CRS 6 Flashcards

1
Q

Discuss the uses and limitations of the laboratory techniques available for demonstrating the parasite

A
  • Heartworm and MFF antigen tests: antigen test takes 7 months do give positive result. Only means infection has occured at some point
  • Thoracic radiological examination: can predict stage of infection and find thromboembolism, can see infiltration of vessels by worms
  • Echocardiogram may show rigth ventricular dilation and wall hypertrophy, parallel linear echodensities produced by worms may be detected in right ventricle, right atrium and pulmonary artery
  • ECG usually unremarkable
  • ELISA: positive means must be a recent infection
  • Tracheal washes show parasites up the parasites themselves
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2
Q

Discuss the approaches to treatment and prophylaxis of Dirofilaria immits

A
  • Kill both adult worms and MFF
  • Prevent transfer to adult dogs
  • To kill adult worm immiticide and caparsolate useful
  • Dead worms may induce significant immune reaction
  • Surgical removal may be necessary (caval syndrome)
  • MFF can be killed using ivermectin, milbemycin
  • Both can be used as prophylactics
  • Ivermectin as heart guard and milbemycin as interceptor
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3
Q

Explain the clinical relevance of vascular parasites

A
  • Catastrophic effects
  • Rapid decline and death
  • Immune inflammatory response that can cause more damage than parasite itself
  • May also be opportunity for parasite to reach brain and reduce blood flow to the area
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4
Q

List important epidemiological factors in lungworm disease of dogs

A
  • Poorly understood
  • Sligs and snails appear to be vectors for parasite when ingested by dog
  • Transmission also associated with kennels and travelling
  • Can be transferred dog to dog (Angiostrongylus vasorum)
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5
Q

List importnat epidemiological facotrs of lungworm disease of cattle

A
  • Dictyocaulus viviparus
  • Calves and yealings turned out to pasture fist time
  • Later half of first grazing season
  • Cattle on permament pastures used for seasonal grazing in EU affected
  • Develop immunity following infection
  • Must be mainteined by exposure each year
  • Hypobiosis of late larval stage has been demonstrated in adult cattle
  • L3 larvae may overwinter on pasture in enough numbers to cause disease following spring
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6
Q

List important epidemiological factors of lungowrm in horses

A
  • Dictyocaulus arnfieldi
  • Mainly when pastures shared with donkeys
  • When field previosuly used for donkeys
  • Not persistent infection in horses
  • Patency lower than that in horses
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7
Q

Suggest relevant diagnositc tests for lungworm

A
  • Clinical signs
  • Faecal egg count
  • Bronchoalveolar lavage
  • Tracheal wash
  • Endoscopy
  • Post mortem
  • Biopsy
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8
Q

Compare the immune response to Angiostrongylus in dogs and Dictyocaulus in cattle

A
  • Eosinophils, neutrophils, mast cells and basophils
  • Immune responses different due to genetic variation between species of parasite and host
  • Immune response to an occult infection also different to an adult infection
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9
Q

Explain the variation in immune response reflecting in clinical signs of angiostrongylosis in dogs

A
  • Clinical signs include coughing, dyspnoea, haemorrhage, pulmonary hypertension, lethargy, exercise intolerance, collapse, neurological signs, ocular signs, lumbar pain or no clinical signs
  • Adult antigen causes type III hypersensitivity, dissemination of immune complexes, complement activation and immune infiltrate in the lungs and other tissues
  • Egg deposition or L1 can cause pulmonary inflammatory/granuloma and pulmonary arteriolar vasoconstriction
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10
Q

Outline ways in which parasitic diseases may be transmitted

A
  • Vectors
  • Ingestion
  • From individual to another individual
  • From parasite laying eggs in animal
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11
Q

List some importnat taxonomic features which enable parasite identification

A
  • Gross morphological structure of adults and eggs
  • Plugs?
  • Smooth or rough shell
  • Thin or thick shell
  • Parasite visible in egg?
  • Colour?
  • Size?
  • Where found?
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12
Q

Describe the life cycle of some respiratory parasites in exotic species

A
  • Snake lung worm (Pentasmid) migrate as larvae from intestinal tract and then as adult to lungs
  • Common intermediate hosts include insects and rodents
  • Ivermectin common treatment but cannot be used for turtle
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13
Q

Discuss some methods used to diagnose respiratory parasites of exotic species

A
  • Clinical signs and history
  • What kind of feed
  • Contact with other animals
  • Faecal egg count
  • Identification of eggs under microscope
  • Post mortem
  • ELISA
  • Biochemical tests
  • Complete blood count
  • Blood smear
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14
Q

Define an acid

A

A proton donor (increases H+ concentration in a solution)

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15
Q

Define a base

A

A proton donor and decreases H+ concentration in solution

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16
Q

Define the term pKa

A
  • Negative log of Ka
  • pKa = pH at which 50% of molecules are ionised
  • Greater pKa = lower dissociation and weaker acid
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17
Q

Define Ka

A
  • Dissociation constant
  • Ka = [H+][A-]/[HA]
  • Stronger acid has a higher Ka
  • Strong acid gives Ka>1, pKa
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18
Q

Define the term buffer solution

A
  • Buffer solution is one that resists a change in pH by accepting or donating protons
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19
Q

Define pH

A

pH = -log10[H+]

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20
Q

State the Henderson-Hasselbach equation and use it to calculate the pH, pKa or [base]:[acid] ratio in a budder solution when given appropriate information

A
  • pH = pKa + log ([A-]/[HA])
  • Many drugs are weak acids or bases
  • Un-ionised drugs cross membranes and enter blood stream more easily
  • Environment will impact upon ratio of ionised to un-ionised
  • Drugs work bes aroun 1pH of their pKa
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21
Q

Explain the need for biological buffer systems

A
  • Need to balance daily input/output of H+ in order to maintain steady state
  • Metabolism of fat and carbohydrates produces H+ ions
  • CO2 combines with water to form carbonic acid
  • Buffers present damage occuring through produciton of waste products
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22
Q

List the different types of acid in the body and give examples for each

A
  • Volatile acid: an acid that can leave solution and enter the atmosphere e.g. carbonic acid in the lung, broken down to CO2 and H2O
  • Fixed acids: cannot leave solution and must be eliminated by the kidney e.g. phosphoric acid
  • Organic acids: by-products or participants in aerobic metabolism e.g. lactic acid
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23
Q

Outline the mechanism of action of a buffer

A
  • Able to accept or donate protons
  • Weka acids or bases exist at equilibrium with the conjugate
  • Resist changes from a stronger solution when added
  • Compounds with pKa values in range of 6.4 - 8.4 most useful
  • Curve is sigmoidal
  • At pH associated with mid range has greatest buffering capacity
  • For each buffer, best capacity extends 1pH unit either side of pKa
  • Can act as open or closed systems
  • Buffers can be proteins, phosphate, carbonic acid, hydrogen, carbon
  • Can also be grouped by location - intracellular (proteins and phosphates) or extracellular (bicarbonate and Hb)
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24
Q

List locations of biologially important buffers and give the components

A
  • ISF: bicarbonate, phosphate, protein
  • Blood: bicarbonate, haemoglobin, plasma protein
  • ICF: proteins, phosphate
  • Urine: phosphate, ammonia
  • Bone: Ca carbonate
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25
Q

Describe protein buffers

A
  • Action depends on ability of amino acids to respond to pH change by accepting or releasing H+
  • Increase in pH, carboxyl group (-COOH) releases H+, acting as a weak acid
  • Becomes carboxylate ion (-COO-)
  • At normal pH, proteins negatively charged and H+ already lost
  • Histidine and cysteine are important donors
  • R groups contain an imidazole ring, can donate H+ if pH climbs too high
  • Albumin contains more histidine residues than globulin
  • Histidine can be donor or acceptor at physiological pH
  • pH decreases, carboxylate ion and amino group act as weak bases and accept
  • Forms amino ion and carboxyl group
  • Only free amino acids have free carboxylate ions and amino groups
  • All amino acids have at least 2 titrable protons therefore 2 pKa values
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26
Q

Indicate the major buffering systems present in mammalian blood and understand the role played by CO2 and haemoglobin

A
  • Haemoglobin, bicarbonate, plasma protein
  • Hb is main one, intracellular
  • RBCs tighlty packed with Hb, cytoplasm contains carbonic anhydrase
  • Hb rich in histidine residues
  • Deoxygenated blood better buffer than oxygenated
  • Imidazole group dissociates less when Hb oxygenated
  • Hb allows exposed or free amino groups and as a resul, Hb can combine with H+ ions
  • Reduces concentration of free H+ ions = buffer
  • Hb plays secondary role supporting the carbonic acid - bicarbonate system in the plasma
  • Increase H+ leads to lower affinity of Hb for oxygen
  • Hb will unload oxygen more readily in capillaries of metabolically active tissues liberating H+ ions and CO2
  • Contribute to more acidic pH environment
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27
Q

Describe the bicarbonate buffer system in the ECF

A
  • Most important
  • Open system
  • pKa is 6.1, poor buffering at normal blood pH of 7.4
  • As is open system, still very effective
  • CO2 dissolves in water, catalysed by carbonic anhydrase
  • CO2 +H2O H2CO3 (H+) + HCO3-
  • If CO2 levels increase, level of bicarbonate stays stable so pH drops significantly
  • CO2 can be breathed off in open system
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28
Q

Explain and compare methods for the evaluation of ventilation and lung function including arterial blood gas analysis and capnography

A
  • Ventilation assessed using capnography, observation of the thorax, observation of bag movement (GA), using a ventilometer of respirometer
  • Blood oxygen can be assessed byestimation from mucous membranes, pulse oximetry or blood gas analysis (pressure exerted on blood by oxygen in the plasma)
  • Oesophageal manometry can also be used to assess pleural function
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29
Q

Explain the purpose of capnography and how it can be used

A
  • Shows ventilation, amount of CO2 produced, crude estimmate for cardiac output, metabolism and integrity of other equipment
  • Goot alternative to blood gas analysis - measure CO2 breathed out
  • Straight from systemic circulation so is accurate and non-invasive
  • Normal circumstances, metabolic rate doesnt alter much
  • Ventilation determines arterial CO2
  • CO2 very soluble so Co2 in alveolar space good approximation of arterial CO2
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30
Q

Describe how pulse oximetry works

A
  • Beams of lgiht shone through capillary beds at 2 different wavelengths
  • Oxyhaemoglobin and reduved haemoglobin absorb light at different rates
  • Makes it possible to work out percentage saturation of oxygen
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31
Q

What are the advantages and disadvantages of pulse oximetry?

A
  • Advantages: non-invasive, fast result
  • Disadvantages: oxygen carrying capacity cannot be determined, not accurate with assisteed oxygenation and smoke inhalation, affected by tongue colour and drugs administered e.g. vasoconstrictive drugs
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32
Q

Describe methods for assessment of direct arterial blood pressure

A
  • Doppler blood flow probe: hear blood flow, ultrasound bounces off moving structures, reflected frequency made audible, done over clipped artery
  • Doppler sphymomanometry: detects presence of flow in distal artery, cuff inflated proximal to flow detector to pressure whcih exceeds systolic arterial pressure. Flow stops. Gradually decrease pressure within the csss and pressure at which flow first returns to heart is systolic presure
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33
Q

Describe methods for the assessment of venous pressure

A
  • Pressure of blood returning to the right side of teh heart
  • Usually reflects volume of blood returning
  • Long cannular insterted through jugular into vena cava
  • Can be connected to a transducer and oscillometer to get automated trace
  • Manometer should be zeroed to right side of heart
  • Extension tube filled with fluid so changes in pressure are visible
  • Can see if heart is functioning properly and can cope with blood returning to heart
  • Can show if there is adequate circulating volume
  • In hypovolaemic animal, movement of water in extension tube will be below 0cm
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34
Q

Describe the methods for assessment of cardiac output

A
  • Mostly in horses under anaesthesia
  • Inject very cold water and measure change in temperature as it travels across the heart
  • Lithium and dyes can also be used to measure the amount of blood that has passed through the heart
  • ECG can also show if there is normal rate and rhythm but not cardiac output (but abnormal rate and rhythm will affect cardiac output)
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35
Q

Discuss advantages and disadvantages of monitoring cardiorespiratory function late in the chain

A
  • Later measurement, reflects things that happen earlier
  • Oxygenation of arterial blood in tissue reflects blood pressure, heart function, lung function and breathing
  • Advantage: can be sure whole system is working
  • Disadvantage: if something is wrong do not know where
  • Measure oxygen delivery by tissue perfusion or blood oxygen content
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36
Q

Explain why it is importnat to measure teh mean arterial pressure and outline how this can be done

A
  • MAP drives tissue eprfusion
  • Low MAP = low perfusion
  • If tissues themselves are constricted then increasing pressure will have no effect
  • Measure MAP by feeling pulse (not very accurate but if can feel a strong pulse then usually adequate)
  • Invasive measurement (cannula in artery)
  • Non-invasive e.g. pressure cuff
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37
Q

Describe the causes of hypoxia

A
  • Problems in uptake of oxygen in arterial blood
  • Impaired ability to carry oxygen in blood
  • Impaired ability of blood to get to tissues
  • Impaired ability of oxygen to get off Hb
  • Uptake hypoxia can be caused by things that reduce normal oxygen transfer to arterial blood, low inspired oxygen and high alveolar carbon dioxide
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38
Q

Describe the causes of hypercapnia

A
  • Can occur when ventilation is not same as respiratory effort or breathing rate
  • Negative pCO2 indicates something is wrong, lowers pH, promotes dysrhythmias and is ultimtely fatal
  • Hypercapnia leads to hypoxia
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39
Q

What is the normal pH of blood

A

7.4

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40
Q

What is the normal pCO2

A

40mmHg

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41
Q

What is the normal pO2 of blood

A

4 times that of the fractional inspired oxygen

42
Q

What is the normal level of bicarbonate in the blood

A

24

43
Q

Define hypoxia

A

Reduced oxygen in each tissue

44
Q

Define hypercapnia

A

INcreased CO2 in arterial blood (paCO2) and is synonymous with hypercarbia

45
Q

What is the aveolar gas equation?

A

PAO2 = PIO2 -1.2(PaCO2)

  • Where PIO2 = percentage of oxygen in teh air x atmospheric pressure
  • PAO2 = average alveolar pO2
  • PaCO2 = average concentration of CO2 in the arterial space
46
Q

List the things that cause the Bohr shift shift to teh right)

A

Decreased pH, increased CO2, increased temeperature, increased 2,3-BPG

47
Q

Describe the clinical assessment of hypercapnia

A
  • unrelaibel since respiratory rate, depth and effort cannot be used to reliably predict the PaCO2 of a patient with possible respiratory distress
  • Patient in respiratory distress can have a high, normal or low PaCO2 as can a patient without
  • PaCO2 only determined by capnography or blood gas analysis
  • Measure partial pressures of oxygen concurrently or measure PaCO2
  • Capnography more reliable, measure CO2 in an expired breath
48
Q

Differentiate causes of hypoxia and hypercapnia arising from ventilation or gas exchange or perusion related disturbances

A
  • Uptake hypoxia caused by reduced normal oxygen transfer to arterial blood for example by high alveolar carbon dioxide (hypercapnia)
  • Disease or thickened alveoli
  • Low inspired oxygen
  • Low atmospheric pressure
  • Ventilation perfusion mismatch
49
Q

Describe how shunts can cause hypoxia

A
  • In normal lung, oxygen enters alveoli and raises saturation from venous level (70%) to 100% by the time it reaches arterial side
  • In shunting, no oxygen gets into alveoli so venous saturation not increased
  • In low SvO2 situations, alveoli unable to raise low venous saturation to normal levels
  • When both problems present, arterial desaturation worsens
  • Lungs diseased and filled with pus and fluid then increasing oxygen administered will not help as cannot be taken up
  • V/Q mismatch taking place
50
Q

Explain how hypoxia (and hypercapnia) can be detected

A
  • Pulse oximetry (SpO2 low in hypoxia)
  • Cyanosis (hypoxia)
  • Lactate
  • Blood gases
  • Blood gas analysis measure pO2mmHg in blood
51
Q

Explain the physiological effectos of hypoxia

A
  • Decreased brain function (including ventilation)
  • Decreased cardiac function
  • Positive feedback (increased heart rate to perfuse tissues, no oxygen so perfusion not increased, increase rate to have an effect)
  • Worsened by concurrent hypercapnia
  • Cardiac dysrhythmia
  • Cardiac arrest
  • Brain cells only survive 3 minutes in oxygen starvation and tissues of major organs only last 15-20 minutes
  • Normal physiological response is to increase ventilation
  • Mild hypoxia with no hypercapnia has no effect on breathing
52
Q

Indicate, briefly, how to manage animals with hypoxia or hypercapnia

A
  • increase oxygen supply
  • Manage underlysin diseases (inotropes for heart failure and intravenous fluids for blood loss)
  • Ventilate to increase VA and PAO
53
Q

Define cyanosis and explain its cause

A
  • Appearance of blue or purple colouration of the skin or mucous membranes (difficult o detect in pigmented skin)
  • Severely hypoxemic
  • Cause may be clear (e.g. air hunger)
  • Poor indicator of hypoxia since other things can affect detection (lighting, colours around animal)
  • More anaemic an animal is, more hypoxis must be before cyanosis detected
  • Threshold for cyanosis is reduced Hb content of 5g/L in capillary
  • Can occur at varying values of arterial oxygen saturation (SaO2) and arterial Hb count
  • If cyanosis present then emergency situation - severely hypoxic, give oxygen
54
Q

Outline transport hypoxia

A
  • Either Hb unable to carry oxygen (carbon monoxide)
  • Or unable to remove oxygen from Hb
  • Anaemia
  • Abnormal Hbs
55
Q

Outline perfusion hypoxia

A
  • Heart failure
  • Low blood volume
  • Extreme vasoconstriction or sepsis
56
Q

List the causes of perfusion hypoxia

A
  • Inability of tissues to take up oxygen such as cyanide posioning
  • Perfusion hypoxia is rare and difficult to detect
57
Q

State the primary causes of blood acid-base disturbances

A
  • Respiratory: increased or decreased CO2
  • Metabolis: increased ordecreased bicarbonate
  • Aemia is change in pH of ECF
  • Osis once know the cause of the disturbance
  • Where both CO2 and HCO3- are altered, more altered one is primary cause and less altered one is compensation
58
Q

Describe the short term physiological compensatory mecahnisms of acid-base disturbances

A
  • Respiratory acidosis: increased renal net acid excretion with resulting increase in serum bicard
  • Respiratory alkalosis: decreased renal net acid excretion with resulting decrease in serum bicarb
  • Metabolic acidosis: hyperventilation with resulting lowering of pCO2
  • Metabolic alkalosis: hypoventilation with a resulting increase of pCO2
59
Q

Describe how the respiratory system operates to regulate blood pH

A
  • if blood pH too low due to increased HCO3-, reacts with H+ to form H2O and CO2
  • Increased ventilation prevents build up of CO2 which would decrease pH by dissociation
  • If blood pH too high, ventilation decreases in order to retain the CO2 and produce more HCO30, lowering pH again
60
Q

Explain how the kidneys excrete acid by reabsorbing HCO3- and excreting acid urine

A
  • Na+/H+ antiporter in luminal membrane of proximal tubule
  • H+ combines with HCO3- to form H2CO3 which breaks down to form CO2 and H20
  • H20 and CO3 passively reabsorbed
  • H20 breaks down to OH- and H+
  • OH- binds with CO2 to form HCO3-
  • In ascending loop of Henle, H+ ATPase pump removes H+, carries out same process
  • HCO3- removed from cell by Cl- antiporter and into the blood
61
Q

Indicate how the changes in blood parameters such as pH, PCO2 and HCO3- you would expect to see in acute and chronic acid-base conditions

A
  • Acute respiratory acidosis: decreased pH, increased PCO2 and increased HCO3-
  • Acute metabolic acidosis: decreased HCO3- (loss by diarrhoea), decreased pH, decreased CO2 (increased ventilation)
  • Chronic respiratory acidosis: increased CO2 and HCO3-, pH not returned to normal
  • Chronic metabolic acidosis: increased renal excretion of H+ as NH4+ so increased pH, increased HCO3-
  • Acute respiratory alkalosis: CO2 decerased, decreased HCO3-, increased pH
  • Acute metabolic alkalosis: increase pCO2, decreased HCO3-, decreased H+ therefore increased pH
62
Q

Describe the basic methods for acid base determination in domestic species

A
  • Blood gas analyser

- derives bicarb from other valuses as well as anion gap and base excess

63
Q

What is teh anion gap and what is the normal value

A
  • Difference between the main measured plasma cations and main measure plasma anions
  • Represents anions not routinely measured such as proteins and phosphates
  • Normal value is 17mmol/L
64
Q

Define the term poikilotherm

A

An animal that has a body temperature across a wide range of environmental temperatures
- Does not have to be an ectoderm e.g. naked mole rat

65
Q

Define the term homeotherm

A

An animal that maintains its body temperature within narrow limits using its own energy

66
Q

Define the term thermoneutral zone

A

The zone where no active control of body is required

67
Q

Define lower critical temperature

A

The lowest temperature at which the body can still function

68
Q

Define upper critical temperature

A

The highest temperature at which the body can still function

69
Q

Define the zone of thermal comfort

A

The range of comfortable environmental temperatures

70
Q

Define thermal set point

A

The point at which active control kicks in. This can be altered in diseases such as influenza

71
Q

Descirbe how heat is generated

A
  • Energy metabolism and ATP from energy use
  • Musce contraction: 1 unit of energy contraction produces 4 units of heat (shivering produces a lot of heat)
  • The liver has the highest heat generation except the brain due to its high metabolic rate
72
Q

Describe how conduction results in heat loss

A
  • Direct transfer between 2 surfaces that are in direct contact
  • Heat gain or heat loss can take place
  • Heat goes from warmer to cooler
  • Air has poor thermal conductivity
  • Conductive losses can take place due to ground contact or contact with cold water
73
Q

Describe how convection results in heat loss

A
  • Heat movement within a fluid or gas
  • Heat exchange takes place between skin and surrounding air
  • Efficiency decreases with increasing environmental temperature
74
Q

Describe how radiation results in heat loss

A
  • Movement of heat without physical contact e.g. solar radiation
  • Animals emit heat by radiation to cooler surroundings e.g. stone stables
  • Grass absorbs radiation whereas sand and clay reflect it
75
Q

Describe how evaporation results in heat loss

A
  • Change from liquid to vapour
  • Efficiency decreases with increasing humidity
  • At 100% relative humidity, evaporation cannot take place
  • Increased by increasing air temperature
  • Heat required to convert fluid to gas
  • Sweating and panting
  • Stimulated by increases SNS
  • Panting energy efficient method of heat loss but leads to dead space in ventilation
  • Wetting can be used to cool animal down
76
Q

Explain the consequences of hyperthermia and understand possible causes

A
  • Hyperthermia malignant
  • Causes enzymes and proteins in the body to denature
  • Can cause death
  • Rapid cooling necessary
  • Can be caused by heatstroke or over working in warm weather
  • Wet with cold water to cool down, not ice cold as this will raise internal temperature due to receptors receiving very cold signals
  • Latent heat of vaporisation to cool animal down
77
Q

Explain the cardiovascular response to cooling and describe potential therapeutic benefits

A
  • Lowered metabolic oxygen demand
  • Animal able to tolerate anoxia for longer
  • May be useful in hypoxic and septic patietns
  • Reduce peripheral diffusion in early stages of laminits
78
Q

Explain the clinical importance and management of thermoregulation in veterinary species

A
  • Important to ensure animals kept at normal temeperature
  • Ability to do so is impaired if ill
  • Too cold, raise using heat pads, blankets, reducing heat loss especially if animal is wet (neonates)
  • Convection should be limited using heat lamps
79
Q

Explain how body surface area:weight ratio affeects an animal’s ability to thermoregulate

A
  • Young animals have a larger surface area to body weight ratio
  • Larger potential surface to lose heat from
  • Young animals more susceptible to abnormal temperature changes which could have detrimental effect on their health
80
Q

Explain how sweating is controlled

A
  • Direct heating of skin can lead to sweating
  • Increase skin blood flow
  • Sweat glands have sympathetic innervation
  • Not abundant in all species
81
Q

Outline the central regulation of temeperature

A
  • Hypothalamus controls core temperature
  • Heat receptors (specialised to be for hot or cold) in skin, central organs and hypothalamus
  • Information received by hypothalamus is compared to reference range
  • Normal range increased during fever
  • Correction of temeperature mediated by thyroid hormone
  • Vascular tone in periphery altered accordingly
  • Too cold: heat redistributed by CV system, blood flow to skin limited, heat loss limited by adipose tissue, feathers and fur
82
Q

In what systems might physiological changes occur at the transition from foetal to neonatal life

A
  • Respiratory
  • Circulatory
  • Temperature control
  • Nutrition
  • Immune function
83
Q

Explain the changes that occur in respiration at the transition from foetal to neonatal life

A
  • Lungs change from fluid filled to air filled
  • Gaseous exchange across alveoli
  • Breathing stimulated by sensory stimuli: squeezing, light and cold
  • Removal of placental oxygen supply and CO2 removal
  • Stimulates first gasping respirations
  • Established functional residual capacity
  • FCR established due to gasps generating high intra-thoracic negative pressure, vercomes surface tension of alveoli, moves gas/fluid interface down bronchial tree into alveoli
  • Problems occur due to small alveoli
  • Take a lot of force to inflate due to high surface tension
  • Most fluid removeed by lymphatic and circulatory resorption within the lungs
84
Q

Explain teh removal of fluid from the lungs by epithelial cells

A
  • incrase in Na, K, and ATPase
  • Enables fluid to leave lungs
  • Adrenaline binds to beta receptors on interstitial membrane of epithelium
  • Cascade ending in increased intracellular cAMP
  • 2 membrane pumps activated
  • Na/K ATPase pumps Na into interstitial space, activated by oxygen and steroids
  • Facilitated entry of sodium into epithelium by ENaC pumps
  • Movement of sodium pulls liquid into intersitial space
  • Removed by lymphatic drainage
  • Induction of ENaC and Na/K ATPase pumps coordinated to work together
  • Rise in adrenaline at birth triggers switch from secretion to absorption
  • Increase in oxygen after birth augments increase in sodium absoption which completes transition to the post-natal stage
85
Q

Explain how liquid absorption can be compromised

A
  • Steroids, thyroid hormones and adrenaline
  • Factors altered in premature delivery
  • Absorption mechanism of lung develops during latter part of gestation
  • Premature infants may not remove liquid as efficiently as a term infant
  • May be important in future lung growth
86
Q

Explain the role of surfactant and the problems that occur post-partum

A
  • Premature - reduced surfactant
  • More surface tension in alveoli, difficult to inflate
  • Surfactant production stimulated by pre-partum rise in cortisol close to term
  • Not complete by full term
  • Respiratory distress syndrome may occur if there is insufficient surfactant
  • Diabetes can lead to reduced production
  • Increased insulin leads to decreased phospholipids, as can hypoxia, hypothermia and acidosis
  • Inadequate surfactant results in inadequate gaseous exchange
87
Q

Compare the immature lung to the mature lung

A
  • Immature: low surfactant, non-conducive to gas exchange, thick blood gas barrier, low compliance, immature epithelial cells, small area for gas exchange, poorly vascularised, high resitance to blood flow
  • Mature is opposite
88
Q

Explain why oxygenation is threatened at birth

A
  • Asphyxia common cause of perinatal loss in neonates
  • Due to reduced blood flow in uterus (contractions)
  • Umbilicus stretched and in some species placenta separates at expulsion
89
Q

Explain the changes that occur in circulation at the transition from foetal to neonatal life

A
  • In foetus, neonate reliant on mother and at birth has to develop own systme in conjuction with own breathing system
  • Umbilical cord crushed at birth, stopping venous return from the placenta
  • Expansion of lungs filling with air causes pulmonary vascular resistance to fall
  • Flow of blood through the ductus arteriosus ceases
  • Oxygenation acts on duct wall to cause muscle contraction
  • Prostaglandings maintain ductal flow
  • Prostaglandin inhibitors may result in premature closure in the foetus causing pulmonary hypertension
  • Right heart pressure falls and foramen ovale closes
90
Q

Explain the thermoregulation changes that occur at the transition from foetal to neonatal life

A
  • Conduction, convection, radiation, evaporation
  • High surface area:weight ratio, wet, little subcut fat, poorly keratinised skin
  • Immature shiverig reflex
  • Non-shiverign thermogenesis in volves brown adipose tissue
  • Contains uncoupling protein 1 (UCP1) which uncouples ATP production from respiratory chain
  • UCP1 peaks at around time of birth
  • Hypothermia is a major cause of neonatal mortality
  • If environment too cold, metabolic rate increases and limited energy reserves used up quickly
  • Once energy reserves ued up, peripheral circulation reduced and metabolism slows
91
Q

Explain the nutritional changes that occur at the transition from foetal to neonatal life

A
  • Establish independent energy intake
  • Most infants root and suckle quickly
  • Full term neonates utilise stores of glycogen and adipose tissue
  • GI tract needs to accomodate to increasing volumes, start to difest and adjust colonisation of bacteria
  • Suboptimal nutrition of the mother can lead to low birth weight and increases susceptibility to disease after birth
  • Neonate has low reserves of adipose tissue, immature renal and hepatic function
  • Depends on colostrum and milk to meet needs
92
Q

Explain the immune changes that occur at the transition from foetal to neonatal life

A
  • Said to be immunologically incompetent
  • Receive passive transfer of antibodies via colostrum
  • Gut transfer can only occur within first 48 hours
  • Initial intake of colostrum critical
  • Naval provides route for infection
  • Sepsis can occur
93
Q

List causes of neonatal loss

A
  • Hypoglycaemia
  • Hypovolaemia
  • Failure of passive transfer of antibodies
94
Q

Describe how hypoglycaemia can lead to neonatal loss

A
  • Low blood glucose due to failure to suckle
  • Neonate unable to suck then tubing may be necessary
  • Can lead to asphyxiation of bacterial proliferation
  • Administering glucose also possible
  • Neonate should be kept warm
95
Q

Describe hypovolaemia in neonatal loss

A
  • Decreased blood volume, decreased volume of blood plasma
  • Diminished blood pressure, bleeding or dehydration
  • Failure to suck means losses not replaced
  • Baroreceptors activated
  • Vasoconstriction occure
  • Reduces perfusion of major organs
  • Nutrients cannot be absorbed
  • Administer parenteral fluid
96
Q

Describe failure of passive transfer of antibodies in neonatal loss

A
  • Failure to tak eoclostrum within 48 hours
  • No access to colostrum
  • Often seen in combination with hypovolarmia and hypoglycaemia
  • If spotted 48 hours then plasma administered IV from dam or another donor
97
Q

List and discribe common causes of lamb losses

A
  • Dystocia: mal presentation, obstruction of birth canal
  • Exposure: hypothermia, adverse weather, shelter reduces this significatnly
  • Born weak: low birth weight, disease present at birth, congenital sway back
  • Inexperienced dams: poor mothers, will not allow offspring to feed, may reject or bully lambs
  • Agalactica: not producing milk
  • Later infectious diseases
98
Q

List and descrieb teh common causes of calf losses

A
  • Dystocia: foetomaternal disproportion, malpresentation, poor supervision of parturition
  • Born weak
  • Exposure
  • Later infectious disease
99
Q

List and describe common causes of foal losses

A
  • Dystocia: head deviation, malpresentation, uterine inertia or torsion
  • Prematurity/dysmaturity (dysmaturity is only one organ being immature)
  • Hypoxic ischaemic encephalopathy
  • Neonatal iseoerythrolysis
  • Sepsis
100
Q

List and describe common causes of piglet losses

A
  • Dystocia: usterine inertia, malpresentation, loss of contractions after first few born, rupture of umbilical cord
  • Low birthweight
  • Later infectious disease
  • Trauma from dam