t

A

extrinsic mechanical or invasive causes such as compression or invasion from an extrinsic lesion

132
Q

what is the best test to confirm the diagnosis of BCS by visualizing a thrombus or obstruction?

A

US w/ duplex flow analysis of the hepatic vasculature

133
Q

BCS can manifest under what circumstances?

A
  • acute w/ acute hepatic failure (5% of patients)
  • acute w/ rapidly worsening liver disease but not yet hepatic failure (20%)
  • subacute (developing over 2-3 months)
  • chronic (manifesting w/ cirrhosis)
134
Q

acute BCS typically p/w

A
  • RUQ pain
  • abdominal distention
  • jaundice
  • ascites
  • hepatomegaly
  • GIB if varices have formed
135
Q

other findings that may be present w/ acute BCS

A
  • edema
  • fever
  • rarely hepatic encephalopathy
136
Q

what are the pathophysiological characteristics of BCS?

A

hepatic vein thrombosis leading to acute liver congestion and painful hepatomegaly d/t trapped blood in the liver –> liver congestion then leads to acute hepatic necrosis and liver enzyme elevation and can progress to acute hepatic failure, acutely, or cirrhosis, chronically

137
Q

what are the most common causes of BCS?

A

= hormonal causes of hypercoagulability (20%)
- OCP use
- current or recent (w/i 2 months) pregnancy

= hypercoagulability from diseases (25-50%)
- myeloproliferative d/o’s
* PCV
* essential thrombocytosis
- SLE
- APS
- IBD
- Bechet
- inherited hypercoagulable d/o’s
* factor V leiden disease
* thalassemia
* protein C deficiency
* protein S deficiency

= space occupying lesions (10%)
- malignancies
* HCC
- benign space-occupying liver lesions
- infections
* liver abscesses

138
Q

treatment goals for BCS

A
  • preventing clot propagation
  • opening the closed vessel if possible
  • relieving the hepatic congestion
  • managing liver failure-related complications
139
Q

first-line therapy in BCS

A

usually AC w/ LMWH or UFH followed by an oral AC

140
Q

in cases of acute BCS, if there is a defined clot, what can be considered?

A

thrombolysis

141
Q

what are other treatment options for BCS?

A

angioplasty and stent placement in the hepatic vein

142
Q

in refractory cases of BCS, what other treatment options can be considered?

A
  • TIPS
  • OLT
143
Q

as part of the risk-benefit evaluation, what is recommended to assess bleeding risk before thrombolysis or AC?

A

EGD

144
Q

what are a couple of the most common causes of drug-induced liver disease?

A
  • acetaminophen
  • amoxicillin/clavulanate

CHEST SEEK Library (11 decks)

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