Term
| What causes an animal to give a respiratory grunt and/or abdominal respiration? |
|
Definition
| Often indicates the presence of thoracic pain often associated with advanced pulmonary diseases and often involves the pleura |
|
|
Term
| What are some Ddx for a a respiratory grunt and/or abdominal respiration? |
|
Definition
Diffuse pulmonary emphysema
Extensive consolidation
Acute pleurisy
Peritonitis
Pleuritis
Pleuropneumonia
Shipping fever
Acute bovine pulmonary oedema and emphysema
Pericartitis
TRP
Abdominal distenstion |
|
|
Term
| What are the constituents of '4 in 1' for treating metabolic diseases? |
|
Definition
Calcium (as calcium gluconate)
Magnesium (as Magnesium hypophoshite)
Phosphorus (as hypophosphite mainly)
Glucose |
|
|
Term
| What dose is recommended for '4 in 1'? |
|
Definition
Around 1 pack, so 500ml S/C or IV with vet supervision. Administer in 125ml
Sometimes another 250-500ml is given after recovery |
|
|
Term
| What is the recommended dose for Ca Borogluconate? |
|
Definition
13.8g ish of 15-20 min
Can give in Ca borogluconate in the 4 in 1 bag comes to about 13.8g |
|
|
Term
|
Definition
| A clinical sytsemic state caused by widespread activation of host defense mechanisms to the presence of toxins in the blood stream produced by bacteria or tissue injury |
|
|
Term
|
Definition
| Toxemia caused by the presence of lipopolysaccaride cell-wall components of gram negative bacteria in the blood |
|
|
Term
| How does endotoxemia cause disease? |
|
Definition
The pathology is the same (mostly) across all bacteria
Endotoxin is present in healthy animals (produced by the SI bacteria) but the volume is small and the intestinal mucosa prevents movement into the blood stream.
Disease happens when
- Hepatic failure causes and increase in plasma conc of toxin
- Damage to the SI mucosal barrier
- Gram negative bacteria gains access to tissue or blood
The effects of endotoxemia are not directly caused by endotoxins, the endotoxins cause the release of cell products. These include
- Cytokines (responsible for the most things)
- Platelet activating factor
- Thromboxane A2
- Prostaglandins
- Leukotrines
- Proteinases
- Toxic oxygen matabolites and vasoactive amines |
|
|
Term
| What are the clinical signs of endotoxemia? |
|
Definition
Increased HR, and then decreased HR (D CO, I peripheral resitance = D organ blood flow, leading to heart and renal failure)
Activation of complement cascade
Neutropenia
Lymphopenia
D GIT motility |
|
|
Term
|
Definition
| Surveillance scheme for monitoring the possible spread of transmissible spongiform encecalopathies |
|
|
Term
| What are the aims of the TSE Scheme? |
|
Definition
Prevent TSE coming into Aus
Increase TSE surveillance
Reduce/eliminate the risk of spread amongst animals and people
Increase public awareness and understanding of TSE |
|
|
Term
| What are the aims of a a'type B surveillance system for TSE? |
|
Definition
To detect 1 case of BSE in 50,000 at a 95% CI.
Involved examining the brains of clinically consitent cases as well as a minimum of 150,000 surveillance points during a seven-year moving window
For sheep this means examing a minimum of 438 eligible neurological cases each year |
|
|
Term
| What samples are needed for the TSE programme? |
|
Definition
2-3 cm length of unfixed cervical spinal cord as well as medulla caudal to the obex for cattle and sheep
Sheep also require the top 3rd of the cerebellum sampled via a coronal/horizontal approach |
|
|
Term
| How do you diagnose coxofemoral dislocation? |
|
Definition
- Gross displacement of the limb
- Determine the direction of the displacement
-Cranio dorsal dislocation? Greater trochanter moves forward and upwards and there is crepitus on abduction and rotation of the femur
- Cranio-ventral dislocation - head of femur is palapated perrecutm
- Caudo-ventral luxation, head of femur may be felt in the obturator foramen |
|
|
Term
| How do you diagnose a spinal fracture? |
|
Definition
Fracture of the tuber coxae - pelvic asymmetry is usually very obvious 'dropped' hip
Other fractures - Dx on rectal palpation, often possible to feel the fracture, though swelling of haemorrhage may get in the way |
|
|
Term
| How do you diagnose limb fractures? |
|
Definition
| Dx in closed fracturs is based on non-wt bearing, limb deviations and crepitus, there may be little deviation, but severe pain |
|
|
Term
| How do you diagnose spinal fractures? |
|
Definition
Difficulty rising or total paralysis, dragging hindlimbs, dorsal aspects of fetlocks on the ground
Ataxia |
|
|
Term
| What are the clinical signs of hypophospataemia? |
|
Definition
Acute recumbency
Inappetent
Weakness
Bone - Osetopenia, osteomalacia, rickets
Shifting lameness, poor growth rate, dull coat, weight loss, reduced milk production, reduction in reproductive performance, pica, kyphosis, lordosis, fractures, haemolysis, phagocytosis, red-brown urine, pallor, pounding jugular pulse, tachycardia, tachypnoea, jaundice |
|
|
Term
| What cows are most at risk for developing hypophosphataemia? |
|
Definition
| Cows 3-10 year of age that are within 6 weeks of calving |
|
|
Term
| How do you diagnose hypophospataemia? |
|
Definition
| A combination of the clinical signs and having a serum level of ~ <2mg/dL |
|
|
Term
| How do you treat hypophosphataemia? |
|
Definition
Monobasic monophosphate should be used as a lot of other solutions are unavailable to mammals
A lactating dairy cow with severe hypoP needs 300ml of 10% monohydrate solution which will provide 7g of phosphate and increases plasma phospate for at least 6hrs |
|
|
Term
| What are some considerations of treating hypoP IV? |
|
Definition
| Should not be given within 2 hrs of Ca as it can precipitate |
|
|
Term
| What is a safer way to treat hypoP? |
|
Definition
Orally, preferred in ruminants WHEN rumen motility is maintained.
Feed 200g of feed grade monophosphate administered in gelatin boluses, drench or ororuminal intubation |
|
|
Term
| How is bovine ephemeral fever transmitted? |
|
Definition
| By biting insects such as mosqueetos and midges |
|
|
Term
| How does bovine ephemeral fever cause disease? |
|
Definition
Virus replications occurs in the vascular system
Causes generalised inflammation and vasiculitis
This results in fibrinous effustion into joints, peritoneal, pericardial and pleural cavities and serous dishcarges |
|
|
Term
| What clinical signs are associated with BEF? |
|
Definition
Sudden onset biphasic fever
Inappetance
Stiffness, muscle tremors, depression, drop in production, salivation
Tachycardia, tachypnoea
Joint effusion and pain
Possible temporary infertility in bulls (up to 6 months)
Possible abortions
Rarely fatal (~1%) |
|
|
Term
| Where is BEF most common? |
|
Definition
Tropical areas!
If there are mosqueetos, there may be disease |
|
|
Term
|
Definition
| Clinical signs, serology, virology, histology |
|
|
Term
|
Definition
| Mostly self resolving, can give NSAIDs for fever, treat any other developing conditions (hypocal etc.) |
|
|
Term
| How do you differentiate between BEF and milk fever? |
|
Definition
Time from parturition (milk fever is usually within 72hrs of parturition)
Treating for hypocal and not seeing improvement |
|
|
Term
| What are the clinical signs of listerosis? |
|
Definition
Mengioencephalitis is the most common manifestation
Abortion
Mastits
Septicaemia
Iritis
Uveitis
Depression
Inapetance
Pyrexia
Neurological sings
Head tilt
facial paralysis
Circling
Proprioceptive defects
Tremor
Collapse
Tongue protrusion
Rumen hypomotility
blindness |
|
|
Term
| How do you diagnose Listeriosis? |
|
Definition
| Clinical signs, CSF analysis, testing of source material such of identification, necropsy, DDx |
|
|
Term
| How do you treat Listeriosis? |
|
Definition
All common antibiotics except cephalosporins (penicillin are often abs of choice). BID at high rates for 4 days
NSAIDs, IVFT, electrolytes, nursing care |
|
|
Term
| What are the clincial signs of PEM? |
|
Definition
Initial depression, apparent blindedd, ataxia, proprioceptive defects, champing of the jaws, frothy salivation, head pressing, aimless wandering, fine muscle tremors, no menace response, present palpebral reflex (differentiates from Pb poisoning) and PLR (centrally-mediated blindness)
Nystagmius, normal rumen function, recumbancy |
|
|
Term
| What animals does PEM affect most commonly? |
|
Definition
| 6-18 months of age, but adults can be affected |
|
|
Term
|
Definition
|
|
Term
| What is PEM associated with? |
|
Definition
|
|
Term
|
Definition
| Clinical signs, history and necropsy (brain histology) |
|
|
Term
|
Definition
| Thiamine hydrochloride IV 10-15mg/kg |
|
|
Term
| What clinical signs are associated with lead poisoning? |
|
Definition
Rapid onset and development
Neurological signs
Sudden death
Staggering, muscle tremors
Blindness, hyperirritability, bellowing, head pressing, spastic twitching of the eyelids, jaw champing, bruxism, salivation, rumen atony, abdominal pain, bloat |
|
|
Term
| How is Pb poisoning diagnosed? |
|
Definition
| Clinical signs, history of exposure, high levels of lead in the blood |
|
|
Term
| How do you treat lead poisoning? |
|
Definition
| Thiamine hydrochloride, DMSA (lower toxicity than Ca-EDTA) and can be used in food producing animals |
|
|
Term
| When are animals most likely to affected by ketosis? |
|
Definition
| During peak lactation (6-7wks post calving). Cows of any age can be affected, but there is a peak at 4th pregnancy |
|
|
Term
| What are the types of ketosis (based on cause)? |
|
Definition
| Primary, secondary, alimentary (from being fed feeds high in ketogenic materials) spontaneous ketosis |
|
|
Term
| What are the types of ketosis (based on presentation)? |
|
Definition
Wasting form - Rapid weight loss, gradual decline in appetite, firm and dry faeces, moderate depression, temp, rr and hr all normal, decrease in number and amplitude of ruminal contractions, possible ping
Nervous form - sudden onset, occur in short bursts which last for 1-2hrs +reoccur @ 8-12hrly intervals, CNS excitement, circling
Subclinical ketosis - subclinical |
|
|
Term
| How can you treat ketosis? |
|
Definition
Gluconeogenic substrate of glucose precursors (propylene glycol and glycerine/glycerol)
Replacement therapy - dextrose
Glucocorticoids
Insulin (do not use as a sole tx) |
|
|
Term
| How can you prevent ketosis? |
|
Definition
Management of BCS, do not allow cows to become over fat (>6/8), you can slim the down over the dry period
Late dry period management
Per-calving management
Monitoring feeding
Feed additives |
|
|
Term
| What management is needed in the late dry period? |
|
Definition
| Transition diets - allow the rumen flora to adapt to the increased amounts of concentrated feed. Aim to feed as much as possible and deliver propionate pre cursors |
|
|
Term
| When does Hypocal commonly cause disease? |
|
Definition
| During lactation, typically 6-8 weeks post calving |
|
|
Term
| What are predisposing factors for hypocal? |
|
Definition
48hrs off feed
Poor quality roughage over winter
Oestrus
Early or mild overeating of fermentable CHO |
|
|
Term
| What are the clinical signs of hypocal? |
|
Definition
| Anorexia, mild tachycardia, reduction in intensity of heart sounds, arrhythmia, ruminal stasis, decrease or abscence of faeces normal temp |
|
|
Term
| How do you treat hypocal? |
|
Definition
Which calcium...
IV calcium borogluconate. Give slowly, stop at 1st heart arrhythimia give rest (of 500ml 23% solution) SC or orally |
|
|
Term
| How can you prevent hypocal? |
|
Definition
Restrict green pasture in the last 2 weeks of gestation
Provide ad lib hay to springers
Supplement Mg of transitional feeding period
Add Ca post calving |
|
|
Term
| What is DCAD and how do you calculate it? |
|
Definition
Dietary cation-anion difference (DCAD)
Sodium + potassium - Chloride + sulphur = DCAD
The equation is (43.5[Na] + 25.6[K]) - (28.2[Cl] + 62.5[S]) = DCAD |
|
|
Term
| How does DCAD relate to acidosis and alkalosis? |
|
Definition
A negative DCAD = Acidosis
A positive DCAD = Alkalosis |
|
|
Term
| How does DCAD relate to hypocal? |
|
Definition
If DCAD is to hight and metabolic alkalosis is induced, the body is not able to respond to parathyroid hormone as wella as possible
A negative DCAD increases tissue receptivity to parathyroid hormone |
|
|
Term
| Why do we use dextrose to treat hypoglycemia? |
|
Definition
| Provides an artificial glucose supply as a short term patch |
|
|
Term
| Why do we use glucocorticoids to treat hypoglycemia (ketosis)? |
|
Definition
| Stimulates the body to increase plasma glucose by changing use, altering partitioning. Steroids block the effects of insulin |
|
|
Term
| Why could insulin be used to treat hypoglycemia (ketosis)? |
|
Definition
| Early lactation dairy cattle are inherently insulin resistant. Insulin is used in the tx of ketosis because of the anabolic effects: decreased fat breakdown, increased fat synthesis, and increased use of ketone bodies as energy sources, which is theorized to decrease the level and consequences of ketonaemia. |
|
|
Term
| What are the clinical signs of hypomag? |
|
Definition
Uncoordination
Hyperaesthesia
Tetany
Tonic-clonic muscle spasms
Paddling
Pyrexia
Frothing at mouth
Bruxism
Spasmodic urination and frequent defecation
Reduced appetite
Sudden deathh |
|
|
Term
| What animals are most at risk of hypomag? |
|
Definition
| Animals on fast growing pastures, often occurs after a period of reduced intake, cattle in the 1st 2 months of lactation, 4-6years of age |
|
|
Term
| How is hypomag diagnosed? |
|
Definition
| Clinical signs, biochemistry, vitreous humor of dead animals |
|
|
Term
| What are the clinical signs of botulism? |
|
Definition
Sudden death, flaccis paralysis, predominant manifestation, forrling, ascending paralysis leading to recumbency and loss of skin sensastion
Bradycardia
Ruminal atony
Rapid condition loss |
|
|
Term
| How is botulism diagnosed? |
|
Definition
| Clinical signs, elimination of Ddx |
|
|
Term
| How long can you wait before separating whole blood without having serious impacts on biochem parameters? |
|
Definition
|
|
Term
| What are the clinical signs of Akabane virus? |
|
Definition
Transient viraemia, no clinical signs in adults
Does affect the nervous system of the foetus in pregnant females. Calves are often aborted, but the ones born alive may:
- Develop arthrogtyposis (affected at 5-6mnths gestation)
- 4-5 mnths you get arthroptyposis and hydrocephaly
- 3-4 mnths hydrocephaly only |
|
|
Term
| Where does Akabane occur? |
|
Definition
| Sporadically in Qld, first spotted in Japan |
|
|
Term
| What are some of preventative measures that can be taken against mycotoxins? |
|
Definition
- Test suspect grain at harvest
- Maintain clean and dry storage facilities
- Use feed acid additives (propionic acid) to control growth
- Effective air exclusion in silage |
|
|
Term
| What are the clinical signs of aflatoxicosis? |
|
Definition
Blindness
Circling
ataxia
Ear twitching
bruxism
Photosensitive dermatitis
Diarrhoea
Abortion
Convulstions in terminal stages (death within 48hrs) |
|
|
Term
| What are the chronic signs of aflatoxicosis? |
|
Definition
Weight loss
Anaemia
Jaundice
Reduced production |
|
|
Term
| How can you diagnose aflatoxicosis? |
|
Definition
ELISA for feed - expensive
Clinical signs |
|
|
Term
| What are the clinical signs of paspalum staggers? |
|
Definition
Continuous trembling of large muscle groups
Jerky, uncoordinated movement
Dangerous to handle
Loss of condition
Total paralysis |
|
|
Term
|
Definition
| The disease caused by ingestion of ergot alkaloids from the fungus Claviceps purpurea |
|
|
Term
| What is fescue foot and what are the clinical signs? |
|
Definition
The disease caused by ingestion of the toxin Ergovaline
Clinical signs include:
- Unilateral or bilateral hindlimb lameness
- Tail and ears may be affected
- Erythema and swelling of the coronary region
- Cattle are alert, but lose condition and may be seen weight shifting or paddling
- Arched back
- Knuckling of the hind pastern
- Progressive lameness
- Anorexia
- Depression
- Tachypnoea |
|
|
Term
| What plant is known to cause prussic acid poisoning? |
|
Definition
|
|
Term
| When is the transition period (in regards to feeding the pregnant cow)? |
|
Definition
| 3 weeks wither side of calving |
|
|
Term
| When do the majority of diseases occur in the post parturient cow? |
|
Definition
| 80% of diseases occurs in the first 4 weeks after calving. |
|
|
Term
| Why does disease occur in the transition period? |
|
Definition
| It is usually a reflection of maladaptation in the transition period. Also consider that there is immunosuppression a week wither side of calving |
|
|
Term
| Why is the transition period so important? |
|
Definition
| It allows us to ease the cow into the lactation period and help her adjust to the sudden changes in metabolic demand |
|
|
Term
| What are the most helpful parameters to measure during 'fresh' cow checks? |
|
Definition
Body temperature
Appetites
Vaginal discharge
These are the most helpful in terms of early indicators of trouble |
|
|
Term
| What are the 4 aims of transition cow management? |
|
Definition
Reduce ruminal distruption
Minimise macromineral deficiencies
Minimise lipid mobilisation disorders
Avoid immune suppression |
|
|
Term
| What the problem with ruminal distruption? |
|
Definition
| Increased chance of developing subacute ruminal acidosis (SARA) as well as lactic acidosis and appetitie suppression |
|
|
Term
| How long does it take to adapt the ruminal papillae to a diet richer in carbohydrates, and what is the adaption? |
|
Definition
| Increased length of ruminal papillae, and it takes 3-6 weeks. |
|
|
Term
| What is the benefit of increasing papillae length? |
|
Definition
| Increase rumen surface area available for absorbtion |
|
|
Term
| How long does it take for the microbial adaptation to take place when changing diets? |
|
Definition
|
|
Term
| How does the microbial population of the rumen adapt to higher concentrate rations? |
|
Definition
| Increasing the proportion of amylolytic bacteria |
|
|
Term
| How does the microbial population of the rumen adapt to higher concentrate rations? |
|
Definition
| Increasing the proportion of amylolytic bacteria |
|
|
Term
| Are changes in metabolism greater due to lactation or partuition? |
|
Definition
|
|
Term
| To decrease the the risk of hypoCal, should you decrease or increase the DCAD? ANd how do you do that? |
|
Definition
| Decrease it, do that by adding anions - chloride and sulphur |
|
|
Term
| How does PTH influence Ca? |
|
Definition
| Decreased pH increases sensitivity to PTH and PTH stimulates an increase in osteoclasts to reabsorb Ca from bone |
|
|
Term
| What are the clinical signs of hypocal |
|
Definition
| Sternal or lateral recumbency, mildly ataxic, nervous, off feed |
|
|
Term
| What are the 3 stages of hypocal? |
|
Definition
1: Mild excitement and tetany, no recumbency, ataxic and nervous
2: Cannot stand, but can support themselves in sternal recumbency, there is ruminal stasis and heart sounds start to decline in intensity
3: Lateral recumbency, progressive loss of consciousness, GI atony, bloat and regurgitation |
|
|
Term
| When does hypo cal occur? |
|
Definition
| Within 1 day of calving (80%) |
|
|
Term
| What are the calcium concentrations associated with the different stages of hypocalcaemia? |
|
Definition
S1 - 1.4-1.9 mmol/L
S2 - 0.9-1.6 mmol/L
S3 - less than 0.9 mmol/L |
|
|
Term
| What treatments can be given for hypocal? |
|
Definition
Calcium borogluconate IV (rapid response)
4 in 1
1g Ca/45kg |
|
|
Term
| What are some considerations when giving Ca IV? |
|
Definition
Too much too fast = cardiac arrhythmias
Precipitates if given less than 30 mins prior to phosphourous |
|
|
Term
| What are the clinical signs of hypomagnesaemia? |
|
Definition
Sudden death
Paddling, stuggling. inappetence, nervousness, agression, ill thrify, diarrhoea |
|
|
Term
| When is hypomag likely to occur? |
|
Definition
| Animals feeding on lush, fash growing pastures that have been heavily fertilised with nitrogen and/or potassium |
|
|
Term
| Which are the worst months for hypomag? |
|
Definition
| June/August (winter, early spring) |
|
|
Term
| WHat are the catagories for ketosis? |
|
Definition
Primary (under feeding)
Secondary (under feeding, intake is inhibited)
Alimentary or ketogenic ketosis (feeds high in ketogenic substances)
Spontaneous (just cos)
2 types, nervous and wasting |
|
|
Term
| Which form of ketosis (presentation, not cause) is more common? |
|
Definition
|
|
Term
| What are the clinical signs of wasting ketosis? |
|
Definition
| Rapid weight loss, loss of production, selective grazing, dull glazed eyes, HR slows, rumen contractions are weakened |
|
|
Term
| What are the clinical signs of nervous ketosis? |
|
Definition
| Rapid weight loss, loss of production, selective grazing, dull eyes, HR slows, excitable, nervous, depraved appetite, bruxism, chewing things, climbing fences, head pressing |
|
|
Term
| How can you diagnose ketosis? |
|
Definition
| Clinical signs and history, lab tests for BOHB concentrations. Ketone bodies in urine and milk, testd cow side with ketostix or sodium nitroprusside |
|
|
Term
| How do you treat ketosis? |
|
Definition
Dextrose (500 mL 40-50% solution)
Corticostroids (40mg dex)
Insulin (300 IU)
Oral Propylene glycol |
|
|
Term
| What are the clinical signs of hypophosphataemia? |
|
Definition
| Decrease in feed intake, GI stasis, recumbeny, very similar to hypocal |
|
|
Term
| How do you diagnose hypophos? |
|
Definition
| Response to treatment, Rib bone and histological composition, Pasture and soil P levels |
|
|
Term
| How do you treat hypophos? |
|
Definition
| Give phosphorous at calcium phosphate |
|
|
