Assessment 2 Flashcards
Intestinal reserve: enzymes
Brush border AND pancreatic oligosaccharides/proteinases
Intestinal reserve: pancreas
Pancreas secretes and excess of enzymes
Intestinal reserve malabsorbed nutrients
Transit slowed if malabsorbed nutrients reach distal portion of GI tract
Colon scavenges malabsorbed carbs as SCFA
Malabsorption clinical presentation
Weight loss/fatigue
Excess calorie intake with no weight gain
Excess flatulence/distension
Diarrhea: oily or liquid
Vit/mineral deficiency
Watery diarrhea comes from
Carbohydrate osmotic effect
Oily diarrhea comes from
Fat malabsorption
Diarrhea can come from
Osmotically active molecules reach colon
Malabsorbed molecules stimulate colon/ion secretion –> osmotic gradient
Diagnostic confirmation of malabsorption
Low beta carotene, cholesterol, TG, Ca
Elevated PT
Evidence of mucosal disease
Low albumin, folate, B12, iron
Malabsorption stool tests
Quantitative fecal collection
Steatocrit: >31% = abnormal
72 hr fecal fat test
100g input, measure output
> 7 = malabsroption
Lactase deficiency
Lactase enzyme not in brush border, lactase buildup in lumen –> osmotic diarrhea
Lactose malabsorption and symptoms
6-20g malabsorbed = flatus
> 20g malabsorbed = flatus+diarrhea
Cystic Fibrosis and pancreas
75% of CF patients have pancreatic exocrine insufficiency by 6 months
60% of remaining patients develop PEI by young adulthood
10% retain pancreatic sufficiency
Chronic pancreatitis
Long term alcohol abuse
Destruction of ducts/acini
Reduction of digestive enzymes
ERCP
Detect ductal abnormalities
MRCP
Detect ductal/parenchymal abnormalities
EUS
Detect ductal/parenchymal abnormalities
Tissue sampling
D-xylose test
Old test - directly asses mucosal function of sugar absorption
Celiac sprue
Immune mediated destruction of enterocytes in response to gluten
Small intestinal villi destroyed
Mature digesting/transporting enterocytes absent
Digestion AND absorption imapired
Celiac sprue antibody
IgA to transglutaminase, endomysium, gliadin
Deaminated gliadin petides
Celiac visual presentation
Decreased folds, scalloping mosaic pattern
Celiac histology stages
Stage 1: inflammation
Stage 2: Deep crypts
Stage 3: Villi/enterocytes destroyed
Clinical manifestation of celiac
Weight loss Bulky/oily stools Flatus/frothy stools Anemia Bone disease Edema/hypoproteinemia Vit B deficiency
Bacterial overgrowth
Deconjugation of bile acids by bacterial enzymes
Consumption of nutrients by bacteria
Damage to enterocytes
Bacterial overgrowth diagnosis
Small bowel culture
Lactulose/glucose hydrogen breath test
Anitbiotic response
Terminal ileum resection and malabsorption
Less than 100cm gone: Excess bile salts in colon = watery diarrhea
100cm gone: Liver cant keep up with bile salt loss = steatorrhea
Fat soluble vitamin absorption
Bile salt defecits > mucosal/pancreatic disease
Folate deficiency
Proximal small bowel disease, alcohol, drugs, congenital effect
Protective mechanisms in pancreas
Synthesis of enzymes as inactive zymogens
Trypsin inhibitor in zymogen granule
Segregation of enzymes
Enterokinase restricted to SI
Acute pancreatitis
Acute inflammatroy condition w/ abdominal pain and increase in pancreatic enzymes
Interstitial (mild): Complete recovery
Necrotizing (severe): Permanent damage
Major etiologies of acute pancreatitis
Alcoholism
Biliary
Idiopathic
Other
Pancreatic divisum
Failure of dorsal and ventral pancreas to fuse
Time course of enzyme elevation - acute pancreatitis
Enzymes 3x UL
Lipase increases faster and to higher degree than amylase, takes longer to decrease
Risk factors of severity
Age Obesity 1st or 2nd episode Organ failure at admission Short interval to admission Pleural effusion CT scan-grade D/E
Diagnostic indicators of acute pancreatitis
Tachycardia/hypotension Tachypnea, hypoxemis Hemoconcentration Oliguria Encephalopathy
Local complications of acute pancreatitis
Fluid collection Necrosis Ascites Erosion into adjacent structures GI obstruction Hemorrhage
Systemic complications of acute pancreatitis
Pulmonary
Renal
CNS
Multiorgan failure
Metabolic complications of acute pancreatitis
Hypocalcemia
Hyperglycemia
Chronic pancreatitis
Pain
Calcification
Pancreatic insufficiency
Etiologies of chronic pancreatits
Alcoholism
Idiopathy
Other - CF, hereditary pancreatitis, hypertriglyceridemia, autoimmune, fibrocalcific
Treatment of chronic pancreatitis
Medical therapy: low fat diet, pain control, pancreatic enzyme supplementation
Surgical therapy
-ERCP, Decompression surgery, resective surgery
Pancreatic cancer and pancreatitis
Increase risk of neoplasm in chronic pancreatitis
May present as acute pancreatitis
Poor prognosis
Cystic neoplasm
No prior pancreatitis
Unexplained pancreatitis with cystic lesion
Fluid analysis, endoscopic US, resection
Inflammatory bowel Disease types
Ulcerative Colitis
Crohns
Ulcerative colitis clinical presentation
BLOODY DIARRHEA Fever Cramping/abdominal pain Weight loss Tenesmus General malaise
Ulcerative colitis location
Mainly distal, 95% rectal involvement
15-25% pan colitis - more likely in children
Crohns disease location
Mainly proximal
40% SI
30% Ileocolonic
30% colon only
Endoscopic chrons appearance
Cobblestone mucoas
Inflammatory polyps
Skip lesions
Crohns clinical presentation
Diarrhea Abdominal pain Bleeding Pyrexia Fistulae Perianal disease More mucus than ulcerative colitis
Age and incidence of IBD
Incidence spike in 20s/30s and again in older age for UC
Differences between UC and Crohns
UC: More malaise, diarrhea, and BLOOD
Crohns: More pain, mucus, pus
Etiology of IBD
Genetic ENVIRONMENT Smoking Dietary Infection/bacteria/gut flora
Indications for surgery (IBD)
Perforation Toxic dilation Massive hemorrhage Chronic ill health Cancer risk
Pharmacological treatments
5ASA
Corticosteroids
Immunosuppressants
Anti TNFa
Anti Adhesion molecules
5ASA targets
Leukotrienes and prostaglandins
Corticosteroid immune system target
trafficking, proliferation, t cell regulation
Intestinal complications of Crohnss
Fistulae Abscesses Adhesions Strictures Obstruction
Systemic complications of Crohns
Arthritis
gallstones
Malabsorption: Lactase/B12
Renal stone
Intestinal complications of UC
Fibrosis Shortening of colon Bleeding Stricture Bowel perforation Toxic megacolon
Systemic complications of UC
Arthritis
Uveitis
Classification of laxatives
Hydrophilic
Stimulant
Secretory
Hydrophilic types
Bulk forming
Lubricants
Hyperosmotics
Hydrophilic intervention
Hydrophilic –> increase water content of stool
Increase stool mass = increase peristalsis
Dietary fiber
Pysllium: Metamucil/konsyl
Methylcellulose
Bulk forming drugs
Psyllium: Metamucil/Konsyl
Methylcellulose: Citrucel
Lubricants
Stool softeners
Ducosate Sodium: Colace
Ducosate Calcium: Surfak
Mineral oil - highly effective but incontinence
Osmotic laxatives
Non absorbable hypertonic ions/agents = increase osmotic gradient
Magnesium salts: milk of magnesia, epsom salt, magnesium citrate
Lactulose - Cephulac
Polyethylene glycol: Golytely, Colyte, Miralax
Stimulant laxatives
Stimulate secretion/peristalsis
Rapid onset
Simulant laxative examples
Phenolphthalein
Bisacodyl (Dulcolax)
Sodum phosphate
Neostigmine - stimulates peristalsis
Lubiprostone
Chloride channel activator
Methylnaltrexone
Opioid receptor antagonist
Does not cross BBB
Glycerin suppositories
Hyperosmotic laxative - draws water into lumen at end of intestine
Very quick
Diarrhea drugs - opioid agonist
Decrease peristalsis
Constipation/dependence
Loperamide
Diarrhea drugs - anti muscarinic
Decrease peristalsis
Anti spasmodic
low doses so no atropine like side effects
Diarrhea drugs - aomatostatin analog
Octreotide
Inhibits secretion
Inhibits gastrin release
Decrease SM contraction
Short half life = frequent dosing = impractical for long term use
Diarrhea drugs - bulk forming agents
Psyllium
Methylcellulose
Aminosalicylates
IBD
Administered as pro drugs, digested by gut bacteria to produce active 5ASA
Can result in toxic byproducts: Sulfapyridine
Corticosteroids
Rectal: hydrocortisone - rapid onset
Oral: Prednisone, methylprednisolone - first pass metabolic steroids
Limit long term use
Immunosuppressive drugs
Azathioprine, 6mercaptopurine
Purine biosynthesis inhibitor
Risk of infection
Methotrexate
Immunosuppressive IBD drug
Folate antagonist
Hepatotoxicity, alopecia, myelosuppression, infection
Cyclosporin
Cyclic polypeptide immunosuppressant
Many toxicities, infection
IBD Biologicals
TNF-1 inhibitor: Infliximab, adalimumab
Natalizumab
Humanized MAB that antagonizes integrin heterodimers
Use for UC patients that dont respond ot other treatment
Diverticula
Sac like protrusion of colonic wall
Diverticulosis
Having diverticulum
80% asymptomatic
Diverticluosis epidemiology
Increases with age
Varies geographically
Risk factors
Inverse relation with fiber
High fat/red meat
Pathophysiology of diverticulosis
Erostion of diverticular wall caused by increased intraluminal pressure
Clinical presentation of diverticulitis
LLQ abdominal pain
Change in bowel habits
Urinary symptoms- dysuria/frequency
Diagnostic tests for diverticulitis
Check white count/urinalysis
Ab CT is best/most sensitivity
Complicated diverticulitis (3 types)
Abscess
Fistula
Obstruction
Abscess diverticulitis
Seen on CT
Patients wont be responding to treatment
Fistula diverticulitis
5%
Colovesical: Between colon and bladder - air coming from urine
Colovaginal
Require surgical repair
Obstruction diverticulitis
Acute - partial obstruction due to inflammation or abscess
Chronic - metal stents treat obstruction
Colonoscopy and diverticulitis
DONT DO RIGHT AWAY
Risk perforation
Do 6 months after recovery to rule out cancer
Diverticular bleeding
Fresh blood with stool through anus
Tagged RBC scan, angiography, surgery
5 I’s of acquisition
Intimacy Inhalation Ingestion Inoculation Injection
Resolution of bacterial infection
Immunity and physical factors (abscesses) contribute to clearance –> does not equal resolution
Enterotixin vs cytotoxin
Enterotoxin: functional alteration
Cytotoxin: Cellular damage
Gastroenteritis enterotoxins
Cholera
E. Coli Labile toxin
Bacillus cereus toxin
Gastroenteritis cytotoxin
Shigella
C. Diff
C. Perfringes
Exotoxin structure
A: Enzymatic activity
B: Binding domain
Cholera toxin
Increase cAMP –> Increase Cl release into lumen –> diarrhea
Shiga like toxins
Released by Enterohemorrhagic E. Coli
Esp: E. Coli O157:H7
Attack endothelial cells
Hemolytic Uremic syndrome
Shiga like toxin attacks endothelial cells –> platelets deposit –> blood cells caught in fibrin deposition –> ischemia –> kidney failure
Salmonella
G(-) bacilli, ferments sugars, oxidase negative
Contaminated food, fecal oral transmission, reptiles
Enteritidis: Does not survive gastric acid, needs high dose
Typhy/Shigaella are more acid resistant
When reach terminal ileum, pili attach to epithelial cells and M cells –> Type II secretion helps salmonella invade and survive
Inflammation/hemorrhage/epithelial injury
Listeria
Internalins: Adhere to epithelial cells
Listeriolysin O: Escape from phagosome
ActA - move to adjacent cell
Injury, inflammation, hemorrhage
Infectious diarrhea types
Intoxication
Non inflammatory
Inflammatory
Intoxication infectious diarrhea
Pre formed toxins in food
Quick onset
Vomiting and watery diarrhea
24hr recovery
Non inflammatory infectious diarrhea
Viruses and non invasive bacteria
2-7 day incubation
Watery, large volume stools
No fever or blood in stool
Focus on SI - vomiting
Inflammatory infectious diarrhea
Invasive or cytotoxin producing bacteria
Fever, tenesmus, blood in stool
Vomiting is less prominent
Intoxication organisms (3)
Staph aureus
Bacillus cereus
C. Perfringes
Staph aureus
G(+) cocci, catalase +
Enterotoxins = superantigens
Cytokine release = serotonin = emesis
Short incubation, vomiting, cramping, no diarrhea
Bacillus cereus
G+ spore forming
Improperly refrigerated food - germinated and toxin produced
Types of bacillus cereus
Emetic: Cerulide toxin - stimulates serotonin
1-6 hr after ingest food
Rice products/starchy food
Diarrheal: Other toxins
6-15 hr after ingestion
Meat, milk, vegetables, fish
Watery diarrhea
C. Perfringes
G+ spore forming
Vegetative cells in food –> Bacteria multiple i gut and sporulate
CPE distrupts tight junctions between enterocytes
Watery diarrhea
Viruses causing non inflammatory diarrhea
Rotavirus
Norovirus
Adenovirus
Astrovirus
Non inflammatory diarrhea Enterotoxin producing bacteria
Cholera
ETEC
Inflammatory diarrheal invasive bacteria
Campylobacter
Shigella
Salmonella
Yersinia
Inflammatory diarrhea cytotoxin producing bacteria
C diff
EHEC
Norovirus
Most common overall
Food/water borne, fecal oral, aerosolized vomit
Abrupt onset, 72hrs
Rotavirus
Ubiquitious - almost all children infected by age 3
2 vaccines developed
ETEC
Enterotoxigenic E coli
Fecal/oral via water
Similar to cholera mechanism
EPEC
Enteropathogenic E coli
Daycare
Type II secretion
Shigella
Overt pathogen, not normal flora
Non lactose fermenting
Diarrhea, dystentery
Human is natural reservoir
Acid resistant
Campylobacter jejuni
Reservoir in GI tract of asymptomatic animals
Undercooked poultry/meats
Mucosal invasion by bacteria and damage
Yersinia (2)
Enterocolitica: Cattle/pig and pseudotuberculosis: rodents/birds
Intimin and type III secretion = close attachment and invasion of macrophages
Survive in peyers patches
Pseudoappendicitis
EHEC
Shiga toxin producing
E Coli O157:H7 - sorbitol negative
Damage microvilli/alter fluid transport
C diff
G+ spore forming
Withstand heat, alcohol, ammonia
On the rise, very effective transmission
Damage to epithelial cells = inflammation
Result from antibiotic use
Obesity BMI range
Obese: >30
Severe obese: >35
Extreme obese: >40
Dieting EWL
14-20%
Weight loss drugs indication and EWL
BMI >30
3-8% EWL
Physician directed weight loss indication/EWL
BMI >30
4-13% EWL
Surgery indications
BMI >40 or >35 w/comorbidities
Failed other treatments
Types of surgery (3)
Restrictive: Smaller stomach
Malabsorbtive: Shorter colon
Combine
Gastric bypass
Make small pouch to bypass stomach
Laparoscopic better than open surgery
Dumping syndrome, vit def, bleed/obstruction/stricture
Sleeve gastrectomy
Risk/benefit much better
Mobilize greater curvature to make stomach smaller
GERD, bleed, stricture
Gastri band
Band around stomach, gastric pouch based on lesser curvature
Need multidisciplinary care and frequent follow up
Hyperplastic polyp
Most common, asymptomatic
Not precursor for cancer, no dysplasia
Inflammatory polyp
Inflammatory pseudo polyp
No malignant potential
IBD or infectious colitis
Juvenile retention polyp
SI, pedunculated, rectal bleeding
Juvenile polyposis
Autosomal dominant
SMAD4, BMPR1A
Increased risk of colon cancer
Peutz-Jeghers syndrome
AD, hamartomatous polyps
LBK1/STK11 gene
Increased risk of colon, pancreas, breast, lung cancer
Cowden Syndrome
AD, hamartomatous polyp
PTEN loss of function mutation
Many extraintestinal manifestations
Cronkhite Canada syndrome
Nonhereditary
Juvenile polyps in elderly patients
Diarrhea, weight loss, 50% fatal
Dysplasia features
Hyperchromatic, elongated, stratified nuclei
Reduced goblet cells
Sessile serrated adenoma
Looks like hyperplastic polyp
No dysplasia but increase cancer risk
Intramucosal carcinoma
Dysplastic cells reach BM and enter lamina propria
Invasion beyond muscularis mucosa = invasive adenocarcinoma
Familial adenomatous polyposis
AD, mutated APC or MUTYH
Many polyps
100% risk for colorectal carcinoma
Colectomy
FAP extraintestinal manifestations
Congenital retinal pigment hypertrophy
Gardner syndrome: FAP + osteomas/cysts/thyroid tumors
Turcot syndrome: FAP + CNS tumors
Hereditaroy non polyposis colon cancer
AD, fewer polyps
MSH1/MSH2 gene mutations: Mismatch repair genes
Right side vs left side adenocarcinomas
Right: Iron deficiency, fatigue/weight loss, ab pan/mass
Left: Rectal bleeding, bowel habit change, LLQ pain
SI Adenocarcinoma
Elderly
Duodenum/ampulla of vater
Biliary obstruction –> jaundice
Carcinoid tumors
Low grade malignant neoplasm
Secrete many hormones
Primary GI lymphoma
Stomach and SI
Risk factor: MALT lymphoma
PTLD
GIST
Gastrointestinal stromal tumor
Arise from ICC
Surgery + anti c-kit
Peyers patch
APC’s, B-cell region, T cell zone
Intestinal epithelial cell immunity (5)
Goblet cells: Mucus
Paneth cells: alpha defensins and antibacterial activity
Enterocytes
sIgA transport
M cell
Specialized epithelial cell usually above Peyers patch
Little to no microvili
Take up particles/molecules and present to Macrophages/DC’s
Dendritic cell
CD103+: Protection/tolerance
CD103-: Identifies pathogenic - proinflammatory, t cell activation etc
Antigen presentation (3)
Direct: Pseudopod of DC travels across enterocyte
Indirect: Goblet cell presents antigen
Indirect: M cell presents antigen
Intraepithelial cell Lymphocyte
Between epithelial cells
Mainly CD8 t cells
Activate due to cellular injury
Lamina propria lymphocytes
CD4 T cells –> cytokines and host defense
Immune suppression: IL10/TGFB
Parasites/allergens: IL4/IL13
Bacteria/pathogens: IFN-gamma, IL17/IL22
B cells and IgA
Secretory: J chain, dimeric
pIgR made by enterocyte
IgA + pIgR travel across cell into lumen –> IgA breaks off and does stuff
Natural IgA
Low affinity
Immunosuppressive, homeostasis, T cell independent
High affinity IgA
T cell dependent
Invasive pathogenic organisms
TLR localizations
Cell surface and intracellular
C type Lectin receptors
Carbohydrate binding domain
Activate inflammation
NBD-NLR
Cytosolic sensor that activate inflammasome
RIG like receptor
Recognize viruses
Norovirus/Rotavirus
Appendicitis cause
Luminal obstruction
Rapid increase in pressure
Appendicitis clinical presentation
RLQ pain
McBurneys point tenderness
Acute Cholecystitis
Impacted stone, >6hrs pain
Murphys sign
Choledocholithiasis
Stone in pancreatic duvt
Bacterial infection
True vs pseudo diverticulitis
True: All layers of organ pushed out
Psuedo: Not all layers
Hinchey staging
1: Small or confined abscess
2: Pelvic abscess
3: Gaseous release but sealed by omentum
4: Fecal discharge
Hinchey staging and treatment
1: Medical management, supportive care and anitibiotics
2: Drainage
3/4: Surgery
Mechanical occlusion of bowel (3)
Luminal obstruction
Intrinsic bowel lesions
Extrinsic bowel disease
Luminal obstruction
Intussusception: bowel in itself
Foreign body
Bezoars
Intrinsic bowel disease
Congenital atresia/stenosis
Stricture
Extrinsic bowel disease
Adhesion from operation
hernia
Extrinsic mass
Volvulus
Paralytic ileum
Impaired gut motilit
Pseudo obstruction
No real blockage
Strangulation
Impaired circulation to obstructed bowel
Intestinal gangrene
Amebiasis: Parasite, location, infective form
Entamoeba histolytica
Colon
Cyst is infective
Amebiasis life cycle
Ingest cyst (survive stomach) –> transform to trophozoite –> invades colonic mucosa –> Cysts/trophozoites passed in feces
Trophozoite invasion of mucosa (amebiasis)
Proteinases
Surface lectins
Channel forming proteins
Amebiasis when enters blood/clinical manifestatiosn
Enters liver via blood stream, can go to lungs
Asymptomatic (E. Dispar)
Dysentery
Giardiasis: Parasite, location, infective form
Giardia lamblia
SI
Giardiasis life cycle
Ingest cyst –> transform to trophozoite in SI –> Colonization –> cysts passed in feces
Giardiasis and mucosa
Attach via sucker/lectin
No invasion
Giardiasis clinical manifestation
Most asymptomatic (endemic areas)
Watery diarrhea
Cryptosporidiosis parasite
Cryptosporidium parvum
Cryptosporidiosis life cycle and pathogenesis
Complicated as shit
Lectin binding but unknown diarrhea mechanism
Cryptosporidiosis pathogenesis
Self limited diarrhea in immunocompetent patients
Chronic diarrhea in immunocompromised patients
Cryptosporidiosis diagnostic test
Acid fast
O&P doesn’t show it
Strongylodiasis parasite, location
Helminthic nematode, SI
Strongylodiasis life cycle
Live in soil and penetrate skin –> travel to lung –> travel up tracheobronchial tree –> cough up and swallow –> mature in SI and lay ova –> hatch and passed in feces (can reinfect in perianal area)
Strongylodiasis and immunocompromised patients
FUCKED
Strongylodiasis pathological manifestation
Larve: pneumonitis, eosinophilia
Adult worms: not a big deal
Strongylodiasis clinical manifestation
HyperinfectionL Diarrhea, GI hemorrhage, meningitis
Enterobiasis
Pinworm, LI
Enterobiasis life cycle
Ingest ova –> eggs hatch –> adults live in cecum –> female lays ova in perianal skin
ITCHY
Taeniasis
Cestode parasitic disease, tapeworm
SI
Taeniasis life cycle
Cattle/pig eat ova –> Get into muscle –> raw food eaten by human –> tapeworm attaches to SI mucosa and grow
Cysticercosis
Cestode parasite
Ingest pork tapeworm ova –> eggs hatch and form in tissue –> can go to brain and fuck everything up
Schistosomiasis
Flatworm helminthic parasite, most significatn worldwide
Schistosomiasis life cycle
Eggs enter water from humans and hatch –> infect snails –> Cercaria released and penetrate skin –> travel to portal veins and grow –> ova deposited and accumulate in tissue
Schistosomiasis pathogenesis adult vs ova
Adult hide from immune system
Ova are immunogenic
Liver and urinary effects
Schistosomiasis clinical manifestations
Bloody diarrhea, hematuria, ascites
Travelers Diarrhea management
Fluids - rehydration
Loperamide (preferred)
Pepto-Bismol
Antibiotics
Antibiotics for TD
Fluoroquinolones - large daily dose (3d)
Rifaximin
Azithromycin
Fluoroquinolones
Broad spectrum
Inhibit DNA gyrase and topoisomerase
Fluoroquinolone adverse effects
Photosensitivity
CNS symptoms
Boxed warnings: tendonitis/rupture, long QTc, neuropathy
Not in children or pregnant women
TD and antiperistaltic agents
Only for mild/watery diarrhea
Avoid in patients with high fever/blood diarrhea
Rifaximin
Mostly excreted - stays in target zone
Bind DNA dependent RNA polymerase - blocks transcription
Only for ETEC, not inflammatory diseases
Macrolides
50S ribosomal subunit inhibitor
Bacteriostatic, conc dependent killing
Block elongation of/exit of peptide from 50S
Macrolide drug interaction
P450 inhibitor
ETEC/EPEC antibiotics
FQ, Azithromycin: 3d
EHEC antibiotic
NONE
Shigella antibiotic
FQ
Azithromycin
Ceftriaxone
Salmonella antibiotic
FQ
Azithromycin
Ceftriaxone
ONLY FOR SEVERE
Campylobacter antibiotic
Macrolide
SEVERE
Listeria antibiotic
Ampicillin
Vibrio antibiotic
Macrolide
FQ
Sulfonamide/Trimethoprim
Folate inhibitors
Block purine production
Broad spectrum
Sulfonamide/Trimethoprim drug interaction
CYP 2C8/9 inhibitor
NOT in 3rd trimester
C diff treatment
Metronidazole: drug of choice for 1st episode
Disrupts DNA of microbial cells
Not in pregnancy
Amebiasis, Giardiasis, BV
Vancomycin
Inhibit cell wall synthesis
Severe C diff
Vancomycin (IV) adverse effects
Nephrotoxicity
Ototoxicity
Red-Man syndrome
C diff follow up
1st relapse: Metronidazole
2nd relapse: Oran vanco, fidaxomicin
Fidaxomicin
Non absorbed macrolide
Inhibits RNA polymerase
C Diff
Equal to or better than Vancomycin