Respiratory Flashcards

1
Q

Dyspnoea at rest?

A

Cardiovascular disease

(Inadequate perfusion of the lungs)

Cardiac disease

congestive heart failure, acute heart failure

Peripheral circulatory failure

shock and dehydration

Increased blood viscosity

•haemo-

concentration including

polycythaemia

and disseminated

intravascular

coagulopathy

Diseases of blood

A

naemia

A

ltered haemoglobin

e.g.

methaemoglobinaemia

in nitrate poisoning

•Nervous system diseases

Paralysis respiratory muscles

•botulism, tick paralysis

Paralysis respiratory centre

•nicotine sulphate poisoning

Neurogenic dyspnoea

• stimulation of respiratory centre by

irritative

lesion

•General systemic states

–pain

–hyperthermia

–acidosis

•Environmental causes

–Very high temperatures, oxygen lack (high

altitude), exposure to toxic gasses

•Poisons

–Nitrate, hydrocyanic acid, urea,

organophosphate

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2
Q

Examination of the Resp Tract

A
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3
Q

Additional tests for respiratory

A

* Percutaneous transtracheal aspiration

  • wide bore needle between tracheal rings
  • insert long plastic catheter: withdraw needle. Leave catheter in place– passed to point approximately 10 cm beyond thoracic inlet
  • infuse 20-40 ml of sterile saline and aspirate back quickly

– culture, cytological examination

* Pleural paracentesis

  • ideally use a teat siphon through a skin stab wound but can use a catheter– insert below fluid line
  • samples for cytology and bacterial culture
  • can be of use in treatment

* Bronchoalveolar lavage (BAL)- may be done using two tubes introduced through the nares– an outer tube which is passed to the level of the trachea and an inner tube which is passed to the level of the bronchus

* Sample obtained can be used for virus isolation and bacterial culture

* Thoracic ultrasonography– pleural and pulmonary surfaces of both lung fields can be examined through the intercostal spaces between the 7th and 11th ribs

  • a 3.5 MHz sector transducer is suitable for this task
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4
Q

Causes of pulmonary congestion and oedema

A

Causes:

* early pneumonia

* Inhalation smoke, fumes

* anaphylactic reaction

* hypostasis in recumbent animals

* secondary causes- CHF

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5
Q

Clinical signs of pulmonary congestion and oedema

A
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6
Q

Treatment for pulmonary congestion and oedema

A

* Adrenalin for oedema due to anaphylaxis

* Antiobiotics if early pneumonia suspected

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7
Q
A
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8
Q
A
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9
Q

What is pneumonia? Causes?

A
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10
Q

Classification of pneumonia

A
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11
Q

Clinical findings of pneumonia

A
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12
Q

Diagnosis of pneumonia

A
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13
Q

Treatment of Pneumonia

A
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14
Q

Aspiration pneumonia– common sequelae to what?

A
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15
Q

Acute undifferentiated bovine respiratory disease?

A
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16
Q

Agents associated with BRD

A
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17
Q

What is the most common cause of illness and death in AUS feedlot cattle?

A
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18
Q

Cause of BRD

A

The major pathogens of BRD are ubiquitous, and

all the major bacterial respiratory pathogens are

commensal

in clinically normal feedlot cattle.

Clinical BRD is the product of the effect of

stressors causing immuno-

suppression, thereby

allowing the colonisation of the lower respiratory

tract by opportunistic pathogens that invariably are

encountered by feedlot cattle.

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19
Q

Risk factors with BRD

A
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20
Q

BRD Clinical findings

A

* Broncho-pneumonia 10-14 days after stress

* In the early stages

  • off feed depressed rapid shallow resp moist cough

* Later stages:

  • febrile (40-41C)
  • deep laboured resp (insp and exp)
  • increased harshness of insp sounds as purulent material gathers in the airways
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21
Q

BRD Clinical findings

A
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22
Q
A
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23
Q

BRD Treatment

A

* Antiobiotics

  • Usually oxytetracycline, ceftiofur, or trimethroprim/ sulphonamide combinations are used in feedlots

* NSAIDs

* Nursing- shelter and high quality feed

* Early detection of new cases and continual reassessment of the results of treatment are necessary

* Value of mass medication of feed supplies of newly arrived cattle to the feedlot

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24
Q

Vaccination against BRD

A
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25
Q

Pneumonic pasteurellosis

A

Combination of:

Viral infections of the respiratory tract

Effects of transportation, temporary starvation,

weaning, fluctuations in temperature, mixing, excess

handling an increase in the total numbers and

virulence of

Pasteurella

in the nasopharynx

Most commonly isolated

Mannheimia

hemolytica

Pasteurella

multocida

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26
Q
A
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27
Q
A

Pasteurellosis

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28
Q

Managing a Manheimia outbreak

A
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29
Q

Monitoring for Manheimia hemolytica

A
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30
Q

Histophilus somni disease complex?

A
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31
Q

Histophilosis respiratory form

A
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32
Q

Histophilosis Septicaemic Form

A
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33
Q

Histophilosis nervous form

A
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34
Q

Diagnosis of Histophilosis

A
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35
Q

Atypical Interstitial Pneumonia

A
36
Q

Interstitial pneumonias include

A
37
Q

ABPEE

A
38
Q

ABPEE clinical findings and necropsy?

A
39
Q

ABPEE Treatment?

A
40
Q

Other interstitial pneumonias

A
41
Q

Contagious Bovine Pleuropneumonia

A
42
Q

Epi of CBPP

A
43
Q

CBPP signs and symptoms

A
44
Q

PM Findings in CBPP

A
45
Q

Control of CBPP

A
46
Q

Enzootic pneumonia of calves

A
47
Q

Enzootic pneumonia of calves signs and symptoms

A

Enzootic pneumonia of calves

Areas of collapse with little bronchiolar reaction

In the later stages a dark red consolidation with

little or no fluid in the lung is detected.

Lesions are bilateral and

histologically

there is

an interstitial pneumonia.

48
Q

Lungworm in cattle

A

Dairy calves are most vulnerable to lungworm

disease, as they are often placed on paddocks

grazed each year by successive groups of

calves

With high stocking rates, pasture challenge

can then reach pathogenic levels within 2 to 4

months.

Usually, only relatively small numbers of larvae

survive to induce low

-grade, asymptomatic

infections in a new group of susceptible calves,

which then start to re-

contaminate the pasture

and recycle the infection

49
Q

Acute verminous pneumonia

A
50
Q

Sub-acute verminous pneumonia

A
51
Q

Lungworm diagnosis

A
52
Q

Infectious bovine rhinotracheitis

A

May also cause an encephalitis in new

born calves

Infectious

pustular

vulvo

  • vaginitis

(IPV),

balano-

posthitis

in adults.

53
Q

Infectious bovine rhinotracheitis signs and symptoms

A

Sudden onset

Anorexia,

Fever up to 42 degrees C,

Severe hyperaemia of the nasal mucosa

-

greyish plaques of necrosis nasal septum

Serous discharge from the eyes and nose

Respiratory rate increased and shallow

Lung sounds are normal on auscultation.

May be short explosive cough

Conjunctivitis is seen in some outbreaks.

54
Q
A
55
Q

Infectious bovine rhinotracheitis calves

A

New born calves systemic form is severe

and highly fatal.

Signs include sudden anorexia, fever,

rhinitis, erosion of the soft palate, acute

pharyngitis.

Broncho-

pneumonia is

common.

56
Q

Infectious pustular vaginitis (IPV)

A

Vaginal examination reveals plaques or

pustules of white necrotic material on the

vulva and vaginal mucosa, and a pool of

odorless

mucopurulent

material on the

vaginal floor.

In bulls, IPV causes a

balanoposthitis.

57
Q

IBR diagnosis

A

Overseas, abortion is a common sequel in

pregnant cows

58
Q

IBR Control

A
59
Q

Oral and laryngeal necrobacillosis

A
60
Q

In a calf

A
61
Q

Oral necrobacillosis- necrotic stomatitis

A
62
Q
A

Quite irritant -

affected animals will often rub their

noses on sticks, thistles

On palpating the nasal mucosa of chronically

infected

granulomatous

nodules of 1 to 4 mm in

diameter and height can be detected in both

nostrils

The severity of the condition in affected cattle

will often wax and wane

63
Q

TB in cattle? Epi?

A

Caused by

Mycobacterium bovis

and is

characterised by the progressive

development of tubercles in any of the

organs in most species.

More about Epi:

* Inf by ingestion is more likely at pasture when faeces contaminate the feed and communal drinking water and feed troughts

* Drinking of infected milk by young animals is a commoin method of spread

64
Q

TB spread in the body

A
65
Q

TB clinical findings

A

* TB mastitis can be of major importance because of its danged to PH

* palpation of the supramammary LNs is essential in all cases of suspected tuberculous mastitis

66
Q

TB clinical pathology

A

Basis of tuberculosis eradication

campaigns is the tuberculin test and a

knowledge of the various tests used, their

deficiencies and advantages, is essential

67
Q

Single intradermal tuberculin

A
68
Q

TB pathology

A
69
Q

TB Diagnosis

A
70
Q

SBE

A

caused by a chlamydia

characterised by inflammation of vascular

endothelium and mesenchymal tissue.

71
Q

SBE Signs and symptoms

A

caused by a chlamydia

characterised by inflammation of vascular

endothelium and mesenchymal tissue.

Later, difficulty in walking stiffness with

knuckling at the fetlocks is evident at first,

followed by staggering, circling and falling

Opisthotonus

may be present but there is no

excitement or head pressing

.

72
Q

SBE Pathology

A

Sporadic Bovine Encephalomyelitis

Pathology:

Chlamydia can be isolated from the blood in

the early clinical

Serological tests, including a complement

fixation test, are available

.

Pathology:

On post mortem a

fibrinous

peritonitis,

pleurisy and pericarditis accompanied by

congestion and

petechiation

are

characteristic.

73
Q

Brisket Disease in Cattle

A

Epidemiology

the low density of the atmosphere at high

altitudes results in an environmental anoxia

most commonly in yearlings.

Brisket disease is reported commonly only

in animals maintained for some months at

altitudes above 1800 metres.

Continued hypoxia can cause sufficient

myocardial weakness to interfere with

cardiac compensation and thus lead to

congestive heart failure.

74
Q

Poisonings which may be associated with dyspnoea

A

A number of poisons cause dyspnoea

as the prominent sign.

Farm chemicals including

methaldehyde

and

dinitrophenols, organophosphates

and

carbamates, urea

Poisonous plants including fast death

factors of algae, the weeds

Albizia

,

Helenium

, Eupatorium, Ipomea,

Taxus

spp., Laburnum

and

Erythrophloeum

spp. can all cause dyspnoea.

75
Q

Nitrite/ Nitrate poisoning

A

Nitrate/nitrite poisoning – common

plant sources

Cereal crops include: immature green oats,

millet, barley, wheat, rye, Sudan grass, corn,

sorghum fodder, mangles, turnips, sugar beet

tops and rape, certain specific plants and water

from deep wells.

Specific plants include variegated thistle,

mintweed and a series of other plants

Nitrate/nitrite poisoning. - epidemiology

Cereal and root crops are likely to contain

high concentrations of nitrate when heavily

fertilised with nitrogenous fertilisers

When growth is rapid during hot humid

weather.

In cattle the maximum methaemoglobin

level usually occurs about 5 hours after

ingestion of nitrate.

76
Q

Findings in nitrate/nitrite poisonings

A
77
Q

Nitrite/nitrate poisoning- pathology

A

Post mortem

  • blood is coffee brown in colour

and clots poorly.

78
Q

Nitrate/ Nitrite Treatment

A
79
Q

Hydrocyanic Acid Poisoning

A

Sources

Many plants contain

cyanogenetic

glucosides

Common pasture plants including

sorghum, Sudan grass and Johnson

grass.

80
Q

Hydrocyanic Acid poisoning epi

A

Epidemiology

High soil concentrations of nitrogen

predispose to higher levels of hydrocyanic

acid in plants.

Wilted, frost bitten and young plants are

likely to more toxic

81
Q
A

Hydrocyanic Acid poisoning

Animals may show signs within 10-

15

minutes of eating the toxic material and

die within a few minutes.

Signs observed include dyspnoea,

restlessness, moaning, recumbency and

terminal clonic convulsions with

opisthotonus.

Mucosae

are bright red in colour.

82
Q

Hydrocyanic Acid Pathology

A
83
Q

Hydrocyanic acid poisoning treatment

A

Treatment

Hydrocyanic acid is taken up by

thiosulphate to form

thiocyanate

which

is not toxic and is readily excreted.

Sodium thiosulphate should also be

given orally to fix the free hydrocyanic

acid in the rumen

84
Q

Poisoning with OPs signs and symptoms

A

Organophosphate compounds and

carbamates

inactivate cholinesterase and

produce a syndrome of salivation, diarrhoea

and muscle stiffness indicative of

stimulation of the parasympathetic nervous

system.

85
Q

Poisoning with OPs Treatment

A
86
Q

Urea Poisoning

A

Urea poisoning

Urea is used as a feed additive for

ruminants as a source of non protein

nitrogen and as a fertiliser

Urea should not constitute more than

3% of the concentrate ration of

ruminants.

Toxic affects are due to the sudden

production of large quantities of

ammonia and signs occur within 20

to 30 minutes of feeding.