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Therapeutics II > admissions and GIB > Flashcards

admissions and GIB Flashcards

1
Q

types of admissions

A
  • planned
  • emergency
  • direct
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2
Q

planned admission

A
  • no immediate threat

- planned elective procedure i.e. hip replacement

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3
Q

emergency admission

A
  • unplanned
  • most likely through ER
  • have been stabilized in ED
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4
Q

direct admission

A
  • usually from PCP
  • avoids ER
  • n/v, neutropenic fever
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5
Q

reasons for admission

A
  • clinical course with significant potential for deterioration
  • urgent surgery or invasive procedures
  • short term IV drugs or transfusions needed
  • inability to care for themself at home
  • unstable pt who needs critical care
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6
Q

what are the two most common causes for admission

A
  • circulatory disorders

- respiratory disorders

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7
Q

sepsis

A
  • life threatening inflammatory disorder
  • high mortality rates with septic shock
  • common sites of infection= respiratory, GU, GI, SST
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8
Q

SIRS

A
  • 2 or more of the following:
  • temp > 38 or < 36
  • HR >90
  • RR > 20, PaCO2 <32
  • WBC > 12 or <4
  • not as bad as sepsis
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9
Q

what does ADCVANDIMALS stand for

A
  • admit
  • diagnosis
  • condition and code status
  • vitals
  • activity
  • nursing
  • diet
  • iv fluids
  • medications
  • allergies
  • labs
  • special
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10
Q

what type of GI bleed is most common?

A
  • upper GI bleed

- 4X more common

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11
Q

where do UGIB occur?

A
  • proximal to ligament of treitz
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12
Q

what lab changes suggest bleed?

A
  • drop in H&H
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13
Q

causes of UGIB

A
  • peptic ulcer*
  • esophagitis, gastritis, duodenitis
  • gastroduodenal erosions
  • mallory weiss tears
  • variceal bleeds
  • tumor
  • angiodysplasia, telangiectasias
  • vascular ectasias
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14
Q

treatment for UGIB

A
  • stabilize pt*, fluid resuscitation, type/screen blood
  • NEED to ID source of bleed
  • monitorl BP, HR, urine output
  • contact GI ASAP
  • high dose IV PPI- reduces rebleed risk for peptic ulcers
  • keep NPO
  • NGT not routinely done
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15
Q

what is oliguria

A
  • urine output < 30 cc/hour
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16
Q

what is the goal Hgb when replacing blood

A
  • Hgb between 7-9%

- keep HCT > 30% in elderly

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17
Q

when would someone get platelets

A
  • if < 50K and active bleed
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18
Q

what are signs of fluid overload

A
  • raised JVP
  • pulmonary edema
  • peripheral edema
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19
Q

triple therapy for H pylori

A
  • PPI + 2 abx
  • clarithromycin
  • amoxicillin
  • flagyl
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20
Q

risk factors for UGIB

A
  • previous bleed
  • alcohol/ liver disease
  • steroids
  • anticoags, NSAIDs
  • severe vomiting
  • aortic surgery- aortoenteric fistulas
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21
Q

factors that influence outcome of UGIB

A
  • CV compromise
  • age > 65
  • coexisting cardio-respiratory disease
  • Hgb < 10
  • hematemesis and melena
22
Q

high risk UGIB pts

A
  • hematemesis or BRB on NGT aspiration
  • shock
  • hemodynamic compromise even with IVF
  • serious comorbidities
  • advanced liver disease
  • admit to ICU
  • after resuscitation, endoscopy should be performed in 2-24 hours
23
Q

endoscopy therapeutic options

A
  • should be performed immed after intubation, hemodynamic stabilization
  • mechanical clip +/- adrenaline
  • thermal coagulation with adrenaline
  • fibrin or thrombin with adrenaline
24
Q

angiography for UGIB

A
  • may be useful in UGIB if bleeding persists and endoscopy does not ID bleed site
  • done by interventional radiology
  • pt needs to be stable
25
Q

variceal bleed mortality

A
  • 50% mortality rate on average
  • 50% rebleed in 10 days
  • 30-50% cirrhosis pts have variceal bleeds
  • 33% survive 3 years post bleed
  • generally very poor prognosis
26
Q

what is the goal pressure for the portal system?

A
  • < 12 mmHg
27
Q

treatment for variceal bleeds

A
  • endoscopy- banding or sclerotherapy
  • octreotide +/- vasopressin
  • tamponade
  • TIPSS surgery
28
Q

general treatment plan for variceal bleeds

A
  • resuscitation and early endoscopy
  • banding +/- sclerotherapy
  • if still bleeding repeat in 5-7 days
  • if you fail- vasoconstrictor +/- tamponade
  • if endoscopy fails X2 then TIPSS procedure
29
Q

prevention of variceal bleeds

A
  • propranolol
  • reduces risk of bleed by lowering sheer force of pressure on vessels
  • prophylactic banding in pts with cirrhosis
  • long acting nitrates
  • soft foods
30
Q

TIPSS procedure

A
  • shunts blood from portal vein to hepatic vein

- usually a bridge to transplant

31
Q

what is TIPSS procedure used for

A
  • refractory bleeding
  • refractory ascites
  • budd chiari
32
Q

complications of TIPSS procedure

A
  • restenosis, occlusion, thromboembolism
  • hepatic encephalopathy
  • hemorrhage
  • cholangitis
  • stent migration
  • HF
  • liver failure
  • infection
33
Q

causes of LGIB

A
  • diverticulosis*
  • angioectasias
  • hemorrhoids
  • colitis- IBD, infectious, ischemic
  • neoplasm
  • post-polypectomy
  • dieulafoy’s lesions
34
Q

predictors of severe LGIB

A
  • HR > 100
  • SBP < 115
  • syncope
  • nontender abd exam
  • bleeding during first 4 hours of eval
  • ASA use
  • > 2 active comorbid conditions
  • > 3 present= 80% risk
35
Q

management of LGIB

A
  • 80% spontaneously resolve
  • lack of standardized approach
  • traditional= elective colonoscopy after bleeding stops, angiography for massive or unstable bleed
36
Q

urgent colonoscopy

A
  • done usu within 6-12 hours of presentation
  • requires rapid purge prep with 5-6 L of go lytely
  • colonoscopy within 1 hour of clear stools
  • not good for unstable pts
  • can ID hemorrhage and perform therapy
37
Q

radiographic studies for LGIB

A
  • tagged RBC scan

- angiography

38
Q

tagged RBC scan

A
  • medicine taggs RBCs
  • IDs area of leaking/ bleeding vessels
  • non-invasive and highly sensitive
  • good if bleed is not brisk” 0.05-0.1 ml/min
  • NOT therapeutic
39
Q

angiography for LGIB

A
  • good choice for brisk bleed who cant be stabilized or prepped for colonoscopy
  • detects bleeds at 0.5-1 ml/min
  • also therapeutic
40
Q

APAP toxicity pathophys

A
  • APAP overwhelms glutathione
  • NAPQI (toxic intermediate) accumulates
  • causes hepatic necrosis and liver damage
41
Q

when are peak plasma levels after APAP OD?

A
  • 4 hours
42
Q

factors predicting hepatotoxicity after APAP OD

A
  • total amount ingested
  • time from ingestion to presentation
  • age of pt
  • alcoholism
  • other enzyme inducing medications
43
Q

complications of APAP toxicity

A
  • jaundice
  • renal failure- hepatic renal syndrome
  • hyperlatatemia
  • metabolic acidosis
  • hypophosphatemia
  • hypo/hyperglycemia
  • cardiac arrhythmias
  • pancreatitis
  • GIB
  • cerebral edema
44
Q

phase 1 APAP poisoning

A
  • 30 min - 4 hours
  • anorexia
  • nausea
  • pallor
  • vomiting
  • diaphroesis
45
Q

phase 2 APAP poisoning

A
  • 24-48 hours
  • less severe
  • RUQ pain d/t hepatic damage
  • elevated LFTs
  • prothrombin may be prolonged
  • renal funciton may deteriorate
46
Q

phase 3 APAP poisoning

A
  • 3-5 days
  • hepatic necrosis
  • jaundice
  • renal failure
  • coag defects
  • hepatic encephalopathy
  • death due to hepatic failure
47
Q

phase 4 APAP poisoning

A
  • 4 days to 2 weeks

- complete resolution or death

48
Q

management of APAP OD

A
  • GI decontamination in first 1-2 hours with ipecac
  • activated charcoal
  • cathartics
  • dialysis not effective
  • four hours post ingestion get levels, plot on rumack-matthews nomogram
  • admin NAC
49
Q

labs to monitor with APAP toxicity

A
  • baseline cbc
  • cr, BUN
  • sugar
  • electrolytes
  • tox screen
  • prothrombin time
  • AST/ALT
50
Q

what is NAC

A
  • antidote for APAP toxicity
  • given PO or IV
  • must finish treatment once started
  • 72 hour protocol: loading dose then maint dose q 4 hours X 17 doses
  • if emesis within one hour of dose then repeat dose

Therapeutics II (8 decks)

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