Gastro

Front 1

LIVER FN:

Detecting hepatocyte injury = TRANSAMINASES

Transaminases - measure activity of hep enzymes such as aminotransferases in the circulation. Usually INTRACELLULAR but released if damaged hepatocytes.

Back 1

Detecting biosynthetic capacity=

- serum ALBUMIN
- PROTHROMBIN TIME (which requires presence of clotting factors prod in liver)

Hypoalbuminemie:
ddx -
*liver probs(hep synthetic disfn)
* nephrotic syndrome
* malnutrition

Albumin:
indicator of chronic liver disease esp in cirrhosis (decreased synthetic fn)

Front 2

PROTHROMBIN TIME

May not be specific to liver disease (can also result from congenital or acquired conditions) including consumption of clotting factors (DICs severe GI bleed)

Prolonged prothrombin due to:
1- defic of vit K (factors 2,7, 9,10) due to inadeq intake, Abs that alter gut flora, malabsorp)

2- poor utilisation of vit K due to advanced parenchymal disease - vit k ineffective.

Test factor 5, because it tests livers actual capacity (not vit k dependent)
Factors 2,7,9,10 we can substitute vit k if low... testing factor V will help distinguish vit k as cause for PT disfn.

Factor v also prognostic

Warfarin is a vit k antagonist
To reverse INR - give konakion

Back 2

Prothrombin time - vit k dependent factors (2,7,9,10)

Front 3

Most common causes of chronic liver disease:

Chronic hep C
Alcoholic liver disease
Non-alcoholic steatohepatitis
Chronic hepatitis B
Auto-immune hepatitis
Sclerosing cholangitis
Primary biliary cirrhosis
Haemachromatosis
Wilsons Disease

Back 3

DEFINITIONS:

Hepatitis - generic term referring to inflammation of the liver.


Cirrhosis - generic term for end stage of chronic liver disease characterised by destruction of hepatocytes and replacement of normal hepatic architecture with fibrotic tissue and regenerative nodules (main causes: hep c, ALD, Hep c + liver disease.


Steastoses - fatty liver (hepatocytes contain macrovesicular droplets of triglycerides). Reversible.

Front 4

Alcoholic hepatitis is a clinical syndrome of JAUNDICE + LIVER FX that generally occurs decades after heavy alcohol use.
Cardinal sign is rapid onset of jaundice.

Back 4

Diagnosis of ALD:

Moderate elevation of AST and ALT (Usually less than 300 - if greater shld prompt suspicion of concurrent liver injury - viral hep, drugs, isch hepatitis)

Compared with viral hepatitis, AST usually more elevated than ALT.

Ratio is usually greater than 2, AST:ALT.

GGT may be elevated.

Bilirubin commonly elevated

WBC often HIGH with polymorphonuclear leucocytosis

PT time (and INR) elevated

Creatinine may be elevated (ominous sign indicating hepato-renal syndrome)

MACROCYTOSIS often present (represents nutritional defic of B12, folate etc)

THROMBOCYTOPENIA result from primary bone marrow hypoplasia or splenic sequestration (due to portal hypertension + splenomegaly)

***Essentials of diagnosis -
AST increased (x2 that of ALT) + elevated INR
+ neutrophilia --->

IN a patient who presents with ascites + hx of heavy alcohol use is indicative of ALC HEPATITIS until proven otherwise.

Front 5

DIFFERENTIAL DIAGNOSIS of ALD:

(also be aware of coexisting disease)
Hep C
Non-alcoholic steatohepatitis
Acute or chronic viral hepatitis
drug induced liver injury
Wilsons disease
auto-immune liver disease
alpha-1 anti-trypsin deficiency
pyogenic hepatic abcess

IMAGING:


liver biopsy
Ultrasound
CT scan
MRI
OGD for varices

Back 5

MGMT TX of ALC HEPATITIS:

Fluid and electrolytes
BSL (ETOH may inhibit gluconeogenesis leading to hypoglyc)
Thiamine (benovar/ becosym)
CIWA (NB no sedatives if encephalopathic)
Magnesium
Assess overall nutritional status esp Albumin
If co-existing gastritis tx with PPI or H2antagonists - if not stop nexium esp if risk of GI bleed (translocation of bacteria)

Evaluate for GI bleeding and treat appropriately- OGD et b-blocker

DRUG tx: Corticosteroids - (post biopsy for dx of ASH)

also IF: Maddrey score more than 32, a MELD score more than 18 or encephalopathy


if dx of ASH then treat for 1 month with 40mg/j corticosteroid, then taper - shown to reduce mortality.
- after 1 week score de Lille to assess whether improvement.
If not then cease - as risk of steroid treatment greater than benefits.
- if no improvement or contraindications to steroid - oxpentifylline (pentoxifylline) is second line tx but not shown to be anywhere near as efficace.


Contraindications to steroid use: seps

Front 6

BILAN ALD:

FSC avec LFT, bili, BSL, alb (et pre-albumin - chronique), crase (esp factor V). bilan anemie.

OGD/biopsie/US.

TX:
becosym/benovar
fluids
coricosteroids if indiq
albumin/supp drinks if required
toresimide/aldactone if ascites/varices

Back 6

MGMT Décompensation d'OH cirrhoses hépatique

Suivi test hépatique
le traitement par les diurétiques (aldactone et frusemide)
Poids tous les jours
Regime hyposodé
angio-CT - exclus CHC et thromobose vein porte
biopsie hépatique trans-jugulaire
OGD - pour varices oesophagienne
bec/ben
Seresta/anxiolytic selon CIWA
score de sevrage
alcoologue
lacitol for >2 stools per day to prevent enceph


facteurs declanchant:
PBS
Infection
reprise de l'alcool
medicamentuese
Saignment gastro-intestinale

Front 7

Liver disease alters coagulation – there are pro and anti coag factors :

Factors increased bleeding risk :
Decreased production of all pro-coagulation factors (eg, factors II, V, VII, IX, X, XI, XIII)
Thrombocytopenia – due to BM supression et ETOH
Altered platelet function (due to portal hypertension splenic sequestration in splenomegaly),
Platelet inhibition by nitric oxide, abnormalities of fibrinogen, and decreased thrombin activatable fibrinolysis inhibitor (TAFI)

Back 7

anti-coag factors:
Increased coagulation/thrombus risk :
Decreased levels of the liver-synthesized anticoagulant proteins C and S,
Decreased antithrombin levels,
Decreased plasminogen,
Elevated levels of endothelial cell-derived factor VIII and von Willebrand factor (vWF)

Front 8

gastro hx:

liver probs -

medications - amoxil, nsaids, paracetamol

travel!

vaccinations - hep?
family vaccinated?

HCC
weight loss, fevers etc

Back 8

Peritonite bacterienne spontanée:
(svt avec les pt cirrhotique)


germes frequents:
e.coli*, strep sp*, klebsiella*

DDx: perforation intestinale
appendicite perforée
abces (autres sources infectieuse)

Symptomes:
Douleur abdominale
fievre
encephalopthaie hepatique
decompensation ascitique
dysfonction haptocellulaire
hemorrhagie digestive haute

Paracenthese diagnostique - leucocytes > 250 et cultures positif.
(il faut aussi exclure un source infectieuse intra-abdominale.)

Si leucs> 250, commence traitment empirique AB en attendant resultats de culture:

cefotaxime/ceftriaxone/piperacillin +tazobactam.
ET

donne ALBUMINE a tous les pts pour prevenir un syndrome hepatorenale

Paracenthesis de controle dans 24-48hrs

Front 9

L'Ictere (jaundice)

L'ictere se manifeste a partir d'une bilirubinemie totale de 35-50

sx:
Ictere
Prurit
Diarhée
Aspect de l'urine:
foncée - ictere hemolytique, OU cholestatique. (increase in urobilinogen ou bili conjugee respectively)

Back 9

TTT ulceres oesophagienne:

IPP 40mg 2x/j pdt 1mois

si h.pylori positif (a noter que IPP pourrait rendre test negatif meme 1 mois apress tt):

amoxyl pdt 5jours

puis

klacid 500mg et flagyl 500mg pdt 5j

* faut penser de recommence/pause aspirines etc

Front 10

Refeeding syndrome:
hypomagnesie
hypokalemie
hypophosphatemie**
volume overload
oedemes

TT: corriger deficits (potassium, phoshate, mg)

Back 10

Hypophophatemie est la cause principal de refedding syndrome et las cause des problemes.

AET: When nutritional replenishment begins and patients are fed carbohydrates, glucose causes release of insulin, which triggers cellular uptake of phosphate (and potassium and magnesium).

Insulin also causes cells to produce a variety of depleted molecules that require phosphate (eg, adenosine triphosphate (ATP) and 2,3-diphosphoglycerate), which further depletes the body’s stores of phosphate [10]. The lack of phosphorylated intermediates causes tissue hypoxia and resultant myocardial dysfunction and respiratory failure.

Front 11

CHILD-PUGH

None (1 point)

Grade 1: Altered mood/confusion (2 points)

Grade 2: Inappropriate behavior, impending stupor, somnolence (2 points)

Grade 3: Markedly confused, stuporous but arousable (3 points)

Grade 4: Comatose/unresponsive (3 points)

Ascites

Absent (1 point)

Slight (2 points)

Moderate (3 points)

Bilirubin

< 2 mg/dL (1 point)

2-3 mg/dL (2 points)

> 3 mg/dL (3 points)

Albumin

> 3.5 g/dL (1 point)

2.8-3.5 g/dL (2 points)

< 2.8 g/dL (3 points)

Prothrombin time prolongation

Less than 4 seconds above control/INR < 1.7 (1 point)

4-6 seconds above control/INR 1.7-2.3 (2 points)

More than 6 seconds above control/INR > 2.3 (3 points)

Back 11

5-6 points:Child class A

7-9 points:Child class B

10-15 points:Child class C

one-year survival rates Child-Pugh class :

A, B, and C cirrhosis are 100%, 80%, and 45% percent