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
List common differentials of diarrhoea in foals, older foals (10-12 months) and adults
Foals - Foal heat diarrhoea (associated with coprophagia and introducing new gut flora, self limiting), rotavirus, salmonella and clostridia
Older foals (10-12months) - Parasitic ( S.vulgaris & cyathostomines), proliferative enteropathy, salmonella, roatvirus, clostridia, nutritional
Adults - Salmonella, NSAID toxicity, carbohydrate overload, clostridiosis , parasitic
What are the two main outcomes of equine diarrhoea treatment
- Fluid therapy - Must replace any fluids lost and account for maintenance needs and ongoing losses. Also take into account any potential loss in metabolites or bicarbonate. Colloids may be useful to regain fluid into vasculature. High possibility of hypovalaemia as Inflammmation of the colon causes increased permeability and loss of albumin, decreasing oncotic pressure and causing oedema
- Adress endotoxaemia - Dead bacteria have their LPS absorbed due to damaged mucosa. causes systemic inflammation as the endotoxins interact with macrophages. Can be followed by CV and GI dysfunction, shock and organ failure.
How is endotoxaemia in horse treated and what are the clinical signs
Clinical signs - Depression, Tachycardia, colic, Fever, diarrhoea, tachypnoea, hyperaemic toxic mucous membranes and decrease white cell count & nuetrophil count.
Treatment includes:
- Preventing movement of endotoxin into circulation (biosponge)
- Neutralise endotoxin before it interacts with inflammatory cells
- Prevent synthesis and release of inflammatory mediators
- Prevent endotoxin induced cellular activation
Whats different between a endotoxaemia infection in a foal and horse
Colon is less develop so whole gram negative bacteria absorbed as apposed to just the LPS. This causes a bacteraemia.
What diagnostic aids can be used to diagnose equine diarrhoea
Faecal ELISA - viral test
Faecal culture - bacterial (salmonella or clostridia)
F.e.c - Parasites (S.vulgaris but PPP is 6months so not really useful)
What are the 4 mechanisms of diarrhoea
- Altered structure or permeability (malabsorption)
- Altered epithelial cell transport (secretory diarrhoea)
- Osmotic effects (maldigestion)
- Altered motility
Parasites such as cyathostomines will cause diarrhoea by mass re-emergence from hypobiosis whereas some bacteria may release soluble toxins causing diffuse damage to mucosa (e.g clostridium)
What is grass sickness
Damage to neurons by C.botulism causing peristalsis to stop. This causes nasogastric reflux and oesophageal ulceration.
Clinical signs include weight loss, constipation, patchy sweating and rhinitis sicca (chronic inflammation of nasal mucosa)
What conditions are amenable via nutritional change
Acute vomiting & diarrhoea Chronic diarrhoea Motility disorders IBD Fibre responsive disorders Chronic hepatic disorder (fatty live) Acute/chronic pancreatitis
What diet changes would you recommend for acute vomiting or diarrhoea
A Low fat, easily digestible diet ( boiled rice and chicken). Diet should only be temporary as it lacks calcium. Meals should be small and frequent.
Why should onions and baby food not be fed to small animals
Onions cause oxidative stress on the RBC’s causing anaemia. Baby food is high in sodium and phosphorus and low in calcium.
What is the difference between soluble and insoluble fibre
Soluble - Attracts water and other nutrients creating a gel like structure, this slows down transit time, decreases nutrient absorption and makes stool softer. Also increases fecal bulk by increasing bacterial load. Also bacteria ferment this soluble fibre producing short chain fatty acids.
Insoluble - Not readily digested therefore speeding up transit time. This causes a decrease in the amount of nutrients absorbed. increases fecal bulk by increasing water.
What are the effects of short chain fatty acids
Decrease inflammation Increase GI hormones Increase sodium and water absorption Increase blood flow Decrease transit time and nutrient absorption
How is pancreatitis managed
With a low protein & fibre diet. Vomiting is managed by enteral feeding. Analgesia’s used to maintain abdominal pain
When evaluating a horse with suspected colic, what are the immediate needs that need to be assessed
Heart rate. Good indicator of the severity of the colic. A heart rate of >80bpm associated with 35-55% mortality and >90bpm associated with 83% mortality.
Signs of pain from least painful to most include:
Recumbancy, pawing, trying to go down, rolling & abrasions.
What history is essential when dealing with colic in horse and what are some good questions to narrow down differentials
SHED-C Signalment (age/sex/breed) History Environment Diet Complain
Important questions would be:
Time of onset of clinical signs
Degree of colic shown (recumbency vs rolling)
Any previous bouts of colic
Any previous treatment
Any changes in management (change in routine/diet)
worming regime
When was faeces last paced (should be 4 times a day)
During physical exam of suspected colic what are you specifically looking for
General demeanor, signs of pain
Temperature (take rectal temp before rectal exam), and respiratory rate
CV status (mucous membranes, pulse quality and skin turgor)
Gut sounds (ileocecal emptying every 1-2 mins in the upper right quadrant of abdomen.
Any abdominal distention
During a rectal exam of a horse, what structures should you be able to palpate and what would be abnormal
20-40% of abdomen can be palpated. Diagnoses often not reached. Work in an anti clockwise fashion.
Firstly the aorta is palpated on the dorsal wall.
Then the caudal pole of the left kidney can be palpated, located just cranial is the spleen.
Retracting your hand slightly and moving ventrally should feel the pelvic flexure of the dorsal/ventral colon which will feel like a mushy mass. On the right side of the abdomen the base of caecum can be felt, the medial teniae are an important landmark.
Abnormal:
Pelvic flexure impaction will feel like dough as aposed to a mushy mass.
Distended SI will feel like bicycle tyres
Nephrosplenic entrapment - The colon will travelling dorsally to the left (follow the ventral tenae). Trapped between the kidney and spleem, hanging over the nephrosplenic ligament
What is a nasogastric tube used for and when should it be used
Should be used routinely when suspected colic because >2L of nasogastric reflux is an indicator of SI obstruction which is a surgical emergency. Tube passed down nasal cavity into the ventral meatus, once into the orophasrynx should cause swallowing reflux, allowing the tube to pass only down the oesophagus.
What use is abdominal ultrasound and abdominocentesis for diagnosing the reason for colic
Abdominal ultrasound allows you to visualise distended stomach, distended duodenum, distended SI, strangulated intestines and visualize the nephrosplenic space
Abdominocentesis is a sterile procedure where peritoneal fluid is withdrawn. Indicator of bowel health, with normal fluid a clear straw colour. Will also have a high protein and Cell count if abnormal. Also high lactate indicates anaerobic metabolism (dead gut, immediate surgery)
What are the possible reasons for distention in the equine abdomen
- Gas - Non strangulating lesion (impaction of displacement)
- Fluid - Stangulating (volvulus, torsion or incarceration)
- Ingesta - Motility dysfuntion (ileus, enteritis, grass sickness)
- Inflammation - Non strangulating lesion ( enteritis, colitis, typhlitis & peritonitis)
- Ischaemia - strangulating (thrombotic, volvulus, torsion, incarceration, parasitic [S.vulgaris], coagulopathy & DIC)
What non strangulating lesions could be responsible for colic in horses
Spasmodic colic - Brief episode of pain that resolves with little or no treatment
Impaction - Impacted feed in the LI. resolves with fluid therapy
Displacement - LI shifts in abdomen without compromising blood supply. Can resolve spontaneously or with surgery
Enteritis/ileus - Inflammation of SI causes hypomotility. increase in nasogastric reflux
Typhlitis - Inflammation of the colon/caecum. Variable amount of diarrhoea –> requires intensive treatment as risk of endotoxaemia is high
Peritonitis - Clinical signs include mild colic, depression, fever. Intensive treatment required
Why is dealing with strangulating lesions critical and what are the different types
Timing is crucial. Within 1hour the intestines will still be viable just distended. However within 3/4 hours compromised intestine with leakage of blood/protein. Withing 6/8 hours likely to be endotoxaemia and ishaemia.
Small intestine - Volvulus, strangulating lipoma, epiploic foramen entrapment, intussusception or diaphragmatic hernia
Large intestine - Colon torsion or intussusception (can be caeco-colic, ileo-caecal or caeco-caecal
What are some key differences between colic caused by SI and LI lesions
SI - Lesion will often cause reflux into the stomach. Also any distention can be felt on rectal (bike tyres)
LI - Can be accompanied by distention of the abdomen. No reflux generally and displacement of LI can be felt on rectal
What are the possible complications associated with post colic surgery
Short term (2-4 weeks) - Anesthetic risk (just under 1% of horse dont make it), Post opertaive colic or ileus (causing reflux), thrombosis, peritonitis, laminitis or incision complications (dehiscence)
Long term - Recurrent colic of incisional hernia
What is the prognosis for the different types of colic
Simple medical colic - Good (90%)
Non strangulating surgery - Good (70-90%)
Stangulating SI - without resection good (60-80%) and with resection guarded (50-70%)
Stangulating LI - Without resection poor (36-83%) and with guarded (50-70%0
What history is important when presented with SA abdominal pain
Vomiting (vs regurgitation) Anorexia (appetite) Diet Urination and defication Non specific - Lethargy and general behaviour Toxic, medcation or foreign body Vaccination and worming history Any recent surgery Acute vs chronis
When presented with SA abdominal pain what are the initial Differentials (vitamin-d)
Vascular - thrombosis & haemorrhage Infection or inflammation - can be immune mediated Toxin/trauma Anomalous Metabolic Iatrogenic/idiopathic Neoplasia/nutrition Degenerative
What causes of colic are classes as surgical emergencies
Pyometra
Dystocia
Vascular emergency - Mesenteric torsion, splenic torsion or intractable haemorrhage
Metabolic emergency - Bile peritonitis or urethral obstruction
Gastric dilation volvulus
Septic peritonitis - Caused by GI, uterine, prostetic abscess or body wall rupture. Also conditions such as intestinal obstruction, intussusception or any penetration to body wall can possibly cause septic peritonitis
What diagnostic plan would be used when presented with SA abdominal pain
Blood test - PCV and TS (plasma protein). Decrease in PCV indicates haemorrhage/anaemia. TS may drop before PCV as Spleen can compensate temporarily for loss of RBC’s.
Blood smear/haematology - neutrophilia/neutropenia with left shift.
Blood glucose - Hypoglycaemia - sepsis, anorexia , addisons, insulin secreting neoplasia.
Biochemistry - Urea, creatinine & USG. measure pancreatic lipase - pancreatitis. Bilirubin and ALT levels.
Right lateral radiograph to see any evidence for GVD (double bubble).
Abdominocentesis - PCV, protein count, septic exudate (looking for intracellular bacteria). Uroperitenium indicated by comparing ratio of peritoneal creatinine: blood creatinine is >2:1. Bile peritonitis if peritoneal bile > Blood bile.
How is small animal abdominal pain managed
Iv fluids - Shock & dehydration.
Antiemetics (maropitant.metoclopramide)
Gastroprotectants - omeprazole
Antibiotics if theres and infection of increased risk of infection
Nutrition
Analgesia - Pure opiods (fentanyl, morphine, methadone) or ketamin infusion, lidocaine infusion.
*Avoid NSAIDS as theres an increased risk GI ulcertaion and kidney injury. Also if going to surgery anaesthetic will reduce blood flow to GI leaving it more prone to damage.
What incision is needed when operating on the LI and what Considerations should be taken
Pelvic split - Essentially the same as ventral midline incision ( xiphoid process to pubis) but incision continuous past pubis and through the pubic synthesis. Holes are drilled either side of the pubic synthesis so that wires can be used to stabilise the joint.
If resection is required, be careful not to remove to much colon which inhibits its absorptive capabilities, also will cause watery faeces. Also try to preserve ileo-cecal junction to preserve absorptive capabilities and prevent retrograde flow of colonic bacteria into SI. Also special importance should be made to preserve the caudal mesenteric, cranial rectal ileocolic vessels. Only ligate small vasa recta vessels.
What are the possible complications associated with colonic surgery in SA
Dehiscence of wound (septic peritonitis) Tenesmus Rectal prolapse Abscess Faecal incompetence Haematochezia (blood on faeces, expected for 1week)
What is megacolon, What are the causes, diagnosis and treatment
Megacolon is a flaccid enlargement of the colon, dilated so much that the smooth muscles no longer an push faecal material. (more common in cats). Secondary megacolon can occur due to pelvic fractures, intrapelvic space occupying lesion, perianal hernia or inappropriate diet.
Diagnosis - Lateral radiograph. present with chronic constipation, tenesmus, vomiting, anorexia and weight loss.
Treatment - If secondary must treat underlying cause. Medical management involves manual evacuation, laxatives. prokinetics (ranitidine) and frequent walks. Possibly change in diet, Increased fibre, low residual diet.
What is the prognosis of Adenomatous polyps & adenocarcinomas
Adenomatous polyps - Surgical resection can cure with a mean survival time of >2 years. But 17% reoccur in 9-12 months and 25% have malignancy transformation within 9-17 months
Adenocarcinomas are difficult to completely excice due to location. associated with a mean survival time of 22 months.
How would you treat SA rectal prolapse
Lubricate and push back in. Place purse string suture around syringe. If any of rectum is necrotic, then u must resect, but resect and suture as you go as the rectum can go back into cavity.
After would give anthelmintics, faecal softener, low residue diet and sedatives.
How would you treat abnormal perianal glands
Normal secretion should be brown, abnormal will be thick white, yellow or green.
Sedate animal and express the anal sac, one finger adjacent to gland and other in rectum. Collect sample for culture/cytology. Antibiotics can be given if theres evidence of systemic infection or abscess.
Sacculotomy may be required. Probe inside and cut along sac. Can see the smooth lining of the sac. Careful not to cut caudal rectal nerves which control anal sphincter ( if one is cut the other side will re innervate therefore important not to cut both).
*tumours of the anal sac are highly metastatic.
What is anal furunculosis
Immune mediated destruction of skin around anus
What are the 3 zones of the hepatic lobule
- Periportal (centroacinar) - Outer portion
- Midzonal
- Centrilobular (periacinar) - Least oxygenated & most susceptible to injury
What are vacuolar hepatopathies and what is lipidosis
Anything with swelling/vacuolisation of hepatocytes (including water (hydrophic) fat (lipidosis) or glycogen ( glycogenosis).
Lipidosis - Occurs during obesity or starvation. Generally when theres an increased demand for energy (pregnancy/starvation or lactation). Can also occur as a result of disease such as diabetes mellitus or ketosis)
What is ‘nutmeliver’ and what causes it
Nutmeg is liver is a congestive hepatopathy caused by venous congestion. Usually caused by RHS heart failure.
What is cholangitis
Inflammation of the bile duct (can be associated with infection or immune mediated)
What viral infections affect the liver, What bacteria affect the liver and what are their routes of infection
Viral - Canine Adenovirus -1 causes a canine infectious hepatitis. Feline herpesvirus -1 causes a feline infectious peritonitis.
Bacteria - Routes of infection include: Direct extension from adjacent tissues, haematogenous (portal vein, hepatic artery or umbilical vein) & abscessation.
Infectious agents include leptospirosis, clostridium novyi type B, salmonella and listeria.
What is Infectious necrotic hepatitis caused by
In sheep is caused by clostridium novyi type B, a soil born bacteria. Bacteria multiplies in areas of hepatic necrosis (caused by liver fluke) and release necrotizing toxin. Pale necrotic foci of necrosis along the migration route of liver flukes,
In dogs, caused by canine adenovirus -1. A viraemia is established & trophism to hepatic parenchyma and vascular endothelium.
Whats the difference between acute and chronic toxic liver disease
Acute intoxication - (e.g trauma or iatrogenic) cause haemorrhage –> increased consumption and decreased synthesis of clotting factors by damaged liver –> jaundice
Chronic intoxication - Continual low dose intoxication (e.g from copper or ragwart
What are the clinical signs of pancreatic hypoplasia
Clinical signs manifest at 1 year. Animal will present with a pot belly (due to fatty ingesta), polyphagia and loss of condition.
What clinical signs of acute pancreatitis, how do you diagnose and treat
anorexia, vomiting, abdominal pain, lethargy, depression and nausea. Diarrhoea is also common with possible fresh blood or melaena due to proximity to the duodenum and colon. Patient can also present in shock, jaundiced or acute renal failure. Cranial abdominal mass can also be palpated.
In cats no significance in amylase and lipase values, would conduct a serum feline pancreatic lipase immunoreactivity test (fPLI). in dogs conduct a Serum canine pancreatic lipase immunoreactivity (cPLI)
Treated by withdrawing food for 1-2 days, place of fluid therapy, analgesic and low fat diet.
What is the clinical signs and cause of chronic pancreatitis
Clinical signs chronic abdominal pain, anorexia and intermittent vomiting and diarrhoea. Cause by multiple bouts of acute pancreatitis, leading to fibrosis and exocrine pancreatic insufficiency. Fluid therapy, analgesics and low fat diet would be recommended.
What neoplasia of the pancreas is most common
Carcinoma, highly invasive, infiltrative with metastases to liver, spleen, adrenals and LN.
What are the possible causes of acute hepatopathies in dogs and cats
Dogs - Infectious (Bacterial, viral and helminth), toxic/drug induced (fungi, mycotoxin, potentiated sulphonamides, neoplasia and genetic (bedlingtons with copped storage disease)
Cats - Inflammatory (neutrophilic cholangitis), neoplasti, hepatic lipidosis, Infectious (FIP) and drug induced (diazepam and phenobarbitone)
What are the possible causes of chronic hepatopathies in dogs and cats
Dog - Inflammatory (eosinophilic & granulomatous hepatitis, idiopathic), cirrohosis, neoplastic, drug related (glucocorticoid or developmental (portosystemic shunt or copper storage disease)
Cat - Inflammatory (lymphocytic cholangitis (treated with corticosteroid), neutrophilic cholangitis ( treated with antibiotics), amyloidosis, neoplasia, Infectious (FIP, toxoplasmosis), congenital (portosystemic shunt) & triaditis (inflammation of the liver, pancreas and SI. only occurs in cats because pancreatic duct in cat enters the common bile duct before entering duodenum).
What is the principle of hepatic treatment
- Fluid therapy - Replace any lost fluids and manage electrolyte and acid balance. Supporting the animal until the liver regenerates. has massive regenerative capability.
- Antibiotic/viral - Eliminate infectious agent
- corticosteroid - For any inflammatory conditions, however lowers immune system
What is the normal physiology of haemoglobin break down
broken down by macrophage to iron (which is recycled) & protoporphyrin. Bilirubin is made (unconjugated), and is transported in the blood bound to albumin. Liver cant excrete because its not water soluble, therefore carries on in circulation until conjugated by liver.
Describe reasons for pre-hepatic, hepatic & post-hepatic jaundice
Pre-hepatic: Always due to Anaemia. Can be immune mediated haemolytic aneamia. Can also be due to microangiopathic (splenic torsion or haemangiosarcoma), babesia or ingestion of onion or garlic.
Hepatic: Dogs - Chronic inflammatory hepatitis, neoplasia, toxic, infectious
Cats - Cholangiohepatitis (acute/chronic neutrophilic/lymphocytic), FIP or hepatic lipidosis
Post-hepatic: Toxic cholangitis, pancreatic disease (pancreatitis, or carcinoma/abscess), bile duct rupture or an infiltrating space occupying lesion
Apart from anaemia or liver pathology, what can cause increased bilirubin in SA
Fever
Starvation
sepsis
Inflammation
Why is +2 bilirubinuria ok in dogs but not cats
Renal enzymes in dogs can conjugate to a limited extent. Unlike cats who have a 9x higher threshold.
What is hepatic encephalopathy, what are the clinical signs and treatment options
Neurological dysfunction due to hepatic disease. Usually due to congenital/acquired systemic shunts.The Aromatic AA’s:BCAA ratio is altered in favour of AAA’s.
Clinical signs: Aimless walking, wall seeking, head pressing, intermitten diarrhoea/vomitting (can be antibiotic responsive), poor growth, polydypsia/uria & in cats can have increased aggression, seizures and copper colored iris. Breed prevalence increased in irish wolfhounds & maltese.
Treatment includes medium protein diet, lactulose, avoid red meat and antibiotics to reduce gut flora ( decreases bacterial protein metabolism and ammonia absorption. Hypertonic fluid could be administered to reduce any cerebral oedema
What are the possible reasons for haemolysis in horses
In foals could be neonatal isoerythrolysis. Also could be due to infection (infectious anaemia), toxins (onions), autoimmune haemolytic anaemia and drugs (penicillin)
Why can not eating for 24 hours cause jaundice in horses
Due to a shortage in ligandin. Ligandin responsible for uptake of unconjugated bilirubin in the liver. Has a very short half life and therefore starvation of 24 hours could cause a shortage of ligandin, and therefor a decrease in conjugated bilirubin causing jaundice. Most common cause of jaundice in horses
What is photosensitization in horses
When theres liver dysfunction a product of bacteria that is normally conjugated in liver is not. Phylloerythrin a photodynamic agent reacts with UV light and causes burning of the skin
Whats a good indicator of liver damage in horses
Bile acids
What is ragwort posining and whats the prognosis
Ingestion of ragwort cumulatively over 4-12 weeks will cause it to be metabolised to pyrole derivates by the liver. This is an anti-mitotic substance, not allowing cells to divide and causing megalocyte production. When these cells die they cause fibrosis.
Prognosis is poor and would expect death within 10 days of clinical signs
What is hyperlipaemia and what breeds have a pre disposition. Also how would you treat
Shetland ponies and minature horses are predisposed to insulin resistance. usually triggered when animal goes into a negative energy balance (e.g during pregnancy, lactation, disease or stress)
Negative energy balance causes the activation of hormone sensitive lipase –> addipose tissue is converted into Fatty acids which are hen converted into triglycerides in the liver. Later converted to very low density lipoproteins –> causes hepatic lipidosis.
Treatment: Reverse negative energy balance (early weaning/abortion), Inhibit furthur fat mobilisation (insulin), Suppportive therapy & increase TG uptake by peripheral tissue (cheparin, increases lipoprotein lipase)
Prognosis is poor
What is the Dentistry COHAT (comprehensive oral health assessment and treatment)
- History (Age, breed - malocclusions, Diet - wet or dry, chew toys, routine oral health visitor or oral health complaint? - animals rarely stop eating due to dental disease)
- Oral exam
- Pre anaesthetic screening
- General anaesthetic
- Radiographs
- Charting & oral exam
- Oral procedure (Scale & polish, Antiseptic treatments)
- Treatment as required (Extractions)
What are the possible complications with a tooth extraction
Pain Soft tissue damage Root retention Wound breakdown Nerve damage Iatrogenic damage - Jaw fracture or ocular damage
Why do the majority of dental cases (95%) not require antibiotics?
Because Peridontal disease bacteria are located in the calculus (tartar) meaning that they impervious to chemical attack. Also during endodontic disease, once the pulp necrosis has occurred, theres no blood supply
what are the advantages of dental charts
- systematic and comprehensive
- Good record that can be updated every oral health check and can be compared to previous
- Legally important
- excellent marketing tool
What are dental probe and sharp explorer used for
Dental probe - Good for assessing how well the gingivae is attached, how deep the pockets arount the tooth are & whether the peridontal ligaments are intact
Sharp explorer - only used on the crown of teeth, useful for probing fractures
What dental problems can be assessed by radiograph
Tooth resorption
Missing teeth that are impacted
Pulp necrosis
Pathology associated with worn/chipped or fractured teeth
What are the two recommended blocks and which two are not
Caudal maxillary block - Place needle behind the 2nd maxillary molar on either side - Blocks all maxillary dental tissues on the side your blocking (affecting the maxillary branch of the trigeminal nerve)
Caudal mandibular block - Block inferior alveolar branch of the maxillary branch of the trigeminal nerve. all dental tissues on the mandibular side ur blocking. needle inserted on the underside of the mandible at the
Do not perform Infra-orbital nerve block. Needle inserted into the infra orbital foramen. infraorbital vein, artery & branches of maxillary trigeminal nerve exit here. Also a risk in brachycephalic breed of inserting needle directly into eye as the foramen is extremely short.
What is peridontal disease, what causes the development of it and what are the key indications
Disease of the supporting structures of the tooth (alveolar bone, peridontal ligaments and gingiva). Peridontal disease is not a normal consequence of ageing and can be avoided by goof oral hygiene
Plaque is essentialy bacteria in their biofilm and their waste products. Plaque then builds up and becomes mineralised forming calculus (acts a retentative surface for further plaque). Plaque builds up in the sub-gingiva causing gingivitis. Progresses causing loss of attachment of the tooth from the gingiva –> peridontal disease.
Key indications are: Plaque/calculus, gingival recession, mobile teeth, gingivitis and halitosis (bad breath)
What is endodontic disease, how is it caused and what are the consequences
Disease of the pulp that occurs due to:
> Tooth fracture
> Tooth wear - chronic - from chewing on objects (When wear of tooth exceeds the rate of tertiary dentine being layed down)or from malocclussions
> Tooth trauma
Uncomplicated tooth fractures that don’t expose the pulp can still cause endodontic disease because theres only a small amount of dentine present, therefore bacterial invasion still possible. Bacterial invasion of the pulp will result in either: Pulpitis, pulp necrosis or alveolar bone invasion.
Trauma to the tooth can result in haemorrhage, which presents as a pink/grey tooth. possible indicator of pulpitis
What 4 indicators would make you suspect pulp necrosis.
- Pulp exposure
- Tooth discoloration - 92% of discolored teeth have irreversible pulpitis –> pulp necrosis
- Pulp chamber and root canal width ( wider canal = no cells laying down tertiary dentine –> pulp necrosis)
- Periapical lucency = Bacterial invasion of the root canal causing inflammation
What disease of the tooth could cause a acute facial cellulitis
A peri-apical periodontitis caused by pulp necorsis (most likely from tooth fracture)
describe dental resorptive disease, the different types and how you would treat
Progressive disease where crown/root destroyed, can’t be stopped.
Classification:
> Type 1 - Focal loss of dental hard tissue, peridontal ligament & root canal present
> Type 2 - Diffuse loss of dental hard tissue, loss of peridontal ligament and loss of root canal
> Type 3 - Mixture of type 1 & 2 (E.g one root is resorbed and the other isn’t)
Treatment - Feline crown amputation with end stage 2 only! (where the peridontal ligament and root canal can’t be visualised). Traditional extraction for type 1 & early type 2.
Why should missing teeth always be radiographed?
Root remnants from previous surgery (must be removed)
Root remnants left from teeth lost from disease
Congenitally missing
Unerupted teeth ( risk of cyst formation)
What is stomatitis & how is it managed
A condition of widespread oral inflammation of the soft tissues. Feline chronic gingivo-stomatitis is a immune mediated disease that’s thought to have some viral component (calicivirus & herpes).
Treatment includes oral hygiene procedure and home care for life (chlorahexidine mouth wast twice daily). Surgical extraction of any badly effected teeth
What are the classifications of malocclusions
Class 1 - Normal rostral-caudual relationship between maxillary and mandibular arches with malposition of one or more teeth
Class 2 - Mandibular arch occludes caudal to normal position (overbite)
Class 3 - Mandibular arch occludes rostral to normal position (underbite)
What are the two types of tooth extraction
Closed - Breakdown of peridontal ligament and then extract tooth. Ideal for single root teeth and made easier by severe peridontal disease. However risk of snapping root alot higher and slower healing, also alot slower and difficult with complicated extractions
Open - Create muco-periosteal flap. Alveolar bone then removed to expose roots. tooth is then extracted and the alveolar socket is lavaged. Then a tension free closure of peri-osteal flap.
Advantages of surgical include faster healing, can lavage the alveolar socket, and complicated extractions are made easier. however if not executed properly risk of flap breakdown and can be more time consuming.
Follow up appointments should be 3-5 days post op and then 2 week after. Dry food diet would be recommended as its less abrasive
