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Food Animal Medicine & Surgery > Circulatory Disorders of Ruminants > Flashcards

Circulatory Disorders of Ruminants Flashcards

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1
Q

Heart rate of a lactating dairy cow is?

A

RR 60-80

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2
Q

Tachycardia - 6 causes

A

Centrally - Cortico-stimulation - catecholamine
Peripherally Increased demand (lactating, eating etc)
Decrease in blood volume
Severe anemia
Decreased cardiac function
Arrhythmia

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3
Q

Bradycardia - 7 causes

A

Hypoglycemia
Decrease in catecholamines
Conserve energy
Vagal stimulation
Hyper/Hypokalemia (if severe causing A/V block)
Increased intra-cranial pressure
Arterial pressure is less than the inter-cranial pressure

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4
Q

Heart rate or rhythm doesn’t fit it what do you do?

A

ECG

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5
Q

Shock - name 7 types

A

Hypo-perfusion
Cardiogenic
Hypo-volemic
Toxic (micovascular failure)
Endotoxic (bacterial toxins on the heart)
Septic (septicaemia with affect on organs & vasculature)
Neurogenic (intense stimulus - emotions, vagal, CNS trauma)

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6
Q

Leptospirosis - 5 types

A

Aerobic motile spirochete

Hardjo (host adapted), pomona (non-host adapted), gryppotyphosa, itcterohemorrhagica, canicola

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7
Q

Host adapted Lepto - causes what?

A

Repro problems, chronic persistent infections

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8
Q

Non-host adapted Lepto - causes what?

A

acute infection in accidental hosts

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9
Q

Epidemiology of Lepto

A

warm & wet
skin abrasions & mucus membranes
Urine, uterine fluids, spread venerially
After recovery can still shed

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10
Q

Leptospirosis - pathogenesis

A

Enters abrasion
Multiplies in blood
Liver/spleen brain
blood vessels/liver damage
Proximal tubules of kidneys/placenta/fetus damage
Recover? antibodies remove everything but eye, uterus & renal system

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11
Q

Leptospirosis - acute

A

calves < 1 month
high mortality (sudden death)
pyrexia, depression, anorexia, petichea, acute hemolytic anemia, hemoglobinurea, super anemic, tachycardic, have shock
(usually caused by pomona)
direct damage to the micro-circulation - blood loss - tachycardia, less O2 carrying –> tachycardia, peripheral vasoconstriction –> edema (damaged blood vessels, hypoxia, cell death, tachypnea & dyspnea

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12
Q

Leptospirosis - sheep

A

rare, but often sudden death

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13
Q

Leptospirosis - adult cattle

A

Usually hardjo

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14
Q

Initial infection of Leptospirosis - adult

A

pyrexia, anarexia, agalactia & stiffness
Recnet in intro? mastitis Agalactia, abortions a few weeks later
Sequelae - persists in repro tract, infertility (fetal infection, but also placentitis) & transmitted venereally
Mastitis - without gland inflammation - possible

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15
Q

Leptospirosis - diagnosis

A

Culture, but only do this in acute cases (pomona)
Dark field microscopy
PCR - don’t tell you the serovar
Serology - can look at a rising titre, but hard to know if the herd is endemic

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16
Q

Leptospirosis - prevention

A

vaccine - server specific
reduces shedding as well
Can do as young as 4 weeks, repeat every 6-12 months, doesn’t prevent abortions or renal shedding
Control - hard to identify carriers, can try to control shedding & spreading & have good hygiene

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17
Q

Cold water hemoglobinurea

A

Happens when you drink a whole lot of cold water - intravascular hemolysis - usually in calves (rumen is buffer). Usually after a period of water deprivation

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18
Q

Cold water hemoglobinurea - pathogenesis

A

Absorb water, decreases, blood electrolytes, decreases osmotic pressure,
RBC are the most fragile at 5 months
occurs within 1 hour of ingestion
tachycardia due to relative O2 deprivation
cell death, vasodilation, edema (pulmonary, brain, death)

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19
Q

Copper poisoning

A 
Acute hemolysis because of chronic copper poisoning
Either primary (lot at once, or chronic) or secondary (plant, toxic)
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20
Q

Copper poisoning - pathogenesis (acute/chronic)

A

Acute - actual chemical damage to the GI mucosa, causing protein to coagulate causing coagulation necrosis, fluid loss, shock & death
Chronic - poorly understood - no clinical signs until critical levels in liver, liver necrosis - releases copper, oxidizes blood cells, methemoglobinemia, heinz bodies, hemolysis
PCV can decrease in 48 hours seriously

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21
Q

Copper poisoning - clinical signs

A

acute - GI issues, diarrhea, dysentary & jaundice, shock, abdominal pain
chronic- pale, jaundice, low appetite, tachycardia, depressed, tachypnea, maybe neurosigns later, anemia, methemoglobinemia, hypoxia & dyspnea

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22
Q

Copper poisoning - clinical path

A

anemia, hemoglobinemia/urea, methemiglobinemia/urea

high copper, high liver enzymes

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23
Q

Copper poisoning - treatment

A

don’t stress
give a chelator - molybdenum to get the copper out.
(if suspected)

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24
Q

Copper poisoning - prevention

A

keep copper low in feed, or if you know about their molybdenum intake, you can give a little more

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25
Q

Heart failure - right or left?

A

right

26
Q

Right-sided heart failure

A

Increase in heart right, decrease in appetite, exercise tolerance
Ventral edema, jugular distension, jugular pulse, extremities cool, elbows abducted

27
Q

Left-sided heart failure - rare

A

Tachycardia, etc similar to right
Increase in pulmonary pressure, probably won’t have many respiratory signs, unless pulmonary edema (frothing at the nares etc)
First sign - might be right sided heart failure

28
Q

Treatment

A

poor prognosis, probably already permanent damange, could try diuretics

29
Q

Arrhythmias

A

Heart disease usually, supra ventricular dysrhythmias rare, but usually a/fib cattle do get normal sinus arrhythmia.

30
Q

Atrial Fibrillation

A

Lose coordinated electrical activity of the atria (sometimes you get AV node ventricular activity)
On ECG, no p-waves, irregular base line (as in f waves) undulating baseline… every once in a while, normal random QRS
Occurs especially with atrial enlargement
Can occur spontaneously with sub-acute or chronic GI disease
If persistent, heart disease or heart failure
Always clinically relevant (toxemia, severe electrolyte imbalances, myocardial abnormalities)

31
Q

Endocarditis

A

Valvular or non-vavluar

A. pyogenes, e.coli or alpho-hemolytic strep

32
Q

Endocarditis - pathogenesis

A

Disturbed blood flow -> damage to endocardium -> platelet adhesion/fibrin clumps -> bacteria can colonize if circulating

33
Q

Endocarditis - Predisposing factors

A

valvular regurg/stenosis, heart disease, none

34
Q

Endocarditis - clinical finding

A

poor doing weight loss, shifting lamens associated with arthritis, fluctuating fever goes away with antibiotics, may or may not have a heart murmur
Usually tricuspid on the atrial surface
Lungs showered, will get cough
Lots of these? pulmonary hypertension, after load increases, right volume overload
Left - renal/myocardial infarcts, maybe septic arthritis

35
Q

Endocarditis - clinical pathology

A

neutrophilia (with or without left shift)
anemia
hyperfibrinogenima
Hypergloblinimia

36
Q

Endocarditis - post mortem

A

vegetative growths that distort the valves
Examine the chordae & the rest of the endocardium (hard to culture)
Other lesions consistent with embolization & abscess

37
Q

Endocarditis - treatment

A

ideally culture first
Start with broad spectrum
Change to what culture says
Continue for more than 14 days

38
Q

Cardiomyopathy - what kind is in bovine?

A

DCM
Inherited - red gene in Holsteins
Diffuse myocardial fibrosis association
Clinical signs = right heart failure

39
Q

DCM - diagnosis

A

R/O other causes of right heart failure
See the clinical signs like this in an otherwise healthy animal
Congestive heart failure and extensive myocardial fibrosis

40
Q

Myocarditis

A

Bacterial - h. somni, a. pyogenes, clostridia

Viral - FMD, bluetongue

41
Q

Myocardial degeneration

A

Toxin (ionophore, bacterial toxemia, gosseypole)

Nutrition (vitamin e & selenium deficiency, excessive molybdenum or sulphates)

42
Q

Myocarditis/Myocardial degeneration

A

Sudden death
Chronic - heart failure, arrhythmias
Vitamin e/selenium -> die when exercised

43
Q

Myocarditis/Myocardial degeneration - clin path

A

Can look at CK
Tropanin 1
Otherwise underlying cause

44
Q

Myocarditis/Myocardial degeneration - treatment

A

Remove/treat underlying cause
Rest, decrease stress
Anti-inflammatories in myocarditis
Don’t treat with anti-arrhytmias

45
Q

Myocarditis/Myocardial degeneration - PM

A

don’t see much histo
Can see a streatked pallor on the myocardium if vitamin/E/selenium
Myocarditis abscess - may see these, patchy though, not diffuse

46
Q

Pericardial disease (TRP)

A

In ruminants usually, pericarditis (TRP in cows)
Sheeps/goats/calves - sequelae of septicemia
Hardware ingested, decreased everything, venous engorgement, elbows are abducted
Undulating disease

47
Q

Friction rubs

A

Important to differentiate from a murmur. These can vary from beat-to-beat and in timing with relation to the beats. (both character & intensity)
Can disappear with the appearance of effusion

48
Q

Triad of diagnostic clinical signs for pericardial disease

A

Muffled heart sounds
Weak rapid pulse
Venous engorgement
(Can do U/S, ECG, large & small alternating QRSs, pericardio-centesis)
Can see fibrin, thickened pericardium, purulence, may see FB. Reticulum communication possible

49
Q

Pericardial disease - treatment

A

antibiotics
drain pericardial sac
Remove FB by surgery

50
Q

Pericardial disease - sequelae

A

Fibrin –> fibrosis, constrictive pericarditis

51
Q

High mountain disease

A 
Chronic heart failure in cows living in high altitude.  
Low atmospheric oxygen
Alveolar hypoxia
Pulmonary vasoconstriction/hypertension
right heart failure
Cor pulmonale
52
Q

High mountain disease - animals affected

A

Holsteins (tunica media is more sensitive) predisposed, sheep & goats pretty resistant
introduced animals

53
Q

High mountain disease - pathogenesis

A

Low O2
Myocardial damage
Need to slowly adapt them.

54
Q

High mountain disease - PM

A

CHF, concentric right ventricular hypertrophy

55
Q

Congenital heart disease

A

Variable incidence, can be simple or complex
Simple - VSD
ASD/PD are less common
Complex - rare (tetraology of fallow), persistent truncus arteriosis etc)

56
Q

Congenital heart disease - Clinical significance

A

Consider the direction of the shunt

Possible extra-cardiac effect could alter cardiac function (e.g. pulmonary hypertension)

57
Q

Left-to-right shunts

A

Increase the workload of both the chambers (left more than right)
Decrease the cardiovascular functional capacity
Cause failure to thrive

58
Q

Right-to-left-shunt

A

similar to L-to-R, but even worse because of hypoxemia

59
Q

Congenital heart disease - Clinical signs

A

variable - from asymptomatic, to gradually progressive to severe/immediate (exercise intolerance) - resp distress
(can do blood gasses, grave prognosis)

60
Q

Simple VSD

A

Loudest very forward on the right

61
Q

Complex VSD

A

Loudest on the left

62
Q

PDA in ruminants is simple or complex

A

Complex in ruminants

Food Animal Medicine & Surgery (9 decks)

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