Digestion 6 Flashcards
(107 cards)
1
Q
List 9 derivatives of the fore-gut
A
- Part of the mouth
- Pharynx
- Oesophagus
- Stomach
- Liver and pancreas
- Major portion of the small intestine
- Thyroid, parathyroid
- And thymus glands
- Trachea and lungs
2
Q
derivatives of the hind-gut
A
Terminal end of the small intestine and the large intestine and cloaca
Anal canal/urogenital sinus
3
Q
2 structures involved with the development of the mouth and what each form
A
1) The Stomodaeum is a midline depression on the ventral surface of the head that is created by the cranial and lateral body folding.
○ enlarges into a definitive oro-nasal cavity. - the mouth and nose
2) The Oral Plate (or pharyngeal membrane) is formed by the fusion of the ectoderm of the stomodaeum and the endoderm of the fore-gut.
○ The oral plate subsequently breaks down and the cranial opening of the digestive tube is established.
4
Q
branchial arches what derived from what does 1st branch, 2-3 branch and 4-6 branch create
A
1st branchial arch divides into the
left and right maxillary processes and mandibular
processes which elongate to form the jaws and mouth - oral cavity
2-3 hyoid bones
4-6 pharynx
5
Q
mesenchymal process what called what includes and what forms
A
fronto-nasal prominences - and they will give rise to the future frontal area of the embryo and the nose.
○ This includes the Frontal process (will give rise to the frontal bones-the forehead) and the left and right naso-lateral and naso-medial processes (will give rise to the nose).
6
Q
what forms the upper jaw, nose, lower jaw
A
The upper jaw - is formed by the naso-medial processes together with the maxillary processes
The nose - is formed by the frontal process together with the naso-lateral processes
The lower jaw - is formed by the fusion of the mandibular process in the midline
7
Q
facial cleft, cleft lip and cleft palate failure of what fusion
A
Facial cleft (lamb)
–Maxillary and lateral nasal processes fail to fuse
Cleft Lip
–Maxillary and medial nasal processes fail to fuse
–May occur in association with cleft palate
cleft palate
- failure of the palatine processes to fuse
8
Q
the palate derives from what three parts and how occurs
A
1) Left palatine process
2) Right palatine process
3) Median palatine process (= inter-maxillary process)
- These three processes fuse together to separate the oral and nasal cavities.
- This hard palate extends caudally as the soft palate that separates the rostral pharynx into the nasopharynx (dorsal) and oropharynx (ventral)
9
Q
tongue formation what 4 mesenchymal swellings and what occurs
A
- Median tongue swelling;
2 and 3. Two distal tongue swellings; - Proximal tongue swellings
1) The median and distal tongue swellings will form the body of the tongue,
2) the proximal tongue swelling will form the root of the tongue.
10
Q
formation of the oesophagus what forms it, what forms epithelial lining, connective tissue and muscle layer
A
- The fore-gut narrows to form the oesophagus
- The epithelial lining of the oesophagus and any associated mucosal glands develop from the endoderm of the primitive fore-gut.
- connective tissue and muscle layer of the oesophagus are derived from accumulating mesenchymal cells partially derived from the splanchnic mesoderm of the primitive gut.
11
Q
formation of the stomach
A
- A dorsal mesentery (the dorsal mesogastrium - greater omentum) develops on the dorsal surface and the ventral mesentery (the ventral mesogastrium - lesser omentum) develops on the ventral surface.
- The developing stomach moves caudally and shifts away from the midline.
○ Thus the stomach rotates towards the left pulling with it the dorsal mesentery and leading to the formation of the greater omentum.
12
Q
4 steps in the formation of the small and large intestines
A
1) Initially the gut grows faster than the body so a hairpin-shaped loop is formed. The remnant of the yolk sac (the yolk-stalk) is at the tip of the loop.
2) Rapid development of the liver forces the loop of gut into the umbilical stalk - this is physiological herniation.
3) Later the intestines return to the abdomen and move into their final position.
4) Further changes involve rotation of the loop and extensive coiling of the cranial arm of the loop to form the duodenum, jejunum and most of the ileum.
13
Q
formation of the anal opening from cloaca and proctadeum
A
- The caudal portion of the primitive gut expands to form the blind cavity of the cloaca.
- The invagination of ectoderm beneath the tail forms the proctadeum.
○ This boundary between the endoderm and the ectoderm forms the cloacal membrane.
○ This degenerates to form the anal opening.
14
Q
Body cavities what are they created from and what creates each of the 3 cavities
A
three membrane-bound cavities know as coeloms initially continuous with each other but later seperated
1) The pericardial coelom
- contains the developing heart
2) The Left and Right pleural canals
- contains the developing lungs
3) The peritoneal coelom
- contains the developing abdominal viscera
15
Q
development of the diaphragm
A
septum transversum
○ Forms part of the diaphragm
○ Other part formed by pleuro-peritoneal folds and pleuro-peritoneal canals that join to form the diaphragm
16
Q
what are the normal drainage routes for the peritoneal fluid
A
1) most peritoneal fluid drains via small stomata (pores) into diaphragmatic lymphatics that form a large plexus in the muscular part of the right ventral diaphragm - pleural plexus on the opposite side of the diaphragm - right lymphatic duct to the thoracic duct - eventual return to the right side of the heart
2) a small proportion of peritoneal fluid drains through the omentum and abdominal viscera via lymphatics and lymph nodes to the thoracic duct
17
Q
What are the 4 normal functions of the mesothelial cells
A
1) line the peritoneal cavity (and the pleural cavity and pericardial sac) - create shiny protective layer
2) produce a polysaccharide that acts as a low viscosity lubricant
3) produce plasminogen activator that results in the lysis of fibrin
4) activated mesothelial cells are capable of phagocytosis
18
Q
How do mesothelial cells respond to mild irritation
A
1) hypertrophy (an increase in size)
2) hyperplasia (an increase in number due to mitotic division)
3) metaplasia (altered differentiation) from a squamous to a cuboidal or columnar cell
19
Q
What is the typical sequence of events following injury to the peritoneal surface and what is the repair not influenced by
A
1) debris removed by phagocytosis (macrophage and mesothelial cells)
2) wound heal via granulation tissue and reconstitution of the mesothelial layer (mitotic division) - repair not influenced by the size of the defect
3) if surface fibrin persists more than 3-4 days post-injury, granulation tissue bridges between the apposed viscera and between the viscera and the cavity wall - fibrous adhesion formation - permanent (dysfunction possible)
20
Q
List 3 decompositional changes that are commonly observed in the peritoneal cavity of dead animals
A
1) diffusion of haemoglobin from lysing red blood cells
2) diffusion of bilirubin from the gall bladder, bile ducts and/or duodenum
3) gas bubbles may develop subserosally over the viscera and in the adjacent mesenteries and ligaments
21
Q
Define internal hernia and external hernia
A
Internal Herniation
= displacement of viscera (especially intestines) through a normal or abnormal hole (foramen) within the peritoneal cavity without formation of a hernial sac
= displacement of viscera with the presence of a hernial ring through a natural opening in the abdominal wall (e.g. the vaginal ring at the inguinal canal) or an abnormal opening
22
Q
what are the components of external hernia and list 5 examples
A
1) hernial sac (formed as a pouch of parietal peritoneum +/- a covering of skin and soft tissues)
2) a hernial ring (the opening in the abdominal wall)
3) hernial contents (usually part of the omentum, a segment of intestine +/- other viscera)
examples
1) ventral hernia of the abdominal wall
2) umbilical hernia
3) inguinal hernia
4) perineal hernia
5) diaphragmatic hernia
23
Q
List 3 common examples of internal herniation
A
1) herniation through natural foramina - incarcerations of the epiploic foramen
2) omental and mesenteric hernias - passage of intestine through tear in greater or lesser omentum
3) pelvic hernia - mainly after castration
24
Q
what is the difference between a direct and indirect inguinal hernia
A
- indirect inguinal hernia (in which viscera herniate into the inguinal canal of the groin between the internal inguinal ring and the external vaginal ring
- direct (or false) inguinal hernia in which herniated viscera pass subcutaneously, outside the inguinal canal
25
what is the most common type of diaphragmatic hernia in domestic animals and usual cause
Acquired Peritoneopericardial diaphragmatic hernia usually caused by external abdominal trauma
26
List 5 potential consequences of abdominal trauma
1) introduction of bacteria from exterior or perforation of the gastrointestinal tract - septic peritonitis
2) Peritoneopericardial diaphragmatic hernia
3) ± leakage of bile or urine into the peritoneal cavity
4) +/- uterine rupture in pregnant animals
5) potential fatal haemorrhage into the peritoneal cavity
27
How would you distinguish an ante mortem from a post mortem perforation of the gastrointestinal tract?
post mortem rupture of viscera - ingesta tends to be localised close to the rupture site, without haemorrhage at the margins of the tear and without evidence of peritonitis
28
What is a common parasite that encysts in the peritoneal cavity of sheep?
cysticercus - the intermediate (metacestode) stage of taeniid tapeworms
- appears as a fluid-filled, thin-walled cyst into which the head and neck of a solitary tapeworm larva is invaginated
29
list 4 possible causes of haemoperitoneum
1) trauma especially to the liver, spleen or kidneys
2) spontaneous rupture of enlarged spleen or liver
3) rodenticide anticoagulant poisoning and other coagulopathies
4) rupture of any friable intra-abdominal or retroperitoneal neoplasm
30
list 2 main mechanisms by which ascites may develop and the examples within
1) reduced removal of peritoneal fluid - due to obstruction of lymphatic drainage
2) over production of peritoneal fluid
1. increased permeability of blood vessels within peritoneal cavity
2. hypoalbuminaemia (
31
what can trigger chemical peritonitis in animals
1) chemical peritonitis - antibiotics, pancreatic necrosis (pancreatic digestive enxymes)
2) bacterial
3) viral - feline infectious peritonitis
32
what are the various routes bacteria may enter the peritoneal cavity and what is the most common route
1) perforation of the gastrointestinal tract (the most common cause in domestic animals)
2) penetrating wounds of the abdominal wall from external enironment
3) rupture of infected segments of the extra-hepatic biliary tree, uterus or urinary bladder
4) seepage through devitalised gastrointestinal or uterine segments prior to rupture
6) haematogenously
7) as an extension from an infected intra-peritoneal organ
8) as an extension from an infected umbilicus in neonatal animals.
33
How does infection with feline infectious peritonitis virus lead to fluid accumulation in the peritoneal cavity of cats
- viral antigen-antibody complexes - phagocytosis by macrophages - deposition in walls of blood vessels - fixation of complement + chemotaxis of neutrophils - vasculitis - increased vascular permeability - peritoneal +/- pleural effusion, with a typically high protein concentration
34
List 4 potential consequences of peritonitis
1) paralytic ileus (paralysis of gastrointestinal motility) - limits mobility of peritoneal exudate but increase fibrinous exudate may lead to permanent fibrous adhesions
2) gas accumulates and fluids and electrolytes
3) absorption of bacterial endotoxins into circulation - toxaemia
4) infectious agents may also spread from the peritoneal cavity via lymphatics - pleuritis or bacteraemia/septicaemia
35
What are the various patterns of fat necrosis that may involve intra-peritoneal and retroperitoneal fat stores in domestic animals and causes
1) enzymatic fat necrosis - release of proteolytic and lipolytic enzymes due to pancreatic necrosis
2) focal or multifocal - unknown triggered by local hypoxia of fate
3) yellow fat disease - caused by diets rich in polyunsaturated fats and low in vitamin E (anti-oxidant)
4) massive fat necrosis in cattle - incidental finding but can be fatal, pathogenesis uncertain
36
What species are peritoneal lipomas common and what are the potential consequences
horses and dogs
| - may cause acute intestinal strangulation
37
What species are mesotheliomas most often diagnosed, what gross features might suggest a mesothelioma? What is the typical behaviour of this neoplasm?
- most often diagnosed in cattle and dogs
- typically appear as multiple, firm nodules or as villous projections from a thickened serosa; can grossly mimic peritoneal carcinomatosis
- virtually all are malignant but tend to implant rather than metastasise
- generally cause ascites
38
define peritoneal carcinomatosis
- carcinomas (malignant epithelial tumours) more often implant on serosal membranes than do sarcomas (malignant mesenchymal tumours)
39
define retroperitoneum and how does retroperitonitis does it manifest in a dog
retroperitoneum = the loose fibrofatty connective tissue immediately external to the peritoneal cavity
- may arise from penetrating wounds, migrating grass awns or other foreign bodies or from sepsis involving the abdominal or pelvic viscera or the mesenteric root
40
which neoplasms commonly involve the retroperitoneum
primary neoplasms - e.g. lipoma, fibrosarcoma, lymphoma, osteosarcoma, renal carcinoma, adrenal tumours
metastatic neoplasms - e.g. carcinomas arising in the urinary bladder, prostate, colon/rectum, anal glands or perianal glands may metastatise to the retroperitoneal sublumbar lymph nodes
41
3 causes of diarrhoea
1) Inflammation (enteritis) due to viruses/parasites/bacteria
2) Inflammatory bowel disease (IBD)
3) Neoplasia
42
3 mechanisms of diarrhoea
1) increases permeability (exudation) result in oedema
2) hypersecretion - net efflux of fluid and electrolytes independent of permeability changes
3) malabsorption - results from villous atrophy no matter the cause
43
bacterial enteritis list 4
1) Salmonella spp. (salmonellosis)- all species, horses+++
2) Clostridium spp.(clostridiosis)-herbivores
3) E. coli (colibacillosis)- all species
4) Mycobacterium paratuberculosis (Johne’s disease)- ruminants
44
salmonellosis what species especially seen in and phases
- Species-specific, present in all species especially horses
1) Acute - causes fibrino-necrotic inflammation
2) Chronic - necro-ulcerative inflammation
3) Septicaemic - when bacteria get into circulation, proliferate and produce toxins
45
clostridiosis what animals most effected, what causes
- Herbivores are more affects - horses
| - Necrosis and haemorrhage - very similar to salmonella
46
Johne's disease what caused by, what animals, what results in
Mycobacterium
- Granulomatous (macrophage rich inflammatory infiltrate)
- Disease of ruminants
- No mucosal damage just inflammatory damage in lamina propria from macrophages which compromises absorptive capacity
47
E.Coli how cause diarrhoea in what animals of what age what results in
- Common cause of diarrhoea in neonates (2 days - 3 weeks)
- Adhere to enterocytes and produce various enterotoxins
○ Enterotoxins trigger electrolytes to be secreted into intestinal lumen and water follows osmotically
- Microscopically intestinal mucosa is normal as not damage by the toxins
48
List 4 viral causes of enteritis, where they effect the villi and what animal cause diarrhoea in
1) Rotavirus: tips and side of villi - each species has own
2) Coronavirus : tips of villi - neonatal calves
3) Parvovirus: crypts - cats and dogs less an a year - usually fatal
4) BVDV: crypts and villi - cattle of all ages
49
name a protozoa that causes diarrhoea, what generally effects and how does it cause diarrhoea
Gardia lamblia
- Infect everything important in puppies and kittens - zoonosis
- Damamges the microvillus border of the villous tips in small intestine leading to malabsorption
50
list parasite that causes diarrhoea, what species most effected and how cause
small strongyles
- Particularly horses and ponies with acute syndrome of sudden weight loss, severe diarrhoea
- Parasite live under mucosa in nodules the of large intestine
- Disease associated with mass emergence from nodules causing leakage of mucosal barrier
51
Name a idiopathic cause of diarrhoea, what species common in and what result
Inflammatory bowel disease
- In dogs and cats
- Cause unknown but there is presence of many lymphocytes and plasma cells suggesting immunologic problem
- Malabsorption and chronic protein-losing enteropathy result from infiltrate in lamina propria
52
what neoplasia can cause diarrhoea, what commonly effect and how cause
Lymphoma
dogs and cats
infiltrate lamina propria and invade submucosa - ulceration may occur
53
Role of mucus and the two layers
not only for lubrication but also creates a surface mucus barrier
1) Inner layer: sterile & difficult to dislodge thickest in stomach - glycocalyx
2) Outer layer: non sterile & can be removed. thickest in regions with greatest bacterial count
54
What are 3 molecules that are components of the mucus barrier and what cells secreted by
1) Secreted mucins ( gel forming glycoproteins - form binding sites for bacteria) - goblet and paneth cells
2) Non-specific antimicrobials ( from Paneth cells)
3) Immunoglobulins
55
what are the other type of mucins present
cell surface mucins.
- These are trans-membrane
○ Cytoplasmic domains involved in cell signalling
○ Extracellular domains long filamentous glycoproteins (sometimes longer than the microvilli)
- Can be shed from the cell surface in response to bacterial contact
56
List 4 steps in the response to enteric pathogens at the cell surface
1) Secretion of stored mucus from goblet cells
2) Engagement of pathogen with cell surface mucin stimulates intracellular signalling through the cytoplasmic domain - may lead to apoptosis of that cell - shedding of cell with attached bacterium
3) If pathogen binds to mucin, the extracellular domain of the mucin is shed, releasing the pathogen from the cell surface
4) Bacteria that do not bind may be excluded by steric hindrance - electrostatic charge of bacterium
57
3 strategies pathogen use to subvert the mucus barrier and how does this
1) Penetration of mucus layer:
- By enzymatic degradation
- By motility (flagella) - more purposeful
2) Avoidance of mucus layer
- entering through cells not protected by mucus
- M cells within peyers patches
3) Alteration to host cell
- Toxins that damage tight junctions
Toxins that suppress mucus production
58
what increases and decreases the amount of mucin secreted by the goblet cells
1) The luminal environment (microbial population, bile salts)
2) Neural factors (eg cholinergic stimuli)
3) Endocrine factors ( vasoactive intestinal peptide VIP, prostaglandins, nitric oxide)
4) Immune factors (cytokines)
59
Describe the 2 components of the mucosal immune system and what called
MALT mucosa associated lympoid tissue)
1) The role of Peyer’s patches in the SI
- M cells on epithelium overlying Peyer’s patches present commensal microbial antigens to underlying immune cells - M cells surveillance cells, communication
- This results in secretion of immunoglobulin into the gut
Peyer’s patches- organised collection of lymphoid tissue directly under epithelium- more common in small intestine - ileum and ileocaecal junction
2) Lymphoid aggregates
Predominantly B cells
60
Life span of the gastrointestinal cells in the stomach, small intestines and large intestines
```
Stomach-
- Surface Mucous cells 3-4 days
- Parietal cells 100 days
Small Intestinal epithelial cell
- 3-4 days
Large intestinal epithelial cell
- 5-7 days
```
61
Parvovirus what does it cause, what and what does it lead
* a “radiomimetic” virus - mimic radiation damage - kills rapidly dividing cells
* Leads to destruction of dividing cells in crypts of small intestine
* Loss of villi--> loss of absorptive surface
* Erosion of mucosa--> exposure of lamina propria and haemorrhage
* Also effects lymphocytes so effects lymph nodes and bone marrow - also rapidly dividing
62
List 3 factors that alter gastrointestinal blood flow and their actions
1) Redirection of blood from gut when blood volume/pressure falls
2) Local factors-
- Prostaglandins cause vasodilation so increase mucosal blood flow - very important and are constantly being produced
3) Drugs
- eg NSAID’s (aspirin, PBZ) reduce prostaglandin levels
63
Drug absorption across the mucosal barrier
- drugs can penetrate the layer but absorption depends on drug crossing lipid membranes
- many drugs are weak acid or bases and therefore pH can alter the charge and the ability to cross the membrane - unionised better
- why some drugs taken before or after food
64
List the 7 fluids that enter the gastrointestinal tract
1) Water
2) Saliva
3) Oesophageal secretions
4) Gastric secretions
○ Acid
○ Mucous
5) Pancreatic secretions
6) Bile
7) Intestinal secretions
65
Saliva what increases production in herbivores and what is the composition of the saliva for ruminants and horses
- the more roughage consumed the more saliva is produced - hay absorbs lots of water so needs more to lubricate ensuring movement
ruminant - rich in bicarbonate and sodium
horse - less bicarbonate but rick in sodium and chloride
66
List the electrolyte imbalances seen in cattle, horses and simple monogastric animals when saliva doesn't reach GIT
Cattle
- lose bicarbonate and sodium
- increase acidic (decreased pH and acidaemia)
- Hyponatraemic (low blood sodium)
- Hyperchloraemic (high blood chloride) - as need bicarb to buffer
- Quickly dehydrated due to loss of fluid within rumen
Horses
- Hypochloraemic (low blood chloride)
- Hyponataemic (low blood sodium)
- Blood becomes alkaline (increase blood pH) however may have initial acidosis due to hypovlaemia and increase in lactate
Simple monogastric
- Much lower concentration of electrolytes
- Volumes produced per bodyweight is smaller so consequences aren't as high magnitude
67
How much saliva does cattle, horses, pigs and dogs produce each day
* Cattle: 100-150 L/day
* Horse: 10-15 L/day
* Pig: 1-2 L/day
* Dog: 2-3 L/day
68
oesophageal secretions what composed of and function
Mainly mucous that assist with passage of food into stomach or rumen
69
gastric secretions what are the 3 phases it is secreted into the stomach, what are the two things it varies with (horses and ruminants)
1) cephalic phase
2) gastric phase
3) intestinal phase
1) vary with diet - carnivores larger amount of digestive enzymes - pepsin
2) varies between species
horses - squamous and glandular part of stomach no mucus from squamous so more susceptible to ulcers
ruminants - forestomach no secretion just absorption, abomasum has secretions
70
pancreatic secretion how secreted what rich in and what species has most continuous secretions
- Secreted in 3 phases as for gastric secretions
○ Horse - most profuse and continuous pancreatic secretions
- Rich in sodium and bicarbonate so is alkaline
○ Works to buffer acidic gastric contents as pass into duodenum
71
Bile secretion what high in what is released stimulated by and species variation in secretion times and volume (pig and horse)
- high in sodium, chloride and bicarbonate
1) Food in duodenum
2) Positive feedback from bile acids returning to liver via portal circulation
- high flow rates however gall bladder allows concentration of bile
- horses and rat without gall bladder continuous secretion
- volume relative across species
pig - 2-3 L/day
Horse - 5L/day
72
small intestine what role in secretion and absorption where this occurs and what essential for
- both secretion and absorption of fluid and electrolytes
- Generally crypt cells have secretory roles and villus cells have absorptive roles
- As crypt cells move up their change from secretory to absorptive
- Essential for preserving water and electrolyte balance
73
movement of nutrients and water into the blood and what occurs with obstruction within gastrointestinal tract
- via transcellular or paracellular absorption into lateral spaces then into vascular system
○ Nutrients enter capillaries by diffusion from lateral spaces and water follows
obstruction - absorption stops and water is secreted into gut lumen resulting in high PCV (total protein), high TS (total solids) and high lactate
74
large intestines overall functions, what occurs in dogs and horses, what are the 3 motility patterns and what results in obstruction
- Absorption and secretion - net fluid absorption
Dogs - water and electrolyte absorption
Horses - water and electrolyte as well as volatile fatty acids absorption
1) Mixing/segmentation
2) Reverse peristalsis/antiperistalsis
3) Peristalsis
obstruction - low electrolyte values in the blood and dehydration - Increased PCV, decreased TS and increased lactate
○ Often cause blood to become more acidic
75
List and describe 7 assessments of the gastrointestinal tract
1) examination of the mouth - dental disease, mucosal lesions
2) ausculation - stethoscope listening to gastrointestinal sounds
3) palpation - externally or through the rectum
4) imaging - X-ray, ultrasound, MRI, CT, endoscopy
5) peritoneal fluid analysis - WBC (infection) + protein (ischaemia)
6) passage or an orogastric/nasogastric tube - horse determine fluid accumulation in stomach prevent rupture
7) cardiovascular parameters - heart rate, temperatures, capillary refill time
76
List the 3 things laboratory evaluation of the GI tract can provide
1) can provide a diagnosis in some cases
2) narrow the list of differentials
3) direct further investigations
77
inflammatory leukogram characterised by
- Marked mature neutrophilia
- Mild monocytosis - monocytes turn into macrophages within the tissues
- Moderate lymphopenia
○ can be involved with acute inflammation most commonly involved with stress
- Super common see all the time due to stressed animals
78
what is a relative increase in RBC most common with
1) secondary fluid loss - dehydration
| 2) pain - adrenalin
79
evaluating Na and Cl and how to confirm if selective Cl abnormalities present
- Chloride is found in a 1:1 ratio with sodium
- Selective loss or gain of chloride in excess of sodium (ie a disproportionate change)
- indicates an acid base disturbance - metabolic alkalosis secondary to vomiting
- to confirm calculate corrected Cl
Cl(cor)= Cl (measured) x (normal Na ÷ measured Na)
normal Na is midpoint of Na reference interval
- if correct Cl not in reference interval then there is selective loss
80
Hypoproteinaemia what characterised by in haematology and biochemistry and what is cause
- Low total solids in blood
- low albumin and total protein in biochemistry
probably gastrointestinal loss
81
hyperkalaemia what likely associated with and what cause
metabolic acidosis - as losing bicarbonate so losing buffering
○ Secondary to hypovolaemia, anaerobic metabolism
○ Bicarbonate is also lost with diarrhoea
82
What are the 3 causes of decrease in cholesterol and how to exclude or confirm them
1. protein enteropathy - losing GIT - look at albumin, total solids and total protien
2. Liver function - makes cholesterol - look at urea and glucose
3. Inflammation - look at electrolyte imbalances and WBC counts
83
what is a degenerative left shirt and what does it suggest
○ bands outweigh mature neutrophils (degenerative left shift - poor prognosis overwhelming inflammatory demand - usually infectious)
84
what biochemistry expect with haemorrhage, liver failure, protein losing nephropathy
•Haemorrhage;
- expect panhypoproteinaemia plus low PCV
•Liver failure;
- expect hypoalb, hypochol, hypoglyc, low urea
•Protein losing nephropathy;
- expect hypoalb, hyperchol plus proteinuria
85
what is in normal peritoneal fluid and what is a fluid wave
- normal peritoneal fluid is not palpable, normally clear and colourless with low volume, has high cell count 10^9 and low numbers of macrophages, lymphocytes, neutrophils, also low protein content
86
What test used to confirm exocrine pancreatic insufficiency, what species used on and are there false negatives
- Serum TLI - only for dogs and cats
○ Trypsin-like Immunoreactivity test
○ EPI is confirmed by subnormal fasting sTLI
§
87
List 2 tests for intestinal function, where absorbed and therefore what possible reasons for decrease amounts
1) Folate (Vit B9)
- Absorbed: proximal SI
- Decreased folate:
○ Prox SI disease (jejnum)
2) Cobalamin (Vit B12)
- Absorbed: distal SI
- Decrease cobalamin:
○ SIBO (↑ binding/use) EPI (low pH plus lack IF), Distal SI disease (ileal)
88
List 6 results from proximal to mid small intestinal obstruction
1) vomiting or regurgitation or reflux - exacerbates fluid and electrolyte losses and can lead to oesophageal ulceration and/or aspiration pneumonia
2) Dehydration or hypovolaemic shock
3) hypochloraemia
4) hypokalaemia
5) metabolic alkalosis - due to loss of hydrochloric acid in vomitus
6) increase in pressure results in ischaemic necrosis and possible intestinal rupture leading to septic peritonitis
89
Distal small and large intestinal obstruction development of symptoms and how compare to small intestinal obstruction
more gradual development of proximal GI distension, with a more chronic clinical course
- fluid, electrolyte and acid-base disturbances are less severe than in proximal to mid small intestinal obstructions -
- vomiting/reflux/regurgitation may not occur or is less severe and luminal fluid proximal to the obstruction may be absorbed gradually over time
90
what may occur in horses with Distal small and large intestinal obstruction
horses - complete obstruction of large bowel - tympany of the caecum and colon due to gas production from bacterial fermentation - rupture
91
what is the most common segmental anomaly and what do these result in
- astresia coli
- may cause stenosis (incomplete occlusion of the lumen) or atresia (complete luminal occlusion)
- progressive abdominal distension due to accumulation of meconium and faeces proximal to the obstruction
92
congenital colonic agangliosis what is it, cause and what animals seen in
absence of ganglia of the myenteric plexus of the distal ileum, caecum and colon - absence of peristaltic contractions - segmental stenosis - colic and death within 48 hours of birth
- autosomal recessive trait in white foals born to parents with multiple spots (“frame overo” pattern of coat colour)
93
List 2 examples of extrinsic obstruction
1) tumours or abscesses
| 2) left dorsal displacement of large colon in horse
94
rectal prolapse what animals common in, what are possible causes and what results in
pigs, sheep and cattle
exposed to oestrogenic mycotoxin from fungi or consumption of oestrogenic pastures
1) the prolapsed distal rectal segment becomes congested and oedematous
2) the mucosa may undergo venous infarction and ulceration
3) the necrotic segment may eventually slough - rectal stricture
95
bezoars and enteroliths what types where most often found, what enteroliths made of and cause
- phytobezoars - most often found in the colon of horses, often as incidental findings
- trichobezoars - occasionally found in the intestines of dogs and cats, often as incidental findings
- enteroliths - rare except in horses
- usually composed of struvite
- usually incidental but can impact at pelvic flexure
- associated with diets rich in magnesium and phosphate
96
what most common parasites found in small intestines for pigs and sheep
pigs, foals - roundworms
| sheep - tapeworms
97
what are the 3 types of foreign bodies and what does each cause
1) sharp foreign bodies - perforation and septic peritonitis
2) blunt foreign body - become impacted and cause local pressure necrosis or at a nidus for enterolith formation
3) linear foreign body - perforation if one end gets fixed and other end moves down - becomes tighter and can cut through segments of intestine
98
small intestine what occurs with what time frame after hypoxia (4 things) same with large intestine (2 things)
1) 5-10mins - sloughing of enterocytes from the tips of the villi to the crypts
2) 30-60mins - necrosis of serosal mesothelium
3) 2-4 hours crypt epithelial necrosis
4) 6 hours - smooth muscle necrosis (may lead to ileus)
colon
1) 1 hours - sloughing surface enterocytes
2) 2-4 hours - necrosis of crypt epithelium
99
What occurs in colon with short term hypoxia (3-4 hours) and more protacted hypoxia
1) short term hypoxia
- survival of at least cells at the base of the crypts - mitotic division - re-epithelialisation of the mucosal surface within 1-3 days
2) more protracted hypoxia
- full thickness mucosal necrosis with ulceration - repair by granulation tissue and re-epithelialisation from surviving epithelial cells at the margins of the infarct - loss of functional absorptive area and risk of stricture
100
What are the 4 things that lead to venous infarction in intestines what is involved and give example
1) intestinal strangulation - pedunculated lipomas in horses
2) intestinal torsion - rotation of intestine across long axis - occurs generally with sudden dietary change to high concentrate ration in horses and ruminants
3) intestinal volvulus - rotation of intestine on its mesenteric axis, horses predisposed due to lack of mesenteric anchorage in large colon
4) intestinal intussusception - telescoping of one segment of intestine into the lumen of a more distal segment, most common in young animals (dogs, lambs, calves, foals)
101
what is the mechanism for intestinal intrussusception
- tension on and compression of mesenteric veins - congestion and oedematous swelling of the telescoped segment (the intussusceptum) - fibrin and neutrophilic exudation - adhesion (rendering it surgically irreducible) - ultimately venous infarction - possible sloughing
102
arterial infarction why less common than venous, what species most common and what caused by
intestines have a parallel arterial blood supply
- most often seen in horses as a consequence of arterial thromboembolism from thrombi in the root of the cranial mesenteric artery caused by Strongylus vulgaris larvae
103
List 4 other causes of intestinal hypoxia and ischaemic necrosis
1) sudden occulsion of portal vien
2) portal hypertension
3) shock
4) NSAIDs - phenylbutazone
104
Intestinal stenosis what are the two main causes and give example
1) reparative fibrosis
- pig survive ulceration from salmonella may develop rectal stricture
2) intestinal smooth muscle hypertrophy - can be caused by physical or function obstruction such as ileus
105
List neoplasms from intestinal tract, cause and most common in what species
1) intestinal adenocarcinoma - malginant tumour of intestinal epithelial, lead to stenosis and metastasise to lymphatics - common sheep with brackenfern poisoning
2) lymphoma - most common in cats - there are T cell and B cell lymphomas dog mostly T cell, horses mostly B cell
3) plasma cell tumour - malignant or benign uncommon but older dogs
4) mast cell tumour - malignant uncommon but sometimes cats and dogs
106
Paralytic (Adynamic) Ileus what is it, causes, what mediated by and clinical sings
lack of normal smooth muscle tone and peristaltic movements of the intestines and/or stomach
causes - abdominal surgery, peritonitis, severe gastrointestinal pain, toxaemia, tetanus
- mediated by sympathetic nerve reflexes
clinical signs: abdominal distension, anorexia, absence of bowel sounds and vomiting
107
List 4 other causes of functional obstruction
1) acquired injury to intestinal autonomic ganglia or nerves
2) equine dysautonomia (grass sickness) - high mortality rate
3) feline dysautonomia
4) canine dysautonomia
