Mindmap

Alimentary System (Bolts)

Bertrand Ng VET377 Pathology Englisch

Mind map: Alimentary system (bolts)

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Alimentary System (Bolts)

John Bolton
- URT Pathology
  - Dysphagia
    - Difficulty Eating
      - Prehension
      - Mastication
      - Swallowing
      - NOT UNWILLINGNESS
    - Associated with Oropharyngeal/Oesophageal Disease
    - Gag Reflex
      - Normal Defence Mechanism
        vs. Foreign bodies
      - From intraoral stimulation
        CN V, IX, X to brain
        impulse elevatese soft palate and constricts pharynx
      - Dysphagia can provoke gagging, but gagging not necessarily dysphagia
    - Clinical Signs
      - Reduced/no food intake
      - Ptyalism (saliva)
      - Halitosis
      - Gagging
    - Evaluate Prehension > Mastication > Swallow
      - Lips, Face, incisor, teeth, tongue = Prehension
        CN V, VII, XII = motor
        CN VII, IX, X (taste), I (smell), II (sight), V (feel) = sensory
      - Teeth, tongue, jaws, muscles = Mastication
        CN V, IX = sensory
        CN VII, XII = motor
      - Pharyngeal and oesophageal function = Swallowing
        Voluntary Phase (Oral)
        Involuntary Phase (Everything below the pharynx)
        Oesophagus
        Dogs and Ruminants: striated
        Horse/Cat/Pig, striated to smooth
        Innervated by vagus, and sympathetic nerves
        Oesophageal Disease
        Inflammation: Infectious
        Viral: Same as mouth/pharynx
        BVDV
        Toxic
        Corrosive agents
        Trauma
        Foreign bodies/iatrogenic
        Intraluminal Obstructions
        Pressure causing necrosis/ulceration
        Neoplasia
        Developmental/Degenerative
        Vascular Ring anomalies
        Congenital/Acquired motility disorder
        Megaoesophagus
        Extraluminal Obstructions also possible
        Persistent Right Aortic Arch
        CN: V, VII, IX, X, XII = Sensory
        Pharyngeal Dysfunction
        Pharyngeal Paralysis: Neuro
        Nasal discharge
        Aspiration Pneumonia
        Achlasia
        Failure of upper oesophageal sphincter to open
        Uncommon
        Acquired (polymyopathy) or Congenital
      - Pathology affecting Function (DAMNITV)
        Toxic
        Uremia/Corrosive Chemicals
        Trauma
        Bones, Wire, Grass seeds, poor dentition
        Inflammation: Infectious
        Bacteria
        Actinobacillus ligniersi
        Wooden Tongue
        Fusobacterium necrophorum
        Necrotic stomatitis/calf diphtheria
        Viral
        Feline rhinotracheitis virus
        Calicivirus
        Vesicular Stomatitides
        FMD, VS
        Erosive Stomatitides
        BVDV, Rinderpest, MCF
        Fungal
        Neoplasia
        Lymphosarcoma
        Fibrosarcoma
  - Regurgitation + Vomiting
    - Regurgitation
      - Usually with oesophageal disease
      - Followed by retch/gag
      - Passive expulsion from pharynx/oesophagus
      - NO nausea/abdominal contraction, conscious effort, bile
    - Vomiting
      - Nausea, Retching
      - Forceful expulsion of stomach contents
      - Antiperistalsis (SI) into stomach, and Retrograde Giant Contractions (RGC)
      - Initiates in Emetic centre in Medulla
        Not a distinct entity (pharmacologic)
        Stimulated by:
        Bacterial toxins
        Upper GI irritation/distension
        Indirectly via other pathways
        Efferent: Vagus, Phrenic, Spinal nerves to abdominal muscles
      - Consequences
        Malnutrition
        Dehydration/Hypovolemia
        Hypochloremia
        Hypokalemia
        Metabolic alkalosis
- Intestines
  - Obstruction
    - Simple obstruction
    - Closed Loop Obstruction
      - External
        e.g incarcerated umbilical hernia
      - Internal
        e.g incarcerated small intestine in epiploic foramen
      - Both stretch and chemical receptors
    - Strangulation Obstruction
      - Examples
        SI Torsion
        Colonic torsion
        Caecal torsion
        Left Displaced Abomasum
        GDV
        Right Sided Abomasal Torsion
      - e.g. Torsion/Pedunculated lipomas
    - Mechanisms
      - Mechanical
        Obturation obstruction
        Typically minimal vasc. damage to wall
        Sometimes pressure necrosis
        Ingested foreign bodies/phytobezoars
        Phytobezoars (fibre/plant material), trichbezoars = hairballs
        Activates Stretch receptors
        Distended intestine proximal to obstruction
        Intussusception
        "Telescoping"
        Common in young animals
        Usually secondary to non--obstructive disease (parasties)
        Hypermotility/irritability
        Retained Meconium (Failure to pass feces in neonates)
        Enteroliths/Faecaliths
        Accumulations of mineral salts, or faeces
        Block Colon in horses
        Impaction
        Many Causes
        Severe constipation (LI) in dogs
        Sand impaction in horses
        Activates Stretch receptors
        Narrowing of Gut Lumen: Intrinsic lesions on wall
        Congenital
        Atresia
        Stenosis of pylorus (rare)
        Acquired
        Inflammatory lesions
        Benign/malignant tumors
        Post anostomotic stenosis
        Narrowing of Gut Lumen: Extrinsic Lesions on wall
        Adhesions
        Previous surgery
        Previous peritonitis
        Herniae
        External (umbilical/inguinal)
        Internal (epiploic forman)
        Extraintestinal masses:
        Abscesses
        Tumours
        Fat Necrosis
        Small intestinal Volvulus (Volvulus/Torsion)
        LI/Colonic Torsion/Displacement
        esp,. Horses
        Left Displaced Abomasum (Cows)
        Gastric Dilation Volvulus (Dogs)
        Right sided Abomasal Torsion (Cows)
      - Paralytic Ileus
        "Functional" obstruction
        Fails to propel contents
        Can affect either SI or LI
        Often follows GI Sx
        Also associated with Electrolyte imbalance, peritonitis, toxemia
        Stretch receptors: pain
      - Vascular Bowel Disease
        "Functional" obstruction
        Associated with arteritis: S. vulgaris parasite
        Severe cases: Segmental infarct of colon
        Uncommon now with antiparasitics
    - Other Signs
      - Reflex Reduced intestinal motility
      - Emptying intestine distal to obstruction
      - Reduced/Intestinal Borborygmi
        Distension of intestine with fluid/gas
        Reflex Neural Inhibition
        Reduced blood supply
        Hypovolemia, electrolyte disturbances
        Endotoxemia
      - Abdominal Distension
        Accumulated gas/fluid proximal to obstruction
        Fluid in small intestine accumulates, may reflux
        Horses cannot vomit, fluid causes pain/rupture
        Vomiting in dogs
        HCl Loss
        Metabolic alkalosis
        Continued fermentation with gas production
        Tympany (esp. horses) large intestine
        Caecal gas cap "ping"
      - Tachycardia
      - Hypovolemic/Endotoxic Shock
      - Diagnostic Tests
        Changes in peritoneal fluid
        Abdominal Ultrasound Examination
- Abdominal Pain
  - Neural Pathway
    - Extreme Stretch and Chemo nociceptors
      - Spinothalamic Pathway
      - Stretch Receptors
        Hollow Organs: Muscular layers b/w muscularis mucosa and submucosa
        Solid Organs: In serosa
        Mesentery: w/ large blood vessels
        Activation
        Distension of Hollow organs
        e.g GI Obstruction
        Forceful muscular contractions
        Urolithiasis/cholelithiasis, intestinal spasms
        Stretching of solid organ serosa or capsule
        Hepatic Congestions
        Stretching of mesentery or mesenteric vessels
        Neoplasia/Volvulus
      - Chemoreceptors
        Hollow organs: Within mucosa/submucosa
        Activation
        Inflammation
        Peritonitis/Abscess/Pancreatitis/G
        Ischemia/Necrosis
        Volvulus/GDV/Infarct/splenic torsion
        by substances and ions
  - Clinical Manifestations
    - Vary: Episodic to Continuous
    - Tends to be more severe with BOTH stretch and chemical
    - Pain varies with lesion
    - Species differences
      - Horses: Obvious
        Agitated, grinding teeth, sweating
        Restlessness, inappetance
        Lateral Recumbency/Dog sitting
      - Ruminants: Hard to determine
        Non-specific: anorexia/depression
        Kicking at abdomen, restless, grunting
        TEST: Positive Grunt Test
      - Dogs: Range (depression, growling to grunts and tense abdomen)
- Diarrhea
  - Refresher
    - Surface Area is super important in digestion
    - Crypts + Cells
      - Produce Enterocytes
        Migrate up to villi
        Die and slough into lumen
      - Secretory
    - Villous Cells
      - Absorptive
    - Enterocytes
      - Cells joined to one another tightly
        Transport
        Intracellular
        Through cell
        Transcellular
        Between the cells
    - Digestion
      - Carbohydrates
        Amylase
        Glucose, Fructose, Galactose
      - Protein
        Pepsin + Pancreatic proteases
        Amino Acids
        Multiple Digestive Pathways
        Luminal Enzymes digest proteins to AA for absorption
        Luminal enzymes digest proteins, brush border enzymes digest to AA for absorption
        Luminal enzymes digest proteins to oligopeptides, taken by enterocytes, broken to AA and absorbed intracellularly
      - Lipids
        Lipase + Co-lipase + Bile Salts
        FFAs + Monoglycerides
  - Intestinal Fluid Balance
    - Water/Electrolyte balance
      - Secretion/Absorption > Input/Output
      - Efficiency of absorption increases down the tract
      - Sodium Transport
        Nutrient Coupled Na Transport
        Downhill gradient from Na/K pump
        Cl absorbed passively (paracellular)
        other ion gradient
        Na - Glucose transporter SGLT1
        Small Intestine
        Sodium Hydrogen Exchanger
        Small Intestine + Colon
        Na exchanged for H
        NHE3 transporter
        Down gradient from Na/K pump
        // Na H and Cl HCO3 exchange
        In Ileum and Proximal colon
        Na absorbed, coupled to Cl-
        HCO3- produced intracellularly
        H+ and HCO3 released
        Na and CL absorbed
        Electrogenic Na Absorption
        Distal Colon
        via Na+ specific, aldosterone sensitive ion channel
        Down Na gradient by Na/K pump and K channel
        Cl- absorbed passively (paracellular)
        other ion gradient
      - Chloride Secretion
        Both SI and LI
        Secreted from crypt cells
        Paracellular movement of Na
        Cl secretion drives fluid secretion
        Main source of Cl for Cl-HCO3 anion exchanger
        Secretion regulated by second messengers
        Stimulation by secratogogues >>> Opening/addition of new Cl channels (Secretory diarrhea)
      - Short Chain Fatty Acids/VFAs
        Colon
        Generated by bacterial fermentation
        Acetate/Proprionate/Butyrate
        Rapid absorption in colon = more Na/fluid resorption
        SCFAs upregulate NHE3 expression
        Enhances entry of SCFA into cells
        Cl butyrate and SCFA HCO3 exchangers coupled to Na/H exchange
        Promote Na/Cl absorption
      - Nett Balance (Small Intestine)
        Absorption
        Water
        Na (active)
        K (passive)
        Cl (exchange for HCO3)
        Non-electrolytes
        Glucose/AA/Lipids/Bile Salts
        Secretion
        Bicarbonate
      - Nett Balance (Large Intestine)
        Absorption
        Water
        Na
        Cl
        SCFAs
        NO NON-ELECTROLYTES absorbed. These are fermented
        Secretion
        K
        HCO3-
      - Water Absorption
        Passive (respond to salts)
        Freely permeable upper small intestine
        Most paracellular
        Very large amounts
  - Pathological Mechanisms
    - Maldigestion/Malabsorption
      - Ingestion of poorly absorbed solutes
      - Villous atrophy (Loss of Surface Area)
        Different types of atropy (Rotavirus/Parvovirus/TGE)
      - Epsom Salts/Sodium Sulfare poorly absorbed
        Maldigesta in intestines
        Causes water to move into lumen (osm D+)
        Maldigested material ferments, increased osmotic drag
        Also poor digestible milk replacer/lactose intolerant puppies
        EPI, or Hepatic Insufficiency
      - LOW VOLUME
    - Secretion
      - Bacterial toxins
        Enterotoxigenic e.Coli (Non-invasive)
      - Inflammatory Mediators
      - Endogenous laxatives
      - Increased ion transport mechanisms (esp. Cl-)
        Both SI and Colon
        No demonstrable intestinal lesions
        Biochemical lesion
        Fluid overload of large intestine
        HIGH VOLUME DIARRHEA
        Diarrheal fluid is isotonic
      - HIGH VOLUME
    - Changes in intestinal Permeability
      - Acute inflammation
        Enteroinvasive Salmonella/e.coli
      - Chronic Inflammation
        Eosinophilic enteritis (Horses)
        Eosinophils infiltrate gut wall
        Thickened gut wall
        Infiltrates mesenteric LN
        Variable granuloma formation in mucosa
        Johne's Disease (Cows)
        Chronic D+/emancipation/hypoproteinemia
        Mycobacterium avium/ss. paratuberculosis
        Histiocytic Ulcerative Colitis (Boxers)
        Granulomas/ulceration in colon
        infiltration with mØs with PAS+ material
      - Often associated with loss of protein
        Protein-losing enteropathies
        Electrolytes and protein move into lumen
        Water moves into lumen/Osmotic D+
    - Changes in intestinal motility
      - Rarely a primary cause of disease
      - Increased motility can cause D+
        secretory diarrhea
      - Decreased motility (SI), possibly SIBO
  - Osmotic Diarrhea
    - PART OF most D+ cases
    - Increased solute = more water into lumen
  - Role of Large Intestine
    - Compensated
      - Gut Flora = large reserve
      - Excess sugar = Converted to SCFA
        Rapidly absorbed = no D+
    - Hypofermentation
      - NO developed flora (newborns)
      - Excess sugar not converted to SCFA
        Less absorption = osmotic diarrhea
    - Hyperfermentation
      - Well developed flora
        Overloaded with carbohydrates
      - Lactic acid produced (pH decreases)
        Osmotic Diarrhea
- Ruminants
  - Fermentation linked to Motility
  - Fermentation
    - Acidosis
      - Excess carbohydrate
        Excess lactate
        Osmotic diarrhea
        Dehydration
        Hypovolemic Shock
        Metabolic Acidosis
        Even more bacteria/endotoxin
        Endotoxic shock
        Lactic acidosis
        D-Lactate
        In rumen and blood
        L-Lactate
        Used by host
        Overwhelmss buffers --> Anion Gap
        Also caused by poor perfusion
      - Death of "Good" bacteria
      - Diagnosis
        Rumen Fluid Collection
        Protozoa normally suspend the fluid, quick settling = protozoa are dead.
        Analyse pH
        gram stain
        Presentations
        Star Gazing
      - Consequences
        Ruminal Stasis
        Due to SCFAs
        Caused by damaged ruminal wall, hypovolemia, metabolic acidosis and toxemia
        Polioencephalomalacia
        Destruction of thiamine producing bacteria
        Thiamine deficiency
    - Ruminal Tympany (Bloat)
      - Free-Gas Bloat
        Fermentation Normal
        Acute
        Chronic
        Failure to Eructate
        Blocked oesophageal opening
        Obstruction of cardia
      - Frothy (Legume) Bloat
        Fermentation Abnormal
        Feeding lush pasture/legume
        Chloroplast membrane protein = stable foam
        traps gas, blocks eructation
        No"ping"
        Thorax compression, cardio failure, recumbency, death
  - Motility
    - Primary Cycle
      - Related to emptying/mixing
    - Secondary Cycle
      - Related to Eructation
    - Regulation via long vagovasal reflexes
      - Vagus nerve up to medulla
        Vagus nerve down to smooth muscle
    - Abnormalities
      - Depression of Gastric Centers in CNS
        anesthetics, drugs, pain, pyrexia
        Traumatic Reticuloperitonitis (TRP/Hardware Disease)
        Cow eats random hard stuff (esp in parturition/pregnancy)
        Collects in reticulum
        Penetrates wall
        Local peritonitis
        Generalised peritonitis
        Migrates through diaphragm: (myocarditic, thoracic abscess)
        Sits harmlessly and dissolves
        Reduce risk with a magnet
        very common
        Clinical Signs
        Decreased milk production
        Fever, Depression, Anorexia
        increased HR/RR
        Cranial abdominal pain (positive grunt test)
        Usually vague w/ localised TRP after 24hours
        Chronic = weight loss, poor lactation, rough hair, vagal indigestion
      - Lack of Excitatory Reflex inputs via tension receptors in forestomach
        anorexia, vagus indigestion
        Vagal Indigestion
        Chronic, vague
        Characterised by disruption to forestomach emptying
        Failure of transport into/through omasum
        Failure of abomasal emptying
        Adhesions between forestomach and peritoneum
        Often secondary to TRP or gut perforation
        Usually no vagus nerve lesion
        mechanoreceptors?
        interferes with sensory signals to the brain
        Disrupted vagal motor signals for normal reticuloruminal motility
        Clinical Signs
        Reduced feed intake, normal water
        Bradycardia, from vagovasal impulse
        Variable rumen sounds (absent/hypermotile)
        Usually increased but ineffective
        "Pearpple shape"
      - Blockade of motor pathways
        secondary to drugs
        atropine
        hypocalcemia
      - Increased inhibitory reflex inputs via epithelial receptors in forestomachs
        ruminal distension, acids, abomasal/small intestinal distension

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Beschreibung: VET377 Pathology Mindmap am Alimentary System (Bolts), erstellt von Bertrand Ng am 15/10/2017.
Erstellt von: Bertrand Ng
Aufrufe: 4
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Alimentary System (Bolts)

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