Alimentary Flashcards
Where is the vomiting center and where does it receive inputs from
Vomiting centre is a collection of nuclei within the medulla oblongata. Receives inputs from cerebral cortex (nervousness, odour, pain and opoids), Vestibular apparatus ( Motion sickness or middle ear infections), Peripheral receptors, Visceral receptors and the Chemoreceptor trigger zone CRTZ ( has no BBB to allow toxins in the blood to cause vomiting)
What are the key receptors in the vomiting centre
Alpha2 adrenic receptors
5-HT1A receptors
NK1 receptors
what are the 3 stages of vomiting
- Nausea - Decrease in gastric tone, duodenal contents reflux into stomach and there is hyper salivation
- Retching - dry heaves
- Vomiting - Epiglottis closes to prevent aspiration pneumonia. abdominal muscles and diaphragm contract. Cardia opens and pyloric stomach contracts. anti peristaltic movements.
What are the causes, clinical signs, treatment and prevention of ruminal acidosis
Cause - Sudden ingestion of of large amounts of fermentable carbohydrates. causes a change in microbes in the rumen due to PH. Main VFA produced no longer acetate, but now Propionate, butryate and lactate.
Clinical signs - Dull or recumbant, ruminal stasis, dehydrated ( due to water being drawn into rumen), sunken eyes, abdominal distention, laminitis and ataxia
Treatment - 5% sodium bicarbonate slow i/v, 5 litres per 450kg of cow per 30 mins
What is SARA
Subacute ruminal acidosis - usually a herd level problem. charactersised by low milk fat and milk yield. Repeated Haemopytsis (coughing blood) and epistaxis ( nose bleed) in the herd is a sign of SARA
What is ruminal bloat, what are the two types and their treatment
Bloat is characterized by enlargement of the left flank (rumen) or abdomen in sever cases. can present as sudden death, recumbency, standing quietly or struggling to breath (dyspnoea).
- Frothy bloat - Froth traps in the rumen that cant be eructed out. Caused by foaming properties of soluble leaf proteins at pasture (e.g clovers and legumes). ]
Treatment includes removing from pasture, and oral treatment of mineral oil (500ml). Future control with buffer feeding
2.Gaseous bloat - Increase in carbohydrate intake or any esophageal obstruction. Also a cow in left lateral recumbency blocks the cardia, not allowing eructing. treatment includes either a stomach tube or puncturing the left paralumber fossa with a red devil trochar. stay sutures required if a rumenotomy done.
what is hardware disease
Traumatic reticulo peritonitits is where a metal object has been ingested and remains in the reticulum, possibly causing: local peritonitis, diffuse peritonitis, pericarditis or liver abscesses. Clinical sings will include increased temperature, decreased milk yield, arched back and decreased rumenal contractions.
Testing for it will include:
-Withers pinch - a cow should flex back ventrally but because in pain wont.
-Pole test
-Eric williams test which u observe a grunt before rumenal contraction
What management issues can lead to LDA and what test could you use to confirm
Left displaced abomasum usually occurs withing 6 weeks post calving. Due to poor management over the transition period ( from dry to post calving). So theres a rapid increase in carbohydrates in the diet to quickly. usually accompanied with a decrease in BCS and increased ketone levels in blood or urine
Define the key differences between primary and secondary GI disease
- Primary GI disease - Primary lesion is in GI (e.g gastritis, gastric foreign body gastric ulcer, pyloric disorder, intestinal obstruction or enteritis). Patients that present may have palpable abnormality or discomfort in abdomen, vomiting with diarrhea, vomiting is related to time of eating or will have normal clinical history and be bright, alert and responsive. Further investigation involves imaging the abdomen NOT biochemistry.
- Secondary GI disease - Due to pathology outside the GI (e.g renal failure, liver disease, pancreatitis, ketoacidosis, hypoadrenocorticism or hypocalcaemia). Animals generally have other clinical abnormalities, intermittent vomiting, metabolically ill and not bright or responsive. Vomiting is a result of toxins acting on the CRTZ. Further investigation involves biochemistry profile.
Exceptions!
a) pancreatitis in dogs - Presents as primary GI disease as it has a acute onset of vomiting after eating, with a dog who is otherwise fit and healthy.
b) Hyperthyroidism in cats - vomit intermittently over long periods
What considerations are taken into account before GI surgery
- Gastric vomiting will lead hypochloraemia, dehydration and possible Hypokalaemiae (insufficient food intake).
- suspected low intestinal obstruction will cause a loss of pancreatic Na+ and HCO-3 (metabolic acidosis) and possible malabsorption
- Chronic vomiting, diarrhoea and weight loss will cause dehydration, hypoaluminaemia and malabsorption/maldigestion
- Haematemesis (vomiting blood) and melaena (blood in poo) will cause anemia (regenrative unless BM is exhausted then it becomes non-regenerative)
Therefore to rectify these Intravenous fluids should be given (possibly i/v Potassium due to hypokalaemia from lack of food). Also if Haematemesis and melaena is present a blood transfusion may be needed if haematocrit is low (along with Fe supplementation)
What is the potential risk for infection with GI surgery and what steps can be taken to minimize these
Up to 5x as many bacteria per ml in LI in comparison to SI, with 79% anaerobes in comparison to 50%.
Prophylactic antibiotics can be given:
-Stomach & SI surgery can give a single broad spec antibiotic with anaerobe coverage ( 2nd gen cephalosporins)
-LI surgery are given 2nd gen cephalosporin and specific anaerobe targeting antibiotic (metronidazole)
Can also isolate GI entry with wet swabs, Lavage the wound and abdomen, change gloves and separate instruments for contaminated part of the surgery
Describe the ability of the GI tract to heal, what measures can be taken to allow optimum heal
The stomach heals rapidly due to abundant blood supply
SI regains 75-80% of tensile strength by 14d where as LI regains 50% tensile in 14d
Stay sutures can be used to manipulate the tissues to avoid any excess pressure. Also atraumatic (debakey) forceps can be used.
PDS II is appropriate suture as its monofilament and absorbable, Continuous or simple interupted suture is appropriate.
Chemotherapy should be delayed 3 weeks prior and any steroid use should be discontinued. any hypoproteineamia should be corrected where possible
What incision is made for an exploratory laparotomy and how would you biopsy the SI, liver and stomach
If no discrete lesions are spotted on exploration biopsy should be taken.
Large incision from the xiphisternum to the pubis ( through the preputial muscle in male dogs). Then follow down the linea alba.
Stomach - Incision between the greater and lesser curvature of the stomach, biopsy can be taken from here. Don’t cauterize any vessels. Repair in 2 layers, simple continuous through submuscosa and mucosa & inverting lambert through serosa and muscularis.
SI - Milk contents and close with atraumatic clamps, incise on the anti mesenteric border. simple interrupted sutures 3-5mm apart. release clamp and check for leak.
Liver - punch biopsy can be done on the liver but a coagulant must be used to fill space.
*careful not to ligate cranial/caudal pancreatico-duodenal artery
What reasons would you have to perform an gastrotomy
Common for gastric foreign bodies which present as abdominal pain, lethargy, vomiting and gastric distention. Post surgery important to feed and give antacids (decrease aciditiy)
If neoplasia is preset must consider: is there metastasis and is resection achievable ( must preserve cardia, bile & pancreatic ducts). Complete resection of leiomyoma (fibroid, benign fibrous smooth muscle neoplasia) prognosis is good, unlike adenocarcinomas which reoccur in weeks.
How would you assess viability of intestines
Pulsations of arterial vessels
Coloration
Wall thickness
Presence of peristaltic movements
What problem may a intestinal neoplasia cause
May cause a partial obstruction, so gasmay not always be present on radiographs. Clinical signs include intermittent vomiting, weight loss and diarrhoea
What is Intussusception, what are the clinical signs and what steps should be taken
Intussusception is when one portion of the GI tract invaginates into another.
Clinical signs: dehydration, depression, abdominal pain and possible palpable tubular structure in abdomen.
Has a 6-27% reoccurence rate 3d-3w post op. Usually give fenbendazole to treat any underlying worming issues
What is the major associated complication associated with GI surgery
Incision dehiscence - break down of the surgical site leading to the contents of the bowl leaking into the body cavity = Septic peritonitis. Bacteria cause vasodilation (hypovalaemia) and increasede capillary permeability. This increases the amount of proteins in cavity, decreasing the vascular oncotic pressure resulting in hypovalaemic shock and DIC. Associated with a 50% mortality rate.
Clinical signs include vomiting, pyrexia, depression, abdominal pain/enlargement, haematemesis and melaena.
To diagnose a blood spear with oil is taken. Intracellular rods can be seen inside hypersegmented neutrophils
Treatment includes stabilizing with fluids, correcting abdominal leak, lavage of abdominal cavity and intensive care
What is FIP, what causes it and what are the two types
Feline infectious peritonitis is cause by mutated feline coronavirus. Has two froms:
- Wet form - Widespread pinhead granulomas and fibrin deposition in serosa of LI and SI
- Dry form - Larger grey granulomatous masses on all abdominal organs
What is Anisognathism in relation to horses
This is where the maxillary aracade is wider than the mandibular
What is the infundibulum
Infolding of enamel from the occlusal surface, with a central core of cement. 2 in each maxillary cheek teeth and none in the mandibular. 1 in each incisor
In an equine oral exam what are you looking for
- Incisors - is there any malocclusion?
- Interdental space - Presence of wolf teeth, canines and any injuries
- Cheek teeth - is there and buccal or lingual ulcers, is there any fractured teeth, is there step mouth (One tooth missing and opposing tooth grows into space, not allowing forward backward motion), wavemouth (high and low points of both arcades making it impossible to chew efficiently) and any signs of peridontal disease
What is infundibular caries
Decay of tooth which leads to decreased cementum in infundibulum which leads to septic pulpitits. Increase risk of fracture. affects 80% of >15years
What is peridontal disease
Diseas eof the gingivae/peridontal ligament and alveolar bone. Begins with gingivitis which leads to pocket formations and diastemas. Food in diastema ferments causing bacteria to enter the pulp cavity
What is an apical tooth infection, what are the clinical signs and how can it lead to sinusitis
Infection at the tip of the roots. Present with asymmetrical swelling and with LN swelling.
Can be due to infundibular caries or pulp exposure from where or iatrogenic (excessive rasping) in 106, 107, 207, 206.
Sinusitis is possible when its teeth 08/07 because roots open into rostral sinus and 10/11 open into caudual sinuses
What xray angle is appropriate for visualizing the quine teeth
Oblique - Reduced superimposition of the mandibular apices. Place plate on the side you wish to examine.
Lateral radiograph wold be use to visualise the paranasal sinuses. teeth apices are superimposed preventing visualisation
How is a sample taken for cytology
Fine needle (22G-24G) biopsy. No negative pressure just insert needle in several times at different angles without exciting the mass. Then use air filled syringe to gently expel onto slide.
Fine needle aspiration only if previous is unrewarding
If lesion is identified as inflammatory via cytology, what is the next classification
Whether its septic or not.
Septic - Degenerative neutrophils (swollen nucleus and lighter in colour), intracellular rod bacteria inside neutrohpil
Non-septic - No bacteria intracellularly (extracellular could be contaminates), neutrophils are normal and lack of degenerate neutrophils
Increase number of macrophages indicates a granulomatous inflammation (mycobacterium)
If under cytology the lesion is not inflammatory, whats the next classification step
Whether the neoplasm is round cell, epithelial or mesenchymal.
Round cell - Small round leuokocytes (lymphocytes, monocytes & plasma cells). common tumours include lymphoma, mast cell tumours, plasmacytoma, melanoma and histiocytomas.
Epithelial - Large cell size with cell to cell junctions, abundant cytoplasm . examples include sebaceous, mammary and liver tumours)
Mesenchymal - individual or clumped cells small to medium in size. Indistinct cell borders, matrix production (collagen/osteoid)
What criteria must be met for malignancy to be suspected in cytology
- Anisocytosis - Variation in cell size
- Variation in nuclear size - odd number of nuclei
- High nuclear to cytoplasmic ratio
- Increased mitotic figures
- Nuclear moulding - One nucleus growing around another
What are NK1 antagonist
NK1 is a receptor in the nucleus tractus solitarius. Effective against emesis induced by central and peripheral receptors. Oral dose required alot higher than sub cut. Treats motion sickness, acute gastric enteritis and cytotoxic induced vomiting. Maropitant
What is metoclopramide
Anti-emetic drug that antogonises D2 & 5HT3 receptors of the chemoreceptor trigger zone (CRTZ) also has pro-cholinegic effects. Used for disorders with central & peripheral activation of vomiting E.g Cancer chemo, gastroesophageal reflux and gastric emptying
What is associated with decrease gastric emptying
Inflammatory GI disorders Gastric ulcers/neoplasia Hypokalaemia Pyloric stenosis Diabetes melitus
What are phenothiazines
Anti-emetic drug that antagonises alpha 1, alpha 2 adrenic receptors, Dopamine 2, Histamine 1 & 2 receptors and muscarinic receptors acting on the peripheral receptors, vestibular, vomiting centre and CRTZ. Off record drug
Why are antihistamines a useful anti-emetic drug
Act on histamine receptors in the CRTZ, involved in motion sickness in dogs but not cats
Describe species differences in anti emetic drug receptors
D2 receptor agonist potent emetic agent in dog but not cat
Alpha 2 agonist is a potent emetic agent in the cat but not the dog (xylazine)
Why would you need to give anti-ulcer drugs
Used when there confirmed gastroc ulceration. Due to disease (renal/liver failure) or NSAID toxicity. used to prevent secondary oesophagitis with sever vomiting.
What are non systemic antacids used for
Anti ulcer drug. Inexpensive but has to be given orally every 4 hours (not practical) and is use symptomatically not as prevention
What are the 3 H2 receptor agonists and what are they used for
Used as an anti-ulcer drug
Ranitidine - Effective at treating gastric ulcers caused by NSAIDS and uraemia (off books)
other two are cimetidine (licenced) and damotidine
What is misoprostol and what is its major contraindication
Used to prevent and treat stomach ulcers from a variety of causes. however causes abortion !
What is omeprazole
Proton pump inhibitor thats not licenced. Used to treat and prevent gastric ulcers.
What are the common differentials for a calve/cow with diarrhoea
Calves - E.coli, Cryptosporidium, Rotavirus, Coronavirus, coccidia, salmonella
Cow - Salmonellosis, coronavirus, acidosis/SARA and mucosal disease
What is ETEC and whats its pathophysiology
Enterotoxigenic E.coli, commonly occuring in calves aged 5days-3weeks. For E.coli to be ETEC must have adhesive fimbrae and enterotoxin.
Liable toxin (LT) - attaches to the brush border of SI cells. Acts on the alpha subunit of Gs, causing intracellular increase of cAMP. This stimulates the activation of Cl- channels, causing secretion of chloride ions into the lumen, followed by Na+ and water.
What is STEC and whats its effects on people
Shiga-toxin E.coli. Shiga toxin encoded in bacteriophage and infects E.coli. Invades enterocytes and is absorbed. Causes a haemorrhagic colitis, vascular damage, oedema and can cause renal failure
Whats the infectious agent responsible for johnes disease, Whats its pathophysiology and hows it controlled
Caused by Mycobacterium avium subspecies paratuberculosis. Usually contracted in the first 4 days of life but no clinical signs until 4th/5th lactation cycle.
initially resides in the ileum. Mcells of the payers patch sample luminal contents and the mycobacterium is presented to macrophages to be phagocytosed. Mycobacterium survives inside the macrophage, multiplies and lyses the cell to infect further macrophages. Large amount of WBC’s recruited to try eradicate, causing thickening of the the intestine, leading to malabsorption, causing diarrhoea due to build up of proteins.
Control relies on preventing infection of young animals by preventing contact to adult faeces and ingestion of infected colostrum.
From appearance what differences are there between small bowel and large bowel diarrhoea
Small bowel - varied consistency, pattern, colour. any blood will be dark or look like coffee granules as its been partly digested.
Large bowel - Tends to be little and often with mucous present. Appetite usually normal. Any blood present will be fresh. Shouldn’t cause weight loss. Tenesmus (cramping rectal pain)
What are possible differentials for acute & chronic small bowel diarrhoea
Acute - Diet related ( overeating, dietary change, spoiled food or garbage), parasites (ascarids, hookworms), protozoa (giardia, coccidia) or infectious (parvovirus, rotavirus or coronavirus)
Chronic - Bacterial (compylobactor, clostridium, giardia or cryptospiridium), parasitic (toxocara or ancylostoma) or diet related ( lactose intolerance, gluten intolerance or dietary hypersensitivity)
What is ARD
antibiotic responsive diarrhoea, patient is responsive to antibiotic treatment. most likely due to dysbiosis (imbalance of bacteria)
What are the different types of Irritable bowel disease
IBD is persistent inflamation of the intestinal mucosa
Subdivided into Lymphoplasmacytic enteritits & eosinophilic enteritis
Some patients respond to antibiotics (metronidazole) and others respond to immuno suppresive drugs (prednisolone)
What are the differentials for large bowel diarrhoea
Large bowel diarrhoea almost always because of primary GI lesion.
Parasitic (trichuris vulpis), Protozoa (giardia), bacterial ( campylobacter, clostridia, salmonella & ARD), diet related ( toxicity, fibre responsive & dietary hypersensitivity) , stress & inflammatory (idiopathic ulcerative, granulomatous and neoplasia)
What diagnostic test can be used to rule out pancreatitis
Serum trypsin like immunoreactivity (TLI) - test for insufficient exocrine pancreatic enzymes
What dietary trials might you use for an animal with diarrhoea
Increased fibre
Hypoallergenic (contain foods not previously exposed to e.g venison and potatoe)
Full response can take 6-8 weeks however change can be noted withing 2 weeks
