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Gastroenterology Flashcards

1
Q

Cause of vomiting

A

motion sickness, ingestion of emetogenic substances, GI obstruction, abdominal inflammation/irritation and extra-gastrointestinal tract disease that may stimulate medullary vomiting centre region, CNS, behaviour

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2
Q

definition of vomiting

A

active, forceful process of ejection of gastric/intestinal content with prodromal signs

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3
Q

signs of vomiting

A

vomiting
dehydration
abnormal behaviour

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4
Q

diagnosis for vomiting

A

History (acute onset of vomiting in unvaccinated puppy could be infectious),
signalment, CBC, biochemistry, pH would be less than 5 (showing gastric acid),
gastroduodenoscopy and biopsy (colonoileoscopy in cats),
faecal exam (parasites),
x-ray and ultrasonography,
cats (FeLV, FIV, hyperthyroidism)

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5
Q

treatment for vomiting

A

Fasting, fluids, antiemetic agent, antiemetic agents, anti-secretory agents, prokinetics
- if animal is stable with vomiting, then symptomatic treatment for 1st 1-2 days

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6
Q

cause of diarrhoea

A

Acute
- caused by diet, parasites or infectious diseases
Chronic
- small intestinal: maldigestion (EPI), nonprotein-losing malabsorptive and protein-losing enteropathy

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7
Q

pathogenesis of diarrhoea

A

Osmotic diarrhoea
- unusually large amounts of poorly absorbable osmotically active solutes in the intestinal lumen
- occurs with malabsorptive disorders where nutrients are maldigested or mal-absorbed, remain within the intestinal lumen and osmotically attract water. EPI is example

Secretory diarrhoea
- abnormal ion transport in intestinal epithelial cells.

Increased mucosal permeability
- causes loss of fluids, electrolytes, proteins and RBC into intestinal lumen
- erosive or ulcerative enteropathies, IBD or neoplastic disorders

Deranged motility
- abnormal ileal and colonic motility patterns may contribute to clinical symptomatology of IBD
- suppression of contractions and stimulation of giant migrating contractions

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8
Q

definition of diarrhoea

A

increase in frequency, fluidity or volume of faeces

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9
Q

signs of diarrhoea

A

weight loss, polyphagia, frequency of bowel movements, volume of faeces, blood in faeces, mucus in faeces, tenesmus, maybe vomiting

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10
Q

diagnosis of diarrhoea

A

signalment, history, FIV, FeLV, faecal panel, radiography, Ultrasound
CBC
- eosinophilia ? secondary to endoparasitism, eosinophilic enteritis, mast cell neoplasia
- anaemia ? from enteric blood loss
- neutrophilia ? stress, inflammation or infection
- lymphopenia is relatively common finding in dogs with intestinal lymphangiectasia
Serum chemistry
- BUN can be increased from dehydration or gastrointestinal bleeding
- panhypoproteinemia, hypocholesterolaemia – protein losing enteropathy
Specialised gastrointestinal function tests
- serum trypsin-like immunoreactivity – exocrine pancreatic insufficiency
- serum cobalamin and folate: measurement of serum Vit B12 and folate concentrations – absorptive function of ileum and jejunum, decreased in IBD or lymphoma
Chronic
- Parasite test (giardia, tritrichomonas – ELISA, snap test but IFA is gold standard)
- failure to lose weight/body condition despite chronic diarrhoea indicates large bowel disease
- weight loss usually indicates small bowel disease

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11
Q

treatment for diarrhoea

A

: dietary therapy (highly digestible, moderately fat-restricted food), antimicrobials (metronidazole 10-15mg/kg q12h), oral protectants (activated charcoal), fluids, motility modifier (iopermaide 0.1-0.2mg/kg q8-12dog, q12 cat), probiotics,
- chronic diarrhoea: oral corticosteroids (for IBD)

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12
Q

differentials for diarrhoea

A

Dietary, inflammatory, infectious, pancreatitis, obstruction, neoplasia, drugs + toxins

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13
Q

when is diarrhoea acute/chronic

A

acute if lasts for less than 14 days, chronic if longer than 14 days

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14
Q

cause of dysphagia

A

results from oral pain, masses, foreign objects, trauma, neuromuscular dysfunction or combination

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15
Q

what is dysphagia

A

difficulty swallowing

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16
Q

signs of dysphagia

A

difficulty of prehension of water and food, drooling, nasal discharge
- repeated, often unproductive attempts to swallow with extension oof the head and neck during swallowing, often accompanied by gagging, retching, odynophagia and ptyalism

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17
Q

diagnosis of dysphagia

A

complete examination of pharynx, X-rays (positive contrast)

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18
Q

how do you differentiate between dysphagia and regurgitation

A

localisation of disease

  • oesophageal dysphagic and salivation must be differentiated from oropharyngeal dysphagia and salivary gland diseases (sialadenitis or Sialoadenosis)
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19
Q

what is regurgitation

A

Expulsion of material from the mouth, pharynx or oesophagus whereas vomiting is expulsion from the stomach and/or intestines

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20
Q

cause of regurgitation

A

obstruction and muscular weakness

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21
Q

pathogenesis of regurgitation

A

passive process that occurs without prodromal signs

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22
Q

signs of regurgitation

A

expelling material from mouth, pharynx or oesophagus

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23
Q

diagnosis of regurgitation

A

watch the animal eating, fluoroscopic evaluation of swallowing barium to differentiate pharyngeal from cricopharyngeal dysfunction
- plain radiograph and later barium contrast

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24
Q

treatment of regurgitation

A

depending on cause: foreign body (surgery), weakness (supportive therapy)

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25
Q

haematemesis

A
  • vomiting of blood (fresh/digested)
  • damage in the oesophagus, stomach or duodenum
  • ingestion of blood from mouth, nose, respiratory tract
  • check haematocrit and plasma total protein concentration to see if blood transfusion needed
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26
Q

melena

A
  • “black stool” digested blood
  • food
  • bismuth compounds
  • upper GI bleeding/respiratory tract bleeding
  • cause: hookworm, GUE, ingested blood
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27
Q

haematochezia

A
  • fresh blood in stool
  • disease of large intestine: colitis, proctitis, large intestine tumour, anal sac disease
  • if has haematochezia and diarrhoea – problem approached in same manner as large bowel diarrhoea
  • acute haematochezia may result from trauma (passing a foreign body)
  • digital rectal exam necessary – express each anal sac repeatedly and examine the contents, biopsy/colonoscopy recommended if unhelpful digital rectal exam
  • barium enema isn’t recommended
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28
Q

tenesmus

A
  • straining to defecate vocalisation, painful defecation – dyschezia
  • cause: perineal inflammation/pain, rectal inflammation/pain, colonic/rectal obstruction in cat (urethral obstruction, rectal obstruction or constipation)
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29
Q

predisposition for faecal incontinence

A

older more than younger

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30
Q

cause of faecal incontinence

A

injuries to spine/tail, anal gland disease and/or intestinal disorder

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31
Q

pathogenesis of faecal incontinence

A

inability to retain faeces in the colon and rectum leading to uncontrolled leakage of faecal material at times other than during conscious defecation

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32
Q

signs of faecal incontinence

A

scooting on floor, defecating in atypical areas, bloated abdomen, tenderness or aversion to being touched near tail, loss of tone and voluntary movement of the tail, weight
weight loss, vomiting, spasms of urogenital diaphragm

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33
Q

diagnosis of faecal incontinence

A

history, CBC, biochemistry, urinary and faecal analysis (infection or parasite)

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34
Q

treatment of faecal incontinence

A
  • changes in diet (low residue diets), warm water enemas, maybe surgical reconstruction
  • anti-inflammatory agents, opiates
  • motility-modifying drugs shouldn’t be used if infectious or toxic cause is suspected and opiates never used with patients with respiratory disease
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35
Q

cause of stomatitis

A

physical insults, uraemia, inadequate host responses to pathogen, renal failure, trauma, immune-mediated disease, upper respiratory, tooth root abscess, etc

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36
Q

pathogenesis of stomatitis

A

Inflammation of the oral tissue that usually begins in the periodontium or the oropharyngeal area

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37
Q

signs of stomatitis

A

decreased appetite, ptyalism, oral haemorrhage, difficulty prehending or chewing food, blood tinged saliva, oral pain, nasal discharge, facial swelling, ulceration of the lips, oral inflammation
- thick, ropey saliva, severe halitosis, and/or anorexia caused by pain

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38
Q

diagnosis of stomatitis

A
  • hemogram and serum chemistry
  • FeLV/FIV testing – all cats with stomatitis
  • oral and dental radiographs
  • tissue biopsy and histopathology – rule out neoplasm
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39
Q

treatment of stomatitis

A

symptomatic and specific
- thorough teeth cleaning and aggressive antibacterial therapy, maybe extracting teeth
- bovine lactoferrin = suggested to ameliorate otherwise resistant lesions in cats

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40
Q

cause of feline lymphocytic plasmacytic gingivitis

A

idiopathic, maybe: feline calicivirus, bortonella henselae, immunodeficiency from FeLV or FIV

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41
Q

signs of feline lymphocytic plasmacytic gingivitis

A

red gingiva around the teeth and/or posterior pillars of the pharynx. Dental neck lesion often accompanies the gingivitis

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42
Q

diagnosis of feline lymphocytic plasmacytic gingivitis

A

biopsy of affected gingiva
- histologic evaluation reveals lymphocytic plasmacytic infiltration
- serum globulins can be increased

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43
Q

treatment of Feline lymphocytic plasmacytic gingivitis/

A

no reliable therapy, proper cleaning and polishing of teeth, ATB, high-dose corticosteroid therapy

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44
Q

prognosis of Feline lymphocytic plasmacytic gingivitis

A

guarded

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45
Q

sialodenitis definition

A

inflammation of the salivary gland

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46
Q

predisposition of sialodenitis

A

rarely clinical problem in dogs and cats

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47
Q

cause of sialodenitis

A

unknown, has occurred as idiopathic event, secondary to chronic vomiting/regurgitation, trauma from penetrating wounds/systemic infection affecting salivary glands, rabies, distemper

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48
Q

signs of sialodenitis

A

painless enlargement of one or more salivary glands. Animals may be dysphagic, fever, depression, reluctance to open mouth and eat

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49
Q

diagnosis of sialodenitis

A

Biopsy, cytology/ histopathology confirm that the mass is salivary tissue and determines whether inflammation or necrosis is present

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50
Q

treatment of sialodenitis

A

if substantial inflammation and pain, surgical removal, if vomiting (treat cause)
- developed abscess should be drained through overlying skin – systemic antibiotics

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51
Q

prognosis of sialodenitis

A

excellent

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52
Q

sialdenosis

A

sialdenosis is a non-inflammatory, non-neoplastic, usually bilateral enlargement of the mandibular salivary gland, associated with regional swelling and exophthalmos but no apparent pain

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53
Q

predisposition of nasopharyngeal stenosis

A

uncommon in cats, quite rare in dog

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54
Q

cause of nasopharyngeal stenosis

A

congenital malformation, response to inflammation from chronic upper respiratory disease or regurgitation into the nasopharynx, foreign body/ any irritant contacting affected area

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55
Q

pathogenesis of nasopharyngeal stenosis

A

pathologic narrowing of the nasopharynx due to the formation of a web of scar tissue which leads to upper airway obstruction

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56
Q

signs of nasopharyngeal stenosis

A

dyspnoea, gagging, sneezing, stridor, retching, vomiting, regurgitation, anorexia, oculonasal discharge

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57
Q

diagnosis of nasopharyngeal stenosis

A

CT or MRI, nasopharyngeal endoscopy (passing a catheter through the ventral nasal meatus)

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58
Q

treatment of nasopharyngeal stenosis

A

surgical options (nasopharyngeal stenosis include excision of the scar tissue, balloon dilation or stent placement)

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59
Q

predisposition of laryngeal paralysis

A

common in dogs, rare in cats
- middle – older, large and giant breeds (Lab, Irish setters, Great Danes)

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60
Q

cause of laryngeal paralysis

A

tumours or lesions in neck or chest, trauma to the throat, hormonal disorders (hypothyroidism and Cushing’s)

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61
Q

pathogenesis of laryngeal paralysis

A

Failure of arytenoid cartilages to abduct during inspiration. Congenital, acquired, unilateral and bilateral forms

vocal fold is narrowed

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62
Q

signs of laryngeal paralysis

A

dynamic upper airway obstruction
dry cough, voice changes, noisy breathing, stridor, collapse, regurgitation and vomiting may occur

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63
Q

diagnosis of laryngeal paralysis

A

based on clinical signs, laryngoscopy (under light LA for confirmation), radiographs are not diagnostic

  • direct or endoscopic laryngoscopy in shallow anaesthesia
  • disease of larynx with same symptoms:
    o Laryngeal neoplasia, obstructive laryngitis, foreign body, trauma, laryngeal collapse, extraluminal masses around the larynx and acute laryngitis
    o Palpation of the area – x-ray
    o Thyroid hormones
    o Acetylcholine receptor antibody test
    o Chest x-ray – aspiration pneumonia?
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64
Q

treatment of laryngeal paralysis

A

relieving signs of airway obstruction
- corticosteroids effected temporarily in mild cases
- severe obstruction may require tracheotomy

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65
Q

complications of laryneal paralysis

A

aspiration pneumonia 8-25% of dogs post op

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66
Q

differentials for laryngeal paralysis

A

myositis, recurrent laryngeal/vagal nerve tumour, inflammation, myasthenia gravis, severe hypothyroidism, trauma

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67
Q

definition of laryngitis

A

inflammation of the mucosa or cartilages of the larynx

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68
Q

predisposition of laryngitis

A

primary occurs more in cats than dogs and secondary more common than primary in both

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69
Q

cause of layrngitis

A

some infections, aspiration of food, inhalation of irritating vapours, barking, trauma. Acute laryngitis can develop into chronic laryngitis, trauma from intubation, infections

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70
Q

pathogenesis of laryngitis

A

inflammation/irritation of the laryngeal mucosa often characterised by edema and hypervascularisation

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71
Q

signs of laryngitis

A

dry short cough, vocal changes, stridor, halitosis, animal may stand with its head lowered and mouth open, swallowing is difficult and painful, bad breath, bluish gums

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72
Q

diagnosis of laryngitis

A

based on clinical signs and laryngoscopy, auscultation

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73
Q

treatment of laryngitis

A

steroids or NSAIDs, oxygen therapy, intubation/ventilation if needed, systemic antibiotics

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74
Q

prognosis of laryngitis

A

earlier the treatment, the better the outcome, if the larynx or any surrounding cartilage areas in the airway include chronic damage, the prognosis is worse

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75
Q

predisposition of laryngeal neoplasia

A

rare in dogs and cats

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76
Q

cause of laryngeal neoplasia

A

genetics, infection, cell malformation, age, environmental pollutants, chronic inflammation

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77
Q

pathogenesis of laryngeal neoplasia

A
  • found on wall of the larynx and can cause respiratory obstruction
  • laryngeal oncocytomas occur most often with young dogs
  • chondrosarcomas of the larynx are mostly of malignant sort and develop in CT of the larynx
  • SCC of the larynx can form in the upper, middle or lower area
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78
Q

signs of laryngeal neoplasia

A

weakness, regurgitation of undigested food/blood, vomiting after eating, dysphagia, dyspnoea, change in tone, respiratory distress, cyanosis, coughing, lethargy, depression, weight loss, halitosis

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79
Q

diagnosis of laryngeal neoplasia

A
  • CBC, biochemistry and urinalysis
  • radiographs of neck and chest, CT
  • FNA on lymph notes
  • endoscopy
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80
Q

treatment of laryngeal neoplasia

A

surgery, chemo

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81
Q

what are the most common neoplasia in dogs and cats

A
  • Most common in dogs: rhabdomyoma, SCC and oncocytoma
  • Most common in cats: lymphoma, SCC and adenocarcinoma
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82
Q

oesphagitis definition

A

inflammation of the MM and/or deeper layers of the oesophagus

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83
Q

cause of oesophagitis

A

GER, foreign body, chemical damage, structural abnormalities, chronic vomiting, invasion by larvae, NSAIDs

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84
Q

signs of oesophagitis

A

regurgitation, increased salivation, painful swallowing, inappetence

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85
Q

diagnosis of oesophagitis

A

haematology, biochemistry, X-ray + contrast, endoscopy

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86
Q

treatment for oesophagitis

A
  • mild form: diet
  • moderate to severe: sucralfate, metoclopramide, antisecretory drugs, ATB
  • hospitalisation of dogs with aspiration pneumonia and cachexia
  • complications – strictures of the oesophagus
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87
Q

GER predisposition

A

dogs that have abdominal surgery

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88
Q

cause of GER

A

incompetence of cardiac sphinter, GA

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89
Q

pathogenesis of GER

A

reflux of gastric contents into oesophagus

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90
Q

signs of GER

A

mucous lesions – prolonged contact with gastric acid, decreased appetite, difficulty swallowing, licking the lips, change in bark, chronic cough, appearance of generalised discomfort, pacing/ restlessness at night

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91
Q

diagnosis of GER

A

Endoscopy, caudal sphincter pressure measurement and 24-hour intraluminal pH determination
- physical exam: localise pain and feel for abdominal mass, obstructions etc
- CBC, biochemistry and urinalysis
- Xray and ultrasound
- diagnosed on endoscopy – shows oesophageal inflammation

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92
Q

treatment of GER

A

fat restrictive. mucosal protectors (sucralfate), PPI (omeprazole/esomeprazole), H2 blockers (ranitidine/ famotidine) and prokinetics (metoclopramide)

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93
Q

predisposition of oesophageal FB

A

: most common in small dogs, less common in cats

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94
Q

cause of oesophageal FB

A

food boluses, toys, hairballs, ETC

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95
Q

pathogenesis of oesophageal FB

A

most common localisation: in front of the aperture thoracis cranialis, the thoracic oesophagus above the base of the heart or cranially from the lower oesophageal sphincter

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96
Q

symptoms of oesophageal FB

A

increased salivation, difficulty swallowing, straining, regurgitation, lethargy, loss of appetite.

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97
Q

diagnosis of oesophageal FB

A

x-ray immediately before endoscopy

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98
Q

treatment of oesophageal FB

A
  • endoscopic removal of a foreign body
  • “pushing” foreign body into the stomach
  • surgery
  • post FB removal: PPI and prokinetic drugs
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99
Q

prognosis of oesophageal FB

A

without perforation usually good, perforation = guarded

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100
Q

oesophageal stricture definition

A

severe, deep inflammation of the oesophagus

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101
Q

cause of oesophageal stricture

A

any cause, especially foreign bodies or severe gastroesophageal reflux

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102
Q

pathogenesis of oesophageal strictures

A

circular narrowing occurs as secondary pathological change due to inflammation of the deeper layers of the oesophageal mucosa

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103
Q

signs of oesophageal strictures

A

regurgitation, hypersalivation, dysphagia, choking, gagging and weight loss, hyporexic

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104
Q

diagnosis of oesophageal strictures

A

intraluminal and extraluminal masses. Contrast x-ray: precision in revealing the exact position, number and extent of change on the oesophagus. Endoscopy

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105
Q

treatment of oesophageal strictures

A

Surgery, balloon catheter dilation, bougienage, stent placement

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106
Q

prognosis of oesophageal strictures

A

very chronic strictures have more guarded prognosis

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107
Q

mega oesophagus predisposition

A

GSD, golden retriever’s, and irish setters

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108
Q

cause of mega oesophagus

A
  • Congenital oesophageal weakness is unknown
  • acquired in dogs: neuropathy, myopathy or myasthenia gravis
  • cats: may be a cause of acquired oesophageal weakness
  • primary: idiopathic and can be congenital or acquired
  • congenital defects: vascular ring anomalies, oesophageal diverticular, congenital myasthenia gravis, idiopathic congenital megaoesophagus
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109
Q

pathogenesis of megaoesophagus

A

severe diffuse oesophageal hypomotility and flaccid dilation of the oesophagus

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110
Q

signs of megaesophagus

A

regurgitation, aspiration pneumonia as a complication

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111
Q

diagnosis of megaoesophagus

A

survey radiographs or barium contrast oesophagram

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112
Q

treatment of megaoesophaugs

A
  • congenital: cannot be cured or resolved by medically therapy
  • acquired: treat underlying disease
  • surgery for vascular ring anomalies
  • frequent small meals and feeding from an elevated position
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113
Q

prognosis of mega oesophagus

A

guarded

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114
Q

hiatal hernia def

A

Diaphragmatic abnormality that allows part of the stomach to prolapse into thoracic cavity

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115
Q

predisposition of hiatal hernia

A

brachycephalic breeds

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116
Q

causes of hiatal hernia

A

can be congenital or acquired in origin

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117
Q

pathogenesis of hiatal hernia

A

protrusion of the oesophagus, lower oesophageal sphincter (LES), and/or part of stomach through oesophageal hiatus into the thoracic cavity

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118
Q

signs of hiatal hernia

A

regurgitation primary symptoms, some are asymptomatic

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119
Q

diagnosis of hiatal hernia

A

Plain radiographs/positive contrast

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120
Q

treatment of hiatal hernia

A

surgery, if signs appear later in life, aggressive medical management of GER (cisapride, omeprazole) sometimes sufficient, if not surgery

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121
Q

prognosis of hiatal hernia

A

often food after surgical repair (congenital cases) or aggressive medical management (acquired)

122
Q

predisposition of gastroesophageal intussusception

A

more common in dogs, especially young, very rare in cats
- rare condition of young dogs (< 3 months)

123
Q

cause of gastroesophageal intussusception

A

many have pre-existing oesophageal disease (idiopathic megaoesophagus)

124
Q

pathogenesis of gastroesophageal intussusception

A

rare hiatal disorder resulting from invagination of the stomach into the lumen of the oesophagus; other abdominal organs may or may not invaginate as well

125
Q

signs of Gastroesophageal intussusception

A

regurgitation, vomiting, dyspnoea and collapse

126
Q

diagnosis of Gastroesophageal intussusception

A

histoy
physical exam
X-ray of neck and chest

127
Q

treatment Gastroesophageal intussusception

A

endoscopic or surgical reduction

128
Q

prognosis of Gastroesophageal intussusception

A

guarded, successuful oucome if prompt diagnosis and intervention

129
Q

predisposition of acute haemorrhagic diarrhoeal syndrome

A

smaller breeds (yorkies, schnauzers, mini pinschers, Maltese)

130
Q

cause of acute harmorrhagic diarrhoeal syndrome

A

unknown, maybe C. perfringens

131
Q

signs of acute haemorrhagic diarrhoeal syndrome

A

more severe than acute g. Profuse haematemesis and/or haematochezia. Rapidly critically ill: severe dehydration, DIC and renal injury

132
Q

diagnosis of acute haemorrhagic diarrhoeal syndrome

A

History
pcv (most have increased)
thrombocytopenia

133
Q

treatment of acute haemorrhagic diarroeal syndrome

A

fluid therapy: aggressive fluid therapy IV (to prevent shock, DIC, renal failure) crystalloids
- same as in acute gastritis, ATB, synthetic colloids, plasma
- antimicrobial therapy has not been found beneficial

134
Q

prognosis of acute haemorrhagic diarrhoea sydnrome

A

good for most animals that are presented on time and receive aggressive fluid treatment on time

135
Q

predisposition for acute gastritis

A

dogs more likely than cats

136
Q

cause for acute gastritis

A

dietary or intolerance, foreign bodies, drugs and toxins. Systemic disease, parasites, bacteria and virus, NSAIDs

137
Q

pathogenesis of acute gastrtis

A

syndrome marked by vomiting of sudden onset presumed to be due to a gastric mucosal insult or inflammation

138
Q

signs of acute gastritis

A

acute onset of vomiting (food and bile), uninterested in food, nauseous, fever uncommon, abdominal pain uncommon

139
Q

diagnosis of acute gastritis

A

history, physical exam, signalment (young animal, often foreign body), response to symptomatic treatment, abdominal imaging, lab testing, US

140
Q

treatment of acute gastritis

A
  • fluid therapy: orally, SC (rare), or IV, diet restriction (24h), 1st give water if no vomiting, small amounts of food, bland diet
  • drugs only if necessary
  • adsorbents (activates charcoal, kaolin-pectin)
  • central-acting antiemetics (maropitant)
  • ACID reducing drugs (H2 blockers, PPI)
  • ATB – rarely indicated
  • foreign bodies: endoscopy, can give emetic (H2O2 per os in dogs, but need to know what foreign body is, if has sharp edges don’t do it)
141
Q

prognosis of actue gastritis

A

for uncomplicated acute gastritis: usually complete recover
- excellent as long as fluid and electrolyte balance is maintained

142
Q

predisposition of GUE

A

more common in dogs

143
Q

cause of GUE

A

metabolic/ endocrine (hypoadrenocorticism, uraemia), inflammatory (uraemic), neoplastic (leiomyoma), drug induced (NSAIDs), hypotension (shock, sepsis), idiopathic (stress, spinal surgery, exercise- induced)

144
Q

pathogenesis of GUE

A

associated with number of primary gastric and non-gastric disorders

145
Q

signs of GUE

A

hyporexia, vomiting, haematemesis, melena, pale MM, weakness, abdo pain, hypersalivation, ulcer performation: signs of septic peritonitis

146
Q

diagnosis of GUE

A

history (finding evidence of GI blood loss), physical exam
- CBC: anaemia, thrombocytosis, decreased iron saturation, eosinophilia, neutrophilic leucocytosis)
- biochemistry and urinalysis (acidic urine)
- serum gastrin and gastric pH
- coagulations
- abdominal imaging, ultrasound (detects gastric thickening), endoscopy (+biopsy)

147
Q

treatment of GUE

A
  • patient status, underlying cause
  • fluid therapy: IV fluids – rate: hydration/perfusion status
  • treatment of dehydration: over 4-24hr
  • fluid deficit (% dehydration x body weight kg)
  • daily physiologic requirements (30xBW/kg)
    same as you would use for ulcer (PPI etc)
148
Q

prognosis of GUE

A

favourable if the underlying cause can be controlled and if therapy prevents perforation of the ulcer

149
Q

predisposition of GDV

A

large deep chested dogs, easting once a day, male

150
Q

cause of GDV

A
  • hepatic portal vein/caudal cava obstruction 
  • impair venous return to the heart 
  • hypovolemic shock 
  • devitalisation of the gastric wall 
  • splenic torsion or avulsion 
  • congestion of abdominal viscera 
  • endotoxemia
151
Q

pathogeensis of GDV

A

caused by poor gastric emptying of solids  produce some degree of chronic gastric distention  subsequent stretching of hepato-gastric and duodeno-gastric ligaments

152
Q

signs of GDV

A

non-productive retching, salivation, abdominal distension, abdominal pain “restlessness”, weakness, collapse
abdominal distension and tympany, tachycardia, mucosal pallor, hypothermia, depression, coma

153
Q

diagnosis of GDV

A

history, physical examination, abdominal imaging  after decompression and shock stabilisation
- lab testing: increased PCV, acido-base and electrolyte abnormalities, increase plasma lactate
- ECG

154
Q

treatment of GDV

A
  • fluid therapy: aggressive, IV fluids, aggressive monitor, potassium
  • decompression: trocarisation: 12-16g catheter, orogastric tube, warm water lavage
  • drugs: broad spectrum ATB-IV, arrhythmia
  • surgery: as soon as animal constitutes an acceptable anaesthetic risk
  • post-surgery: monitor the patient
155
Q

predisposition for chronic gastritis

A

common in dogs: 35% of dogs with chronic vomiting, 26-48% asymptomatic dogs
- more common in cats than dogs

156
Q

cause of chronic gastritis

A

immune, H.pylori, ollulanus tricuspis (cause granulomatous gastritis in cats)

157
Q

types of chronic gastritis

A
  • lymphocytic plasmacytic (immune and/or inflammatory reaction to variety of antigens)
  • eosinophilic (allergic reaction probably to food antigens)
  • atrophic (chronic gastric inflammatory disease and/or immune mechanism)
158
Q

signs of chronic gastritis

A

hyporeixa and vomiting

159
Q

diagnosis of chronic gastritis

A

histologic exam of gastric biopsies, US

160
Q

treatment for chronic gastritis

A
  • lymphocytic plasmacytic = sometimes responds to dietary therapy, if inadequate = prednisolone
  • canine eosinophilic gastritis = responds well to strict elimination diet if not prednisolone
  • atrophic = difficult to treat, diets low in fat and fibre might help, also might respond to anti-inflammatory, antacid and/or prokinetic therapy
161
Q

prognosis of chronic gastritis

A

often good

162
Q

cause of acute enteritis

A

parasites, virus, fungus, IBD, ingestion of toxins, neoplasia, boarding at a kennel, scavenger

163
Q

def of acute enteritis

A

inflammation of SI

164
Q

signs of actue enteritis

A

Diarrhoea of unknown cause (common, especially in puppies and kittens), vomiting, dehydration, fever, anorexia, depression, crying and/or abdominal pain

165
Q

diagnosis of actue enteritis

A
  • history, physical and faecal examinations (faecal flotation and direct faecal exam)
  • if animal febrile, has haemorrhagic stool and part of outbreak enteritis = CBC (to identify neutropenia), faecal ELISA (parvo), serological analysis (FeLV, FIV), blood glucose (hypoglycaemia), serum electrolyte (hypokalaemia)
  • abdominal imaging
166
Q

treatment of acute enteritis

A
  • symptomatic therapy
  • opiates most effective antidiarrheals
  • bismuth subsalicylate – useful for diarrhoea in dogs with mild to moderate enteritis
167
Q

prognosis of actue enteritis

A

depends on animal’s condition
- very young/emaciated animals and those with SIRS or intestinal parasites are more guarded
- if intussusception occurs secondary to acute enteritis, the prognosis is guarded

168
Q

predisposition of colitis

A

Middle-aged dogs, no sex predilection. Cats: middle aged and more commonly purebred
- granulomatous colitis is rare, breed- specific IBV of young boxers and French bull dogs
- eosinophilic colitis tends to be in animals younger

169
Q

cause of colitiis

A

Food intolerance, ingestion of toxins/foreign bodies, bacterial infections, uncontrolled drug therapy, ATB, IBD, neoplasia, changes in bowel position, IBS

170
Q

pathogenesis of colitis

A

often presents as chronic, large bowel diarrhoea of unknown origin

171
Q

signs of colitis

A

diarrhoea (mucus, haematochezia, tenesmus and occasionally pain), increased urgency and frequency of defecation, weight loss and vomiting occur but are uncommon

172
Q

diagnosis of colitis

A

history + clinical examination, faeces, x-ray (contrast), CBC and biochemistry, endoscopy and rectal examination
- excluding other infectious disease

173
Q

treatment of colitis

A
  • rehydration
  • diet – easily digestible, fibre-rich food (colitis), probiotics
  • symptomatic – antiemetics, electrolyte correction, analgesia
  • ATB: metronidazole (6-10mg/kg BID), amoxicillin (10-20mg/kg BID/TID), tylosine (10-20mg/kg SID/BID/ 3-6 months), enrolxacin (5mg/kg SID)
  • sulfasalazine – colitis
174
Q

prognosis of colitis

A

short term is good, long term for complete resolution without relapse appears poor
- idiopathic lymphocytic plasmacytic colitis respond to dietary and medical changes
- stricture formation and extensive fibrosis = more guarded
- eosinophilic colitis in dogs – good, in cats more guarded
- hypereosinohpilic syndrome is progressive, fatal and has no effective treatment in animals
- histiocytic colitis of boxers - grave

175
Q

predisposition of ileus

A
  • most common in young (about 70% less than 1 yr old)
  • neoplasia more in middle-aged to old
  • intestinal torsion (volvulis) – large breeds
176
Q

cause of ileus

A

foreign bodies, bowel invagination, mesenteric torsion and neoplasia

177
Q

pathogenesis of ileus

A

temporary arrest of intestinal peristalsis, temporary and reversible obstruction in the intestines

  • intraluminal (foreign body), mural (neoplasia, abscess), extramural (adhesion, hernia, neoplasia)
  • proximal to the site of the obstruction is the extension of the intestinal segment and the accumulation of gas and liquid content
  • paralytic ileus: consequence of primary disease, electrolyte imbalance or anaesthesia
178
Q

signs of ileus

A
  • depends on location, severity and cause of the obstruction
  • acute vomiting (or chronic cases = faecal vomiting)
  • sometimes no defecation, sometimes watery to bloody diarrhoea
  • dehydration, hypovolemia, shock, bowel necrosis, sepsis and death
179
Q

diagnosis of ileus

A
  • history and palpation of the abdomen, x-ray and ultrasound
180
Q

treatment of ileus

A

surgery (removing the cause of obstruction/bowel resection), rehydration, ATB, analgesic, motility promoters (metoclopramide EXCLUSIVELY WITH PARALYTICAL ILEUS)

181
Q

predisopisiotn of constipation/obstipation

A

older, overweight cats with chronic kidney disease or previous episodes of constipation are at increased risk of constipation

182
Q

constipation + obstipation definitiation

A

Constipation: infrequent or difficult evacuation of stool from the rectum or colon
Obstipation: intractable constipation refractory to control or cure; implies a permanent loss of colonic function

183
Q

cause of constiaption

A

dehydration, neuromuscular control (spinal damage, electrolytes, opioids), consequence of other diseases (colitis, perineal hernia, disease of spine, prostate hypertrophy)

184
Q

signs of constipation

A

absent or painful defecation for days – week, anorexia, vomiting and weight loss, watery or mucus material from the rectum

185
Q

diagnosis of constipation

A
  • colon can be palpated distended with faeces
  • digital rectal examination – can detect strictures, foreign bodies, pelvic trauma etc
  • serum biochemistry panel – serum T4 level
  • radiography or endoscopy
  • neurological examination
186
Q

treatment of constipation

A
  • rehydration
  • removal of impacted faeces is required to reduce toxic and inflammatory stress on the bowel wall
  • enemas are used to remove impacted faeces
  • laxatives and prokinetic agents, lactulose, paraffin oil, bisacodyl
187
Q

predisposition of mega colon

A

common in cats and less in dogs

188
Q

cause of mega colon

A

idiopathic dilated megacolon and hypertrophic megacolon
Idiopathic dilated megacolon
- functional disturbance of the colonic smooth muscle followed by a more permanent loss of colonic function
- in cats, behavioural or environmental factors (stress and poor litter box hygiene)
Hypertrophic colon
- develops as a sequela of an obstructive lesion

189
Q

pathogenesis of mega colon

A

persistent colonic dilatation and hypomotility , colon becomes chronically nelarged

190
Q

signs of mega colon

A

chronic constipation or obstipation, weight loss, vomiting, anorexia, tenesmus, lethargy, dehydration

191
Q

diagnosis of mega colon

A

abdominal x-ray, in cases of megacolon, colon will be 1.5x length of L7

192
Q

treatment of mega colon

A

fluid therapy, clear out colon, adequate exercise, high fibre diet, nutritional supplements, subtotal colectomy, laxative (lactulose) and prokinetic agents (cisapride)

193
Q

prognosis of mega colon

A

50% recurrence rate. Prognosis with surgery in cats excellent

194
Q

definitions of tenesmus

A

frequent attempts or straining to pass faeces. Occurs with urinary problems and shouldn’t be confused with constipation

195
Q

pathogenesis of tenesmus

A

if faecal material isn’t passed, it becomes extremely desiccated, making it more difficult to be passed and more likely to obstruct the colon and rectum

196
Q

signs of tenesmus

A

constipation can lead to absorption of toxic intestinal products

197
Q

predisposition of IBD

A

GSD, German boxier, yorkies, cocker spaniel, purebred cats, dogs 2-7 years

198
Q

cause of IBD

A

adverse reactions to food, idiopathic IBD and ATB responsive diarrhoea, environmental factors, food, immune system, genetics

199
Q

pathogenesis of IBD

A

in dogs: small and large intestine, cats: small intestine (triaditis)

200
Q

signs of IBD

A

chronic vomiting and diarrhoea
Clinical diagnosis of IBD is considered only if affected animals have:
- Persistent - >3 weeks in duration, gastrointestinal signs (anorexia, vomiting, weight loss, diarrhoea, haematochezia, mucous faeces)
- Failure to respond to symptomatic therapies (parasiticides, ATB, gastrointestinal protectants alone)
- failure to document other causes of gastroenterocolitis by thorough diagnostic evaluation
- histologic diagnosis of benign intestinal inflammation

201
Q

diagnosis of IBD

A
  • thickened bowel loops may be detected during abdominal palpation if the small bowel is concurrently involved
  • digital examination of the anorectum may evoke pain or reveal irregular mucosa, and blood pigments and mucous may be evident on the exam glove
  • CBC, biochemistry, urinalysis are often normal in mild cases of large bowel IBD
  • elimination of known digestive symptoms: history, exam, bloods, faecal analysis, cobalamin
  • x-ray, US, endoscopic examination
202
Q

classification of IBD

A
  • lymphocytic plasmacytic enteritis
  • chronic lymphocytic-plasmacytic colitis
  • immunoproliferative enteropathy in basenji
  • diarrhoea syndrome in Norwegian elkhound (lunde hund)
  • eosinophilic form of IBD
  • histiocytic ulcerative colitis
  • granulomatous enterocolitis
203
Q

treatment of IBD

A
  • dietary therapy: dietary modification
  • glucocorticoids:
    o prednisolone In dogs after failed dietary management,
    o sulfasalazine/metronidazole: adjunctive therapy to dietary modification in feline
    o dose of glucocorticoids may be reduced by 25% at 1-2 weeks intervals
  • azathioprine:
    o purine analogue that inhibits lymphocyte activation and proliferation
    o used as adjunctive therapy with glucocorticoids
    o cats need to be monitored for side effects, including myelosuppression, hepatic diseases and APN
  • cyclosporine: in some cases of refractory IBD
  • chlorambucil: in some difficult or refractory cases of feline IBD
  • sulpasalazine:
    o highly effective prostaglandin synthestase inhibitor – dog
  • ATB: metronidazole: mild-moderate IBD in both dogs and cats. Side effects: anorexia, hypersalivation, vomiting
  • probiotics, anti-diarrhoeal agents, restoration of normal motility, exercise, behavioural modification
  • additional therapy: physical therapy
204
Q

prognosis of IBD

A

short term, good to excellent. Prognosis for cure is poor and relapses should be anticipated

205
Q

IBD in cats

A

triaditis” cholangitis, pancreatitis and IBD in cats

liver, pancreas and small intestines

206
Q

differentials of IBD

A
  • allergy or intolerance to certain ingredients in foods
  • gastrointestinal parasites
  • intestinal dysbacteriosis
  • hyperthyroidism in cats
  • infectious peritonitis in cats FeLV, FIV
  • fungi
  • neoplastic diseases: lymphoma, adenocarcinoma
  • EPI
207
Q

cause of liver failure

A

sudden injury, poisoning and infection, endocrine imbalance

208
Q

pathogeneis sof liver failure

A

sudden loss of liver function, often associated with neurologic signs and clotting abnormalities

209
Q

signs of liver failure

A

ascites, digestive ulcers, lack of blood coagulation, HE
vomiting, excessive thirst, frequent urination, bloody diarrhoea, jaundice, ulcers, aggression, poor coordination, blindness, seizure

210
Q

diagnosis of liver failure

A
  • lab work: blood and urinalysis
  • X-rays and ultrasound: hepatomegaly and diagnosis of cancer, cysts or vascular abnormalities
  • medical history
211
Q

treatment of liver failure

A

treat underlying cause, fluids, diet changes, antibiotics
- diuretics, Vitamin K

212
Q

prognosis of liver failure

A

dependent on diagnosis, some conditions are good

213
Q

what is heaptic fibrosis

A

When scar tissue forms and continuously replaces the normal tissue. Not associated with an underlying condition. Characterised by decrease in the size of the liver and particular condition can show changes in blood vessels between the intestines and liver

214
Q

predisposition of hepatic fibrosis

A

young dogs, under 2 years

215
Q

cause of hepatic fibrosis

A

activation of myofibroblasts can cause hepatic fibrosis – causes inflammation, oxidative stress

216
Q

signs of hepatic firbosis

A

ascites, abdominal distension, weight loss, diarrhoea, jaundice, PUPD

217
Q

diagnosis of hepatic firbosis

A
  • physical exam: urinalysis, stool sample
  • blood: bilirubin and cholesterol should be abnormal and liver enzymes, anaemia, and WBC high
  • radiographs
  • abdominocentesis
218
Q

treatment of hepatic firbosis

A

no proven treatments, address the underlying cause, when cause is unknown: anti-inflammatory or immunosuppressive agents, low protein diet
- colchicine: inhibits microtubule polymerisation: inhibits inflammation and fibrosis: dogs: few case reports + significant GI side effects

219
Q

prognosis of hepatic fibrosis

A

cannot be cured, so dependent on compliance of owner

220
Q

what is HE

A

Neurological dysfunction in patients with liver disease

221
Q

cause of HE

A

Pss
cirrhosis
hepatic lipidosis

222
Q

pathogeensis of HE

A
  • ammonia crosses the BBB
  • brain is very sensitive to toxic effects of ammonia, but doesn’t possess urea cycle, so NH3 is detoxified by conversion to glutamine by astrocytes
  • excessive NH3 and glutamine build up results in osmotic stress of astrocytes with cell swelling and cerebral oedema
223
Q

signs of HE

A
  • subtle, non-specific signs: anorexia, depression, weight loss, lethargy, nausea, fever, hypersalivation (especially in cats)
  • CNS signs: non-localising, trembling, ataxia, hysteria, dementia, circling, head pressing
224
Q

diagnsosi of HE

A

based on symptoms (history and physical examination)
- blood (maybe anaemic)
- biochemistry: elevated liver values, high bilirubin, high kidney, low albumin, low glucose and electrolyte abnormalities
- urinalysis – abnormally dilute urine
- bile acid test if liver disease
- X-ray: to see for enlarged: liver, spleen, tumours
- US, CT or MRI

225
Q

treatment of HE

A

supportive therapy and non-meat protein-based diets and lactulose + metronidazole
- mannitol (reduce swelling on brain), L-ornithine L-aspartate (LOLA) to decrease ammonia levels
- seizures: anticonvulsant (diazepam, levetiracetam or phenobarbital)
- enema may be used to reduce colon bacteria

226
Q

cause of ascites

A

organ failure or low protein levels (nephrotic syndrome), CHF, right heart failure, chronic liver failure, portal hypertension, kidney failure, malnutrition, hypoalbuminaemia, lymphoma, peritonitis

227
Q

pathogenesis of ascites

A

fluid and blood can leak back into abdominal cavity from diseases organs, from parasitic migration, from leaks in the tricuspid valve in the heart, or from blocked blood vessels due to high blood pressure so It then accumulates

228
Q

signs of ascites

A

distension of abdomen, lack of appetite, difficulty breathing, abdominal discomfort + pain, lethargy, coughing

229
Q

diagnosis of ascites

A
  • fluid thrill test – palpating the abdomen which may reveal the presence of fluid wave
  • CT and ultrasound
  • abdominocentesis
  • faecal exam, urinalysis, X-ray, ECG, echo, biopsies
230
Q

treatment of ascites

A
  • spironolactone 2mg/kg PO q24 (can be increased to 4mg/kg PO q 24)
  • furosemide – 1-2mg/kg PO q12
  • mild restriction of sodium
  • abdominocentesis should be avoided
231
Q

prognosis of ascites

A

with concurrent treatment, can be reduced and managed but it can return if cause not resolved

232
Q

predisposition of acute hepatitis

A

less common than chronic hepatitis

233
Q

cause of actue hepatisis

A

infectious or toxic (leptospirosis, E.canis, clostridium, drugs, idiopathic), aflatoxin

234
Q

signs of acute hepatitis

A

acute onset of: anorexia, vomiting, PUPD, dehydration, HE with depression, jaundice, fever, cranial abdominal pain, ascites and splenomegaly

235
Q

diagnosis of actue hepatitis

A

history, clinical signs and findings
- liver histopathology confirms but often not obtained until recovery or post-mortem
- marked increased in ALT and AST
- jaundice and increased in markers of cholestasis
- hyperbilirubinemia, hypoglycaemia and hypokalaemia

236
Q

treatment of acute hepatitis

A

supportive measures and allowing liver to recover, corticosteroids aren’t indicated and may worsen prognosis, plasma transfusion

237
Q

prognosis of acute hepaitits

A

poor, if they recover from acute phase have a good chance of complete recovery

238
Q

differentials for acute hepatitis

A

CAV-1 and Leptospira

239
Q

predisopsition of corhinc hepatitis

A

Cocker spaniels, dalmatian, Doberman pinschers, springer spaniels, great Dane, labs, Samoyed, standard poodle, young-middle aged

240
Q

cause of chronic ahepatitis

A

mutation of gene involved with copper storage disease, mostly idiopathic

241
Q

pathogenesis of chronic hepatitis

A

relates to the loss of hepatic mass resulting in loss of function and late in disease process, development of portal hypertension

242
Q

signs of chronic hepatitis

A

no clinical signs until late in the disease process

243
Q

diagnosis of chronci hepatitis

A

take liver biopsy, diagnostic imaging and aspiration of bile and culture
- persistently elevated liver enzymes

244
Q

treatment of chronic hepaitis

A

treating underlying cause, supportive liver function and animals nutritional and metabolic needs
- with idiopathic hepatitis = nonspecific and attempts to slow progression of clinical signs
- choleretics: ursodiol – modulates bile acid pool in biliary stasis
- antioxidants: Vitamin E
- glucocorticoids/ other immunosuppressive drugs
- antifibrotics/antibiotics

245
Q

predisposition of feline inflammatory infectious hepatic disease

A

any cat, any age sex or species

246
Q

cause Feline inflammatory infectious hepatic disease

A

viral, bacterial, fungal, parasites, poisoning, gall stones, stress, environmental cause, dietary, immune system, certain medications

247
Q

signs of Feline inflammatory infectious hepatic disease

A

lethargy, vomiting, weight loss (unspecific signs), fever, abdominal swelling, jaundice, increased thirst, increased urination, dark urine, changes in behaviour, grey/white faeces

248
Q

diagnosis of Feline inflammatory infectious hepatic disease

A

FNA, abdo US, biopsy, blood, urinalysis, faecal exam, bile acids

249
Q

Feline inflammatory infectious hepatic diseasetreatment of

A

ATB according to culture (ampicillin, amoxicillin and clavulanate), NSAIDs, IV fluids, feeding therapy and supplementation and nutritional support

250
Q

prognosis of Feline inflammatory infectious hepatic disease

A

poor if advanced

251
Q

predisposition of lymphocytic hepatitis

A

older cats with history of hyperthyroidism

252
Q

cause of lymphocytic hepatiis

A

related to thyroid disease or immune system dysfunction

253
Q

signs of lymphocytic hepatitis

A

unspecific signs: nausea, inappetence, lethargy, vomiting and jaundice, diarrhoea

254
Q

diagnosis of lymphocytic hepaitis

A

X-rays, ultrasound, liver biopsy, CBC, biochemistry, urinalysis

255
Q

treatment of lymphocytic hepatitis

A

ATB while awaiting culture results, prednisolone, supportive

256
Q

predisposition of infectious feline hepatobiliary disease

A

young-middle aged cats

257
Q

cause of infectious feline hepatobiliary disease

A

micro and macro hepatic abscesses, polymicrobial growth in >50% cats
bacterial infections: secondary to ascending intestinal bacteria: klebsiella, listeria, salmonella, brucella, yersinia…
- viral infections: FeLV, FCV, FIP and FIV
- liver flukes: platinosomum spp

258
Q

signs of infectious feline hepatobiliary disease

A

acute vomiting, diarrhoea, anorexia and lethargy, abdominal pain, fever, icterus

259
Q

diagnosis of infecitious feline hepatobiliary disease

A

iver biopsy (tru-cut-type/ FNA)to differentiate from effusive FIP, increased ALT, AST, GGT and ALP

260
Q

treatmetn of infectious feline hepatobiliary disease

A

ATB at least 6 weeks

261
Q

predisposition of hepatic vascular anomalies - PSS

A

mostly young animals before 1-2 yr. and acquired 3 year. More common in dogs than cats
- Persian and Himalayan cats
- extrahepatic: terriers, maltese, mini schnauzers
- intrahepatic: irish wolf hound

262
Q

pathogenesis of PSS

A

acquired (multiple extrahepatic, secondary to fibrosis, secondary to arteriovenous malformations)

congenital: macrovascular PSS (intrahepatic – large breeds, extrahepatic- small), primary portal vein hypoplasia, disturbances in outflow

Extrahepatic PSS
- abnormal communications between portal vein or one of its contributors and the caudal vena cava

Intrahepatic PSS
- may be left sides: persistence of the fetal ductus venosus after birth
- right sided/centrally located in the liver” anomalous vessels

263
Q

signs of PSS

A

HE, vomiting, anorexia, pica, diarrhoea, ptyalism (cats), melena, haematemesis, pollakiuria, ascites, anaemic, neurologic
smaller in structure, failure to gain weight, copper coloured irises (cats)

264
Q

diagnosis of PSS

A
  • based on neurological signs
  • blood: anaemia, microcytosis,
    o low: albumin, glucose, cholesterol urea,
    o high: serum liver enzyme activities
  • urinalysis: low USG, ammonium biurate crystalluria, proteinuria
  • serum bile acids
  • ammonia and ammonia tolerance test
  • Xray, US, scintigraphy, CT (liver atrophy)
265
Q

treatment of PSS

A

medical (supportive, prognostic 50% euthanised within 10Mo) surgical (shunt attenuation: ligation, aneroid constrictors, cellophane bands)

266
Q

predisposition of feline hepatic lipidosis

A

cats prone to mild to moderate steatosis when anorexia and in response to toxic insults
- younger to middle age female cats and obese

267
Q

cause of feline hepatic lipidosis

A

obesity, anorexia and stress, environmental differences
- Secondary hepatic lipidosis is seen in cats that are not obese, usually due to neuroendocrine responses to stress

268
Q

pathogenesis of feline hepatic lipidosis

A

massive accumulation of fat in hepatocytes leading to acute loss of hepatocyte function
- excessive peripheral lipid mobilisation to the liver, deficiency of dietary proteins and other nutrients that would usually allow fat metabolism and transport out of the liver

269
Q

signs of feline hepatic lipidosis

A
  • primary: after 6-7 weeks of anorexia and/or loss of more than 25% BW
  • secondary: cholangitis, pancreatitis, IBD, neoplasia, DM, hyperthyroidism
  • acute loss of hepatocyte function and hepatocyte swelling
  • cats usually jaundiced and have intermittent vomiting and dehydration
  • depression, ptyalism
270
Q

diagnosis of feline hepatic lipidosis

A
  • palpable hepatomegaly on physical exam
  • biochemical: increased BHB, increased circulating triglycerides, NEFA and VLDL
  • lab (GGT normal, hypokalaemia, hyperglycaemia)
  • histopathology of a wedge biopsy
  • use FNA
271
Q

treatment of feline hepatic lipidosis

A

early intensive feeding, high protein diet, rapid institution of tube feeding, treat any concurrent inflammatory disease, fluids (to address electrolyte abnormalities)

272
Q

prognosis of feline hepatic lipidosis

A

good as long as feeding is rapidly and effectively instituted
- older age was a poor prognostic indicator
- secondary hepatic lipidosis may do slightly worse than primary

273
Q

predisposition of liver tumour

A

Primary liver tumours: rare to infrequent (older animals), dogs: meta changes much more frequent, uncommon in cats,
- unlike in cats, malignant tumours are more common than benign, with metastases – spleen, pancreas and GI

274
Q

cause of liver tumour

A

no predisposing factors have been identified, except maybe primary copper storage

275
Q

signs of lvier tumour

A
  • primary malignant tumours of liver are usually seen in older cats (10-12yrs) and no obvious gender predisposition
  • lethargy, vomiting, weight loss, ascites or jaundice
  • 50% of cats with liver tumours are asymptomatic
276
Q

diagnosis of liver tumour

A
  • diagnostic imaging (hepatomegaly), cytology and histology
  • high liver enzyme activity and bile acid concentration and mild anaemia and neutrophilia are common but non-specific findings
277
Q

treatment of liver tumour

A

primary tumour relies on surgical removal if they are resectable
- primary hepatic tumours generally have a poor response to chemotherapy
- radiotherapy isn’t wise as normal liver tissue is very radiosensitive

278
Q

rognosis of liver tumour

A

benign tumours is good after resection but poor for cats with any type of malignant liver tumour. However, most cats with lymphoma of the liver respond to chemotherapy

279
Q

predisposition of acute pancreatitis

A

terriers, schnauzers, domestic short hair, middle aged dogs and cats

280
Q

cause of acute pancreatitis

A

mutations of trypsin which can predispose to pancreatitis

281
Q

pathogenesis of acute pancreatitis

A

inappropriate early activation of trypsinogen inn the pancreas as a result of increased autoactivation of trypsinogen

282
Q

signs of acute pancreatitis

A

vomiting, anorexia, diarrhoea, abdominal pain, lethargy, dehydration, hypovolemic shock, DIC, MODS, mild abdominal pain, jaundice

283
Q

diagnosis of acute pancreatitis

A

presence of typical clinical signs, elimination of possible diff. dg, elevated PLI, typical ultrasound lesions, histopathology, fluid analysis (abdominal effusion)
- routine lab: CBC, electrolytes and urinalysis doesn’t help but helps with information and treatment
- TLI (trypsin like immunoreactivity) and PLI (pancreatic lipase immunoreactivity)

284
Q

treatment of acute pancreatitis

A

fluid, electrolytes, analgesia (fentanyl patch, tramadol) , food, antiemetics (maropitant, ondansetron, thiethylperazine), gastroprotection’s (H2 blockers: famotidine, ranitidine, PPI: omeprazole, sucralfate), ATB (cefotaxime, ciprofloxacin, metronidazole, clindaymycin), insulin, surgery

285
Q

prognosis of acute pancreatitis

A

mild with moderate pancreatitis: proper treatment, prognosis is favourable, severe: bad

286
Q

predisposition of chronic pancreatitis

A

rare and not that important in dogs, but most common form of pancreatitis in cats
- idiopathic: most common middle-aged dog, king Charles, cockers, collie or boxers, domestic short hairs mostly affected
- autoimmune: English cocker spaniels

287
Q

pathogenesis of chronic pacnreatitis

A

characterised by destruction parenchyma, irreversible changes. Leads to progressive/permanent impairment of exocrine and endocrine

288
Q

signs of chronic pancreatitis

A

vomiting, inappetence, colitic diarrhoea, pain on palpation, may develop jaundice

289
Q

diagnosis of chronic pancreatitis

A

clinical signs unclear or identical to AP, other tests be aware CP as possible D pathohistology
- gold standard: histology
- ultrasound lower sensitivity because there’s less oedema than in acute pancreatitis
- measure serum Vitamin B12 – supplemented if low

290
Q

treatment of chronic pancreatitis

A

analgesia, food, immunosuppressants

291
Q

prognosis of chronic pancreatitis

A

depends on successful neutralisation of pain as well as treatment of both DM and EPI

292
Q

predisposition of EPI

A

both dogs and cats, young GSH, rough collies

293
Q

cause of EPI

A

pancreatic acinar cell atrophy or destruction due to pancreatitis, can be autoimmune

294
Q

pathogensis of EPI

A

unctional diagnosis that results from lack of pancreatic enzymes. Approx 85-90% of the exocrine secretory pancreas must be non-functioning before signs of EPI are evident
- primary to pancreatic acinar atrophy (D): young GSD, autoimmune, rough collies and English setters
- secondary to end stage chronic pancreatitis (C,D): cats, middle aged/older small breed dogs (Charles, cockers)

295
Q

signs of EPI

A

voluminous faeces, often pale and steatorrhea, high defaecation frequency, weight loss, hyperphagic, chronic small intestinal diarrhoea, ravenous appetite, cats (hyporexia and lethargy)

296
Q

diagnosis of EPI

A
  • CBC, biochemical profile, urinalysis
  • TLI – trypsin like immunoreactivity
    o dog <2.5 ug/L and compatible clinical signs
    o cat < 8 ug/L
  • Cobolamine (decreased B12), folate
  • ELISA faecal elastase test
297
Q

treatment of eEPI

A

Specific
- exogenous enzymes: powdered pancreatic extracts, rarw chopped pancreas
- diet: low on fibre, restricted fat, vitamin supplementation B12
supportive
- antacid therapy
- treatment of concurrent disease

298
Q

prognosis of EPI

A
  • quite good, especially in dogs which respond well to initial therapy > 5 years
  • complicated EPI or recurrent acute phases of acute pancreatitis, prognosis is reduced
  • +DM the treatment is becoming more challenging and more expensive
299
Q

vascular ring anomaly

A

Congenital malformations of the great vessels and their branches that entrap the intrathoracic oesophagus and other intrathoracic structures

Cause: persistent right aortic arch – ligamentum arteriosum continues to develop from the left side and forms a fibrous band that crosses over the oesophagus to connect the main pulmonary artery and anomalous aorta

Signs: cause clinical signs of oesophageal obstruction

Diagnosis: survey thoracic x-ray shows severe dilation of oesophagus

300
Q

gastric neoplasia

A

Predisposition: uncommon in dogs and cats, dogs 6-9 years, cats 10-12, gastric leiomyoma tend to occur in older dogs, slight predominance for male dogs and cats to develop GI neoplasia
- most common in dogs: adenocarcinomas
- most common in cats: lymphosarcoma

Signs: vomiting, haematemesis, melena, anorexia, weight loss

Diagnosis:
- routine lab testing helps exclude non-gastrointestinal origins
- anaemia
- x-ray, ultrasound, endoscopy
- definitive diagnosis is based on cytological or histology demonstration of neoplastic cells – FNA

Treatment: chemotherapy, surgical resection

Prognosis: poor to grave

301
Q

delayed gastric emptying

A
  • most commonly recognised manifestation of gastric motility disorders

Cause: by outflow obstruction (congenital stenosis, FB, neoplasia granuloma, polyps)or defective propulsion (gastric disorders, gastritis, ulcer, neoplasia, peritonitis, pancreatitis)

Signs:
- vomiting (projectile – with pyloric stenosis)
- abdominal distension, weight loss, melena, abdominal discomfort, distension, bloating and anorexia

Diagnosis: suspect DGE when a pet vomits food at least 8 hours, often 10-16 hours after a meal
- dependent of the cause
- Lab: CBC, Biochem, serum gastrin and gastric pH
- abdominal imaging: plain and contrast
- ultrasonography
- endoscopy (before barium contrast)

Treatment:
- directed at underlying cause
- diet: food that facilitates gastric emptying, small amounts, frequent intervals, semi-liquid, protein and fat restricted
- prokinetic drugs: cisapride, erythromycin, metoclopramide)

Internal (12 decks)

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