Mind map

Alimentary System (Nahiid)

Bertrand Ng VET377 Pathology English

Mind map on alimentary system: routes of entry, defense mechanisms, clinical signs and diagnostic tests

Mind map: Alimentary system

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Routes of Entry
- Ingestion
- Direct Extension
- Expectorated from lungs and swallowed
- Systemic blood borne infections
- Parasitic migration
Defense Mechanisms
- Physical
  - Normal motility
  - Vomiting/Diarrhea
  - Saliva/mucus/gastric juice/bile
  - Gastric pH
  - Intestinal Proteolytic enzymes
  - High epithelial turnover/barrier
  - Gut flora/fauna (biofilm)
- Innate
  - Mast Cells, mØs, neutrophils, paneth cells
  - Autophagy
  - PRRs
  - Complements, defensins, TLRs
- Adaptive
  - Immunoglobulins
  - DC, T, B, Plasma cells
Clinical Signs
- Non-specific (region)
  - Malaise/Lethargy/weakness
  - Inappetance/anorexia/pain
  - Dehydration
  - Hemorrhage/melena
  - Lower tract disease
    - Abdominal pain/colic
    - Polyphagia/hyperphagia
- Upper (includes forestomachs)
  - Dysphagia
  - Ptyalism
  - Halitosis
  - Bloat in ruminants
    - And D+ secondary to lactic acidosis
  - Upper Tract
    - Halitosis + Ptyalism
      - Inflammation
        Stomatitis/Gingivitis/Cheilitis/Glossitis/Pharyngitis/Tonsillitis
      - Morphological changes
        Cattarrhal (mucous), fibrinonecrotic, granulomatous
        Vesicular
        Proliferative
        Erosive/ulcerative
    - Viral Vesicular Stomatitides
      - Viruses, form vesicles, erode, granulate and heal
      - All 4 lesions look the same
        can rupture and look like erosion/ulcer stomatitides
        BVDV, bluetongue, malignant catarrhal
      - FMD, V. Exanthema, Swine VD, VS
      - Endothelial damage
        Thrombosis, vasculitis
        ischemic necrosis
        oedema/hemorrhage
    - Proliferative Lesions (Oral cavity)
      - Neoplasias
        Benign
        fibromatous epilus of periodontal ligament origin
        common (can be multicentric), contain bone
        Acanthomatous ameloblastoma
        invasive, no metastasis
        Malignant
        SCC
        v. invasive
        Fibrosarcoma
        Malignant melanoma
        rapid metastasis
      - Papillomas
        Spontaneous or viral (young dogs and cattle)
      - Gingival Hyperplasia
      - Viral Papular Stomatitis
        Scabby mouth/orf
        Bovine papular stomatitis
    - Teeth and gums
      - very common
      - Malocclusions
      - Teeth development anomalies
        Enamel/dentin defects (CDV/BVDV)
        Adontia/oligodontia/polyodontia
      - Dental attrition and abnormal wear
      - Feline Odontoclastic resorptive lesions (idipathic)
      - Periodontal Disease
        Plaque
        bacterial mass + organic matrix
        Caries/infundibular impaction
        gingivitis/periodontitis/pulpitis/alveolar osteomyelitis
        Calculus
        mineralised plaque
    - Rumenitis
      - Basically means lactic acidosis
        Inflammation
        Degeneration/coagulative necrosis of ruminal epithelium
        Stellate scars
      - Can be secondary to mechanical/chemical injury
      - Primary viral diseases
        BVDV/MCF/FMD/bluetongue
      - Sequelae
        Secondary bacterial/mycotic infection
        Fusobacterium -> Haematogenous to liver -> Abscess
        Aspergillus -> Haematogenous to liver -> Hepatitis
- Lower
  - Vomiting/nausea
  - Diarrhea
  - Haematochezia
  - Dyschezia/constipation/tenesmus
  - Gas bloat/borborygmi/eructation/flatulence
  - Faecal incontinence
  - Lower Tract
    - Monogastrics/abomasum
      - Critical functions
        motility
        pyloric outlet patency
        mucosal integrity
      - Clinical Signs
        Anemia/Haematemesis/melena/inappetance/weight loss
        Melena = significant blood loss in short period of time
        Stays in stomach/small int. long enough for digestion
        Anemia with hypoalbuminemia
        GIT blood loss
        Vomiting
        Hypovolemia
        metabolic acidosis
        HypoK/HypoChloremia
        abdominal pain (colic/bruxism)
        Decreased appetite and weight loss
        Abdominal Ostertagiosis
        L3,4,5 in abomasal glands
        Glandular hyperplasia/metaplasia
        Increased luminal pH, less pepsin, fermentation
        osmotic diarrhea
        Adults damage mucosa -> inflammation
        Weight loss, diarrhea, hypoproteinemia
    - DAMNITV
      - Inflammation
        Gastritis/Enteritis/Colitis/Proctitis
      - Morphological Changes
        Catarrhal/fibrinonecrotic/granulomatous/necrotic/haemorrhagic
        Ulcerative/erosive
        Poorly understood: imbalance b/w acid secretion and protection
        mucosal barrier breached, acid/pepsin damage deeper tissue
        inflammation/pain
        SEVERE: perforation (septic peritonitis)
        Secondary to neoplasia (lymphoma) in all species
        Common in foals and pigs (dogs often subclinical)
        Pigs: Fatal hemorrhage, deep ulcers
        Mast Cell tumors (histamine release) -> haematemesis/melena
        Foals: cannot vomit, idiopathic, ill thrift and pain
        Adults: often subclinical
        Calves: dietary changes/stress/irritation
        Proliferative (Hyperplasia/Neoplasia)
    - Intestinal Disease
      - Clinical Signs
        Varied, wide
        Acute/explosive to chronic/intractable
        Altered appetite
        Vomiting
        Diarrhea
        Pathological Mechanisms
        Malassimilation
        Results in weight loss: despite big appetite
        Also pyrexia/pain
        Maldigestion
        Incomplete breakdown of large molecules
        Not absorbed, accumulate in lumen
        Osmotic diarrhea
        Rapid fermentation
        More osmotic pressure, decreased pH worsens absorption
        Worse diarrhea
        e.g. poor milk replacer, lactose intolerance, EPI, impaired bile salt mechanism
        Can lead to low Vitamin K
        Coagulopathy
        Produced by fermentation and gut microbes
        Malabsorption
        Structural abnormalities in mucosa impairing absorption
        ALWAYS due to intestinal disease
        villous atrophy
        Canine Parvovirus
        Targets crypt epithelium -> necrosis
        increased intraluminal osmotic load
        Diarrhea
        enhanced fermentation
        Usually accompanies maldigestion
        Hypersecretion
        More ions: bacterial toxins/inflamm. mediators/endogenous laxatives
        e.g enterotoxigenic collibacillosis
        non invasive, blocks NaCl absorption
        Increased intestinal permeability
        Acute inflamm (bacteria), chronic, neoplasia, lymphatic obstruction
        Acute
        Enteroinvasive enteritis (salmonella/bacteria)
        Swine dysentery, Clostridium perfringens, coccidia
        Mechanisms increasing tissue pressure (e.g. chronic)
        Johne's Disease/Eosinophilic enteritis etc.
        IBD, fungal enteritis
        Starlings (Oedema) mechanics
        Fluid to lumen
        Severe loss = plasma protein loss
        Hypoalbuminemia/hypoproteinemia
        Protein-losing enteropathy (PLE)
        e.g. Intestinal lymphangiectasia in dogs (congenital), or lymph obstruction
        Changes in intestinal motility
        Rarely primary cause of diarrhea
        Increased motility = possibly diarrhea
        Decreased motility = SIBO (Small intestine)
        Causes of change in gut flora
        hypomotility
        neonates before gut flora establish
        antibiotics
        EPI
        Leads to
        Bile Salt depletion -> Fat malassimilation
        osmotic diarrhea
        Decreased cobalamin (binding and inactivation of vitamin to bacteria)
        Increased folate due to increased bacteria
        Can lead to intussusception
        Consequences
        Dehydration, hypovolemia
        Shock/inadequate perfusion
        Hypoglycemia, ketoacidosis, decreased pH
        loss of pH dependent enzymes
        Acidosis, fecal bicarb loss
        From loss of kidney perfusion
        Electrolyte imbalance, intracellular more H+, less K+
        lose control of myocardial contraction
        Vicious cycle --> Hypovolemic shock
        Dehydration/lethargy/depression
        Weight loss/ill thrift
        Tenesmus (Cramping rectal pain)
        Abdominal distension
        Abdominal pain
        Borborygmi/flatulence
      - Small vs Large
        Small
        Mild increase in frequency
        Increased fecal volume
        Melena
        No fecal mucus
        Large
        Alot more frequent defecation
        Decreased fecal volume
        Fecal mucus present
        Hematochezia
      - NSAIDS and Ulcers
        Inhibits prostaglandin (pg) synthesis
        alters circulation
        Delays GIT healing (turnover and mucus)
        more gastrin, increased acid production
        Horses: Gastroduodenal/colitis
        Dogs: Colonic perforation
      - Proliferations
        Usually dogs and cats
        Benign or Malignant
        Hyperplastic polyps
        Epithelial: Adenoma/carcinoma
        Stromal: gastrointestinal stromal tumor, leiomyoma
        Round Cell tumor: Lymphoma, mast cell tumor
    - Omentum/Peritoneum
      - Inflammation (Peritonitis
        Clinical Signs
        Abdominal Pain
        Ascites
        Usually due to multiple organ disease
        Aseptic abdominocentesis to characterise fluid
        Peritonitis
        Causes:
        Rupture
        Systemic Infection (FIP)
Gastric Ulcerations
- Erosion: loss of epithelium, BM intact
  - heals fast
- Ulcer: loss of epithelium and BM
  - Second intention healing + scarring
  - Leads to perforations/strictures/stenosis in tubular GIT organs
Diagnostic Tests
- Minimum Database
  - Haematology/Biochem/Urinalysis
    - Albumin + Globulin
      - Panhypoproteinemia usually with PLE
        Compare with hepatic insufficiency/PLN (hypoalbuminemia alone typical)
      - Insensitive indicators of protein loss
      - Increased protein usually dehydration
        Hyperglobulinemia can be inflammation
    - Serum Bile Acids
      - SIBO increases unconjugated SBA
    - Na/K
      - Electrolyte abnormalities
        Vomiting, obstructions, secretory diarrhea
    - Liver Enzymes
      - Leakage and Induced enzymes
        Primary GI disease with secondary hepatopathy
        Link with SBA to differentiate primary GI with primary hepatopathy
    - Cholesterol
      - Increased cholesterol with PLN (ddx for hypoalbuminemia)
      - Decrease seen with diseases causing fat malabsorption (ddx hepatic insufficiency)
    - Urea and Creatinine
      - V+/D+/inappetance all associated with dehydration and pre renal azotemia
        increased urea/creat, hypersthenuria
      - Increased urea can be gastric/upper intestine hemorrhage
    - Ca and Mg
      - Decreased Ca/Mg seen with PLE (reduced Ca can be hypoalbuminemia)
    - Cats with Chronic GIT Disease
      - Serum T4 hormone, FeLV, FIV status are useful
- Diagnostic Imaging
  - US/XR
    - Obstructions/Neoplasia
  - Endoscopy/Biopsy
    - Gold Standard, but invasive
  - Scintigraphy/Fluoroscopy
  - CT/MRI
- Serum markers of function/inflamm
- Fecal samples
  - Infectious agents
    - Faecal Culture and Sample
      - Suspect a specific pathogen
        Isolate and ID
        Test Ab susceptibility
      - Use when Acute GI signs: haemorrhagic D+, pyrexia, inflamm leukogram, neutrophils
        Screening test for chronic
      - Fresh feces, do not refrigerate/store with formalin fixed
    - Adjunct Isolate Testing
      - Specific enteropathogens with GI disease
        Most are commensals, must be isolated
      - Test for virulence genes
      - Test for toxins
      - Determines isolate's clinical importance, or typed for epidemiologic surveys
    - Faecal PCR
      - Detects DNA/RNA, not cells
        DNA extraction is hard, can have false negatives
        Looking for set pathogens
      - Higher sensitivity
        DNA contamination is a problem
        False positives possible
      - Only use a lab with expertise in this
    - Canine Faecal Parvoviral Antigen (ELISA)
      - ELISA: Fresh Feces > Swab
      - For Young, unvaccinated, exposed
      - Use if: D+, anorexia, haematemesis, melena/haematochezia, pyrexia, leukopenia, neutropenia
      - False Negatives: Virus shed briefly in feces, small window
        If tested too early. Retest later if suspected
      - False Positives: modified live vacc
    - Fecal Parasite Testing
      - Dependent on quantity/quality of feces
      - Fecal Egg Count
        Quantitative
        Not for trematode eggs or some tapeworms
        Use with worm egg count guides (livestock)
      - Fecal concentration (cysts/ova)
        Qualitative
        Incl. Giardia
    - Immunofluorescence Antibody Test
  - Small Animals
    - Wet microscopy
    - Gram Stain
    - Occult blood
    - Concentrations for cysts and ova
  - Large Animals
    - Fecal Egg Count
- Assessing GIT Function
  - Permeability Testing
    - Dz causes epithelial damage
      - Increased intestinal permeability
        Movement of antigens/pathogens through mucosa
      - Use of Markers
        Exogenous non-metabolisable probes
        No degradation/metabolism
        If appear in serum/urine, THEN increased permeability
        Not useful to localise sites
        CANNOT tell decreased absorption
        Sugar Probes
        Metabolised/degraded
        Mixtures of sugar probes can localise
        More in serum/urine = permeability increased
        Less = decreased absorptive capacity
  - Evaluation of Intestinal Protein Loss (PLE)
    - Serum albumin and total plasma protein
      - Panhypoproteinemia usually
        sometimes only hypoalbuminemia
        Compare with A:G ratio/conc.
      - Rule out: blood loss, PLN, hepatic failure, exudative dermatopathy
    - Faecal a-1 proteinase inhibitor in fecal samples
      - Validated for K9/F9 only in USA/Europe
        Lost with albumin in PLE, so increased fecal concentration = PLE
        Potential early indicator of PLE in dogs
    - 51Cr albumin recovery in fecal samples
      - Gold standard
      - IV radioactive substance
        hard to do (radioactive)
  - Biomarkers of Gastric/Intestinal Inflamm.
    - Serum Gastrin
      - For dogs/cats with unexplained gastric erosion/ulcers/hyperplasia
      - Chemiluminescence immunoassay - LH serum serum immediately, freeze
        Persistent increase with CS = suggests gastrinoma
        Secretin stimulation test to confirm Dx
        Proton pump inhibitors can interfere
        Check about patient meds first
    - Faecal Occult Blood
      - If GI bleeding suspected but NOT apparent
        e.g. NO melena/haematochezia
      - Poor sensitivity/specificity
        Take 3 consecutive motions
      - Detects pseudoperoxidase activity (Hb/Myb)
        But ALSO dietary haemoglobin (meat)
    - Plasma Pepsinogen
      - Zymogen of gastric protease pepsin
        From chief cells
      - Use in Ruminants
        Indicates abomasum damage
        Increases with ostertagiasis (esp. type II)
        Can also increase with azotemia
    - Ruminal Fluid pH
      - Acidosis
      - Normal = 6.5 - 7
    - Lactate in Horses with colic
      - Simultaneously measured blood lactate
        Indicates strangulation/ischemia
        Serial blood lactate measurements > 1 measurement
        prognostic indicator of postop recovery
    - Others
      - Increased plasma L-lactate
      - Plasma citrulline
      - Inflamm. markers (CRP etc.)
  - Evaluation of GIT motility
    - Radiography
    - Ultrasound
  - Assessment of Intestinal function/pathology
    - Lab detection of malassimilation
      - Fecal Analyses
        microscopy of smears
        Cytology --> Infectious agents/neutrophils
        Fecal fat, starch, fibre
        Unassimilated materials
        Strictly Qualitative
        Cheap, but unreliable/rare
        Total fecal fat
        Steatorrhea
        Fecal proteolytic (trypsin) activity
        ID fecal proteases (mostly pancreatic)
        Unreliable, superseded by TLI to r/o EPI
      - Trypsin-like immunoreactivity (TLI)
        Canine
        Sensitive/specific to K9 EPI
        Feline
        Species specific
        Decreased renal excretion can also increase TLI, but those are mild even in severe renal failure
      - Intestinal absorption/tolerance tests
        Detect increased intestinal permeability relative to reduced SA/enterocyte dysfunction
        Feed and sample serum for absorbed substance
        Lipid assimilation tests
        Inaccuracies can be delayed gastric emptying, or poor micelle formation from low bile salts
        Carbohydrate assimilation tests
        Inaccuracies due to delayed emptying, reduced SI blood flow, abnormal motility, decreased GFR etc.
  - Assessment of SI dysbiosis (SIBO)
    - Serum Cobalamin (B12)
      - EPI decreases availability
      - SIBO, bacteria binds to B12, prevents absorption
      - Absorbed in ileum, severe SI disease decreases absorption
    - Serum Folate
      - Carriers necessary for absorption
      - Only in proximal SI
      - Increase with SIBO and EPI
      - Artefact: Increases with haemolysis: red cell folate
    - Breath Hydrogen
      - Detects Carbohydrate malabsorption, or SIBO
        Bacteria in GI metabolises carbs to Hydrogen (not mammalian cells)
      - Increased H with increased LI fermentation/SIBO
      - BUT: variation in measured values, no standardised protocol, not readily available
        Limited utility
- Cytology
  - Neoplasia vs. Inflamm.
  - ID aetiological agents
  - Techniques
    - FNA
    - Impressions
    - Scrapings
  - Avoid ulcerated areas
- Exploratory Laporotomy
- Biopsy/Adjunct Methods
  - Endoscopic biopsy
    - Take multiple, quality matters
    - Place on mount in mesh cassette in formalin jar, NOT on gauze/free

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Description: VET377 Pathology Mind Map on Alimentary System (Nahiid), created by Bertrand Ng on 22/10/2017.
Created by: Bertrand Ng
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Alimentary System (Nahiid)

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