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Collège Royal 2019 > Gastro > Flashcards

Gastro Flashcards

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Royal College: Emergency Medicine flashcards
1
Q

Chez qui doit-on suspecter une étiologie plus dangereuse lorsque la RC est une douleur abdominale?

A

Age older than 60 years old

Previous abdominal surgery including obesity surgery

History of inflammatory bowel disease

Recent instrumentation (eg, colonoscopy with biopsy)

Known abdominal/pelvic/retroperitoneal malignancy

Active chemotherapy

Immunocompromised, including low dose prednisone

Fever, chills, systemic symptoms

Women of childbearing age

Recent immigrants

Language or cognitive barrier

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2
Q

Diviser les structures abdominales en forgut, midgut, hindgut

A

Foregut structures (stomach, duodenum, liver, gallbladder, and pancreas) are associated with upper abdominal pain.

•

Midgut derivatives (small bowel, proximal colon, and appendix) are associated with periumbilical pain.

•

Hindgut structures (distal colon and genitourinary tract) are associated with lower abdominal pain.

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3
Q

Décrire le métabolisme normal de la bilirubine

A

Bilirubin is generated from heme products, primarily senescent red blood cells. A small portion is derived from myoglobin and maturing erythroid cells. Within the reticuloendothelial system, heme is oxidized to biliverdin, which is then converted to bilirubin. Unconjugated bilirubin forms a tight but reversible bond with albumin in circulation. It is passively taken into the hepatocytes, where it undergoes glucuronidation and at this point has become conjugated bilirubin. This conjugated fraction is secreted into the biliary system and emptied into the gut. Colonic bacteria metabolize the majority of the bilirubin to urobilinogen and stercobilin. Stercobilin is excreted in the stool (causing the stool to turn brown), and urobilinogen is reabsorbed and excreted in the urine. The remaining conjugated bilirubin is deconjugated and reenters the portal circulation to be taken up again by the hepatocytes (enterohepatic circulation). In the laboratory, conjugated bilirubin and unconjugated bilirubin are reported as direct and indirect fractions, respectively.

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4
Q

Quel est le danger d’une accumulation de bilirubine non conjuguée?

A

Bilirubin is generated from heme products, primarily senescent red blood cells. A small portion is derived from myoglobin and maturing erythroid cells. Within the reticuloendothelial system, heme is oxidized to biliverdin, which is then converted to bilirubin. Unconjugated bilirubin forms a tight but reversible bond with albumin in circulation. It is passively taken into the hepatocytes, where it undergoes glucuronidation and at this point has become conjugated bilirubin. This conjugated fraction is secreted into the biliary system and emptied into the gut. Colonic bacteria metabolize the majority of the bilirubin to urobilinogen and stercobilin. Stercobilin is excreted in the stool (causing the stool to turn brown), and urobilinogen is reabsorbed and excreted in the urine. The remaining conjugated bilirubin is deconjugated and reenters the portal circulation to be taken up again by the hepatocytes (enterohepatic circulation). In the laboratory, conjugated bilirubin and unconjugated bilirubin are reported as direct and indirect fractions, respectively.

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5
Q

Dxd ictère selon le type de bilirubine augmenté

A
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6
Q

Décrire les stades d’encéphalopathie hépatique

A
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7
Q

Comment faire le dx de cholangite?

A
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8
Q

Cause la plus fréquente de dysphagie neuromusculaire

et la 2e

A

Cerebrovascular accidents causing pharyngeal weakness with failure of the cricopharyngeus muscle to relax is the most common cause of neuromuscular dysphagia.

2e: myopathies inflammatoires - poly/dermatomyosite

Ne pas oublie dysphagie 2nd anormalie a. sous-clavière droite qui comprime l’oesophage, cause dyspnée et dysphagie, souvent asx ad 40 ans

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9
Q

Nommer 5 syndromes causant de la dysphagie oesophagienne motrice (pas obstruction mécanique)

A

Maladie du collagène

Sclérodermie

CREST

Syndrome paranéoplasique

Chagas

Intrinsèque: achalasie, spasme oesophagien, nutcracker, hypertonicité shincter oesophagien inférieur

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10
Q

Facteurs de risque généraux de saignements digestifs hauts et bas

A

Medication use

•

Aspirin

•

Nonsteroidal antiinflammatory drugs

•

Steroids

•

Anticoagulants (warfarin, heparin)

•

Chemotherapeutic agents

History of peptic ulcer disease

Known liver disease, cirrhosis

Advanced age (>60 yr)

Alcoholism

Current smoker

Chronic medical comorbidities

•

Congestive heart failure

•

Diabetes

•

Chronic renal failure

•

Malignancy

•

Coronary artery disease

History of abdominal aortic aneurysm graft

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11
Q

Nommer 10 causes endocriniennes de diarrhée

A

Carcinoid syndrome (serotonin)

Hormonal hypersecretion

Hyperthyroidism (thyroid hormone)

Medullary carcinoma of the thyroid (calcitonin)

Pancreatic cholera (VIP)

Somatostatinoma (somatostatin)

Systemic mastocytosis (histamine)

Zollinger-Ellison syndrome (gastrin)

Endocrine Pathology

Adrenal insufficiency

Diabetes enteropathy

Hypoparathyroidism

Pancreatic insufficiency

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12
Q

Nommer des facteurs de risque d’avoir une diarrhée non bénigne

A
  • Immunosuppression, MII, VIH, greffé, homosexuel, maladies chroniques
  • Antibiotiques
  • Voyage, exposition eau contaminée
  • Expositions animaux, reptiles, aliments crus
  • Résidence personnes âgées, épidémie, hospitalisation, garderie
  • Diarrhée chronique
  • Instabilité HD, fièvre, rectorragie
  • Proctite, ulcérations colonique
  • PTT-SHU
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13
Q

Nommer des causes 2nd (non fonctionnelles) de constipation

A
  • Immobilité, diète, déshydratation
  • médication: opiacés, anticholinergiques, antipsychotiques, antidépresseurs, BCC, fer, antiparkinsonniens
  • Hypercalcémie, hypothyroidie, hypokaliémie, hypomagnésémie, diabète
  • Atteinte moelle épinière, SLA, sclérose en plaques, parkinson
  • obstruction intestinale, rectocèle, prolapsus, intussusception
  • abus, troubles alimentaires, troubles de l’humeur
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14
Q

Nommer les catégories de laxatifs

A
  • Bulk - fibres/metamucil
  • Osmotic: Mg, lait magnésie
  • Sucres peu absorbés: sorbitol, Peg lyte
  • Stimulants: senna, bisacodyl
  • Émollients: docusate sodium
  • nouveaux agents: ex méthylnatrexone (pour constipation induite par opiacés)
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15
Q

Décrire le syndrome de Plummer-Vinson

A

which is characterized by anterior webs (membranes oesophagiennes), dysphagia, iron deficiency anemia, cheilosis, spooning of the nails (koïlonychie), glossitis, and thin friable mucosa in the mouth, pharynx, and upper esophagus.

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16
Q

Nommer 20 causes de dysphagie

A
  • Neuro/immuno: AVC, SEP, SLA, sclérodermie, myasthénie grave, dystrophies musculaires, neuropathie diabétique, dermato/polymyosite, alzheimer, parkinson
  • Infectio: botulisme, tétanos, diphtérie, polyomyélite, rage, chorée Sydenham
  • mécanique: CE, néo, membranes, oesophagite, compression vasculaire, ostéophyte, goître, masse médiastinale, diverticule Zenker
  • Tr motilité: spasme, achalasie, nutcracker
  • métabo: Diabète, alcool, RGO, Sjogren, hypomagnésémie, thyrotoxicose
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17
Q

Nommer des traitements possible de l’achalasie

A

BCC

Nitrate

Botox

Dilatation pneumatique LES

Chirurgie

Autres troubles de motilité: possible utilité des anticholinergiques

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18
Q

Durée maximale acceptée pour obstruction incomplète par CE oesophagien (pas batterie/objet coupant)

A

24 hrs

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19
Q

3 méthodes d’extraction de CE a/n oesophage supérieur

A
  • Pince McGill, sonde Foley avec retrait, bougienage pour avancer CE a/n estomac
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20
Q

Traitement possible pour bolus nourriture impacté

A

Glucagon non recommandé

Boisson effervescente: pas mieux que placebo

Gastroscopie

(nitrate, bcc)

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21
Q

Durée et taille des objets

A

Considérer retrait du CE si

  • plus de 5cm de long ds estomac
  • plus de 2.5 cm de large ds estomac
  • objet ds estomac plus de 3-4 sem
  • objet à la même localisation a/n intestin plus de 1 sem
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22
Q

Décrire la triade de Mackler

A

Pathognomonique de la perforation oesophagienne spontanée

  • vomissement
  • dlr thoracique
  • emphysème sous-cutané
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23
Q

Décrire les signes visibles au RX pulmonaire en cas de perforation oesophagienne

A

Emphysème sous-cutané

Ép pleural D (si perfo haute) ou G (si perfo basse)

Infiltrats pulmonaires

PTX

Pneumomédiastin

Médiastin élargi

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24
Q

Facteurs de risque de RGO

A

Nourriture: chocolat, gras, menthe, alcool, caféine

Augmentation pression gastrique: obésité, valsalva, grossesse + oestrogènes/progestérone

Tr motilité oesophagienne

Rx: nitrates, BCC, anticholinergiques

Retard vidange gastrique: gastroparésie, db, obstruction gastrique, maladies neuromusculaires

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25
Q

Nommer les critères dx d’oesophagite eosinophilique

A

Sx dysfonction oesophagienne

> 15 eosino/ch sur biopsie

sx réfractaire IPP

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26
Q

Nommer 5 médicaments responsables d’oesophagite à Rx

A

Biphosphonates

Fer

Antibio - surtout tétracycline

ASA et AINS

KCl

Quinidine

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27
Q

Nommer 10 sx extraoesophagiens du reflux

A
  • Asthme, toux
  • voix rauque, mal de gorge, globus
  • otalgie
  • halithose
  • érosions dentaires
  • gingivite
  • hoquet
  • laryngospasme
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28
Q

Tx RGO

A

Style de vie: perte de poids et tête de lit (2 seuls démontrés), sinon diète, exercice, éviter valsalva

IPP

Anti-H2

Sucralfate

Misoprostol

Agent prokinétique: maxeran

Chx

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29
Q

Tx oesophagite éosinophilique

A

Cortico PO

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30
Q

Décrire comment le syndrome de Zollinger-Ellison induit des ulcères

A

Tumeur sécrétant de la gastrine

Gastrine stimule les cellules pariétales à sécréter des H+ et induit une prolifération des cellules pariétales

L’hyperplasie des cellules pariétales augmentent la sécrétion d’acide et favorise les ulcères

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31
Q

Nommer 2 “protocoles” pour traiter H Pylori

A

Triple Therapy (10- to 14-day treatment regimen)

Clarithromycin, 500 mg bid

Plus

Amoxicillin, 1 g bid

Or

Metronidazole, 500 mg bid (if penicillin-allergic)

Plus

A PPI

Quadruple Therapy (10- to 14-day treatment regimen)

Bismuth subsalicylate (Pepto-Bismol), 525 mg PO qid

Plus

Metronidazole, 250 mg PO qid

Plus

Tetracycline, 500 mg PO qid

Plus

PPI or ranitidine, 150 mg PO bid

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32
Q

Distinguer le volvulus gastrique primaire de secondaire

A

A primary (or subdiaphragmatic) volvulus occurs when the stabilizing ligaments are too lax or are congenitally abnormal in such a way that the stomach is able to twist on itself. Approximately one-third of cases are of this type.

Secondary (or supradiaphragmatic) volvulus occurs in patients with diaphragmatic defects such as a paraesophageal hiatal hernia, elevated diaphragm, gastric ulcer or carcinoma, diaphragmatic paralysis, extrinsic pressure on the stomach from other organs, or abdominal adhesions. The combination of one of these factors and ligamentous laxity makes a volvulus more likely.

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33
Q

Décrire la triade de Borchardt

A

The combination of severe epigastric pain and distention, vomiting followed by violent nonproductive retching, and inability to pass a nasogastric tube (Borchardt’s triad)

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34
Q

Facts about hepatitis

A

Hépatite D nécessite la production de HbsAg (donc Hép B chronique)

Hépatite fulminante plus fréquente avec Hép B + Hép D (coinfection)

AST/ALT: de 10 à 100x la normale, ALT > AST, Direct and indirect bilirubin levels are elevated almost equal proportions. Alkaline phosphatase and lactate dehydrogenase levels may be elevated but are rarely more than 2 to 3 times normal.

On a 2 semaines pour donner les immunoglobulines en cas d’exposition à hép B chez qqn non vacciné. Si vacciné, mais pas HbsAb ou HbcAb - redonner vaccin mais pas immunoglobulines.

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35
Q

Décrire la signification des différents anticorps/antigènes des hépatites virales

A

Anti-HBcAg antibody generally is the best indicator of previous HBV infection, whereas anti-HBsAg antibody is the best marker for immunity to HBV.

The presence of anti-HDV in conjunction with IgM antibody to HBcAg suggests coinfection with HDV and HBV. Anti-HDV in association with IgG antibody to HBcAg supports the diagnosis of superinfection.

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36
Q

Décrire la prophylaxie post-exposition en cas d’expostion à l’hépatiteA-B-C-D

A

Close personal contact :ISG, 0.02 mL/kg IM

Day care center

Employee: ISG, 0.02 mL/kg IM

Attendee: ISG, 0.02 mL/kg IM

School contactsNone

Hospital contactsNone

Workplace contactsNone

Food-borne source

Within 2 wk of exposure: ISG, 0.02 mL/kg IM

After 2 wk of exposure: None

After common source outbreaks have begun to occurNone

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37
Q

Décrire la progression de l’Atteinte hépatique par l’alcool

A
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38
Q

Décrire les laboratoires retrouvés en cas d’hépatite alcoolique

A

Élévation AST> ALT, rarement supérieur à 10 x la normale

Élévation bilirubine

Leucocytose 10-20

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39
Q

Décrire le tx des hépatites alcooliques

A

Évaluer le score MDF (Maddrey’s Discriminant Function for Alcoholic Hepatitis), Score utilise le PT et la bilirubine

Si score sup 32, et absence de sgmt GI, sepsis, hépatorénal, cortico 40mg PO die.

Alternative: pentoxifylline

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40
Q

Décrire les types de cirrhose avec la structure hépatique associée

A

Cirrhose de Laennec - alcoolique - processus diffus, atteinte des lobules en entier

Cirhose post nécrotique - non homogène, zones saines et zones atteintes - infectieux/ métabo/ Rx

Cirhose biliaire - 2nd atteinte obstructive des canaux intra hépatiques/canaux biliaires

Cirrhose cryptogénique - stéatose hépatique devient une cause de + en + importante

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41
Q

Traitement de l’ascite

A

Ascites

Alcohol cessation in patients with alcohol-induced liver disease
Baclofen, 5–10 mg tid, for management of alcohol cravings
Diagnostic paracentesis in patients with new-onset ascites
Hepatology follow up within 1 wk of hospital or ED discharge
Sodium-restricted diet
Diuretic use—spironolactone
Spot urine sodium/potassium ratio to monitor sodium restriction
Fluid restriction for sodium level < 125 mmol/L
Caution in pressure lowering agents: ACE inhibitors and ARBs
Avoid nonsteroidal antiinflammatory drugs (NSAIDS)
Consider liver transplantation referral.

Refractory ascites

Oral midodrine, 7.5 mg tid for refractory or recurrent ascites
Caution with beta blockers, such as propranolol
Serial paracentesis
Postparacentesis albumin infusion (6–8 g/L removed) for large-volume paracentesis (removal of >5 L)
Consider referral for transjugular intrahepatic portasystemic shunt stent or surgical shunt placement.
Immediate referral for liver transplantation

Spontaneous bacterial peritonitis

Paracentesis with fluid PMN count < 250 cells/mm3 and infectious signs and symptoms requires parenteral cefotaxime, 2 g q8hr
Paracentesis with fluid PMN count > 250 cells/mm3 requires parenteral ceftriaxone, 2 g die

(cefotaxime supérieur à ceftriaxone selon uptodate)
Signs of secondary peritonitis—obtain ascitic fluid for total protein, glucose, Gram stain, LDH, carcinoembryonic antigen (CEA) and alkaline phosphatase testing.
Obtain CT scan.
Repeat paracentesis for for patients at increased risk due to nosocomial or recent antibiotic exposure.
Albumin, 1 g/kg body weight in the setting of PMN >250 cells/mm3, renal insufficiency (blood urea nitrogen > 30 mg/dL or creatinine > 1 mg/dL)

Hepatorenal syndrome (HRS)

Obtain urinary neutrophil gelatinase-associated lipocalin to aid in the diagnosis
Albumin infusion plus vasoactive midodrine or octreotide for type I HRSa
Albumin infusion plus norepinephrine for type I HRSa in the intensive care setting
Urgent referral for liver transplantation for type I or II HRSa

42
Q

Nommer des précipitants d’encéphalopathie hépatique

A
  • Sgmt GI
  • Infection - SBP
  • Iléus- constipation
  • déshydratation, hypovolémie
  • sédations
  • IRA
  • thrombose veineuse
  • désordres électrolytiques
43
Q

Traitement encéphalopathie hépatique

A

Tx condition sous-jacente

Éviter sédatifs

LActulose 30-60 g / jour ad 3-4 selles/jour

Antibio : rifaximin ou neomycine ou flagyl ou vanco PO

glycerol phenylbutyrate

Dialyse à l’albumine

nutritional intake of 25 to 40 kcal/kg/day with dietary modification of protein. Protein intake should be approximately 1 to 1.5 g/kg/day.

44
Q

Dx/tx de la péritonite associée à la dialyse péritonéale

A

dialysate WBC more than 100 cells/mm3 and confirmed by culture.

In patients with symptoms suggesting peritonitis, dialysate should be collected for analysis and culture, and treatment should be initiated. Consideration of catheter removal is also warranted.

Antibio, favoriser intrapéritonéal > IV sauf si pt septique

Intrapéritonéal: en continu vs intermittent dans l’échange le plus long (min 6 heures)

vancomycin or cefazolin, plus cefepime/ceftazidime/genta or aztreonam.

45
Q

Tx cholestaste de grossesse

A

symptomatique

Vitamine K

46
Q

Décrire les 2 types de cholélithiases pigmentaires

A

Noir: associé à l’hémolyse, contenu élevé en bilirubine de calcium

Brun: associé à des infections bactériennes > parasites, contenu aussi élevé en calcium

47
Q

Nommer 3 germes pouvant causer une cholécystite emphysémateuse

A

E.Coli

Klebsiella

Clostridium perfringens

48
Q

Nommer 4 germes associés à la cholangite

A

E coli

Klebsiella

Enterococcus

Bacterioides

49
Q

Nommer la pentade de Reynold

A

Dlr HCD

Fièvre

Ictère

Hypotension

AEC

50
Q

Nommer 5 “cocktails” antibio pour la cholangite

A

Tazo

Ceftri/flagyl

Cipro/flagyl

Levaquin/flagyl

Mero

51
Q

Nommer 4 germes associés à la cholangiopathie du VIH

A

CMV

Microsporidia

Mycobacterium avium complex -MAC

Cryptosporidium

52
Q

Traitement des abcès hépatiques

A

Cefotaxime + metronidazole

Ampicillin + gentamycin + metronidazole

Ciprofloxacin or levofloxacin or moxifloxacin + metronidazole

Piperacillin-tazobactam

Impinem or meropenem, or doripenem or ertapenem

Drainage si plus de 3 cm

Si amibe: flagyl 750 mg IV TID x 7-10 jours

53
Q

Nommer 15 causes de pancréatite

A

Toxico-métabolique

Alcool

Hypercalcémie

Hypertriglycéridémie

Urémie

Médication : sulfa, acide valproique, cortico, salicylates…

Venin scorpion

Obstruction

Pancréas divisum - malformation congénitale

Tumeur

Biliaire

Post-trauma

Post-ERCP

Dysfonction ampoule

Diverticule duodenum

Infectieux

EBC, CMV, VIH, oreillons, cocsackie, varicelle

TB, Salmonella, Campylobacter, Legionella, Mycoplasma

Ascaris

Vasculaire

Hypoperfusion

Vasculite

Embolie

Hypercoagulabilité

Autres

Db - Acidocétose

Idiopathique

Héréditaire

Auto-immun

54
Q

Nommer 2 types de complications post pancréatite

A

Interstitial Edematous Pancreatitis

•

Acute peripancreatic fluid collection—homogeneous fluid collection adjacent to pancreas; seen within 4 wk of symptom onset

•

Pancreatic pseudocyst—homogeneous fluid collection with well-defined wall; seen >4 wk from symptom onset

Necrotizing Pancreatitis

•

Acute necrotic collection—heterogeneous collection of fluid and necrosis; intrapancreatic and/or extrapancreatic

•

Walled-off necrosis—heterogeneous collection of fluid and necrosis with well-defined wall; intrapancreatic and/or extrapancreatic; seen >4 wk from symptom onset

Autres

bowel necrosis, splenic or portal vein thrombosis, gastrointestinal bleeding, or gastric outlet obstruction.

55
Q
A
56
Q

Nommer 5 causes d’élévation de l’amylase autre que l’atteinte pancréatique

A

Atteinte hépatique

Atteinte salivaire

Trauma

Brûlures

Néoplasie

VIH

Cholécystite

IRA

57
Q

3 indications de TDM en pancréatite

A

CT is only recommended in the following circumstances: (1) in cases of diagnostic uncertainty—for example atypical abdominal pain—or normal pancreatic enzyme levels in the setting of high clinical suspicion;

(2) to rule out other suspected intra-abdominal pathology—for example, bowel obstruction or aortic aneurysm;
(3) to assess for complications in patients who fail to respond to appropriate therapy after at least 48 hours

58
Q

Décrire la classification d’Atlanta en pancréatite

A

Légère: peu ou pas d’atteinte d’organe

Modérée: dysfonction d’organes transitoires ( à 48hr), complications locales ou systémiques

Sévère: dysfonction d’organes persistante

59
Q

Nommer les critères de Ranson

et 2 autres scores possibles

A

At Admission

Age > 55 yr

WBC > 16,000/mm3

Glucose > 11

AST > 250 IU/L

LDH > 350 IU/L

At Admission (if biliary cause)

Age > 70 yr

WBC > 18,000/mm3

Glucose > 12

AST > 250 IU/L

LDH > 400 IU/L

At 48 Hours

Hematocrit drop > 10%

BUN rise > 2 mmol/L

Calcium < 2 mmol/l

PO2 < 60 mm Hg

Base deficit > 4 mEq/L

Fluid sequestration > 6 L

At 48 Hours (if biliary cause)

Hematocrit drop > 10%

BUN rise > 0.8 mmol/L

Calcium < 2 mmol/L

Base deficit > 5 mEq/L

Fluid sequestration > 4 L

The bedside index for severity in acute pancreatitis, BISAP,

urée, AEC, SRIS, age, ép. pleuraux

Compared to other scoring systems, it has lower sensitivity and similar specificity.

Harmless Acute Pancreatitis Score (HAPS),

in patients with no peritonitis (no rebound or guarding) and normal hematocrit and creatinine levels, there is a very low risk of mortality, necrosis, or need for hemodialysis or ventilatory support.

60
Q

Tx pancréatite

A

Tx support

Tx hypocalcémie si calcium ionisé bas

Remplacer hypoMg peut corriger HypoCa

Pas d’indication de NPO

61
Q

Nommer les classes de pancréatite chronique

A

Toxico-métabolique

Obstructif

Auto-immun

Génétique

Post-nécrotique, post pancréatite récurrente

Idiopathique

62
Q

Comment imager une pancréatite chronique

A

The initial diagnosis of chronic pancreatitis is made by one of several imaging modalities, including CT, MRCP, or EUS

63
Q

Nommer des FR de néo pancréatique et la distribution des types de Néo

A

Tabac +++

Alcool

Diabète

Pancréatite chronique

Obésité

Approximately 85% of cases are adenocarcinoma. About 10% are neuroendocrine tumors such as gastrinomas (Zollinger-Ellison syndrome), insulinomas, and glucagonomas.

64
Q

Nommer 15 causes SBO et test de choix pour dx

A

1,2,3,

Adhérences, tumeurs, hernies

Extrinsèque: Néoplasie, volvulus, hernie, adhérences

Paroi: Néoplasie, hématome, strictures (MII), radiation

Intraluminal: CE, infectieux (ascaris), bezoars, lithiase, intussusception

TDM avec contraste IV sans contraste PO (plus cher, inefficace, entraine retard dx, inconfort, peut induire vo et aspiration)

65
Q

Tx obstruction intestinale maligne

A

Si non candidat à la chirurgie

TNG

Cortico

Octreotide 200-900 mcg / jour divisé TID

66
Q

Décrire la vascularisation mésentérique

A

These become the celiac trunk, superior mesenteric artery (SMA), and inferior mesenteric artery (IMA), respectively. The celiac trunk arises from the anterior aspect of the abdominal aorta and branches into the common hepatic, splenic, and left gastric arteries. These vessels supply the distal esophagus to the duodenum at the entrance of the bile duct. The SMA normally arises 1 cm below the celiac trunk and runs toward the cecum, terminating as the ileocolic artery. The SMA supplies the distal half of the duodenum to the proximal two-thirds of the transverse colon. The IMA originates approximately 6 to 7 cm below the SMA and gives rise to the left colic artery, sigmoid arteries, and hemorrhoidal arteries. Anatomically, this vessel provides blood flow to the distal third of the transverse colon to the rectum.

67
Q

Nommer des FR de thrombose veineuse mésentérique

A

Thrombophilie: surtout V Leiden, aussi antithrombine, déficit prot C et S

Polycythémie vraie, thrombocytose essentielle

Hypertension portale, insuffisance cardiaque, insuffisance rénale

Inflammation locale: pancréatite, MII, néoplasie

Contraceptifs oraux

Trauma, post splénectomie

68
Q

Signes à la RX d’ischémie mésentérique

A

Pneumatose intestinale

Thumbprinting

Air a/n système porte

69
Q

Nommer des FR d’échec au tx conservateur de l’appendicite

A

Présence fécalith

Tumeur

Abcès

Collection liquide péri appendicite

Appendicite > 1.1 cm

70
Q

expliquer les 4 mécanismes pathophysiologiques de la gastroentérite

A

one of four mechanisms—ingestion of preformed toxins, adherence of the infectious pathogens to the intestinal cell walls, invasion of mucosal cell walls, and production of enterotoxins and cytotoxins.

71
Q

Nommer des facteurs épidémiologiques et les pathogènes associés

A
72
Q

Critères pour demander culture de selles en cas de GE

A

Stool cultures should be sent for patients with severe illness, fever of 38.5° C (101°F) or higher, dysentery, persistent diarrhea for 14 days or longer and for patients who are immunocompromised or who have been recently hospitalized or placed on antibiotics.

73
Q

Tx GE bactérienne

A

Shigella (sonnei, flexneri, dysenteria)

Pas de tx si non sévère, sauf si S dysentérie.

Ciprofloxacin, 750 mg daily for 3 days; azithromycin, 500 mg daily for 3 days

Complications: SHU, Reiter, convulsions, encéphalopathie

Salmonella (typhimurium, enteritidis, typhi)

Entérite bactérienne la + fréquente

 Nontyphoid : pas de tx sauf severe colitis and for infants younger than 3 months, adults older than 50 years, and those at risk for severe disease, including those who are immunocompromised, with sickle cell disease, and with prosthetic grafts

For severe cases (fever, bloody diarrhea, bacteremia)—

levofloxacin (Levaquin) ou Cipro, 500 mg daily for 7–10 days

Azithro 1g puis 500 die x 6 jours

Associé au syndrome de Reiter dans 2% des cas

Typhoid Fluoroquinolone daily for 7 days; ou si hospit, ceftriaxone IV , 1–2 g for 7 days

Campylobacter( jejuni, coli) :

pas de tx empirique si HD stable, attendre culture.

Azithromycin/ Erythro, 500 mg daily for 3 days ou Cipro (mais résistance ad 20%)

Induit Guillain-Barré 1/1000

Vibrio cholerae et non colera spp

The difference between cholera and noncholera Vibrio spp. versus V. parahaemolyticuslies in the mechanism of pathogenesis. V. parahaemolyticus produces disease via toxins that cause intestinal mucosal destruction, whereas cholera and noncholera Vibrio strains produce an enterotoxin in vivo that stimulates enterocyte adenylate cyclase, disrupting mucosal fluid absorption and leading to a secretory diarrhea.

Vibrio vulnificus, associé fruits de mer, induit septicémie, cause de mortalité importante. Doxy + ceftazidime, ou levaquin ou cipro

Dose unique Cipro 1 g, Azithro 1g ou Doxycycline, 7 mg/kg up to 300 mg once

Vibrio—noncholera - Vibrio parahaemolyticus

Associé au fruits de mer/poisson cru, eaux salées

Majorité de requièrent pas de tx, tx seulement si prolongé/sévère

Ciprofloxacin, 750 mg daily for 3 days; azithromycin, 500 mg daily for 3 days

Ceftriaxone

Enterotoxigenic Escherichia coli:

Ciprofloxacin, 750 mg daily for 3 days, rifaximin 200 mg tid for 3 days; azithromycin, 1 g once

Shiga toxin–producing E. coli; E. coli O157:H7

No treatment, supportive care only; antibiotics increase risk for HUS

Yersinia enterocolitica:

Supportive care; in severe cases,

TMP-SMX (Bactrim) 1 co DS BID

Doxy + aminoglycoside ou fluoroquinolones

Peut mimer appendicite

Manifestations immunes fréquentes: arthrite, Reiter, érythème noueux

Clostridium difficile : Metronidazole, 500 mg tid for 10 days; vancomycin, 125 mg PO qid for 10 days

Staphylococcus aureus: Supportive care

Clostridium perfringens: Detection of spores in stool; production d’entérotoxine, Supportive care

Bacillus cereus;

Food may be cultured, produits spores

2 types d’entérotoxines (1 émétisante et l’autre diarrhée)

Supportive care;

for severe cases—vancomycin, 125 mg qid; or clindamycin, 500 mg tid for 7–10 days

74
Q

Tx GE parasites

A

Giardia lamblia: Stool microscopy for ova and parasite;

Tinidazole—2 g PO single dose
Metronidazole—500 mg PO bid or 250 mg tid for 5–7 days
Nitazoxanide—500 mg bid for 3 days
Alternative agents
Albendazole—400 mg once daily for 5 days
Mebendazole—200 mg PO tid for 5 days
Quinacrine—100 mg PO tid for 5 days
Paromomycin—10 mg/kg PO tid day for 5–10 days

Entamoeba histolytica: Stool microscopy, culture, immunoassay

Metronidazole—500–750 mg PO tid for 7–10 days;
Tinidazole—2 g PO once a day for 3 days;
Nitazoxanide—500 mg PO bid for 3 days
Intraluminal infection
Paromomycin—25–30 mg/kg PO tid for 7 days
Diiodohydroxyquin—650 mg PO tid for 20 days for adults
Diloxanide furoate—500 mg PO tid for 10 days for adults

Cryptosporidium: Stool microscopy, culture, immunoassay

Nitazoxanide—500 mg PO bid for 3 days

Cyclospora cayetanensis: Stool microscopy, stool culture, acid-fast stain, fluorescence microscopy

Trimethoprim—trimethoprim-sulfamethoxazole (TMP-SMX), one double-strength 160/800 mg tablet PO bid for 7–10 days

75
Q

Décrire le pattern des GE bactériennes à pathogène invasif

A
76
Q

Décrire présentation GE bactériennes non invasives

A
77
Q

Décrire présentation clinique GE virales

A
78
Q

Décrire présentation clinique GE parasites

A
79
Q

Décrire l’intoxication au scombroide

A

Poissons les + fréquemment impliqués: mahi mahi, thon, tassergal (blue fish)

Scombroid fish poisoning results from the ingestion of heat-stable toxins produced by bacterial action on the histidine present in the dark meat of the fish. The bacteria responsible are normal constituents of the surface marine flora, rather than contaminants. The histidine decarboxylase activity of these organisms produces histamine and histamine-like substances, which cause the symptoms of scombroid fish poisoning. High levels of histamine in the fish correlate directly with the occurrence of the illness.

In general, the problem is caused by improper refrigeration by the supplier rather than being the fault of the restaurant serving the fish

While eating the fish, the patient may note a metallic, bitter, or peppery taste, although many affected fish do not have an abnormal odor or taste. Symptoms usually develop abruptly within 20 to 30 minutes and consist of facial flushing, diarrhea, severe and throbbing headache, palpitations, and abdominal cramps. Other manifestations may include dizziness, dry mouth, nausea and vomiting, and urticaria

Tx: diphenhydramine, 50 mg IM or IV, or cimetidine, 300 mg IM or IV, usually relieve all symptoms promptly

80
Q

Décrire l’intoxication au ciguatera

A

More than 400 fish species that frequent coral reefs have been implicated as ciguatoxin carriers, but fewer than 50 are commercially important; these include amberjack, barracuda, grouper, king mackerel, parrotfish, sea bass, snapper, sturgeon, surgeonfish, and ulua.

Ciguatoxin is produced by the marine dinoflagellate Gambierdiscus toxicus, which attaches itself to marine algae and is passed up the food chain. The lipid-soluble toxin accumulates in the tissues of the larger predacious coral reef fish

Ciguatoxin has anticholinesterase and cholinergic properties, but its neurotoxicity is mediated by its effect on sodium channels

The GI symptoms (eg, nausea, vomiting, profuse watery diarrhea, crampy abdominal pain, diaphoresis) tend to appear first and resolve over the first 24 hours. The constellation of neurologic symptoms consists largely of dysesthesias and paresthesias around the throat and the perioral area—burning feet, which may resemble alcoholic peripheral neuropathy, loose painful teeth, and sometimes CNS changes, such as ataxia, weakness, vertigo, visual hallucinations, and even confusion and coma.

Cold allodynia, defined as dysesthesia experienced on contact with cold water or cold objects, is almost pathognomonic of ciguatera poisoning and often is incorrectly referred to as cold-hot temperature reversal. Another classic feature is a return or a worsening of all the symptoms after ingestion of alcohol.

Ciguatera poisoning lasts an average of 1 to 2 weeks, but at least 50% of victims are still symptomatic at 8 weeks.

Pruritus may be managed with a histamine H1 receptor antagonist, such as diphenhydramine 25 mg PO qid, or cetirizine, 10 mg once daily. Amitriptyline, 25 mg bid, can bring about a dramatic reduction in the pruritus and dysesthesias, two of the most disturbing and protracted symptoms.

81
Q

Décrire prévention et tx diarrhée du voyageur

A
82
Q

Pathogènes impliqués chez le VIH

A

In HAART-naïve populations, Cryptosporidium and CMV infections are the two most common causes

Chronic high-volume watery diarrhea often is indicative of small bowel disease from one of the coccidia, Cryptosporidium and Cystoisospora belli.

CMV and MAI also produce a chronic illness in those with CD4+ counts less than 100/mm3

Microsporidia fréquent si < 100

Salmonella infections, especially with S. typhimurium, are common in immunocompromised hosts. Patients with AIDS who acquire Salmonella enteritis are at increased risk for bacteremia and metastatic focal infection compared with normal hosts

Entérite bactérienne la + fréquente: C diff

Patients with a fulminating clinical course usually have a disseminated infection, such as infection with CMV or MAI complex. Massive weight loss is also associated with diarrhea caused by infection with those two organisms and the coccidia Cryptosporidium and Cystoisospora. Voluminous watery diarrhea usually is a result of one of the coccidial organisms, including Cyclospora and Isospora. Patients with a proctocolitis-like picture most often have herpes simplex virus or CMV infection

Ciprofloxacin, 500 mg PO, may be empirically initiated while the evaluation is in progress. If Giardia or C. difficile is suspected, metronidazole, 500 mg PO, should be added. If CMV colitis is suspected, foscarnet, 90 mg/kg IV, should be given

83
Q

Critères dx colon irritable et tx

A

Recurrent abdominal pain or discomfort at least 3 days/mo in the previous 3 mo associated with two or more of the following:

  1. Improvement with defecation
  2. Onset associated with a change in frequency of stool
  3. Onset associated with a change in form (appearance) of stool

Facteurs qui ne concordent pas avec dx colon irritable:

onset of symptoms after the age of 50 years, unintentional weight loss, anorexia, bloody stools, nocturnal diarrhea, or family history of significant colon disease

Tx:

dycyclomine

Loperamide / lax-a-day

Rifaximine

ISRS, TCA

84
Q

Nommer 3 combinaisons d’antibio possible pour diverticulite

A

Trimethoprim-sulfamethoxazole, one double-strength tablet bid, andmetronidazole, 500 mg q6h or

•

Ciprofloxacin, 500 mg bid, and metronidazole, 500 mg q6h, or

•

Amoxicillin-clavulanate, extended-release, 1000/62.5 mg, two tablets bid

85
Q

Nommer dxd obstruction colique

A

Néoplasie colique

Volvulus

Diverticulite

Carcinomatose péritonéale

Hernie incarcérée

Adhérences

Pseudo obstruction

Fécalome

Strictures

86
Q

Nommer les MII et leurs associations extra intestinales

A

CU: Arthropathies inflammatoires, cholangite sclérosante (et atteinte oculaire, dermato, osseuse)

Crohn: spondyarthropathies, uvéite, stomatite aphteuse, érythème noueux

87
Q

Indices de MII chez les enfants avec dlr abdo

A

Diarrhée

Rectorragies

Perte de poids

Paleur, fatigue

Atteinte oculaire/arthrite

Fistules/abcès périanaux

ATCD familiaux

88
Q

Nommer les critères qui distinguent la sévérité de la CU et Crohn

A

Ulcerative Colitis

Mild Disease

•

Fewer than four stools/day

•

Stools may contain some blood

•

No systemic signs of toxicity (eg, fever, tachycardia, anemia, elevated erythrocyte sedimentation rate)

Moderate Disease

•

More than four stools/day

•

Minimal signs of toxicity

Severe Disease

•

More than six bloody stools/day

•

Signs of systemic toxicity

Crohn’s Disease

Mild to Moderate Disease

•

Patient ambulatory and able to eat

•

No dehydration

•

No toxicity

•

No significant abdominal pain or mass

•

Weight loss of 10%

Moderate to Severe Disease—Any of the Following

•

Mild disease that has failed to respond to treatment

•

Patient may have some systemic toxicity, significant weight loss, anemia

•

Fever, some abdominal pain or tenderness, intermittent nausea or vomiting

Severe Disease

•

Persistence of symptoms during corticosteroid or biologic (eg, infliximab) therapy

•

High fever, persistent vomiting

•

Intestinal obstruction

•

Rebound tenderness

•

Cachexia

•

Abscess

89
Q

Nommer des signes d’ischémie colique au TDM

A

CT features suggestive of CI include thumbprinting, wall thickening, and luminal narrowing and inner wall hypoperfusion, the so-called double halo sign

90
Q

Tx rectocolite radique

A

Lavement avec cortico

LAvement avec sucralfate

water-absorbing stool softeners to reduce mucus-containing diarrhea are helpful.

91
Q

Décrire l’anatomie du rectum

A

The superior, middle, and inferior hemorrhoidal arteries provide the blood supply to the anorectum. They arise from the inferior mesenteric, internal iliac, and internal pudendal arteries, respectively. The superior hemorrhoidal veins drain into the portal system, and the inferior hemorrhoidal veins drain into the caval system. Lymphatic drainage is to the inferior mesenteric nodes above the dentate line and to the inguinal nodes from all areas of the anorectum.

92
Q

Décrire la classification des hémorroides

A
93
Q

Tx fissures anales

A

WASH regimena

• bains de siège, analgésie, stool softeners, high fiber diets

Nitroglycerin ointment (0.4%) bid or tid

•

Nifedipine gel (0.2%) bid with lidocaine (1.5%)

•

Botulinum toxin (surgical consultation)

•

Anal dilation performed with the patient under general anesthesia

•

Surgical excision

94
Q

Type et traitements des abcès rectaux

A

Horseshoe Abscess

A large, communicating, horseshoe-shaped abscess forms in the ischiorectal, intersphincteric, or supralevator space. Surgical management is necessary.

95
Q

Traitement hydradénite suppurée

A

Traitement de support

  • éviter macération, porter linge ample, éviter trauma
  • tx comorbidités, contrôle glycémie, perte de poids, arrêt tabagique
  • clinda topique
  • antibio systémiques à long terme (doxy, clinda)
  • rétinoides
  • immunosuppresseurs
96
Q

DxD incontinence fécale

A

Traumatique: lésion médullaire, trauma obstétrical, lésion sphincter, lésion nerveuse post-op

Neurologique: neuropathie autonome (db), lésion nerveuse post-accouchement, démence, lésion médullaires

Mécanique: CE, néoplasie, fécalome, hémorroides

Ped: hirschprung, encoprésie, congénital, myéloméningocèle, spina bifida

Autres: diarrhée, laxatif, MII, procidence

97
Q

DxD pruritus ani

A

Acronyme ITCH

Infection: VPH, HSV, syphilis, parasites/bactéries/fongiques, gale

Topique irritation: mauvaise hygiène, fissure, fistule, skin tags, hémorroides

Cutané: dermatite séborrhéique, psoriasis, lichen plan, lichen scléreux, néo cutané, dermatite contact (savons, cortico)

Hypersensibilité: IRC, Db, Dysthyroidies, polycythémie, déficit fer/vit A/ vit D, caffeine, tea, beer, spicy foods, citrus fruits, quinidine, intravenous hydrocortisone, colchicine, tetracycline

98
Q

DxD lésions anales chez les patients séropositifs

A

Common Conditions

Anal fissure

Abscess and fistula

Hemorrhoids

Pruritus ani

Pilonidal disease

Common Stds

Gonorrhea

Chlamydial infection

Herpes

Chancroid

Syphilis

Condyloma acuminatum

Atypical Conditions

Infectious

TB, CMV infection, actinomycosis, cryptococcosis

Neoplastic

Lymphoma, Kaposi’s sarcoma, squamous cell carcinoma

Other

Idiopathic anal ulcer

99
Q

DxD et tx lésions ulcératives anales

A
100
Q

DxD et lésions non ulcérativse anales

A
101
Q
A

Collège Royal 2019 (23 decks)

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