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Farm Flashcards

1
Q

predisposition of simple indigestion

A

most common in cattle, rare In sheep and goats

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2
Q

cause of simple indigestipn

A

sudden changes in food or “mistakes” of nutrition

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3
Q

aetiology of simple indigestion

A
  • any dietary factor that can alter the intraruminal environment (spoiled or frozen feed too)
  • introducing urea to a ration
  • accumulation of excessive quantities of relatively indigestible feed that can impair function
  • turning cattle onto a lush cereal grain pasture… etc
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4
Q

signs of simple indigestion

A

anorexia and moderate drop in milk production, rumen is fully, firm and dough, faeces are normal to firm but reduce and can be soft-watery and foul smelling

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5
Q

diagnosis of simple indigestion

A

history, often multiple animals affect, hypocalcaemia present, rule out ketosis, rumen fluid analysis: reduced activity and concentration of large and small protozoa

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6
Q

treatment of simple indigestipn

A
  • re-establish normal GI motility, pH and flora: by ruminal transfaunation
  • feeding long-stem fibre
  • parenteral calcium solution
  • evacuate the GI tract
  • correct suspected dietary factors
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7
Q

prognosis of simple indigestion

A

good

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8
Q

acute ruminal lactic acidosis aetiology

A

most severe form of indigestion, cattle can accidentally gain access to large quantities of grain, improper mixing of TMR (total mixed ration)

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9
Q

cause of grain overload

A

: sudden change to a diet containing higher levels of finely ground, rapidly fermentable feeds

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10
Q

pathogenesis of grain overload

A
  • within 6 hours of ingestion, easily fermentable and high – sugar + starch concentrate is broken down to VFA, D and L lactic acid
  • number of gram-positive bacteria  increased amount of lactate  rumen falls to <5  destroying protozoa, cellulolytic organisms  impairs rumen motility  osmotic pressure rise substantially  results in movements of excessive quantities of fluid into the rumen  causing rise of fluid ruminal contents and dehydration
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11
Q

consequence of acidosis and dehydration

A

haemoconcentration, cardiovascular collapse, renal failure, muscular weakness, shock, death

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12
Q

pH < 5.5

A
  • low ruminal pH causes chemical rumenitis
  • endotoxin and bacteria escape into the portal circulation
  • septic emboli, dissemination in the liver, lungs, joints and kidney and laminitis3
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13
Q

signs of grain overload

A

anorexia, drastically decreased milk production, dehydration, subnormal temperature, elevated heart, elevated respiratory rates, totally static and enlarged rumen, cool skin surface, diarrhoea, or loose manure, weakness, ataxia, recumbency, abdominal pain, laminitis, coma and death

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14
Q

diagnosis of grain overload

A

history, confirmed by CE, assessment of rumen pH,
- CBC: neutropenia with left shift
- biochemistry: marked azotaemia
- metabolic acidosis
- rumen fluid analysis: sedimentation rate is fast, with a delayed or absent secondary flotation, decreased number of protozoa

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15
Q

treatment with grain overload

A

slaughter for salvage should be considered, restoration of rumen microenvironment
Mild cases
- rumen lavage with large tubes, application of large volume of warm water (15-20x), emptying the rumen via gravity flow, magnesium hydroxide diluted with water PO, laxative and charcoal IR
Serious cases
- rumenotomy and washed rumen, with water and emptied several times to remove as much lactate as possible
- fresh hay
- ruminal transfaunation, parenteral calcium, flunixin meglumine, procaine penicillin G at least 5 days
- thiamine

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16
Q

prognosis of grain overload

A
  • good – quality hay and no grain should be given during the convalescent period, then introduced gradually, if good appetite returns within 3 days, prognosis = good
  • some bacterial endotoxins can escape into circulation causing embolic infection of liver, lungs and other organs, resulting in fever and in some cases, death
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17
Q

cause of SARA

A

feeding of excessive quantities of concentrate with low level of well-structured fibrous roughage

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18
Q

pathogenesis of SARA

A

results from continued indigestion of these feeds over a prolonged period rather than sudden exposure without adequate adaption

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19
Q

signs of sARA

A

reduced or cyclic feed intake, decreased milk production, reduced milk fat, poor BCS, loose faeces

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20
Q

diagnosis of SARA

A

assessing rumen fluid samples or from telemetric rumen pH boluses sensors

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21
Q

treatment of SARA

A

no specific treatment, rather secondary conditions may need to be treated and the focus should be on prevention

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22
Q

cause of ruminal alkalosis

A

prolonged anorexia, poorly digestible roughage, simple indigestion, moudly food, spooield silage- coliform + proteins, high protein diets

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23
Q

pathogenesis of ruminal alkalosis

A

excessive ammonia, high protein diet  ammonia concentration rises  decomposition of proteins releases large amounts of ammonia that is absorbed into the blood  liver detoxifies it by converting it to urea  when the amount of absorbed ammonia is high  intoxication occurs
- alkaline ruminal fluid pH occurs most commonly when microbial fermentation is reduced while the animal continues to ingest saliva

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24
Q

signs of ruminal alkalosis

A

inappetence, anorexia, ruminal hypomotility, recurrent tympany, occasional diarrhoea with odour, weakness, salivation, tachypnoea, polyuria, CNS excitation, muscle tremors, incoordination, abortions

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25
Q

diagnosis of ruminal alkalosis

A

history, CE, rumen fluid analysis (pH 7.8, blackish green, strong odour and poor protozoal activity)

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26
Q

treatment of ruminal alkalosis

A
  • normalisation of rumen pH via food changes, antihistamines, vitamins, Ca, 5% acetate
  • supportive therapies: anticonvulsant therapy (phenobarbital, pentobarbital), IV fluid
  • urea poisoning: rapid intervention
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27
Q

prognosis for ruminal alkalosis

A

prognosis is poor for recumbent animals

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28
Q

define tympayn

A

over distension of the rumen, resulting in left-sided abdominal distension in both dorsal and ventral quadrants

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29
Q

frothy bloat

A
  • resulting from stable froth of dietary origin (usually higher in chloroplast membrane fragments and soluble protein)
  • coalescence of the small gas bubbles is inhibited
  • intraluminal pressure Increases because eructation cannot occur
  • cattle – grazing legume
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30
Q

free gas bloat

A
  • occur secondary to over ingestion of grain, which promotes excessive VFA production, lower pH and then lactic acidosis with rumen stasis
  • in calves with clostridial abomastitis-rumenitis
  • oesophageal motility, vagal indigestion, hypocalcaemia, listeriosis, tetanus
  • oesophageal obstruction due to foreign body
  • stenosis of oesophagus or compression in lymphadenopathy or abscess
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31
Q

signs of tympany

A
  • acute onset, commonly develops in 1st 3 days after on bloat producing pasture
  • typically left sided distension extending dorsally to the midline with a full paralumbar fossa
  • rectal examination: ruminal distension extending into the right abdomen dorsally and ventrally
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32
Q

diagnosis of tympayn

A
  • frothy bloat is usually obvious clinically – not relieved by a stomach tube
  • free-gas bloat is accompanied with signs of causative disorder – confirmed if stomach tube can be passed easily and relieves bloat
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33
Q

treatment of tympany

A
  • relief of the ruminal distention and correction of the primary cause
  • decompression with stomach tube
  • additional treatment with antifoaming agents: poloxalene, polymerised methyl silicone (3.3$ emulsion, cattle 30-60mL, sheep 7-15mL), vegetable oil alone, mineral oil
  • trocarisation for emergency relief: trocar and cannula can be inserted into the rumen through a small incision, if trocar fails then rumenotomy
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34
Q

prevention of tympany

A
  • feeding hay before turning cattle on pasture
  • mature pasture are less dangerous than rapidly growing pastures
  • continual administration of an antifoaming agent during the risk period
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35
Q

ruminal drinking

A

Calves – have failure of the reticular groove reflex (milk flows into rumen + is fermented to lactate)
3–8-week-old dairy calves fed with milk mostly by bucket

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36
Q

aetiology of ruminal drinking

A

milk in reticulorumen is fermented and lactic acid is produced, drop in pH of rumen, absorption of organic acids  metabolic acidosis
Chronic rumenitis  hyperkeratosis/parakeratosis  impairment of ruminal motility  chronic and recurrent bloat

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37
Q

cause of ruminal drinking

A

stress

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38
Q

pathogenesis of ruminal drinking

A

fails to close  milk flow directly into the rumen and is fermented to lactic acid

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39
Q

signs of ruminal drinking

A

depression, ataxia, weakness, diarrhoea/clay like faeces, dehydration

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40
Q

diagnosis of ruminal drinkin

A

history, CE, passage of stomach tube may cause reflux of a grey fetid fluid

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41
Q

treatment of ruminal drinking

A

removal of the contents and lavage with warm water via stomach tube. Flunixin meglumine (NSAIDs) to reduce inflammation from endotoxemia

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42
Q

prevention of ruminal drinkning

A

feeding small volume of milk from a nipple-bottle. Closure of reticular groove can be triggered by allowing the calf to suck a finger before the milk is offered

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43
Q

predisposition of traumatic reticuloperitonitis

A

dairy cattle, occasionally in beef, rarely in sheep and goats

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44
Q

cause of traumatic reticuloperitonitis

A

cattle don’t use lips to discriminate between fibrous feed + metabolic objects

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45
Q

pathogenesis of traumatic reticuloperitonitis

A

consequence of perforation of the reticulum with ingested foreign objects like nails and pieces of wire
- after ingestion, objects fall directly into the reticulum or pass into the rumen and in 24-48hr are propelled into the reticulum
- by ruminal contractions subsequently carried over the ruminoreticular fold into the cranioventral part of the reticulum
- reticulo-omasal orifice is elevated above the floor, which tends to retain heavy objects in the reticulum
- honeycomb like reticular mucosa traps sharp objects
- contractions of the reticulum promote penetration of the wall by the foreign object

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46
Q

signs of traumatic reticuloperitonitis

A

Local peritonitis:
- decreased milk production, sudden reticulorumen, atony, anorexia, increased temp, HR + RR, arched back (pain)
Diffuse peritonitis:
- fever, increased HR + RR, total rumen + GI stasis, grunting – diffuse persistent pain
Pleuritis
- depression, increased HR, pyrexia, muffled lung sounds
Pericarditis
- muffled heart sounds, splashing sounds, pericardial friction, jug vein distension

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47
Q

diagnosis of traumatic reticuloperitonitis

A

History, CE
- CBC
- Biochem: plasma fibrinogen, haptoglobin, amyloid A, total plasma protein
- metabolic alkalosis
- pain tests
- metal detectors, abdominal US and radiography

haptoglobin and amyloid A for inflammatory markers

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48
Q

treatment of traumatic reticuloperitonitis

A
  • conservative medical treatment: oxytetracycline, antibiotics therapy (3-7days)
  • symptomatic therapy (oral fluids, ruminotorics, calcium solutions, oral electrolyte)
  • rumen transfuantes, magnet, stall rest
  • metabolic alkalosis: potassium chloride orally
  • surgical treatment: rumenotomy with manual removal of object from reticulum, drainage of reticular abscess into the lumen of reticulum
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49
Q

prevention of traumatic reticuloperitonitis

A

avoiding the use of bailing wire, keeping cattle away from sites of new construction, apply prophylactic magnets and electromagnetic plates

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50
Q

cause of vagal indigestion

A

traumatic reticuloperitonitis (anterior/posterior functional stenosis)

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51
Q

pathogenesis of vagal indigestion

A

Lesions affecting the ventral vagus nerve and its branches (injury, inflammation, or pressure) cause complex clinical signs of indigestion with intermittently or constantly ruminal distension

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52
Q

signs of vagal indigestion

A

decreased: appetite, milk production and HR but normal temp and RR
- L dorsal + R ventral distension distension = ‘papple’ shape
- fever, salivation, swelling abscess, neoplasia

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53
Q

diagnosis of vagal indigestion

A
  • history of primary disorder, CE
  • clinical pathology:
    o persistent lymphocytosis  lymphosarcoma
    o elevated serum globulin may suggest reticular or liver abscess
    o metabolic alkalosis
  • abdominal US
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54
Q

treatment of vagal indigestion (chronic indigestion)

A

surgery (rumenotomy), emptying the rumen, removing the foreign bodies, lancing abscess into reticulum, supportive therapy

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55
Q

prognosis of vagal indigestion

A

usually pooe

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56
Q

predisposition of abomasa displacement

A

during first 6 weeks of lactation, bull and calves at any age, most common in pluriparous cows, in 1st calf heifers, lactating cattle of any age

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57
Q

cause of abomasa dis[lacemetn

A

multifactorial, excessive production of VFA (increases gas production in abomasum), abomasal hypomotility (hypocalcaemia, ketosis, hypokalaemia, retained placenta, mastitis, metritis, indigestion)

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58
Q

LDA

A
  • partially gas distended abomasum  displaced upward along left abdo wall lateral to rumen
  • fundus and greater curvature of abomasum primarily displaced
  • which passes underneath rumen and retained
  • abomasum obstruction is partial  mild metabolic alkalosis
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59
Q

RDA

A

hypomotility, gas production and displacement of partially gas filled abomasum

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60
Q

abomasa volvulus

A
  • serious, life threatening
  • rotation of abomasum on mesenteric axis, impairs circulation and causes ischemia
  • large quantity of chloride-rich fluid accumulates in abomasum
  • moderate-severe dehydration
  • it doesn’t follow in all cases of RDA
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61
Q

signs of abomasal displacement

A
  • anorexia, decreased milk production, dull appearance, mild dehydration, TRIAS normal, rumen motility normal, LDA (ping 9-13th rib), RDA (ping 10-13th, dilated caecum, presence of fluid – splashing and tinkling sounds)
  • AV: depressed, tachycardia
  • if fever and pneumoperitoneum in cow with LDA  abomasal perforation
  • weakness, toxaemia, ping louder, caudal abomasum palpable rectally
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62
Q

diagnosis of abomsal dispalcemtn

A
  • history: recent parturition, partial anorexia, decreased milk production
  • rectal exam
    o LDA  medially displaced rumen and left kidney
    o RDA  occasionally palpable
    o insert 9cm 18G spinal needle 2 inches below bottom of “ping” and aspirate, if pH < 5 = abomasal fluid
  • KB in milk and urine
  • hypocholermic, hypokalaemia, metabolic alkalosis
  • US
  • L – lactate concentration: with AV <2mmol/L
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63
Q

treatment of abomasa displacement

A
  • medically: oral laxatives – after eat as much hay as possible to fill rumen with roughage
  • ruminotoric, antacids
  • cholinergic medications
  • supportive therapy: calcium solution, potassium chloride, electrolyte solution
  • rolling: only for simple LDA, never for RDA or AV
  • surgically: right flank omentopexy, left flank abomasopexy, right paramedian abomasopexy, left paralumbar abomasopexy
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64
Q

prevention of abomasa displacement

A
  • ensuring rapid increase in rumen volume after calving
  • maintaining adequate roughage in diet, feeding total mixed ration
  • avoid rapid dietary changes and post parturition hypocalcaemia
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65
Q

predisposition of abomasa ulcers

A

dairy cattle and calves (first 4-6 weeks after parturition), prolonged inappetence, high volumes of milk, NSAIDs

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66
Q

cause of abomasa ulcers

A

multifactorial, intensive management, highly acidic, high-energy, finely ground diets consisting of concentrates and silage, high milk production, stress

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67
Q

pathogenesis of abomsal ulcers

A

when the thick layer of mucus that protects abomasum from digestive juice is reduced  digestive acids eat away at the tissues that line the abomasum  ulcer

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68
Q

classification of abomasa ulcres

A
  • Type 1: is an erosion or ulcer without haemorrhage
  • Type 2: is haemorrhagic
  • Type 3: is perforated with acute localised peritonitis
  • Type 4: is perforated with acute diffuse peritonitis
  • Type 5: is perforated with peritonitis within the omental bursa
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69
Q

signs of abomasa ulcers

A

mild abdominal pain, bruxism, tachycardia, melena, severe haemorrhage (pale MM, cold)
- perforating ulcers (localised peritonitis): anorexia, fever, pain, rumen hypomotility/stasis
- diffuse peritonitis: anorexia, complete stasis, fever, cold skin, dehydration, grunt or groan
- progression to recumbency

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70
Q

diagnosis of abomsal ulcers

A
  • history, CE
  • occult blood test of faeces to confirm melena
  • PCV can be used to determine degree of haemorrhage
  • X-rays, US
  • inflammatory exudate and evaluation of peritoneal fluid (confirms peritonitis)
  • WBC, serum albumin and TP = low
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71
Q

treatment of abomsal ulcers

A
  • local peritonitis: stall rest, broad spectrum ATB, histamine type 2 blockers IV, PPI
  • corticosteroids and NSAID are contraindicated as they may contribute to further ulceration
  • bleeding ulcers: blood transfusion and fluid therapy
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72
Q

prognosis of abomsal ulcers

A
  • localised peritonitis: good, takes about 1-2 weeks recovery
  • diffuse peritonitis: grave – if they recover, usually have massive abdominal adhesions
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73
Q

prevention of abomasa ulcers

A

avoid prolonged periods of inappetence and low abomasal pH

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74
Q

abomasa impaction predisposition

A

pregnant beef cows during winter month, rare in dairy, calves (idiopathic)

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75
Q

cause of abomasa impaction

A

probably related to abomasal hypomotility or dietary impaction due to ingestion of poorly digestible material

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76
Q

signs of abomasal impaction

A

complete anorexia, scant faeces, moderate distension of abdomen, weakness, weight loss, decreased milk production, grinding teeth

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77
Q

diagnosis of abomasa Impaction

A
  • Rectal exam: enlargement of the rumen dorsal and ventral sacs
  • metabolic alkalosis and haemoconcentration
  • objective: during right/left side exploratory laparotomy or rumenotomy
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78
Q

treatment of abomasa impaction

A
  • idiopathic abomasal impaction massage via right flank laparotomy and administration of mineral oil, coffee or magnesium products
  • rumenotomy: empty rumen and infuse mineral oil directly into abomasum through orifice, often poor prognosis
  • prokinetic agents: erythromycin, bethanechol, lidocaine constant rate
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79
Q

prognosis of abomasa impaction

A

good if primary disorder or dietary impaction treated early, but often poor

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80
Q

predisposition of Abomasitis, abomasal tympany and abomasal ulceration in calves

A

beef calves, lamb and dairy calves, more common in bucket fed calves than bottle

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81
Q

cause of Abomasitis, abomasal tympany and abomasal ulceration in calves

A

clostridium perfingens type A, sarcina, salmonella typhimurium DT104

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82
Q

signs of abomasitis, abomasal tympany and abomasal ulceration in calves

A

acute abdominal bloat, anorexia, shock, diarrhoea, distension of both sides, gas filled abdomen

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83
Q

abomasitis, abomasal tympany and abomasal ulceration in calves diagnosis

A

metabolic acidosis, respiratory acidosis
- low serum chloride, azotaemia, elevated PCV
- immature and toxic-appearing neutrophils
- US: fluid + gas may be seen throughout right and left ventral abdomen
- oedematous and thickened wall of abomasum

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84
Q

treatment of abomasitis, abomasal tympany and abomasal ulceration in calves

A

intensive: colloids, crystalloids, systemic antibiotics

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85
Q

prevention of abomasitis, abomasal tympany and abomasal ulceration in calves

A

routine disinfection of equipment, feeding milk at body temperature, isolation of affected calves, use of bottle rather than bucket

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86
Q

cause of obstructive diseases of SI

A
  • intussusception of jejunum and ileum
  • volvulus of duodenal sigmoid flexure or caecocolic
  • luminal occlusion of jejunum (blood clot, mural thickening, extramural mass, herniation)
  • atresia coli, recti and ani
  • faecal impactions of small intestine
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87
Q

signs of obstructive diseases of SI

A

acute onset of anorexia and GI stasis, milk production in lactating cows drops suddenly, abdominal distension, colic, absence of manure production

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88
Q

diagnosis of obstructive diseases of SI

A
  • rectal examination: distended loops of bowel may be palpable and intussusception and fibrous bands
  • fluid may be heard on simultaneous ballottement and auscultation of right side of abdomen
  • US: distended loops of small bowel
  • biochemistry: hypokalaemia, hypocholermic, metabolic acidosis
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89
Q

treatment of obstructive diseases of SI

A
  • right sided exploratory laparotomy
  • supportive therapy
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90
Q

prognosis of obstructive disease of SI

A

varies, economically may dictate slaughter

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91
Q

what is fat necrosis

A

Hard masses in the mesentery and omentum that gradually causes partial or complete extraluminal intestinal obstruction

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92
Q

predisposition of fat necrosis

A

usually over conditioned middle-aged to old

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93
Q

pathogenesis of fat necrosis

A

fat necrosis  rectal constriction occurs  establishing a risk for iatrogenic rectal injury during rectal palpation

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94
Q

signs of fat necrosi

A

partial anorexia, loose manure, occasional abdominal distension or mild colic

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95
Q

diagnosis of fat necrosis

A

rectal exam: hard mass around S.I, rectum or colon. US: biopsy or exploratory laparotomy to confirm

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96
Q

treatment of fat necrosis

A

exploratory laparotomy and surgical removal

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97
Q

prognosis of fat necrosis

A

bad

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98
Q

predisposition (+ predisposing factors) of caecal dilation and volvulus

A

dairy cattle, early lactation
: hypocalcaemia, indigestion and endotoxemia

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99
Q

cause of caecal dilation and volvulus

A

hypocalcaemia, endotoxemia secondary to metritis or mastitis and indigestion

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100
Q

pathogenesis of caecal dilation and volvulus

A
  • In simple caecal dilatation, the caecum distends with gas and fluid and the apex begins to rise in the abdomen from its normal location toward or into the pelvic inlet
  • Further distension of the caecum leads to rotation of the caecum (CW direction) as viewed from the right side or a ventral or dorsal retroflexion
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101
Q

signs of caecal dilation and volvulus

A

inappetence, reduced manure production, mild/moderate abdominal distension, < milk production, colic, dehydration

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102
Q

diagnosis of dilation

A
  • right sided ping by simultaneous percussion and auscultation (paralumbar fossa to 1-3rd rib cranial)
  • right paralumbar fossa appears “full”
  • rectal: dilated caecum easily palpable in right caudal abdomen, apex of caecum is directed into pelvic inlet
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103
Q

diagnosis of volvulus

A
  • signs more remarkable + metabolic alkalosis
  • large ping in R caudal abdo
  • rectal = dilation + volvulus, maybe distended ileum
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104
Q

treatment of caecal dilation ad volvulus

A
  • medical: caecal dilatation with stable patients
    o laxative ruminotoric (mixed with warm water using a stomach tube)
    o transfaunation
    o calcium and potassium solution
    o diet: avoid highly fermentable feeds
    o treatment must continue for 3-7 days
  • surgical treatment: right flank laparotomy followed by typhlotomy
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105
Q

what is downer cow syndrome

A

Non-ambulatory cattle recumbent for at least 24 hours without obvious reason

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106
Q

predisposition of downer cow syndrmoe

A

dairy cows (with previous episodes of milk fever), beef (after prolonged/difficult calving), delay of >4hr in treatment for recumbent milk-fever cows, hypophosphatemia and/or hypokalaemia

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107
Q

cause of downer cow syndrome

A

ischemic myopathy of large muscles of pelvic limb, ischemic neuropathies, secondary to prolonged recumbency, traumatic injury

108
Q

compartment syndrome (downer)

A

Compartment of the body is composed of muscle and nerves within an anatomically defined area that is surrounded by a rigid muscle fascia layer  6 hours

mechanical constriction of the venous draining leads to ischaemic muscle and nerve necrosis.

109
Q

crush syndrome (downer)

A

Refers to the sum of the systemic effects of extensive muscle tissue injury and is attributed to the massive release of muscle-tissue breakdown products into the blood circulation

muscle breakdown releases myoglobin, which can cause renal failure, and potassium which can cause heart failure.

110
Q

signs of downer cow

A

Alert downer:
- unable to stand, sternal recumbency, normal mental status, appetite and thirst normal/mildly decreased
Non-alert:
- persistent recumbency, altered mentation and vital signs, unable to maintain sternal recumbency, abnormal position of legs
Creeper cows
- alert recumbent, cows unable to bear weight on hindlimbs but use forelimbs to crawl

111
Q

diagnosis of downer cow

A
  • increased serum activity of CK and AST
  • Serum P and K conc may be decreased/increased
  • proteinuria, myoglobinuria
  • ischemic necrosis, edema and haemorrhage of large medial thigh muscle
112
Q

treatment of downer cow

A
  • roll animal from side to side every few (24)hrs
  • NSAID  fluid and electrolyte therapy  hoist cows making them stand
  • hip lifters, body slings, water flotation tanks
113
Q

prevention of downer cow

A

treat all high risk cows with Ca salts PO to decrease change of milk fever

114
Q

control of downer

A

observed 12-24hr before and after calving, if recumbent – don’t delay treatment for more than 1 hr, can treat all high risk cows with calcium salts orally to prevent clinical milk fever

115
Q

gastric ulcers in swine predisposition

A

sows and growing pigs

Usually pars oesophagus of stomach

116
Q

cause of gastric ulcer in pig

A
  • multifactorial
  • nutritional factors (low protein, low fibre and high energy diet, high level of wheat, high levels of unsaturated fats, low zinc, high iron, copper and calcium)
  • physical aspects of feed (size, pelleted, high moisture)
  • managemental factors (irregular feeding patterns, transportation, increased stocking density, poor management, inconsistent temperature, excessive aggression)
117
Q

signs of gastric ulcer in pig

A

Anaemia, dehydration, grinding of the teeth, dark faeces, vomiting, healthy animals found dead and very pale, nutritional deficiencies

118
Q

diagnosis of gastric ulcer in swime

A

clinical signs and PM exams, ulceration always differential in pale sow, faecal exam for blood and parasites and exam of stomach at slaughter

119
Q

treatment of gastric ulcer in pigs

A

separating the pig, pale/anaemic (Vit K and antihematinics), access to fibre, ranitidine

120
Q

prognosis of gastric ulcer in pig

A

poor

121
Q

heat stroke cause in pig

A

extreme temperature and water shortages

122
Q

signs of heat stroke in pig

A

panting, lethargy, reduced feed intake, reduced growth and milk production, diarrhoea, increased water consumption, increased urination, rectal temp 43C<

123
Q

diagnosis of heat stroke in pig

A

increased respiration and loss of appetite

124
Q

treatment of heat stroke in pig

A

wallows, cool, wet towel on the neck, consider diluted vinegar on skin as it evaporates quickly, dibble cold water into rectum, feed electrolyte rebalancing solutions (never use cold/freezing water as sends them into shock)

125
Q

prognosis of heat stroke in pig

A

good with cooling down, otherwise death

126
Q

cause of Porcine stress syndrome

A

stress or transport myopathy, anaesthetics, depolarising muscle relaxants, following muscle activity

127
Q

pathogenesis of porcine stress syndrome

A

Group of conditions associated with autosomal recessive gene (acute stress induced sudden death ((malignant hyperthermia)), pale soft exudative muscle, dark firm dry meat, back muscle necrosis
- after muscle activity metabolism changes to anaerobic, acidity in muscle increases, temp increases

128
Q

signs of porcine stress syndrome

A

muscle tremor, muscle rigidity, inability to walk, rapid respiration, hyperthermia, acute right heart failure, death within 20 minutes

129
Q

diagnosis of porcine stress syndrome

A

accelerated onset of rigor mortis (5 mins), halothane test, genetic testing (PCR)

130
Q

treatment of porcine stress syndrmoe

A
  • malignant hyperthermia (under anaesthesia) – by hyperventilating with oxygen
  • metamizole, beta-blockers, bicarbonate and cooling
  • farm animals, treatment is not possible
  • hetero- and homozygous carried should be culled
131
Q

prognosis of porcine stress syndrome

A

variable, can appear as sudden death

132
Q

cause of back muscle necrosis

A

porcine stress syndrome

133
Q

pathogenesis of back muscle necrosis

A

degenerative changes take place in the back muscles along each side of the spine

134
Q

signs of back muscle necrosis

A

sudden onset after exercise, severe pain in lumbar muscles, incoordination, lameness, dog sitting position, temp normal, discolouration of skin over the affected area

135
Q

diagnosis of back muscle necrosis

A

PCR

136
Q

treatment of back muscle necrosis

A
  • inject with phenylbutazone/other painkiller
  • inject with corticosteroids provided animal isn’t pregnant
  • if temperature – injection of long-acting penicillin
137
Q

predisposition of nutritional myopathy in pig

A

animals 3- 7weeks of age, no breed or sex predilections, pigs 5-06okg

138
Q

cause of nutritional myopathy in spig

A

ingestion of plants high in inhibitors or vit E, fed diets from plants that grown in selenium deficient soils or soils containing selenium antagonists

139
Q

pathogenesis of nutrtional myopathy in pig

A

generalised myopathy in skeletal muscles

140
Q

signs of nutritional myopathy in pig

A

ataxia, stiff gait, staggering gait, weakness, paralysis, depression, anorexia and recumbency prior to death, chronic cases have lameness and shedding of hooves

141
Q

predisposition of mulberry heart disease

A

weavers and growers

142
Q

cause of mulberry heart disease

A

vit e deficiency

143
Q

signs of mulberry heart disease

A

alternating areas of necrosis and haemorrhage throughout the myocardium, pericardial sac is distended with fluid and fibrin strands, straw-coloured fluid often present in pleural cavity and lungs are oedematous

144
Q

prolapse of rectum predispotiion

A

growing pigs (8-20weeks)

145
Q

cause of prolapse of rectum

A

increase in abdominal pressure, sex hormone levels, trauma, tail docking, diarrhoea, respiratory disease (excessive coughing), cold weather, slippery floors, stalls with steep slope

146
Q

pathogenesis of prolapse of rectum

A

causes increase in abdominal pressure which forces rectum to the exterior

147
Q

signs of prolapse of rectum

A

initially red coloured mucosa of rectum protrudes from anal sphincter, after few days it gets swollen and damaged and often haemorrhagic, often cannibalised

148
Q

treatment of prolapse of rectum

A

reposition of the prolapse, purse string/mattress suture, return the pig to the pen, long acting ATB

149
Q

prognosis of prolapse of rectum

A

sudden onset of death

150
Q

consequence of prolaspe of rectum

A

sometimes scarring leads to strictures

151
Q

predisposition of salt poisoning

A

uncommon in piglets

152
Q

cause of salt poisoniing

A

water shortage/deprivation with normal or excess salt in the diet

153
Q

signs of salt poisoning

A

develop in 24-48h, inappetence and dehydration, trying to drink from nipple drinkers
- nervous signs: fits, animals wandering around appearing blind, head pressing, incoordination
- signs of meningitis
- nose twitching just before a convulsion starts

154
Q

diagnosis of salt poisoning

A

clinical signs with documented lack of water, brain histologically at PM

155
Q

treatment of salt poisoning

A

response to treatment is poor when pig develops fit
- dehydration: rectal with flutter valve, oral, peritoneal infusion

156
Q

prognosis of salt poisonnig

A

bad if condition progressed

157
Q

prevention of salt poisoning

A

daily routine check of all water sources in the pens

158
Q

predisposition of thin sow syndrmoe

A

BCS between 1 and 2

159
Q

cause of thin sow syndrome

A

quantative or qualitative inadequate nutrition of sows

160
Q

pathogenesis of thin sow syndrome

A

gradual decline in BCS, slow progression over a period of months, sow depletes body fat  later muscle protein is degraded

161
Q

signs of thin sow syndrmoe

A

very thin sow

162
Q

diagnosis of thin sow syndrome

A

clinical signs, group faeces sample for parasitology and blood, eliminate chronic disease

163
Q

treatment of thin spw syndrome

A

immediately raise feed intake, very thin sows should be housed in warm, extremely lean sows can have irreversible condition

164
Q

prognosis of thin sow syndrome

A

progessive leading to death

165
Q

predispositon of hypoglycemia in pigs

A

weak, new-born pigs who don’t nurse regularly
- gluconeogenetic enzymes aren’t developed in 1st days after birth

166
Q

cause of hypoglycaemia in piglets

A

sow factors (nutrition, presence of disease, fewer functioning mammary glands)

167
Q

signs of hypoglycemia in piglets

A

tachycardia, tremor, nervousness, vocalisation and irritability, hypothermia, mental dullness, confusion, depression and seizure

168
Q

diagnosis of hypoglycmei In piglets

A

loss of condition, weak vocalisation, faltering gait, cold skin and recumbency

169
Q

treatment of hypoglycemia in piglets

A

: immediately remove piglet and warm up, feed piglet with sow, colostrum/20% dextrose solution by syringe or stomach tube every 20minutes then reintroduce

170
Q

cause of iron deficiecny anaemia in piglets

A

large excess of other trace minerals can decrease iron absorption, low iron stores, sows have a low permeability of the transplacental barrier, pigs raised in confinement without access to soil/faeces

171
Q

iron def in piglets pathogenesis

A

rapid expansion of plasma volume due to colostrum, insufficient iron supply = microcytic hypochromic anaemia

172
Q

signs of iron deficiency anaemia in piglets

A

poor weight gain and pale, anaemic, tissue hypoxia, hypothermia, GI inflammation, decreased appetite, stunted growth, tremors, pulmonary edema, death

173
Q

diagnosis of iron def anaemina in pig

A

based on clinical signs, lack of iron supplements and Hb levels in blood below 8g/100ml
- CBC + Biochem will show reduced serum iron and transferrin saturation + low haematocrit

174
Q

treatment of iron def anaemia in pig

A

injected with iron dextran

175
Q

pthogenesis of selenium

A

absorbed in SI  increased by good vitamin A + E levels
 decreased by large dietary quantities of Ca, Cu, Vit C, unsaturated fats

176
Q

signs of selenium

A

retained placenta, nutritional muscular dystrophy, poor growth, weakness, mastitis, metritis

177
Q

diagnosis of selenium

A

serum selenium concentrations reflect dietary intake over the past 2-4 weeks, whole blood selenium reflective of dietary selenium intake over the past 100+ days, liver biopsy is the most accurate method

178
Q

treatment of selenium

A

diets containing 0.1-0.3ppmof selenium, injectable Vit E and selenium

179
Q

zinc predisposition

A

growing pigs

180
Q

zinc cause

A

fed diets high in phytic acid, more than recommended amount of calcium

181
Q

zinc signs

A

parakeratosis + dermatitis, decreased milk production, decreased growth and decreased hair on head and legs

182
Q

zinc diagnsosi

A
  • sample all constituents of the diet
  • serum or plasma should be properly collected into tubes specifically designed for trace mineral
  • haemolysis (RBC have high zinc concentrations)
  • liver samples yield the most reproducible measurements of the zinc status of the animal
183
Q

copper cause

A

primary deficit in forage (alkaline soils, liming of soil), secondary (high conc of dietary cadium, iron and selenium and zinc)

184
Q

signs of copper

A

depressed growth rate after weaning often with diarrhoea, lighter or faded-looking hair or fleece colour with poor quality
- Microcytic anaemia, depressed milk production, heart failure, infertility, increased susceptibility to disease, enlarged joints, lameness

185
Q

diagnosis of copper

A
  • copper status in blood or liver tissue
  • liver storage gets depleted first, so levels fall
  • blood – easier to collect, but delayed significance
186
Q

treatment of copper

A
  • copper glycinate injection
  • addition of copper sulphate or copper lysine in salt/mineral mix
  • standard salt mix
  • ruminal boluses (copasure) releases Cu for 6 months
187
Q

prognosis of copper

A

good
Extras: sheep have liver reserves for 6 months

188
Q

cause of cobalt

A

Used by rumen bacteria in formation of B12
Cause: deficient in highly organic or poorly drained soils

189
Q

pathogenesis of cobalt

A

low phosphorus and copper, chronic parasites play roles in pathogenesis

190
Q

signs of cobalt

A

loss of appetite, emaciation, anaemia, wasting diseases, ulcer discharge, pale skin and fatty liver

191
Q

diagnosis of cobalt

A
  • difficult
  • serum/urinary methylmalonic acid increased
  • serum vitamin B12 and liver cobalt concentration depressed
  • dietary levels below 0.06ppm should be considered deficient
192
Q

iron

A

Predisposition: rare in grazing animals and adults

Cause: can be exacerbated when fed milk replacer low on iron, young animals in total cofinement

Signs: microcytic hypochromic anaemia

Treatment: IM iron dextran, dietary requirement 30-40ppm

193
Q

iodine predisposition

A

more common in certain geographic regions

194
Q

cause of iodine

A

availability is reduced by methylthiouracil, nitrates, perchlorates, soybean meal and thiocyanates, Rubidium, arsenic, fluorine, calcium and potassium interfere with iodine absorption

195
Q

signs of iodine

A

goitre, poor growth, depressed milk yield, pregnancy toxaemia, reproductive abnormalities

196
Q

diagnosis of iodine

A

measure serum or plasma thyroxine levels

197
Q

treatment of iodine

A

3-6 drops of iodine daily for 7 days, mixed mineral feed supplements, iodine to the skin of a pregnant female once each week for preventing iodine deficiency-induced hypothyroidism

198
Q

viatmin A is needed for

A

growth, skeletal development, normal reproduction + vision
liver store is enough for 6 months, plants contain carotenoid precursors of Vit A,
- supplements with oxidising agents (Cu or Fe) can decrease Vit A actvitiy

199
Q

cause of Vitamin A

A

supplements that also contain oxidising agents may result in Vit A that is of severely reduced activity

200
Q

signs of Vitain A

A

weight loss, depressed immune function, microoftalmia in calves, night blindness, decreased fertility, and hair loss

201
Q

vitamin D

A

Predisposition: heavy wooled lambed (reduced sunlight)

Cause: reduced sunlight exposure

Pathogenesis: needed for bone integrity

Signs: rachitis

Treatment: exposure to sunlight or supplemented if housed 24/7, plants fresh + hay contain sufficient D2 and D3 levels

Disease: = rachitis

202
Q

vitamin K

A

Cause: corn, feeds containing high levels of sulphur and onions decrease vitamin E availability

Pathogenesis: needed for blood clotting and vision

Signs: white muscle disease, depressed immune function, subfertility

Treatment: no need to supplement in healthy rums as rumen produces it

Extras: farm animals can synthesis Vitamin B

203
Q

vitamin E

A

Needed for: maintaining cell membrane integrity (is an antioxidant)
Deficiency: white muscle disease, decrease immunity and decrease fertility
Treatment: no need for supplementation in healthy ruminants, lambs given Vit E and selenium injections in deficient areas

204
Q

predisposition ketosis

A

periparturient period of cow (due to marked nutritional, metabolic, hormonal and immunological changes)

205
Q

pathogenesis of ketsosi

A
  • feed intake doesn’t meet energy demand 
  • insufficient ruminal production of propionic acid 
  • not enough glucose = hypoglycaemic 
  • hypoglycaemia causes metabolism of FA and glycerol supplies 
  • FA and glycerol’s are oxidised to form Acetyl-CoA 
  • excess of Acetyl-CoA is converted to KB  KETOSIS
206
Q

prevention ketosis

A
  • avoid overcrowding
  • inappropriate stall design for lying time
  • first lactation heifers should be housed in separate fresh pen to reduce social stress
  • nutritional management
207
Q

type 1 ketosis

A

Predisposition: between 3-6 weeks post calving, component-fed herd, primary (starved, not enough food), secondary (decreased intake due to disease/stress)

Cause: overcrowding, stress, limiting factor = supply of glucose precursors,
Pathogenesis: blood KB conc, becomes very high and blood glucose very low

Signs:
- clinical ketosis = both hyperketonaemia and abnormal clinical signs
o reduced feed intake (1st sign), decreased milk production, rapid weight loss, emptying appearing abdomen, acetone breath, normal TRIAS, rumen motility, weakness
- subclinical ketosis: BHB values greater than threshold without clinical signs
- secondary ketosis: occur due to decreased appetite caused by other diseases (eg, peritonitis, metritis, septic mastitis)

Diagnosis:
- KB in blood, urine or milk
- physical exam
- without clinical signs, results indicate subclinical ketosis
- urine KB conc are always higher than in milk
- positive milk tests for BHB usually indicate clinical ketosis

208
Q

type 2 ketosis

A

Predisposition: fat cows are at higher risk

Cause: cow develops NEB and begins mobilising body fat prior to/ at calving, stress (hepatic lesions)

Pathogenesis: NEB  decease glucose  glucagon, ACTH, catecholamine, glucocorticoids = increase, insulin decrease  lipase activation

3 forms:
- subclinical
- chronic fat mobilisation after early periparturient ketosis
- ketosis in obese ow with massive lipid accumulation in liver

Aetiology:
- insulin + glucose increase but insulin resistance because they’re obese
- obese = increased lipolysis in peripartal period = decrease DMI  NEB, increased adipose sensitivity  mobilise fat very quickly under stress
- excessive mobilisation of fat  increased fatty liver infiltration  ketone production  decreased DMI
- NEB  decreased glucose  increased glucagon, AcTH, catecholamines + glucocorticoids  lipase activation

Signs:
- non-specific: depression, anorexia, weight loss, weakness, hypoactive rumen motility, decreased milk production, enlarged liver on palpation
- dystocia, retained placenta, endometritis, mastitis, SARA, hypocalcaemia puerperalis, abomasal dislocation, ketosis, HE

Diagnosis:
- nonspecific clinical signs
- lab tests
o CBC: leukopenia
o Biochem: increased (NEFA, BHB, pyruvate, AST, ALT, LDH, SDH, GGT and ammonia), decreased (triglycerides, cholesterol, insulin, glucose, albumin)
- US on liver
- very persistent ketosis
- blood ketone conc are not as high as type 1

Treatment – really hard to treat
- non-encephalopathic severe ketosis type II
o 1-2 weeks after calving
o constant rate infusion (CRI) – 5-10% dextrose + balanced electrolyte solution containing supplemental KCl
o IV insulin 200IU q24-36h P21
o force feeding
o 12g/day niacin PO
o if not working after 3- 5 days, milk 1 min 2xday until NEB broken
- Hepatic encephalopathy in severe ketosis type II
o advanced cases, euthanasia is recommended
o depressed consciousness

209
Q

type 3 ketosis

A

Cause: feeding ketogenic silages. Hay crop silages are chopped too wet/low in water soluble carbs (favour growth of clostridium)

Pathogenesis: clostridium  ferment some carbs to  butyric acid (instead of desired lactic acid)

Diagnosis:
- silage fermentation (VFA) analysis confirms present and amount of butyric acid in silage
- silage with clostridial fermentation – can smell

Treatment: divert, dilute and destroy
- divert this feed away from the pre- and post-fresh cows, can be fed to replacement heifers, late lactation cows and/or far-off dry cows
- aerating the forage prior to feeding with it, silage that are over 2% butyric acid should be destroyed
- 50% dextrose solution (IV)
- propylene glycol (PO) should be given as a drench and not mixed in feed, overdosing = CNS depression
- glucocorticoids: dexamethasone/isoflupredone acetate (stimulate hepatic gluconeogenesis)
- neurological form of ketosis: IV glucose + PO chloral hydrate

210
Q

preganncy tozemia and fatty liver syndorme in ewes and does predisposition

A

during last month of gestation, multiple foetuses. Females with poor BCS or over conditioned

211
Q

cause of fatty liver syndrome / pregnancy toxemia

A

stress, anorexia caused by other diseases

212
Q

pathogensis of pregnancy toxemia and fatty liver syndrme

A

anorexia or lack of sufficient energy intake  NEB  animals mobilise body stores of fat and transport them to the liver  hypoglycaemia, hyperketonaemia  fatty liver

213
Q

signs of pregnancy toxemia

A

decreased appetite, anorexia, dullness, altered behaviour, recumbency, constipation, bruxism, acetone breath, frequent urination, incoordination, circling, dystocia

214
Q

diagnosis of pregnancy toxemia

A

presence of multiple foetuses, clinical signs
- Increases serum BHB levels
- positive urinalysis for ketone and protein biochemistry: hypoglycaemia, azotaemia, occasionally hypocalcaemia, hypokalaemia

215
Q

eamtnet of pregnancy toxemia

A

Early cases (before onset of recumbency)
- propylene glycol PO
- single injection of 50% dextrose, followed by balanced electrolyte solution with dextrose + calcium borogluconate
- potassium, flunixin meglumine
Recumbent animals
- comatose animals – human euthanasia

216
Q

prevention of pregnancy toxemia

A
  • good feeding management
  • adequate feeder space for pregnant animals
217
Q

cause of hypocalcaemia/mik fever

A

usually 3rd lactation

218
Q

pathogenesis of hypocalcemia

A
  • need for Ca during dry period is low so GI absorption + mobilisation from bone decreases
  • late pregnant cow needs 30g/d Ca, lactating around 50g/da
  • huge sudden demand for Ca which test homeostatic mechanism
  • occurs when cows don’t extract enough Ca from bones to diet to replace Ca lost in milk
219
Q

signs of hypocalcemia

A

Stage 1 : cows still standing, hypersensitivity, excitation, ears twitching, muscle tremor, mild ataxia, open mouth breathing
Stage 2: sternal recumbency, depression, dry muzzle, decreased temp, cold extremities, heart sounds quieter, tachycardia, smooth muscle paralysis
Stage 3 : lateral recumbency, disturbance of consciousness, complete flaccid muscle paralysis, ruminal bloat, filiform pulse

220
Q

diagnosis of hypocalcemia

A
  • ca: normal 2.2-2.5 mmol/L, milk fever = < 1.9, stage 1 = 1.4-1.9, stage 2 = 0.9-1.6, stage 3 = < 0.9
  • p, Mg decrease, CPK and AST increase
  • stress leukogram: neutrophilia, lymphopenia, eosinopenia

emergency = flaccid paralysis

221
Q

treatment of hypocalcemia

A

ca-borogluconate IV (500ml slowly over 10-20mins) , slow application for teat canal: ca-propionate, give Vit D, wrap knees

222
Q

prognosis of hypocalcemia

A

favourable in simple cases, grave if: cow lying down for long time, mastitis, musculoskeletal trauma, ischemic muscle necrosis

223
Q

prevention of hypocalcemia

A

dietary cation anion difference, diet high in Na + K and low in Cl + sulphur, vit D 1 week before calving, Ca gel PO after calving, PTH IM 6 days before parturition

224
Q

redisposition of parturient paresis

A

occurs 6 weeks prior and 10 weeks after birth

225
Q

cause of parturient paresis

A

: exact cause unknown, stress

226
Q

signs of parturient paresis

A

ataxia, tremor, constipation, rumen atony, tachycardia, tachypnoea, bloat, depression, opisthotonos

227
Q

diagnosis o f paturient paresis

A
  • low level of Ca in goats and sheep in high lactation with multiple foetus, decreased P, increased/decreased Mg
  • history, clinical signs + response to therapy
228
Q

treatment of parturient paresis

A

Ca-borogluconate 50-150ml IV or 50-150ml IV in 1L glucose

229
Q

differeitnatil of parturient paresis

A

pregnancy toxaemia and fatty liver syndrome in ewes and does

230
Q

prevention of parturient paresis

A

avoid alfalfa, application Ca postpartum, avoiding stress and parasite control

231
Q

hypomagnesia predisposition

A

dairy and beef cattle during 1st 2 months after calving
low Mg + high N, K in rapidly growing grass causes hypoMg + HypoCa resulting in tetanic signs

232
Q

cause of hypomagnesiua

A

animals grazed on lush grass pastures or green cereal crops

233
Q

types of hypomagnesiua

A

Grass Tetany (grass staggers)
- in dairy cows during the spring
- grazing cold grass with deficient content of Mg
- grazing wheat, barley/oats treated with potassium and nitrogen fertilisers that reduce the absorption of Mg from rumen
- stress  adrenaline  hypoMg
Winter tetany
- animals are fed with a food deficient in Mg
- stress-extreme low temperature
Transport tetany
- low Mg in food and stress of prolonged transport
- typically in cows and ewes in late pregnancy
Milk tetany
- calves feeding only with milk
- milk < mg but resorption is good
- diarrhoea in calves contributes

234
Q

signs of hypomagnesiua

A

: hyperexcitability, muscular spasms, convulsion, nystagmus, respiratory distress, collapse, elevated temp, tachycardia, loud cardiac sounds, tachypnoea, tetanic spasm

235
Q

diagnosis of hypomagnesia

A

emergency, clinical signs, low Mg in serum and CSF, often hypo Ca and hypo P

236
Q

treatment of hypomasnesia

A

sedation with xylazine, ca borogluconate + hypophosphate IV

237
Q

prevention of hypomagnesia

A

mineral blocks, optimal intake of energy, prevent fertilisation with the K, avoiding stress

238
Q

differentials of hypomagnesia

A

rabies, nervous ketosis, coccidiosis, hypoCa, tetanus, strychnine poisoning, salt poisoning, enterotoxaemia in calves, bloat, acute poisoning heavy metals

239
Q

what is rickets

A

Disease of bony growth plate, failure of both vascular invasion and mineralisation in the area of provisional calcification of metaphysis of the long bones

240
Q

predisposition of rickets

A

dogs, cats, pig, young, growing animals

241
Q

cause of rickets

A

dietary insufficient (phosphorus/ Vit D), abnormal calcium:phosphorus ratio, animals fed all meat diets, during winter

242
Q

signs of rickets

A

bone pain, stiff gait, swelling in the area of metaphysis, lameness, pathologic fracture, limb deformity

243
Q

diagnosis of rickets

A

radiographic exam: thickening metaphysis

244
Q

treatment of rickets

A

correction of the diet, exposure to sunlight increases Vit D3 precursors, high quality commercial food

245
Q

prognosis of rickets

A

good in absence of pathologic fractures/irreversible damage to the physis

246
Q

predisposition of osteomalacia

A

older cows

247
Q

cause of ostemomalacia

A

cattle grazing on arid, infertile soils deficient in phosphorus, horses (bran/miller/big head disease), keeping animals indoors

248
Q

pathogenesis of osteomalacia

A

similar to rickets but seen in mature bones, accumulation of excessive unmineralized osteoid on trabecular surfaces

249
Q

signs of osteomalacia

A

nonspecific shifting lameness, spinal deformation, rough hair coat, weight loss, pica, limb deformities, spontaneous fracture

250
Q

diagnosis of osteomalacia

A

history, CE, diet should be evaluated for calcium, phosphorus and Vit D content, X-ray (generalised demineralisation of the skeleton and fractures of long bones)

251
Q

treatment of osteomalacia

A

proper nutrition prevents occurrence of significant bone damage and fracture

252
Q

prognosis of ostemomalacia

A

favourable only in initial stage of the disease, medicine containing Ca, P and Vit D

253
Q

predisposition of urolithiasis

A

feed a lot and range cattle, steers but also in some sheep and goats

254
Q

cause of urolithiasis

A

high concentrate diets (increased solidification) , grazing on silica-rich soil, high in calcium, Vit A deficiency, hypervitaminosis, reduced water intake, chronic UTIs

255
Q

pathogensis of urlothiasis

A

magnesium ammonium phosphate most common calculi

256
Q

signs of urolithiasis

A

urethral obstruction, tenesmus, colic, inappetence, sandy calculi, bloody urine

257
Q

diagnosis of urolithiassi

A

history, CE, rectal exam, abdominal US, radiography

258
Q

treatment of urlothiasis

A

catheterisation usually impossible in most bulls (sigmoid flexure), surgical treatment: urethrostomy or urethrotomy

259
Q

prognosis of urolithiasis

A

increase urinary chloride excretion, decrease urine pH, decrease dietary cation-anion difference, provide calcium: phosphorus ratio 2:1, free access to a source of non-frozen water

260
Q

prevention of urolithiasis

A

correction of underlying cause, removal from offending pastures of feedstuffs
- to prevent struvite calculi:
o increase urinary chloride excretion, decrease urine pH, decrease dietary cation-anion ratio, free access to caean, non-frozen water

261
Q

cause of pyelonephritis

A

Corynebacterium renale, E.coli, trueperella pyogens, stap and pseudomonas
- Physical/ chemical damage to the mucosa in the lower portion of the UT (dystocia or puerperal infection, bladder paralysis or catheterisation may predispose the cow to pyelonephritis)

262
Q

pathogenssis of pyelonephritis

A

ascending infection from lower urinary tract

263
Q

signs of pyelonephritis

A

urinary blood clots or fibrin, pyuria
- Acute pyelonephritis: fever, anorexia, decrease in milk production, sometimes colic, arched stance, stranguria, polyuria, haematuria
- Chronic pyelonephritis: anorexia and weight loss, poor hair coat, poor production, diarrhoea, polyuria, stranguria, anaemia

264
Q

diagnsosi of pyelonpehritis

A
  • history of recent parturition, CE
  • Rectal exam (palpation of left kidney for enlargement, loss of lobulation and pain)
  • US – kidney, ureters and bladder
  • Endoscopic detection of cystitis
  • urine exam: fibrin, blood clots, pus and haemorrhage
  • positive blood and protein reactions on reagent test strips
265
Q

treatment of pyelonephritis

A
  • catheterisation, urine sample for urine culture penicillin
  • if c.renale identified – penicillin
  • E.coli  ceftiofur
  • azotaemia is present - gentamicin
266
Q

prognosis of pyelonpehritis

A

good for cows with acute pyelonephritis that are treated with long-term antimicrobial therapy, severe bilateral and azotaemia is guarded

267
Q

extra of pyeloneprhtisi

A

calves can get septic nephritis + renal abscessation from umbilical artery infection

Internal (12 decks)

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