Gastro Flashcards
Chez qui doit-on suspecter une étiologie plus dangereuse lorsque la RC est une douleur abdominale?
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
Diviser les structures abdominales en forgut, midgut, hindgut
Foregut structures (stomach, duodenum, liver, gallbladder, and pancreas) are associated with upper abdominal pain.
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Midgut derivatives (small bowel, proximal colon, and appendix) are associated with periumbilical pain.
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Hindgut structures (distal colon and genitourinary tract) are associated with lower abdominal pain.
Décrire le métabolisme normal de la bilirubine
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.
Quel est le danger d’une accumulation de bilirubine non conjuguée?
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.
Dxd ictère selon le type de bilirubine augmenté
Décrire les stades d’encéphalopathie hépatique
Comment faire le dx de cholangite?
Cause la plus fréquente de dysphagie neuromusculaire
et la 2e
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
Nommer 5 syndromes causant de la dysphagie oesophagienne motrice (pas obstruction mécanique)
Maladie du collagène
Sclérodermie
CREST
Syndrome paranéoplasique
Chagas
Intrinsèque: achalasie, spasme oesophagien, nutcracker, hypertonicité shincter oesophagien inférieur
Facteurs de risque généraux de saignements digestifs hauts et bas
Medication use
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Aspirin
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Nonsteroidal antiinflammatory drugs
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Steroids
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Anticoagulants (warfarin, heparin)
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Chemotherapeutic agents
History of peptic ulcer disease
Known liver disease, cirrhosis
Advanced age (>60 yr)
Alcoholism
Current smoker
Chronic medical comorbidities
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Congestive heart failure
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Diabetes
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Chronic renal failure
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Malignancy
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Coronary artery disease
History of abdominal aortic aneurysm graft
Nommer 10 causes endocriniennes de diarrhée
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
Nommer des facteurs de risque d’avoir une diarrhée non bénigne
- 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
Nommer des causes 2nd (non fonctionnelles) de constipation
- 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
Nommer les catégories de laxatifs
- 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)
Décrire le syndrome de Plummer-Vinson
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.
Nommer 20 causes de dysphagie
- 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
Nommer des traitements possible de l’achalasie
BCC
Nitrate
Botox
Dilatation pneumatique LES
Chirurgie
Autres troubles de motilité: possible utilité des anticholinergiques
Durée maximale acceptée pour obstruction incomplète par CE oesophagien (pas batterie/objet coupant)
24 hrs
3 méthodes d’extraction de CE a/n oesophage supérieur
- Pince McGill, sonde Foley avec retrait, bougienage pour avancer CE a/n estomac
Traitement possible pour bolus nourriture impacté
Glucagon non recommandé
Boisson effervescente: pas mieux que placebo
Gastroscopie
(nitrate, bcc)
Durée et taille des objets
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
Décrire la triade de Mackler
Pathognomonique de la perforation oesophagienne spontanée
- vomissement
- dlr thoracique
- emphysème sous-cutané
Décrire les signes visibles au RX pulmonaire en cas de perforation oesophagienne
Emphysème sous-cutané
Ép pleural D (si perfo haute) ou G (si perfo basse)
Infiltrats pulmonaires
PTX
Pneumomédiastin
Médiastin élargi
Facteurs de risque de RGO
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
Nommer les critères dx d’oesophagite eosinophilique
Sx dysfonction oesophagienne
> 15 eosino/ch sur biopsie
sx réfractaire IPP
Nommer 5 médicaments responsables d’oesophagite à Rx
Biphosphonates
Fer
Antibio - surtout tétracycline
ASA et AINS
KCl
Quinidine
Nommer 10 sx extraoesophagiens du reflux
- Asthme, toux
- voix rauque, mal de gorge, globus
- otalgie
- halithose
- érosions dentaires
- gingivite
- hoquet
- laryngospasme
Tx RGO
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
Tx oesophagite éosinophilique
Cortico PO
Décrire comment le syndrome de Zollinger-Ellison induit des ulcères
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
Nommer 2 “protocoles” pour traiter H Pylori
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
Distinguer le volvulus gastrique primaire de secondaire
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.
Décrire la triade de Borchardt
The combination of severe epigastric pain and distention, vomiting followed by violent nonproductive retching, and inability to pass a nasogastric tube (Borchardt’s triad)
Facts about hepatitis
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.
Décrire la signification des différents anticorps/antigènes des hépatites virales
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.
Décrire la prophylaxie post-exposition en cas d’expostion à l’hépatiteA-B-C-D
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
Décrire la progression de l’Atteinte hépatique par l’alcool
Décrire les laboratoires retrouvés en cas d’hépatite alcoolique
Élévation AST> ALT, rarement supérieur à 10 x la normale
Élévation bilirubine
Leucocytose 10-20
Décrire le tx des hépatites alcooliques
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
Décrire les types de cirrhose avec la structure hépatique associée
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
Traitement de l’ascite
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
Nommer des précipitants d’encéphalopathie hépatique
- Sgmt GI
- Infection - SBP
- Iléus- constipation
- déshydratation, hypovolémie
- sédations
- IRA
- thrombose veineuse
- désordres électrolytiques
Traitement encéphalopathie hépatique
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.
Dx/tx de la péritonite associée à la dialyse péritonéale
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.
Tx cholestaste de grossesse
symptomatique
Vitamine K
Décrire les 2 types de cholélithiases pigmentaires
Noir: associé à l’hémolyse, contenu élevé en bilirubine de calcium
Brun: associé à des infections bactériennes > parasites, contenu aussi élevé en calcium
Nommer 3 germes pouvant causer une cholécystite emphysémateuse
E.Coli
Klebsiella
Clostridium perfringens
Nommer 4 germes associés à la cholangite
E coli
Klebsiella
Enterococcus
Bacterioides
Nommer la pentade de Reynold
Dlr HCD
Fièvre
Ictère
Hypotension
AEC
Nommer 5 “cocktails” antibio pour la cholangite
Tazo
Ceftri/flagyl
Cipro/flagyl
Levaquin/flagyl
Mero
Nommer 4 germes associés à la cholangiopathie du VIH
CMV
Microsporidia
Mycobacterium avium complex -MAC
Cryptosporidium
Traitement des abcès hépatiques
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
Nommer 15 causes de pancréatite
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
Nommer 2 types de complications post pancréatite
Interstitial Edematous Pancreatitis
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Acute peripancreatic fluid collection—homogeneous fluid collection adjacent to pancreas; seen within 4 wk of symptom onset
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Pancreatic pseudocyst—homogeneous fluid collection with well-defined wall; seen >4 wk from symptom onset
Necrotizing Pancreatitis
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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.
Nommer 5 causes d’élévation de l’amylase autre que l’atteinte pancréatique
Atteinte hépatique
Atteinte salivaire
Trauma
Brûlures
Néoplasie
VIH
Cholécystite
IRA
3 indications de TDM en pancréatite
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
Décrire la classification d’Atlanta en pancréatite
Légère: peu ou pas d’atteinte d’organe
Modérée: dysfonction d’organes transitoires ( à 48hr), complications locales ou systémiques
Sévère: dysfonction d’organes persistante
Nommer les critères de Ranson
et 2 autres scores possibles
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.
Tx pancréatite
Tx support
Tx hypocalcémie si calcium ionisé bas
Remplacer hypoMg peut corriger HypoCa
Pas d’indication de NPO
Nommer les classes de pancréatite chronique
Toxico-métabolique
Obstructif
Auto-immun
Génétique
Post-nécrotique, post pancréatite récurrente
Idiopathique
Comment imager une pancréatite chronique
The initial diagnosis of chronic pancreatitis is made by one of several imaging modalities, including CT, MRCP, or EUS
Nommer des FR de néo pancréatique et la distribution des types de Néo
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.
Nommer 15 causes SBO et test de choix pour dx
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)
Tx obstruction intestinale maligne
Si non candidat à la chirurgie
TNG
Cortico
Octreotide 200-900 mcg / jour divisé TID
Décrire la vascularisation mésentérique
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.
Nommer des FR de thrombose veineuse mésentérique
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
Signes à la RX d’ischémie mésentérique
Pneumatose intestinale
Thumbprinting
Air a/n système porte
Nommer des FR d’échec au tx conservateur de l’appendicite
Présence fécalith
Tumeur
Abcès
Collection liquide péri appendicite
Appendicite > 1.1 cm
expliquer les 4 mécanismes pathophysiologiques de la gastroentérite
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.
Nommer des facteurs épidémiologiques et les pathogènes associés
Critères pour demander culture de selles en cas de GE
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.
Tx GE bactérienne
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
Tx GE parasites
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
Décrire le pattern des GE bactériennes à pathogène invasif
Décrire présentation GE bactériennes non invasives
Décrire présentation clinique GE virales
Décrire présentation clinique GE parasites
Décrire l’intoxication au scombroide
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
Décrire l’intoxication au ciguatera
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.
Décrire prévention et tx diarrhée du voyageur
Pathogènes impliqués chez le VIH
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
Critères dx colon irritable et tx
Recurrent abdominal pain or discomfort at least 3 days/mo in the previous 3 mo associated with two or more of the following:
- Improvement with defecation
- Onset associated with a change in frequency of stool
- 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
Nommer 3 combinaisons d’antibio possible pour diverticulite
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
Nommer dxd obstruction colique
Néoplasie colique
Volvulus
Diverticulite
Carcinomatose péritonéale
Hernie incarcérée
Adhérences
Pseudo obstruction
Fécalome
Strictures
Nommer les MII et leurs associations extra intestinales
CU: Arthropathies inflammatoires, cholangite sclérosante (et atteinte oculaire, dermato, osseuse)
Crohn: spondyarthropathies, uvéite, stomatite aphteuse, érythème noueux
Indices de MII chez les enfants avec dlr abdo
Diarrhée
Rectorragies
Perte de poids
Paleur, fatigue
Atteinte oculaire/arthrite
Fistules/abcès périanaux
ATCD familiaux
Nommer les critères qui distinguent la sévérité de la CU et Crohn
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
Nommer des signes d’ischémie colique au TDM
CT features suggestive of CI include thumbprinting, wall thickening, and luminal narrowing and inner wall hypoperfusion, the so-called double halo sign
Tx rectocolite radique
Lavement avec cortico
LAvement avec sucralfate
water-absorbing stool softeners to reduce mucus-containing diarrhea are helpful.
Décrire l’anatomie du rectum
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.
Décrire la classification des hémorroides
Tx fissures anales
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
Type et traitements des abcès rectaux
Horseshoe Abscess
A large, communicating, horseshoe-shaped abscess forms in the ischiorectal, intersphincteric, or supralevator space. Surgical management is necessary.
Traitement hydradénite suppurée
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
DxD incontinence fécale
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
DxD pruritus ani
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
DxD lésions anales chez les patients séropositifs
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
DxD et tx lésions ulcératives anales
DxD et lésions non ulcérativse anales
