Haemolymphatic and Alimentary Pathology Flashcards
(161 cards)
0
Q
What does the bone marrow normally look like at post mortem?
A
In normal adult animals, the marrow is low cellularity and dominated by fat with a thin rim of active marrow peripherally.
1
Q
What is Haematopoiesis?
A
Haematopoiesis concerns the development of erythrocytes, thrombocytes, granulocytes (neutrophils, eosinophils and basophils), monocytes and lymphocytes. All these cell lines complete some or all of their development in the bone marrow. When there is demand for haematopoeisis, extramedullary haematopoiesis can occur in other organs (spleen and liver).
2
Q
What is hyperplasia of bone marrow?
A
In Functional hyperplasia there is an increased cellularity of the marrow because of increased production by the haematopoetic cells. Fatty white marrow is converted to cellular red areas beginning in the endosteal zone. Hyperplasia may be in response to a fall in the number of peripheral cells or to an increased demand in inflammatory conditions.
3
Q
What is the name for the bone marrow itself becoming inflamed?
A
Myelitis
4
Q
What is involution of bone marrow?
A
Involution may be due to many causes such as plant and chemical poisons, radiation, bacterial toxins, ageing and viral diseases, causing hypoplasia or aplasia in one or more cell lines. Marrow fat is relatively resistant to lipolysis but in severe starvation it becomes watery, translucent and pink.
5
Q
What is Anaemia and how does it occur?
A
Anaemia can result from either an increased rate of destruction or loss of RBCs, or alternatively from a decreased rate of production (non -regenerative). The signs of anaemia are referable to reduced oxygen supply to the tissues. May be Haemorrhagic, haemolytic.
6
Q
What are the major pathological features of Anaemia?
A
Pallor: Due to reduction in haemoglobin
Pulmonary oedema: Depends on the severity of the anaemia
Cardiac changes: If anaemia is chronic, myocardium is flabby, friable and pale.
Liver changes - periacinar hepatic necrosis if acute anaemia.
Spleen - Varies according to cause and course of disease e.g acute haemorrhagic (contracted); acute haemolytic (enlarged and meaty).
Muscle - In chronic anaemia, muscles pale in proportion to loss of myohaemoglobin.
7
Q
Describe nodular hyperplasia of the spleen
A
Very common in old dogs - producing demarcated encapsulated swellings. The spleen will have a nodular enlargement and firm consistency. The tissue comprises hyperplastic foci of lymphoid cells or mixed lymphoid cells with areas of EMH.
8
Q
Describe Primary haemangioma and haemangiosarcoma
A
Common neoplasms of older dogs (especially large breeds). They are frequently large with areas of haemorrhage and necrosis and may rupture spontaneously or due to palpation causing life threatening intra abdominal haemorrhage. Metastases to lungs and wider are frequent with haemangiosarcoma.
9
Q
When is contraction of the spleen seen?
A
Can be marked in association with catecholamine release, shock (e.g hypovolaemia, cardiogenic).
10
Q
Describe splenic Rupture?
A
Quite common in the dog (RTA). It may be fatal or additional splenic fragments may form in the surrounding tissues. Congenital accessory splenic fragments may also be found in the omentum.
11
Q
What are siderofibrotic plaques? (gamna-gandy bodies)
A
Common lesions in older dogs - yellow, dry encrustations on the capsule - probably sites of previous local haemorrhage with subsequent deposits of Fe, Ca and fibrosis.
12
Q
What is Haemosiderosis?
A
RBC breakdown - formation of haemosiderin and some haemosiderin will therefore normally be found in spleen. Excessive amounts can occur e.g in haemolytic anaemia, chronic heart failure.
13
Q
Describe Infarcts of the Spleen
A
These tend to occur in the more peripheral zones of the spleen where perfusion is poorer or in diseases which cause vasculitis.
14
Q
What is the definition of lymphadenopathy?
A
A regional or generalised lymph node enlargement of unknown/unspecified cause.
15
Q
What is lymph node hyperplasia?
A
Hyperplasia of B and or T cell compartments secondary to immunological reactions/infections.
16
Q
What is lymphadenitis?
A
It can result when an infectious agent is present in the lymph node - e.g equine strangles. May be accompanied by lymphangitis.
17
Q
What is anthracosis of the lymph nodes?
A
Seen as black discolouration of the medulla of the bronchial nodes of dogs in industrial areas.
18
Q
Why is melanin pigment sometimes seen in lymph nodes?
A
It can be seen in association with pigmentary incontinence - pigment is taken by macrophages to draining lymph nodes.
19
Q
When would degeneration of the thymus occur?
A
Lymphocytolysis can occur in association with a number of viral diseases e.g canine distemper virus, equine herpes virus 1. The thymus is composed of both lymphoid and epithelial tissue, thymic involution is part of the normal ageing process.
20
Q
Describe common Neoplasms of the thymus
A
Thymic lymphosarcoma - cats, young cattle and dogs. Signs relate to the space occupying effect of the tumour.
Thymoma - less common, generally slow growing and rarely metastasise. They may be predominantly lymphocytic, predominantly epithelial or mixed.
21
Q
Where is stratified squamous epithelium found in the alimentary tract?
A
Lines the mouth, oesophagus, the non-glandular part of the stomach in the pig and horse, the fore-stomachs of ruminants and the anus. This is keratinised in ruminants, the horse and the pig.
22
Q
Which epithelium lines the stomach/abomasum through to large intestine?
A
Simple columnar glandular epithelium. This consists of a single layer of cells overlying the lamina propria. in the stomach the glandular epithelium is composed of simple tubular glands with five cell types; Stem cells at the neck, mucous neck cells, parietal cells, chief cells and neuroendocrine cells.
23
Q
What lines the large intestine?
A
The large intestine, caecum and colon is lined by a thick layer of glandular mucous epithelium containing many mucus secreting goblet cells. No villi are present in the large intestine. The large intestine absorbs more water and secretes fewer enzymes than the small intestine.
24
Describe the secretions of the alimentary tract and their functions.
Saliva - flushing effect and antibacterial components, e.g lysozyme, secretory IgA. Mucus - inhibits contact with mucosa, protects surface. Acid - parietal cells in stomach. Digestive enzymes - salivary amylase, pepsin from gastric chief cells, pancreatic and small intestinal enzymes. Bile secretions - kill some pathogens.
25
Describe the Epithelial defence mechanisms of the alimentary tract?
forms mucosal barrier; tight junctions between epithelial cells prevent entry of macromolecules and pathogens but allow ions and water to diffuse through. Stratified squamous epithelium: multilayered, relatively high cell turnover, may have a keratinised surface layer at some sites.
26
What is the function of the commensal flora of the alimentary tract?
Act as barrier to pathogens - they secrete volatile fatty acids and compete with pathogens for nutrients. They are essential for digestion in herbivores. Any disequilibrium of microflora can lead to disease.
27
What are the cell mediated and humoral defences in the alimentary tract?
Lamina propria contains macrophages, B and T lymphocytes, plasma cells, mast cells. Epithelium - intraepithelial lymphocytes. Lymphoid aggregates - peyer's patches, gut associated lymphoid tissue. Antibody production (IgA), regional lymph nodes, omental macrophages.
28
hat is a diphtheritic membrane?
Composed of fibrin and necrotic material; secondary bacterial invasion.
29
What is erosion?
Loss of superficial Mucosa
30
What is an ulcer?
Loss of deep mucosa.
31
Describe Erosion and ulcer in mucosa lined by stratified squamous epithelium.
Erosion - Loss of partial thickness of epithelium. Ulcer - full thickness epithelial defect in which there is loss of the entire epithelium down to or deeper than the basement membrane.
32
Describe erosion and ulcer in mucosa lined by simple glandular epithelium.
Erosion: loss of epithelium and partial thickness loss of lamina propria. Ulcer: full thickness mucosal defect in which there is loss of epithelium and the entire lamina propria, sometimes extending into the submucosa.
33
What are vesicles?
Vesicle formation is a common response to systemic viral infections that target stratified squamous epithelial cells. It is also seen at mucocutaneous junctions in autoimmune diseases and as a response to thermal injuries. Hydropic degeneration occurs in cells, which swell and undergo necrosis, leaving a fluid filled space (vesicle).
34
What is brachygnathia?
Short maxilla/mandible
35
What is prognathia?
Abnormal prolongation of maxilla/mandible
36
Describe cleft palate/palatoschisis
Inadequate growth of palatine shelves leaves a central defect. Communication of nasal and oral cavities may result in aspiration pneumonia and problems with suckling. Affects hard and/or soft palate.
37
What is a hare lip/cheiloschisis?
Absence of part of lip rostral to nasal septum.
38
What is Stomatitis?
Inflammation of the membranes of the oral cavity
39
What is glossitis?
Inflammation of the tongue.
40
What is wooden tongue?
Granulomatous inflammation caused by actinobacillosis - actinobacillus lignieresii, a chronic lesion of bacterial origin.
41
What is lumpy jaw?
A chronic lesion of fungal origin - caused by actinomycosis - actinomyces bovis in cattle. The mandible becomes enlarged due to chronic osteomyelitis.
42
Describe Calf diphtheria
Caused by Fusobacterium necrophorum, necrosis predominates with coagulative necrosis and surrounding granulation tissue affecting the gingival and oral mucosa.
43
Describe some examples of disease which cause oral ulceration?
Feline calicivirus and feline herpesvirus infections. Mucosal disease caused by bovine viral diarrhoea virus in which ulceration of the oral cavity, muzzle and more distal alimentary tract occur. Immune mediated diseases - autoantibodies directed against epithelial cell surface antigens e.g pemphigus vulgaris.
44
Describe an example of a disease with papular lesions.
Proliferative papular lesions e.g contagious pustular dermatitis (orf) in sheep and oats, with firm raised papules and pustules on lips and oral mucosa. There is hydropic degeneration, mixed inflammatory cell infiltration and secondary bacterial invasion.
45
Describe two common examples of Epithelial Neoplasia's In the oral cavity.
Papillomas - are benign epithelial tumours with raised, sometimes cauliflower like lesions on the lips and oral mucosa. There is a thick squamous epithelium over a branching Pedunculated fibrous stroma. Squamous cell carcinomas - are malignant epithelial tumours common in cats, often on the ventrolateral tongue. They are locally invasive. Composed of elevated firm white plaques.
46
What is a melanoma?
A tumour of pigment producing melanocytes. Most common oral neoplasm in dog and nearly always malignant in the oral cavity. They grow rapidly and are not always pigmented. (amelanotic melanoma). Oval or spindle shaped melanocytes with variable melanin content.
47
What are Epilus?
A group of benign neoplasms of periodontal origin affecting gingivae. Particularly in brachycephalic dog breeds. They are firm lesions on gums, surrounding teeth, especially in carnassial/canine region. Dense collagenous and sometimes ossified tissue covered with stratified squamous epithelium which descends into dermis in cords.
48
What is segmental aplasia?
Rare failure of fusion. Band of fibrous tissue where distal oesophagus should be.
49
What is Achalasia?
failure of cardiac sphincter to open.
50
What is mega-oesophagus and what are its possible causes?
Dilated oesophagus lack peristalsis, accumulates ingesta due to underlying neuromuscular disorder but lower oesophageal sphincter is usually normal. May be idiopathic - developmental disorder of vagus nerve/motor nucleus. Acquired - neurological - dysautonomias (grass sickness), myasthenia gravis. Acquired - muscular - myodegeneration (nutritional myopathy).
51
Describe potential Obstructions of the oesophagus.
Intraluminal- Foreign body e.g root veg. Most likely at cardiac sphincter, thoracic inlet. May cause inflammation, necrosis, ulceration and perforation. Bloat in ruminants. Stricture on healing.
Intramural - within the wall - inflammatory lesion, -abscess, granulation, neoplasm - narrowing.
Extrinsic - vascular ring anomaly - persistent right aortic arch constricts oesophagus and leads to megaoesophagus cranially. Also pressure from abscess, haematoma, neoplasm.
52
Describe the possible causes of inflammation of the oesophagus (oesophagitis).
Reflux oesophagitis - damage from gastric acid due to gastro oesophageal reflux or vomiting. This results in erosion of epithelium which may progress to ulcers.
Infectious agents - e.g actinobacillosis, feline calicivirus.
53
Describe possible neoplasia's of the Oesophagus.
Papillomatosis in cattle - bovine papillomavirus type 4. (transforms to squamous cell carcinoma with bracken fern toxins)
Squamous cell carcinoma - in cat especially
Leiomyoma - benign tumour of smooth muscle
54
Describe primary and secondary ruminal tympany
failure to expel fermentation gases. Primary 'frothy bloat' is due to formation of stable foam in the rumen - due to ingestion of excess high protein or high concentrate/low roughage diet. Secondary - mechanical/functional obstruction of oesophagus - accumulation of gas. Rumen distended with gas/feed. Blood is dark and clots poorly. Congestion, oedema and subcutaneous haemorrhage of head and neck tissues.
55
What is ruminal acidosis?
Caused by grain overload - excess carbohydrate - increased gram positive cocci - increased volatile fatty acid and lactic acid production - drop in pH <5 = acidosis. Gross PM findings - porridge like contents, ruminitis may develop and allow thromboemboli to travel to the liver - hepatic abscessation. may be Focal erosions/ ulcerations.
56
What is traumatic reticulitis?
Ingestion of sharp objects e.g wire/nails - can either fall to the floor of the reticulum - insignificant or contractions force foreign body into wall. Mild suppurative or granulomatous reticulitis/peritonitis. Foreign body may penetrate cranial wall - encouraged by rumen contractions - acute peritonitis, local fibrous adhesions. Progresses through diaphragm. Inflammatory process around reticulum may also lead to vagus indigestion and ruminal stasis.
57
What is ruminitis?
bacterial or mycotic ruminitis - fusobacterium necrophorum or fungi - opportunist pathogens which take advantage of acidotic lesions and other disturbances of rumen flora. Multiple dark red areas of swollen papillae. Coagulative necrosis of papillae, marked neutrophil infiltrate, sero fibrinous exudate. Thromboembolic spread to form areas of coagulative necrosis and abscesses in the liver.
58
Describe neoplasia's of the ruminant forestmachs
Papillomatosis - bovine papillomavirus type 4 - usually Pedunculated structures in the reticulum/rumen of cattle. Squamous cell carcinoma - thought to develop from Papillomas in cattle in associated with ingested carcinogens in bracken fern.
59
Describe potential causes of obstruction in the glandular stomach/abomasum.
Foreign body/functional obstruction - bones, stones, hair/wool balls, plant material, neurologic causes include dysautonomia, end stage liver disease, vagal indigestion. Pyloric stenosis - dog, foal, - congenital hypertrophy of pyloric muscle causes delayed gastric emptying and persistent vomiting/regurgitation. Acquired following healed ulcers.
60
Describe how the abomasum can become displaced
Ventral and to left of rumen (LDA) - dairy cattle
To right of rumen (less common)- Constriction of blood vessels and trauma to vagus nerve resulting in Abomasal distension with blood stained fluid and gas, congested mucosa, infarction. May rupture - peritonitis, shock, death.
61
What is gastric dilatation and volvulus? (GDV)
Occurs in large deep chested dogs and pigs. Aetiology is obscure but usually exercise post feeding/aerophagia. Stomach is distended with as, causing increased pressure on thoracic viscera and blood vessels. Stomach and spleen rotate on long axis and occlude oesophagus and venous return - congestion, oedema and necrosis of gastric mucosa. May rupture.
62
What is haemorrhagic gastritis/abomasitis?
Can be caused by clostridial diseases eg clostridium septicum in sheep - acute abomasitis with red, thickened, necrotic haemorrhagic mucosa. Coagulative necrosis of mucosa and deeper structures with fibrin, oedema, haemorrhage and sometimes emphysema.
63
What causes hypertrophic gastritis/abomasitis
Chronic hypertrophic gastritis in dogs - thought to be due to chronic retention of gastric fluid and bile reflux. Marked mucosal thickening and convolution of rugae. There is marked epithelial hyperplasia, loss of parietal/chief cells, dilatation of mucous glands and mixed inflammatory cell infiltrates in the lamina propria.
64
What is ostertagiosis?
may cause Hypertrophic gastritis - cattle/sheep - encysted larvae cause mucosal nodules. Glandular hyperplasia, loss of parietal/chief cells, chronic inflammation associated with lymphocytes, plasma cells and eosinophils.
65
Describe a Cause of Atrophic Gastritis?
Chronic atrophic gastritis in dogs - aetiology uncertain. Reduced mucosal thickness and loss of rugae, but may be difficult to appreciate grossly. mucosal thinning and loss of gastric glands, diffuse mixed inflammatory infiltrate in the lamina propria.
66
Describe the pathogenesis of ulceration
Hypersecretion of acid and/or impaired mucosal barrier - e.g glucocorticoids, prostaglandin inhibitors (nSAIDS), epithelial damage by infectious agents/trauma. Mucosal barrier is disrupted - pepsin and acid cause necrosis - erosions/ulcers. Erosion of underlying blood vessels - haemorrhage.
67
Describe the appearance of ulcers.
Ulcers appear as round, linear or irregular cavity with a rim which is hyperaemic and raised. The base may contain grey necrotic debris/fibrin. Heal by granulation and fibrosis or perforate. If at pylorus, healing may result in stenosis. Sharply demarcated defect in the epithelium with Fibrinopurulent exudate on surface and granulation tissue beneath and sometimes thrombosis of underlying blood vessels.
68
Describe some common neoplasia's of the glandular stomach.
Adenocarcinoma - malignancy of mucosal epithelium. Most common gastric neoplasm. Thickened, pale tissue, ulcerated or fungating. Locally aggressive and spreads via lymphatic vessels to lymph nodes, lung and liver. Squamous cell carcinoma - common in horses. Large cauliflower like mass, metastases and transcoelomic spread. Leiomyoma / leiomyosarcoma - smooth muscle neoplasms forming nodular masses. Lymphoma - Diffuse infiltration of neoplastic lymphocytes.
69
What is Diarrhoea?
increase in bulk (and usually fluidity) of faeces. Diarrhoea occurs if colonic absorption is impaired due to mucosal damage. Excess fluid from small intestine may also lead to diarrhoea but if the colon is normal colonic absorption of the excess water often compensates.
70
Describe secretory diarrhoea
Secretions exceed absorption - caused by deranged mechanism due to bacterial toxins eg E. coli. Toxins inhibit NaCl and water absorption by villus enterocytes and increase secretion of Cl- from crypt cells - excess fluid in small intestine.
71
Describe malabsorptive Diarrhoea
Increased osmotic pressure due to unabsorbed digesta - H20 moves into lumen.
72
Describe Diarrhoea caused by increased mucosal permeability
Interstitial fluid moves into lumen. Caused by increase in hydrostatic pressure e,g right sided congestive heart failure, increased plasma volume or decreased oncotic pressure.
73
What is Protein Losing enteropathy (PLE).
Dietary protein and protein from shed enterocytes is normally almost completely absorbed. PLE = excess loss of protein into intestinal lumen, which can lead to hypoproteinaemia - Severe inflammatory disease, increased mucosal permeability, lymphangiectasia ( loss of protein rich lymph due to obstruction of intestinal lymphatic vessels.)
74
Describe congenital segmental anomalies of the intestine
Incomplete - stenosis or complete occlusion (atresia) of lumen. Common examples are atresia ani and atresia coli.
Hernia - Usually umbilical, common in neonates of all species - often insignificant but may involve small intestine.
75
Describe potential functional obstructions of the intestine
Intestinal ileus - intestinal stasis post surgery, metabolic disease - flaccid/ distended with gas/inesta.
Grass sickness - fluid in small intestine, stomach and large intestine impacted, degenerative lesions in autonomic nerve ganglia including enteric plexuses.
76
Describe potential Physical obstructions of the intestine
Intraluminal -Food impaction - ingesta/faeces which dehydrate. May be primary or secondary to functional obstructions. Foreign bodies - e.g sand impaction, parasites, tapeworms.
Intramural - Neoplasia - lymphoma, adenocarcinoma etc may cause annular stenosis. Also scar tissue, abscesses, granulomas.
77
Describe possible extrinsic obstructions of the intestine
Adhesions - follow peritonitis, perforation, surgery - fibrinous adhesions mature to fibrous adhesions that may restrict intestinal motility.
Neoplasia - in structures adjacent to intestine eg pancreatic tumour spread to duodenum. Pedunculated lipomas in equine mesentry. Prostate enlargement compresses rectum in dog.
78
What is a Hernia?
Displacement of small intestine through a normal or pathological foramina. Mos hernias are external, i.e contents pass through a hernia ring in abdominal wall and are covered with parietal peritoneum, soft tissue and skin = hernial sac. Can be reducible (freely movable - no sequelae) or may cause incarceration - small intestinal contents trapped Obstruction of venous drainage with oedema, congestion. Adhesions between contents and sac.
79
What is a volvulus?
Twist about the long axis of the intestine.
80
What is torsion?
Twist across the long axis of the intestine e.g colon in horse.
81
What is intussusception ?
Telescoping of one segment of bowel into another. Small intestine, caecum, colon. Aetiology: foreign body, intramural abscess/tumour, heavy parasitism, previous intestinal surgery, enteritis, other motility disorders. Compression of mesenteric vessels causes obstruction of venous drainage from the intestine and venous congestion/stagnation > swelling and inflammatory exudate from serous surface > fibrinous fibrous adhesions forming between surfaces.
82
What are the effects of intestinal hypoxia?
Cause may be obstruction of efferent veins, blockage of afferent arteries or reduced blood flow through unobstructed circulation - all have similar effects on the intestine. Separation of epithelium from basement membrane, > villous destruction, > necrosis of crypt cells, > all mucosa necrotic, > sloughed.
83
What is venous congestion/stagnation?
Most common cause of intestinal hypoxia/necrosis are strangulating lesions including intestinal displacements, intussusception etc. Intense oedema, congestion, haemorrhage and eventually dark red/black discolouration of intestine.
84
What is arterial thromboembolism?
Non strangulation infarction, mainly in horses. e.g strongylus vulgaris larvae migrating in cranial mesenteric artery in horse cause arteritis with thickening of arterial wall due to fibrin and debris. A hypersensitivity reaction leads to vasoconstriction - may encourage thromboemboli and ischaemic necrosis of intestine.
85
Describe inflammation of the intestine.
May involve small or large intestine (enteritis) or more specifically the caecum (typhlitis) colon (colitis) or rectum (proctitis). Enteritis means inflammation of the intestine whereas diarrhoea means the passage of faeces with increased bulk and or fluid content. Enteritis can occur without diarrhoea.
86
Describe the process of epithelial renewal in the small intestine
Epithelial progenitor cells in the crypts continually divide and the new epithelial cells move up towards the surface. Enterocytes are usually shed after 2-8 days. Minor loss of epithelial cells > lateral migration of adjacent cells. More major loss > villus contracts and cells migrate across inter crypt surface. Dynamic equilibrium - enterocyte production in crypts = shedding from surface into lumen.
87
What is villus atrophy?
A common lesion seen in small intestinal disease - causing malabsorption of nutrients and water. Occurs when enterocyte loss > enterocyte production in crypts.
88
Describe villus atrophy with intact/hypertrophic crypt glands
Insult affects villus enterocytes leading to increased loss. Mild insult villi may fully regenerate. Severe insult leads to immature cells on villus that secret water and electrolytes into lumen. eg Rotavirus, coronavirus, coccidia, nematodes
89
Describe villus atrophy with damage to crypts
The primary insult is to crypt cells, therefore production is impaired, eventually leading to insufficient cells for villi. Enterocytes lost to lumen are replaced by increasingly immature cells -> severe malabsorbtion. If damage severe, erosions/ulcers may form which may eventually heal. Damage can be long-term. E.g parvovirus, lymphoma, some chemotherapy.
90
Describe the secretory and osmotic diarrhoea - Colibacillosis
Enterotoxigenic E. coli causes neonatal and post- weaning diarrhoea in ruminants and pigs. Bacteria adhere to enterocyte receptors and toxins stimulate loss of NaCl and water in intestinal secretions. Intestinal loops filled with gas and fluid, mucoid contents, flaccid wall, mild congestion. Bacteria on epithelial surface, mild inflammation in lamina propria.
91
Describe clostridial enterotoxaemia (haemorrhaghic enteritis)
Mainly affects SI. Clostridium perfringens type A-E, produce exotoxins which damage. distended gas filled SI with focal or diffuse congestion and haemorrhages. Coagulative necrosis of villi, oedema, and haemorrhage and influx of inflammatory cells. Lamb dysentery (type B) - haemorrhagic enteritis, necrosis, ulcers, fibrinous peritonitis, sudden death. Pulpy Kidney - type D - sudden death, subserosal haemorrhages, intestinal inflammation.
92
Describe Canine parvovirus (haemorrhagic gastroenteritis)
Virus targets crypt cells and lymphoid areas, especially in the small intestine. Intestine is congested and haemorrhagic with blood in lumen. Necrosis of crypt epithelial cells, shortened villi, many neutrophils in lamina propria. May be fibrinous exudate on surface of mucosa.
93
What is Johne's Disease?
Mycobacterium avium subspecies paratuberculosis infects mucosal macrophages and causes chronic granulomatous enteritis in ruminants. Diffuse thickening of intestinal mucosa (especially ileum.) Distended lymphatics, mesenteric lymph nodes enlarged, many large macrophages in mucosa submucosa and lymph nodes containing acid fast organisms.
94
What is feline infectious peritonitis??
The wet form causes widespread white miliary granulomas and fibrin deposition including serosa of intestine. Also high protein exudate in the peritoneal cavity. The 'dry' form- larger grey granulomatous masses causing thickening of the wall of small and large intestine. Multifocal pyogranulomas on serosa and throughout wall, with infiltration by lymphocytes, plasma cells and macrophages with fewer neutrophils.
95
Describe the Necrotising enteritis Salmonellosis
Catarrhal inflammation, yellow fibrinous exudates on mucosal surface, mucosa necrotic and sloughs (diphtheric membrane). Infiltration of lamina propria with neutrophils, macrophages, plasma cells and lymphocytes. Enlarged peyers patches with necrosis of overlying epithelium.
96
Describe Coccidiosis?
Causes a Necrotising enteritis - eimeria and isospora spp. of protozoan intracellular parasites which infect enterocytes of young animals. Mucosal hyperaemia, thickening and necrotic embrane on surface. May see pinpoint white foci of coccidial developmental forms. Acute cases have marked haemorrhage. Necrosis of epithelium and crypts, hyperaemia, mixed inflammatory cells in lamina propria. May progress to ulceration.
97
What is cyathostomosis?
Causes an ulcerative enteritis in horses - small strongyles. Laval development in nodules in the mucosa/submucosa of caecum and colon can cause diarrhoea if mass emergence. Encysted larvae appear grossly as pinhead grey to red mucosal nodules. Larvae surrounded by fibrous capsule and mixed inflammatory cells. When they emerge there is intense eosinophil, neutrophil and macrophage infiltration and oedema.
98
Describe An enteritis associated with villus atrophy
Feline parvovirus - dilated small intestine containing red/brown fluid and fibrinous exudates sen grossly. On histopathology, crypt epithelium damaged, crypts dilated. Fibrin and debris on surface. Progresses to erosion of villous epithelium and villous atrophy. Intestinal lymphoid follicles depleted.
99
What is lymphocytic/plasmacytic enteritis?
Causes inflammatory bowel disease and will result in malabsorption. Common in dog. Idiopathic but may be due to response to dietary antigens. Can develop into lymphoma.
100
What is lymphangiectasia?
The most severe protein - losing enteropathy and diarrhoea in dogs Due to lymphatic obstruction - congenital or acquired (following granulomatous infiltrate or neoplasia). Small intestine and large intestine may be affected. Dilatation of lacteals, oedema of intestinal mucosa and distention of mesenteric lymphatic vessels and lymph nodes. Accumulation of lipid laden macophages and granulomatous response around distended lymphatic vessels.
101
What is an intestinal adenocarcinoma?
Malignancy of epithelial cells from intestinal mucosa. Annular form may cause stenosis of lumen with proximal muscle hypertrophy and dilatation. Spread via lymphatic vessels to lymph nodes, lung, liver or Transcoelomic spread. Small white plaques on serosa and adjacent tissue e.g diaphragm.
102
Describe potential causes of peritonitis
Chemical e.g bile, urine, pancreatic enzymes. Bacterial e.g penetrating wound, intestinal rupture, abscess, surgery. Viral - feline infectious peritonitis. Parasitic - Strongyle migration, Fasciola hepatica.
103
What is the seqelae to peritonitis?
Hyper motility initially -> hypomotility (ileus.) Impaired cardiovasculuar function and acid base imbalance - due to sequestration of fluid and protein in exudate. Hypomotile intestine and bacterial exotoxins/endotoxins. May resolve, become chronic active or lead to adhesions.
104
Name the parasitic cysts sometimes found in the peritoneum.
```
Cysticercus tenuicollis (taenia hydatigena) in ruminants - liver, mesentry, peritoneum - large fluid filled cysts.
Cysticercus ovis (taenia ovis) - sheep, diaphragm - small, firmer.
Hydatid cysts - echinococcus granulosus - any mammal.
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105
What are Mesotheliomas?
Neoplasia - malignant. Arise from the serosa, multiple small nodules, mainly catle and dogs, can be congenital in calves.
106
How can lipomas affect the intestine?
In horses - arise from the mesentery, can become large and pedunculated and may lead to strangulation of the intestine.
107
What are the Functions of the Liver?
Metabolic processing of blood from the intestinal tract. Detoxification, degradation and biliary excretion of endogenous wastes, toxic molecules. Processing and activation of some xenobiotic agents. Synthesis of plasma proteins, including albumin, globulins etc. Storage of glycogen, fats, iron copper and vitamins, Processing of vitamin D. Removal of bacteria and spent erythrocytes. Excretion of bile containing bile salts, bilirubin, cholesterol, bicarbonate, detoxified chemical wastes.
108
What are bile acids and how are they formed?
Bile acids are formed from cholesterol in the liver. The primary bile acids are converted to bile salts and are essential for the digestion and absorption of dietary fats - they act like a detergent, breaking up large fat globules into smaller droplets to form an emulsion with a higher surface area for lipases to act on. Bile salts also contribute to the formation of micelles; these are minute fat particles which are soluble in water and can be readily absorbed.
109
How is bilirubin formed?
Bilirubin is formed by the metabolism of haem breakdown products. When effete erythrocytes are removed from the blood by macrophages, the Fe ion remains in the macrophage bound to iron binding proteins. The remainder of the haem molecule is oxidised to biliverdin and thhen reduced to bilirubin within the macrophage. The water insoluble bilirubin is then released into blood where it binds to albmin.
110
What happens too Bilirubin on reaching the liver?
Hepatocytes remove the insoluble unconjugated bilirubin and conjugate it to glucuronic acid to form water soluble conjugated bilirubin which is actively excreted into the bile caniculi. In the small intestine, bilirubin glucuronide is converted into urobilinogen, most of which is oxidised by bacteria to urobilin.
111
What are liver enzyme and function tests?
Liver enzymes are often measured in the clinic and may be increased because of necrosis, increased synthesis or decreased clearance from the plasma. They are divided into those indicating hepatocellular damage and those indicating biliary disease/cholestasis.
112
What is Alanine aminotransferase ?
ALT is almost liver -specific and a highly sensitive indicator of hepatocellular damage in dogs and cats.
113
What is Aspartate aminotransferase?
Increases in AST tend to parallel those of ALT. AST is of less value since it is a ubiquitous enzyme with particularly high concentrations in muscle.
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What is glutamine deydrogenase?
GLDH - GLDHis used in large animals as an indicator of hepatocellular damage as they have very little ALT in their hepatocytes.
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What is alkaline phosphatase?
AP is attached to the canicular membranes of hepatocytes and the membranes of billiary epithelial cells. It is increased when there is intrahepatic or posthepatic cholestasis. However, in addition to the hepatic AP isoenzyme, there are several others including bone AP and intestinal AP. It can be used in most species.
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What is gamma-glutamyl transferase? (GGT)
GGT is also a membrane bound enzyme associated with the biliary tree. AP and GGT follow a similar pattern in liver disease. GGT is mainly used in large animals and cats.
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Describe bilirubin as a liver function test?
Increased serum bilirubin occurs where there is decreased uptake from the plasma by the liver although it is not specific and may be increased due to haemolytic disease.
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Describe the use of bile acids as a liver function test
These assess liver function rather than damage or cholestasis. Increased serum bile acids occur where there is decreased uptake from the plasma by the liver.
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What is Icterus (jaundice)?
If bilirubin is formed more rapidly than excreted it accumulates in body giving mucous membranes, sclera and skin a yellow hue. Pre hepatic:excessive breakdown of erythrocytes - liver cannot excrete bilirubin fast enough. Hepatic: the liver itself is diseased and cannot excrete even the normal bilirubin load. Post hepatic: there is damage/obstruction of the gall bladder/common duct which prevents bile from being excreted into the small intestine.
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What is oedema/ascites/anasarca?
If the liver is unable to synthesise the normal plasma proteins, there will be a reduction in the plasma oncotic pressure. As a result the body is unable to retain as much fluid within the vascular tree which accumulates in the body cavities and subcutaneous spaces.
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Describe clotting disorders/haemorrhage/immune dysfunction with relation to liver problems.
If the liver is unable to produce clotting factors, fibrinolytic proteins, complement proteins, acute phase proteins etc there may be poor or inappropriate haemostasis and immune dysfunction.
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What is hepatic encephalopathy?
If the liver s unable to detoxify and remove nitrogenous compounds from the body these may build up in the bloodstream and have a significant effect on brain function.
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How can liver disease cause metabolic disease and dysfunction?
If the liver is unable to process dietary components of the portal blood, store glycogen, fat, vitamins etc, detoxify endogenous or exogenous toxins, this will have a range of physiological and clinical implications.
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What is the difference between liver damage and liver failure?
Liver damage does not imply clinically apparent disease whilst liver failure has serious clinical implications. Clinical manifestations of liver disease may be remote from the liver itself. The liver has great functional reserve capabilities and up to 70% of the parenchyma can be lost and the organ can still recover function through regeneration (hepatocyte hyperplasia).
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Describe possible incidental post mortem changes?
The liver is prone to rapid post mortem change because of its density, vascularity and proximity to warm GI tract. Typical post mortem changes include the following - change in consistency, softening and friability, gas bubble production, black discolouration due to bacterial breakdown of haemoglobin pigment, green discolouration due to bile leakage, microscopic dissociation of hepatocyte cords, pyknosis of nuclei and lysis of hepatocytes.
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Describe the normal Liver microanatomy
The hepatic lobule - a roughly hexagonal unit based on radiating sinusoids draining into a central vein with portal tracts at the corners. Portal tract contains : portal venule, hepatic arteriole, bile ductule and sometimes lymphatic vessels. Portal venules/hepatic arterioles drain along sinusoids into central vein.
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Describe hepatocellular swelling
First manifestation of cell injury and is due to their inability to maintain normal homeostasis. Energy production decreases and membrane pumps fail due to lack of ATP - therefore accumulate intracellular water. Non specific mitochondrial and other organelle swelling. When severe may develop cytoplasmic vacuoles.
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What is Fatty change of the liver?
Lipid accumulates in the cytoplasm of injured hepatocytes due to their inability to metabolise/function normally. This may follow hydropic degeneration. Hepatocytes appear pale due to fatty change.
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What is steroid induced hepatopathy?
Hepatocytes distended by feathery cytoplasmic vacuoles due to excessive glycogen accumulation in the presence of high levels of corticosteroid. Ballooning degeneration may be evident. Corticosteroid may be exogenous or endogenous.
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What is lipidosis/steatosis?
May be detectable as pale yellow friable greasy organ. Hepatocyes distended by discrete circular lipid vacuoles which displace the nucleus to the periphery of the cell. Primarily due too the massive uptake of fatty acids frmo bloodstream following excessive mobilisation of adipose tissue.
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What is Amyloidosis?
Primary type in dogs and cats. Secondary type usually follows chronic inflammation. Affected livers are enlarged, pale and firm with rounded borders. Histologically amyloid protein is deposited extracellularly around portal tracts and along sinusoids in space of disse.
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Describe the factors which influence the pattern of hepatic necrosis.
Mode of action of the agent - directly affects hepatocellular or biliary cells or secondary to interference with blood supply or biliary tract damage. Severity and duration of action of agent - mild or short duration - reversible. Severe/constant > irreversible. Route of access of agent - umbilical vein in foetus, portal vein, hepatic artery, transcoelomic, biliary system.
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Describe single cell necrosis and focal necrosis of the liver.
Single cell necrosis: coagulative necrosis of individual cells and immediate neighbours. E.g some viral hepatitis. Focal necrosis is usually a microscopic change in hepatocytes/biliary cells randomly distributed without obvious relationship to lobular pattern. Often of minimal significance. Viral and bacterial agents most common.
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Describe Zonal necrosis: centrilobular vs periportal
Centrilobular hepatocytes are vulnerable to hypoxic damage because of relatively low gradient of oxygen in centre of lobule. Also susceptible to toxic insult by toxins requiring hepatic biotransformation. Periportal necrosis is commony seen in toxic damage where the toxin is preformed.
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What is massive necrosis?
This refers to the complete necrosis of individual lobules and may be isolated or multiple. It implies a more serious and/or longer duration insult but despite the name it does not necessarily mean that the whole organ is affected. It means whole lobules not whole liver.
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Describe the Hepatocyte responses to inflammation
Hypertrophy of surviving hepatocytes. Renegerative hyperplasia/nodular regeneration of existing mature hepatocytes in response to live injury - ability varies with species and age. Hyperplasia may be diffuse but often occurs as nodules. Nodular hyperplasia is a very common incidental finding in older dogs. Discrete unencapsulated nodules of hepatocytes which retain good lobular and cord architecture.
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What is oval cell proliferation?
A response to inflammation - Regeneration of new hepatocytes and bile ducts by proliferation of bipotential stem cells called oval cells located in the terminal bile ductules. Often just see proliferation of bile duct type cells.
138
Describe hepatic atrophy as a response to inflammation
Atrophy of the whole liver, individual lobes or parts of lobes. Pressure on liver parenchyma e.g external/internal space occupying lesions. Anoxia/hypoxia - insidious oxygen deprivation. Impairment of bile flow - chronic biliary disease.
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Describe healing by fibrosis & centrilobular fibrosis/biliary fibrosis
Localised or generalised deposition of extracellular connective tissue matrix as a healing response to hepatic injury. Centrilobular fibrosis - prolonged hypoxia, cell death and fibrosis of centrilobular zones e.g caused by chronic venous congestion in cardiac failure. Biliary fibrosis - chronic periportal inflammation, cholangitis and/or biliary obstruction.
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What is post necrotic scarring?
Following a single episode of widespread massive hepatocellular necrosis, the parenchyma and connective tissue scaffold is damaged and there is post necrotic collapse. The area cannot regenerate and is replaced with fibrous tissue.
141
What is diffuse hepatic fibrosis?
On going hepatocyte necrosis which overwhelms the regenerative capacity e.g chronic toxic injury, chronic inflammation or metabolic disorder. Widespread fibrous tissue deposition. Also get deposition of connective tissue matrix within space of Disse - the overlying sinusoidal lining cells loose their fenestrations and become impermeable.
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What is Cirrhosis of the liver?
Diffuse, irreversible end stage hepatic disease. The combination of hepatocyte Destruction, nodular regeneration, biliary hyperplasia, bridging fibrosis and portal centrilobular vascular anastomoses.
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Name potential mechanical/traumatic conditions of the liver
Displacement - usually associated with acquired diaphragmatic hernia e.g trauma due to road traffic accidents in dogs and cats. Rupture - associated with compression trauma eg RTA.
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What are porto-systemic shunts?
Anomalous development of the portal vein either prior to the liver (Extra-hepatic) or within the liver (intrahepatic). Seen mainly in dogs and cats. FEatures are liver and portal vein hypoplasia and microscopically evident loss of portal venules and proliferation of hepatic arterioles. May present clinically with hepatoencephalopathy.
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What is telangiectasis?
Ectasia (dilatation) of groups of sinusoids filled with blood. Incidental finding seen most commonly in cattle and cats. Common in bovine abattoir specimens.
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Describe the effect of vascular obstruction on the portal vein?
Total rapid obstruction results in death as a result of Hypovolaemic shock with sequestration of blood in the splanchnic bed. Partial or slowly progressive occlusion leads to atrophy of lobe of liver, depending on development of accessory portal circulation. Where this accessory circulation is inadequate, portal hypertension develops -> congestion and ascites.
147
Describe the effect of vascular obstruction of the hepatic vein?
Para-caval or caval abscessation may occur in cattle. Partial or slow obstruction is more likely and results in chronic venous congestion with development of centrilobular fatty degeneration and atrophy with fibrosis.
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What is an acquired portosystemic vascular shunt
Collateral blood vessels bypass the normal route of blood flow through the liver. Most commonly identified in dogs & cats secondary to portal hypertension. Portal hypertension may develop following severe hepatic disease, occlusion of the hepatic vein or portal vein, primary portal vein hypoplasia.
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What is Acute hepatitis?
Hepatitis is inflammation of the liver parenchyma. Bacterial can be - salmonella, Escherichia coli, listeria monocytogenes, campylobacter fetus, clostridium piliforme, Leptospirosis. Viral - infectious canine hepatitis, Feline infectious peritonitis, protozoal - toxoplasma gondii, fungal - aspirgillus fumigatis, trematodiasis - acute fascioliasis - immature fluke migration. Toxic - adverse drug reactions in some individuals.
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What is chronic hepatitis?
When the action of inflammatory cells cannot overcome antigenic stimulus. Typically, chronic inflammatory responses consist of a mixture of granulation tissue, nodular regeneration and fibrosis, together with cellular reaction. e.g copper associated hepatopathy, crhonic copper toxicity, ragwort.
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What is cholangiohepatitis?
Inflammation of the biliary tree and hepatocellular parenchyma. Inflammation starts in the bile ducts and extends into the parenchyma e.g chronic fascioliasis in ruminants or bacterial cholangiohepatitis from ascending infections from the intestine to the bile ducts. In cats, chronic cholangiohepatitis often occurs in association with chronic pancreatitis and/or enteritis.
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What is cholangitis?
Affects intra/extra hepatic ducts. Usually an ascending infection. Note chronic lymphocytic cholangitis - a feline condition characterised by excessive aggregations of lymphocytes in portal tracts, together with bile duct proliferation and portal fibrosis.
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What is cholecystitis?
Inflammation of the gall bladder
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What is cystic mucinous hyperplasia?
Hyperplasia of the gall bladder wall and lining epithelium with abundant mucin production. May become severely distended and can rupture. Rarely causes obstruction.
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What is Cholelithiasis
Uncommon in domestic animals but may be found as an incidental finding at the abattoir in cattle. Usually form in the gall bladder. Complete obstruction leads to extrahepatic cholestasis and jaundice. Leakage of bile into portal areas causes inflammation and fibrosis. Leakage into the peritoneum causes a severe peritonitis.
156
Describe possible hepatic Neoplasias
Hepatocellular carcinomas are more common than adenomas. Cholangiocellular tumours (cholangiocarcinomas and cholangioadenomas), vascular tumours (haemangiosarcoma), metastatic neoplasia to liver (more common than primary neoplasia. Multicentric neoplasia - liver may be infiltrated by neoplastic cells in Multicentric neoplasia.
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What does pancreatic disease usually manifest as?
Alimentary tract signs (maldigestion), concurrent biliary duct obstruction resulting in jaundice, metabolic disease.
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What is pancreatic acinar atrophy?
Seen in dogs - juvenile onset especially young GSDs, autosomal recessive inheritance, likely autoimmune, with large numbers of lymphocytes and plasma cells targeting exocrine pancreas followed by fibrosis. Islets are normal. Most common cause of Exocrine pancreatic insufficiency in dogs.
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What is chronic interstitial pancreatitis?
Extension of process that commences in the ducts, usually ascending infection of intestinal flora but also migrating parasites. Often occurs concurrently with cholangitis and enteritis in cats. Histologically see hyperplasia of pancreatic ducts and inflammation.
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What is acute pancreatic necrosis?
Small breed dogs - activation of trypsinogen to trypsin within the pancreas. Trypsin further activates a cascade of pancreatic proenzymes leading to autodigestion and tissue damage. Occurs due to fusion of zymogen granules with lysosomes. Leads to necrosis of the pancreas, adjacent connective tissues and abdominal fat. Blood vessels are also involved, leading to haemorrhage, thrombosis, ischaemia.
