GI/Liver Flashcards

1
Q

Post op jaundice causes

A

Prehepatic: hematoma abs, hemolytic transfusion rxn (increased indirect unconjugated bili-delayed or acute

Hepatic:

  • Chonic dz (viral hepatitis)
  • Ischemic or hypoxic injury/sepsis (would see abnl LFT’s/coags/plts indicating liver dysfunction)
  • Drug induced (can detect this from reviewing records for drugs such as a-methyldopa, Tylenol, chloramphenicol, isoniazid, sulfonamides, and of course r/o halothane for anes record.)
  • Inborn errors of metabolism (gilberts-unconjugated hyperbillirubemia), crigler Najjar (decreased or absent gluonyl transferase, unconjugated hyerbili), n dubin johnson-conjugated hyperbil
  • Intrahepatic cholestasis

post hepatic

Cholecystitis, Common Bile duct stone, Pancreatitis (would see conjugated hyperbiirubinemia)

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

Etio of hemodyamic changes during esophagectomy

A

cardiac/great vessel compression

vagal stimulation

hemorrhage

dysarrthymias

PTX

epidural

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

synthetic liver fxn tests

A
  1. Albumin 2-3 week half life 3.5-5.5
  2. PT: measures 2 7,,10 (7 half life 4-6 hrs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

halothane hepatitis etiologt

A

hepatitis 2/2 oxidatitve metabolites such as trifluroacetic acid, and they induce autoimmine response or hve direct hepatotoxic effect

RF: F middle age, obese, repeated exposure

iso des 1:300,000 vs halothane 1:35,000

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

Functions of the liver

A
  1. metabolism carbs, fats proteins
  2. synthesis of serum proteins-albumin/clotting factors
  3. metabolism of drugs hormones, toxins (Phase 1-oxidation/reduction (benzo barbs), Phase 2 (conjugation-morphine)
  4. production urea and bile (absorption ADEK)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

factors that effect HBF

how to preserve hepaptic blood flow intraop

A
  1. hypotension (RA GETA
  2. vasoconstriction of HA or GI/splanchnic circ 2/2 sympathetic stim
  3. BB that block B2 mediate HA vasodilation
  4. alpha agonists that cause HA and PV vasoconstriction
  5. excessive PEEP or postive pressure (increased hepatic venous pressure, decreased venous return
  6. H2 blocks decrease HBF
  7. direct surgical compression

maintain euvolemia, avoid hypotension, use iso (reduces portal flow least), min sympathetic stim, avoid BB and alpha agonist if possible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is cirrhosis?

Head to toe effects

A

heapatic necrosis, fibrosis, and nodal regeneration/ leading to portal HTN >10mmHg. causes ETOH, hepatitis, toxins

Anesthesia:

1) paralysis: may need more larger initial dose due to larger VD, decreaed proetin binding larger free fraction may off set this, and impaired metabolism few doses may be needed
2) citrate intoxication more likely w blood
3) psueocholinesterase def

Neuro: encephalopathy AMS, asterxisis, hyperreflexa, wernicke korsakoff (more permeable BBB, ammonia broken down from blood in GI tract or transfusion)

Cards: hyperdynmaic state =high mixed venous(increased CO, low SVR, anemia, systemic shunts), systemic AV shunts

resp: decreased FRC and restrictive dz from ascites, increased AV shunts, plerual effusions, inhibition of HPV (from vasodilating substances - VIP, glucagon)–>hypoxemia, resp alkalosis

GI: Portal HTN causing 1) ascities (2/2 portal HTN, hypoalbumin, renal rentention of fluids),2) varices/hemorrhids, aspiration risk

renal: decrease renal perfusion, sodium retentiom. (increase in total body andvolume but decrease in effective volume, HRS (prerenal oliguria w NA retention, azotemia, and ascites

Heme: thrombocytopenia (splenic sequestration), anemia (bleeding, RBC destruction, malnutrition, SBP

Electrolytes: hyponatremia (dilutional), hypokalemia (diuresis or hyperaldosteronism), hypoalbumin, hypoglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

esophagel cancer considerations

A

cardio: often after ETOH and smoker, high risk post op a fib
pulm: smokers often, chronic aspiration–>pulm fibrosis,

GI: nutrional status poor (increased MM), liver fxn, aspiration risk (obstruction, altered motility and spincter dysfunction

chemo: doxorubicin (cardiomyopathy, belomycin lung, radiation (pnumonitis, pericarditis

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

medical management of PHTN and varicela hemorrhage

A

BB (propranolol), or isosorbide if BB not tolerated, TIPS

variceal bleed: vasoconstriction-somatostatin, octreotide (lower portal pressures) via vasocosnstrction; vasopressin, sclerotherapy, ligataion, balloon tamponade,

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

causes of hepatitis

A

ETOH,

halothane, amiodarone,

rifampin, INH

steriods, OCP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

concerns with chronic alcoholics

A

Anesthesia: intoxiciation effect on MAC

neuro: AMS, encephalopathy, wernicke korsaoff (ataxia, confusion, occular issues; tx thiamine), withdrawl (sezizures DT)
cards: acute HTN tachy; cardiomyopathy, arrythmia
resp: smoker?
gi: ulcer, cirrhosis, aspiration risk
heme: pancytopenia

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

goals fir a cirrhoric pt

A

preop

  1. determine extent of multisystem dz
  2. optimize the pt: encepalopathy volume status, hyperdynamic state, hypoxemia, coaguopthy, anemia, electrolytes,
  3. delay if active hepatitis

intraop

  1. increased aspiration risk
  2. anesthetic that accounts for impaired hepatic drug clearance, increased VD, decreased protein binding, and altered MAC
  3. careful fluid management: low oncotic pressure predisposes to pulm edema need adeuquate hydration to preserve hepatic and renal perfusion
  4. have blood available to treat bleeding and coagulopathy from thrombocytopenia

post op

  1. AMS withdrawl or enceph
  2. same as above
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Labs for cirrhotic

A
  1. CBC plt, PT PTT -pancytopenia from plt sequestration, anemia from bleeding, malnutriion and RBC destruction, coagulopathy from factor def
  2. electrolytes: BUN cr, glucose, na, K-hyponatremia from dlution, hypokalemia from diuresis and hyperaldosteronism, hypoglycemia from severe liver failure, azotemia from dehydration or HRS
  3. LFT for baseline values and albumin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

why are cirrotics hypoxic

A
  1. atelectasis, restrictive lung dz, low FR from ascites
  2. attenuation of HPV via vasodilators, intrapulmonary A shunts
  3. plerual effusions,
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Stages of liver transplant/complications

how to reduce reperfusion

A
  1. preanhepatic- dissection

bleeding

  1. anheppatic-liver is seperated from circulation and replaced w donor
    - clamp IVC above and below, hepatic artery, PV
    - CO drops, distal venous pressure increases
    - consider V-v bypass
    - complications-embolism of air/clots, bleeding/coagulopathy, hypothermia, citrate intoxication, acidosis, RF, brachial plexus injury
  2. transplanted liver connected to circulation
    - clamps removed, HA reanastamosed, CBD reconnected
    - complications: hyperkalemia, acid metabolites/vasoactive suvstances kfrom lower body,cold blood, cytokines
    - flush graft prior to reperfusion, current any current met acidosis to counter acid load from graft, admin calcium ro counter effects of K on heart, admin vasopressors/inotropes to correct any prexisting hypotension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how can veno-venous bypass be used during transplant, complications

what is a piggyback technique

when to use techniques

A

maintains venous return to heart during IVC clamping by diverting blood from IVC via pump (no oxygenator) to axillary vein/ SC/IJ.

minimizes hypotension/improved hemodynamics, improved preload/cardiac filling

reduction pulm edema (less blood and fluid admin)

splanchnic decompression–>faster return of guyt moility

potential decrease post op renal dysfunction

limited metabolic impairment interstitial edema, ischemia, and acid metabolites in lower extxremities,

air/clot embolism, vascular/brachial plexus injury, hematoma

improved surgical field

donor IVC is attached to recipients

cardiac dz, severe pHTN, or when clamping IVC results in severe hemodynamic instability, others believe in volume loading and pressors

17
Q

Post op liver transplant complications

A

neuro: seziure (cyclospirone), encephalopathy
cards: hypo/hypervolemia, CHF (PPH, fluid overload)
resp: pleural effusion, R phrenic nerve injury, TRALI, pulm edema

GI: vascular or anastomitic leak, hepatic or PV thrombosis

renal: ARF (ATN prerenal, drug toxicity, HRS)
metabolic: metabolic alkalosis, hypokalemia (critrate metabolism)
heme: hemorrhage, coagulopathy, infections, rejection (1-6weeks)

18
Q

causes of coagulopathy during liver transplant

A

massive blood transfusion: fdilutional coagulopathy

fibrinolysis-increase in tissue plasminogen activator (tissue plasmiogen activator inhibitor decreased)

hypothermia

DIC

residual heparin

inadequate clotting factor synthesis

uremia

19
Q

What does meld consist of, what does it mean, and what does it exclude

A

INR bili, creatinine

6-40 higher the score the higher the short term mortality

excluded fulminant liver failure and life expectany <7 days -status 1 (higher priority)

20
Q

Triad of hepatopulmonary syndrome

A

Pa02<70 on RA or A-a >20

liver dz

intrapulmonary vascular dilations

21
Q

BENEFITS of paracentesis

How to replace fluid

A

cards: increased CO (relieves compression on IVC
pulm: improved pulm compliance and pulm case exchange (reduced VQ mismatch)-reduction of ascitc pressure on diaphrgam

GI; decreased risk of gastric aspirations (decreased ascetic fluid compression of stomach)

-50% immediate rest of 6 hrs: 6-8g/L

22
Q

def of portopulm HTN

A

PPH: PAP>25 or PVR >240 dynes/sec/cm^5, (3 woods) in presence of normal PCWP

mild 25-35

moderate 35-45

severe >45

>35 and >250 increased risk of periop death from R heart failure or hepatic failure

severe >50 can be considered contraindication to liver transplant

23
Q

confusion in cirrhotics

A
  1. intoxication
  2. wernicke encep (b1)
  3. chronic subdural ICP increase
  4. worsening encephalopathy (bleeding)
24
Q

etiology reperfusion syndrome

reduce effect

A
  1. excessive K load from graft
  2. release vasoactive substances and metabolic metabolites,
  3. cold blood on heart
  4. release of cytokines
  5. flush graft before reperfusion
  6. correct any current met acidosis:: bicarb
  7. calcium to counter effect K on heart
  8. inotropes and vasopressors to correct any preexisting hypotension
25
Q

Carcinoid triad

dx

caricinoid syndrome

preop optimization

A

Flushing diarrhea, cardiac involvement (TR PS-serotonin induced fiborsis), broncoconstrition

urine 5-HIAA: hydroxyindoleacetic acid (breakdown product of serotonin), chromogranin A elevated

  • complex sx that occur when carcinoid tumor releases excessive amounts of hormones (serotonin, histamine, bradykinin) into systemic circulation (met to liver substances bypass portal circ or occur outside the GI tract
  • somtaostatin analog-octreotide to decrease serotonin secretion, optimize fluid status

anxiolytic (reduce stress induced release vasoactive substances), H1 and H2 blockers to attenuate the effect of histamine,, alpha and BB blockeer to prevent catecholamine mediated release of vasoactive sustances, steriods

serotonin antagonist for nausea-zofran

26
Q

ASPIRATION PNEUMONITIS

pathophy of aspiration pneumonitis

when do admin abx

A
  • Aspirated material causes damage to surfactant producing cells (atelectasis), pulmonary capillary endothelium –>pulm edema
    1. bacterial infection based on cx and sensitivity
    2. high liklihood of negative or anerobic organism such as w feculent aspiration
    3. clinical course fails to improve after several days
27
Q

triad of compartment syndrome

A

increased abdominal pressure, abdominal distenion, evidence of end organ dysfunction

28
Q

What to do during aspiration

A

Head down, suction mouth, intubate, then suction bf PPV to avoid distal disemmination

  • baseline ABG and CXR
  • bronch for particulate
  • tx any broncospasm

monitor for 24-48 hrs

-no abx or steriods

29
Q

Considerations for ETOh abuse

A

withdrawl: tremors 6 hrs, seizures 1-1.5 days,

delerium tremens-AMS, autononmic instability (fever tachycardia HTN) 3 days, agitation

30
Q

Issues with cricoid

how it should be approached

A
  1. esophageus is displaced laterally in some pts (not compressed against vertebral bodies
  2. may reduce LES tone increasing risk of aspiration
  3. may increase dificulty of intubation
  4. may practioners apply excessive or insufficinet force–>ineffective or increased difficulty on intubation

proper application of cricoid may reduce risk of aspiration in high risk pt, but I would reduce or eliminatw if I felt it was interferring w rapid intubation.

31
Q

why hydrophilic opioids used for thoracic epidural during esophectomy

A

covers larger number off dermatomes