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DVM 2 - 1 > HLI 1 > Flashcards

HLI 1 Flashcards

1
Q

What occurs with too much coagulation and too little

A

Too much: Thrombosis

Too little: Fibrinolysis

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2
Q

What are the two main features of hemostasis

A

1) pactivated platelets

2) coagulation pathway leading to production of fibrin

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3
Q

What are the 4 main stages of hemostasis

A 
Tissue/vessel injury 
1. Vasoconstriction - reduce blood flow - not stop due to important substances within the blood needed for clotting
- Inherent response to injury 
- Neural - sympathetically induced 
- Platelet-reinforced - release activators 
2. Platelet activation 
- Adhesion and Aggregation 
3. Coagulation 
- Blood clot 
○ Thrombin generation 
○ Fibrin polymerization 
4. Fibrinolysis 
- Blood clot dissolution 
5. Vascular patency restored
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4
Q

Platelet characteristics and what created from

A
  • Shed from megakaryocytes
  • Lack nucleus
  • Store secretory products in granules
  • High concentration of actin and myosin - contraction
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5
Q

What are the steps in activation, adhesion and aggregation of platelets

A
  1. Endothelial injury occurs resulting in the exposure of collagen which activates platelets and attracts vW factor from the blood (released by endothelial cells as well as megakaryocytes)
    - Platelets can also be activated by von Willebrand (vW) factor and tissue factor
  2. Activated platelets express vW factor receptors and secrete Vw factor themselves which binds to the platelets
  3. The exposed sub-endothelial collagen binds vW factor which is attached to the platelet leading to a high avidity bond (high strength)
    - Other stimuli such as adenosine diphosphate (ADP), 5-HT and thromboxane A2 can initiate aggregation via specific receptors
  4. Platelets also release number of factors (activators which activate more platelets) as well as vasoconstrictors such as serotonin and epinephrine and other factors to enhance coagulation
    Activation of platelets + coagulation pathway makes the permanent plug
    - Actin and myosin contracts which compacts and strengthens the plug
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6
Q

What limits platelet aggregation

A
  • Endothelium released prostacyclin and nitric acid that inhibit platelet aggregation
    This is activated by chemicals produced by the platelets themselves
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7
Q

What are the 3 main steps in the coagulation pathway

A

1) Cascades - intrinsic, extrinsic and common
2) cleavage of fibrinogen
3) cross linking through transglutaminase enzyme

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8
Q

Give a general overview of how the coagulation cascade works

A
  • Involve clotting factors that concentrate on activated platelets by binding to calcium ions via Gla domains that are attached to the surface of platelets due to the expression of negatively charged phospholipids
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9
Q

List the 5 thrombin roles in the coagulation pathway

A

1) Stimulates conversion of fibrinogen to fibrin
2) Stabilises the fibrin meshwork
3) Enhances the activation of the reaction converting prothrombin to thrombin
4) Enhances platelet aggregation
5) Anti-coagulant as well - activates protein C which inactivates clotting factors VIIIa and Va (8 and 5)
- Self-limiting

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10
Q

Vitamin K was it is needed for and what out-competes it

A
  • Essential for formation of clotting factors II, VII, IX, X (television channels)
  • These molecules all require gamma carboxylation after synthesis
  • Reduced vitamin K is a cofactor in carboxylation of glutamate
    Warfarin has similar structure to Vit K and competitively inhibits it - anti-clotting
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11
Q

How does the cross-linking of fibrin occur in the final stage of hemostasis

A
  • Initial soft plug characterised by H bonding

- Covalent cross linking mediated by transglutaminase (factor XIIIa 13) of fibrin adds strength

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12
Q

What limits clot formation at the site of injury

A
  1. Diluted by blood flow
  2. Removed by liver
  3. Anticoagulant mechanisms
    - Tissue factor pathway inhibitor
    - Thrombomodulin - modulates thrombin
    - Anti-thrombin III - inhibits thrombin actions
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13
Q

Characteristics of anti-thrombin III and Thrombomodulin

A

Anti-thrombin III
- Inactivates thrombin by forming a complex with it (irreversible)
- Can also block other factors such as Xia and Xa
- This is enhanced by heparin
Thrombomodulin
- Forms complex with thrombin
- Acts as a co-factor with Ca++ for thrombins activation of protein C
- Protein C and Protein S inactive factors Va and VIIIa through proteolytic cleavage

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14
Q

How does fibrinolysis occur

A

1) plasminogen is activated by tissue plasminogen activator and only when biund to fibrin (self-limiting)
2) plaminogen is cleaved into plasmin
3) plasmin degrades fibrin into peptides dissolving the blood clot

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15
Q

Characteristics of arterial and venous thrombus

A

Arterial thrombus (white)
• Platelets plus white blood cells in a fibrin mesh
• Usually associated with vessel wall damage (atherosclerosis)
• Breaks off leading to blood vessel obstruction (eg myocardial infarction)
Venous thrombus (red)
• Fibrin, platelets and red blood cells
• Usually associated with blood stasis (eg DVT with air travel)
• Breaks off leading to embolus lodging in lungs or brain

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16
Q

Why is it important to control haemostasis and thrombosis

A
  1. Hypercoagulability
  2. Blood stasis
    - Atrial fibrillation - saddle thrombosis in cats
    - Deep vein thrombosis - pulmonary embolism
  3. Vessel damage
    - Atherosclerosis
    ○ In coronary vessels–> myocardial infarction
    ○ In carotid arteries –> stroke
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17
Q

List and describe the 3 main drugs that affect fibrin formation

A
  1. Procoagulant drugs eg vitamin K
  2. injectable anticoagulants eg heparin, low-molecular-weight heparins
    - Used acutely for short term action
    Heparin
    - Enhances activity of antithrombin III which inactivates thrombin and Xa
    - Not orally available
  3. Oral anticoagulants eg warfarin
    - Used for prolonged therapy
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18
Q

What are the two types of rodenticide poisoning

A 
• First generation rodenticides 
- multiple feed poisons- lower efficacy but safer 
- shorter half life
• Second generation rodenticide
- feed poisons- higher efficacy
- longer half life
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19
Q

List the 3 drugs that affect platelet adhesion and activation

A

1) ADP receptor antagonists
2) Thromboxane synthesis inhibitors eg aspirin)
3) Glycoprotein IIb/IIIa receptor antagonists

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20
Q

What are the actions of aspirin

A

1) thromboxane synthesis inhibitor (decrease platelet adhesion and activation)
2) irreversible cyclo-oxygenase inhibitor
3) decreased vasoconstriction

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21
Q

what occurs with low dose aspirin therapy

A

90% aspirin cleared first-pass metabolism in liver therefore
- Endothelial production of prostaglandin I2 (PGI2) is preserved
○ beneficial vasodilation is preserved so maintain perfusion in essential tissues
- Platelets are exposed to aspirin as they circulate in the portal vein - causes irreversible inhibition of COX (hence thromboxane synthesis) in exposed platelets –>Decreased platelet aggregation

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22
Q

List the 2 fibrinolytic drugs, their actions and how used

A

1) streptokinase - activates plasminogen and used intravenously
2) alteplase (only in humans) - More active on fibrin bound plasminogen so “CLOT SELECTIVE”, human recombinant tissue plasminogen activators

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23
Q

How do bruises and haematomas resolve and what pigments contribute to gross discoloration

A

extravasated blood cells and coagulated fibrin are removed by lysis and especially by phagocytosis onset hours after haemorrhage

1) acute phase - red-blue due to poorly oxygenated haemoglobin
2) subacute phase - blue-green due to formation within macrophages of biliverdin and bilirubin
3) chronic phase - gold-brown due to formation of haemosiderin and some lipofuscin pigment

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24
Q

What factors determine the clinical significance of haemorrhage

A

1) location - fatal, brain, heart - intra and extra-cerebral, rapid haemopericardium - cardiac tamponade
2) rate and volume of blood loss - 20% of total blood volume or slow loss of larger volumes may have little impact on healthy animals
○ loss of 20-40% of blood volume -> haemorrhagic (hypovolaemic) shock
Loss more than 50% - DEATH

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25
Q

what is the most common cause of haemorrhage in domestic mammals and what are other 4 potential causes

A

physical trauma

  1. gastric dilation volvulus
  2. ectoparasites (fleas
  3. endoparasites - hookworms
  4. active inflammation
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26
Q

list 3 clinical signs would make you suspicious that an animal has a defect in primary haemostasis

A
  1. bleeding immediately after venipuncture
  2. small volume bleeds from multiple sites
  3. petechiae and ecchymoses
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27
Q

list 3 clinical signs make you suspicious that an animal has a defect in secondary haemostasis

A
  1. delayed bleeding after venipuncture
  2. large volume bleeds from multiple or localised sites
  3. haematomas common
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28
Q

List the four major mechanisms responsible for defects in primary haemostasis

A

1) platelet deficiency (thrombocytopenia)
2) platelet dysfunction (thrombocytopathy, thrombopathy or thrombopathia)
3) von Willebrand’s disease (deficiency of von Willebrand factor)
4) damage to small blood vessels

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29
Q

What are the 5 major mechanism for thrombocytopenia and which mechanism is most likely to lead to clinically significant thrombocytopenia in cats and dogs and their underyling conditions

A

1) Decreased platelet production - most common in cats due to retroviral infection (especially feline leukaemia virus (FeLV)) and/or myeloproliferative or lymphoproliferative disease
2) platelet destruction - most common in dogs due to immune-mediated destruction
3) consumption (utilization) of platelets
4) platelet sequestration
5) massive acute haemorrhage

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30
Q

What role does Von Willebrand factor play in primary haemistasis

A
  • in damaged blood vessels with high shear rates (e.g. arteries and arterioles), vWf is essential for platelet adhesion to collagen (i.e. without vWf, the platelets will be dislodged by blood flow)
    ○ vWf also contributes to platelet aggregation
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31
Q

What species most commonly affected with von willebrand’s disease, breeds and how inherited

A

Dogs
- doberman pinscher, german shepherds, goldern retrievers, poodles
3 forms of inherited vWD all ave autosomal recessive patterns

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32
Q

what clinical signs would you expect to see in a dog with von Willebrand’s disease

A

May be subclinical or cause mediate bleeding
bleeding doesn’t usually occur until the plasma concentration falls below 20% of normal
can lead to severe haemorrhage
More severe defect type 1-3, type 2 and 3 may get haematomas

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33
Q

List 5 blood vessel disorders that can manifest as petechiae and ecchymoses
in the skin and/or mucous membranes

A
  1. bacteraemia
  2. infectious vasculitis
  3. immune-mediated vascuilitis
  4. fragility of blood vessels
  5. vitamin C deficiency in guineapigs
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34
Q

List the 4 major mechanisms responsible for defective secondary haemostasis and which mechanism is most common

A

1) inherited coagulation factor deficiencies
2) Vitamin K antagoism or definciency - most common
3) hepatic parenchymal disease
4) excessive fibrinolysis or fibrinogenolysis

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35
Q

In which domestic animal are inherited coagulation factor deficiencies most often recognised and why are purebreds animal most often affected

A

Dogs

generally X-linked recessive trait - inherited and most purebreeds are highly inbreed

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36
Q

Why can some animals have a hereditary deficiency of a particular coagulation factor and
either never bleed excessively or suffer only from minor haemorrhage

A

severity of bleeding is usually inversely proportional to the activity of the clotting factor affected
eg: - factor XI deficiency (haemophilia C) usually causes only mild bleeding because factor X can be activated by the extrinsic system

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37
Q

whihc of the inherited coagulopathies predispose to severe haemorrhage

A

most severe haemorrhage is associated with inherited deficiencies of factor I, II or X of the common pathway (all of these are rare), factor VIII or IX of the intrinsic pathway, or combined factor deficiencies

38
Q

Why do haemophilia A and B mainly affect male animals?

A

haemophilia A (inherited factor VIII deficiency) and haemophilia B (factor IX deficiency) are both X-linked recessive disorders

39
Q

Which coagulation factors are deficient in the inherited coagulopathy recognised in Devon
rex cats?

A

Devon rex kittens with inherited mutation of the gene encoding γ-glutamyl carboxylase and hence deficiency of the vitamin K-dependent factors (factors II, VII, IX and X) often bleed severely in the neonatal period

40
Q

How can large animal species become poisoned by coumarin-type anticoagulants?

A

via ingestion

41
Q

In what circumstances might a dog develop deficiency of vitamin K? How common is vitamin K deficiency

A

rare

1) prolonged anorexia or malnutrition
2) oral antibacterial - kill bacteria found in the stomach that synthesise
3) Chronic lipid maldigestion/malabsorption syndrome - exocrine pancreatic insufficiency

42
Q

what role does the liver play in haemostasis

A

most of the coagulation factors are synthesised by

Factor II can be synthesised by multiple cell types

43
Q

How much of the hepatic functional mass needs to be compromised before an animal is likely
to be predisposed to haemorrhage due to inadequate synthesis of coagulation factors

A

functional mass of hepatocytes has been reduced to ≤ 30% - lose 70%
most animals with hepatic disease of this severity do not bleed spontaneously
○ instead, they are at risk of uncontrollable haemorrhage if haemostatic capacity is challenged (e.g. if a liver biopsy is undertaken!)

44
Q

In which condition is excessive fibrinolysis a contributor to defective secondary haemostasis
in domestic animals

A

rarely cause of bleed except when DIC (disseminated intravascular coagulation occurs)

45
Q

In which condition is excessive fibrinolysis a contributor to defective secondary haemostasis
in domestic animals

A

rarely cause of bleed except when DIC (disseminated intravascular coagulation occurs)
- excessive fibrinogenolysis -> inability to generate fibrin when needed -> haemorrhage

46
Q

List 3 ways to treat haemorrhagic shock

A

1) cyrstalloids - hypertonic solution - cheap, reliable
2) synthetic colloids
3) blood transfusion

47
Q

List 8 characteristics that a canine blood donor needs

A

1) Good temperament
2) Easily accessible jugular veins
3) No other health problems
4) Vaccinated, heart worm prophylaxis
5) - ≥ 25kg to allow collection of full unit (450ml)
6) Negative for blood borne diseases in your area
7) Should never have received a transfusion - may have acquired antibodies to certain blood types
8) Blood typed

48
Q

List 4 characteristics that a feline blood donor needs and what is needed in the clinic

A

1) ≥ 5kg body weight (for 50 mL to be collected)
2) No other health problems
3) FeLV/FIV/Mycoplasma negative
4) Ideally indoor cat
- Donors of both blood groups required

49
Q

What is the difference between cats and dogs in terms of blood types

A
  • dogs do NOT have naturally-occurring alloantibodies unless have already received a transfusion
  • cats DO have naturally-occurring alloantibodies - similar to humans
50
Q

Canine Blood types what is the system, how many types, which one is tested and what is different with greyhounds

A

Dog erythrocyte antigen (DEA) system
- 8 blood types
- DEA 1.1, 1.2, 3…8
Test for DEA 1.1 as it is the one that causes the biggest reaction against - positive or negative for this blood type
Greyhounds don’t have DEA 1.1 so generally more compatible

51
Q

What is the general rule of thumb in giving blood transfusions for dogs

A
  • Negative blood to negative or positive recipient
  • Positive blood to positive recipients (if give to negative get Ab production - now sensitized and if give positive again haemolytic reaction occurs
52
Q

What are the feline blood types, which is common in Aus and what are Siamese and Devon Rex mainly

A

A > B&raquo_space; AB (very rare)

  • Siamese always A
  • Devon Rex commonly B
  • Type B rare in the US, common in Australia
53
Q

Describe the Different Blood types in cats, do they have antibodies against different groups and what transfusion can they receive

A

Type A - 20% weak anti-B antibodies - usually not life-threatening, cells survive 5-6 days
Type B - can have very strong anti-A antibodies - transfusion of A into B leads to severe haemolytic reaction resulting in death (30%)
Type AB - no alloantibodies to A or B so should be transfused AB but can give A, cannot give B due to strong anti-A antibodies

54
Q

What is cross-matching in terms of blood transfusion and the 2 types

A
  • Mixing donor and recipient blood and looking for agglutination or haemolysis - Evaluates absolute compatibility between donor and recipient at that point in time
  • Major cross-match
    ○ Recipient plasma with donor red blood cells
    ○ Protects against lysis of the transfused red cells
  • Minor cross-match
    ○ Recipient red blood cells with donor plasma
    ○ Protects against lysis of the recipient red cells
55
Q

How often can animals donate blood, and what type of blood collection systems and collection methods are used

A

Should be able to donate up to once per month however generally every 3 months
- Blood collection system
○ Open vs closed
○ Closed - no entry to the environment in the tubing that connects the needle to the bag
○ Open - butterfly catheter put together yourself - not sterile so not good for storage
- Blood collection method
○ Suction vs gravity

56
Q

What is the thing to help us remember the coagulation pathway

A

When you walk IN to a store $12=11.98
IN = intrinsic, 12, 11, 9, 8
EX 3+7 = 10
Common 10 = 5 x 2 x 1

57
Q

What is the main anticoagulant that is used and what blood is needed for it to work

A

Citrate

- for fresh whole blood only

58
Q

at what temperature do you administer the transfusion and in what time period do you give the blood

A

Warm to room temperature

  • Water bath (37 °C)
  • Do not heat > 39°C
    1. Start slowly (2-5ml/hr) for 20min to allow early recognition of transfusion reactions
    2. Check patient demeanour and TPR every 5 minutes
  • As fast as you need in per acute, life-threatening situations
    3. Give remainder over 4 hours
    4. Check patient every 30min
59
Q

List the 3 types of whole blood and what they are used for

A

1) Fresh whole blood (FWB)
- RBCs, plasma proteins, all coagulation factors + some functional platelets
2) Stored whole blood
- RBCs, plasma proteins, stable coagulation factors but will lose the platelets
3) Autotransfused blood
- RBCs, plasma protein and clots!!
- result from with sepsis and neoplasia
Indicated in:
- Haemorrhagic shock
- Coagulopathy coupled with anaemia

60
Q

Packed Red Blood cells when used

A
  • Anaemia where intravascular volume is normal
  • Haemolysis (e.g., IMHA)
  • Decreased production
  • Slow, chronic loss
    • Low grade GI bleeds
    • Fleas
    ▪ FFP
61
Q

What conditions would you give a blood transfusion

A

1) look at cardiac output, haematocrit
2) hypovolaemia
3) acute anaemia sooner than chronic
4) PCV about 20% - compromised 02 Delivery

62
Q

How much blood do you need to give when giving a transfusion

A

As much is needed to establish cardiovascular stability - replace what has been lost

63
Q

What is Fresh Frozen plasma good for

A
  • All clotting factors, antithrombin and anti-inflammatory proteins
  • Thaw slowly in warm water bath
  • Disorders of secondary haemostasis
    ○ Rodenticide, SIRS/sepsis, DIC
  • 20ml/kg is a good starting point
64
Q

Hypoprotinaemia do you give blood transfusion

A

no just treat underlying disease

65
Q

What are some clinical signs of acute haemolytic reactions related to blood transfusions

A

○ Haemoglobinaemia/-uria
○ Vasoconstriction
○ Acute kidney injury
○ Systemic inflammatory response syndrome (SIRS)
Fever, restlessness, collapse - can be life-threatening
treat with IV fluids

66
Q

List the 3 ways you assess primary haemostasis

A

1) platelet count - thrombocytopaenia
2) buccal mucosal bleeding time
3) test for Van WIlliberg disease - genetic test via saliva sample

67
Q

Platelet count what tube used, what is the range in which bleeding occurs and what step also needs to be done if abnormally low

A

anticoagulant - citrate
normal 200-500x10^9
bleeding when 50x10^9
If abnormally low need to verify by doing a blood smear - if platelet clumps may not be identified as individual platelets, also large platelets (Cats) may not be identified as platelets

68
Q

Buccal mucosal bleeding time what does it measure, possible issues and when do it

A

Measures platelet function
could cause an issue with creating more bleeding, also dogs may not tolerate it
- If significant issue with primary haemostasis the bleeding time will be prolonged
- Only do if platelet count comes back normal or too high but everything else is saying it is a primary haemostatic disease - possibly a rarer one

69
Q

List the 3 tests of secondary haemostasis and what pathways they assess

A

1) ACT - intrinsic and common
2) APTT (factor 3 or tissue factor) - intrinsic pathway and common - more accurate than ACT
3) PT - extrinsic only - more accurate than ACT
Do APTT and PT together

70
Q

What level of functionality of coagulation factors does ACT and APTT and PT detect
What is normal ACT time and when used

A

ACT - function decreased to 5-10%
normal 60-65s used mainly with snake bites
APTT and PT - function decreased to less than 30%

71
Q

What occurs at the following body temperuatures

  1. 34 degrees
  2. 27-29 degrees
  3. 45 degrees
A
  1. mammals lose ability to regulate temp
  2. cardiac fibrillation and death occur
  3. fatal brain lesion can occur
72
Q

Core vs peripheral body temp

A

core generally higher than peripheral therefore rectal temp changes lag behind core

73
Q

What occurs with chronic exposure to cold

A
  • The basal metabolic rate is increased by thyroxine (released when it’s cold) and the effect of catecholamines on fat to release more energy
  • Neonatal have brown fat
    ○ Specialised vascular mitochondrial rick fat located between the scapulae
    ○ More sensitive to catecholamine induced metabolism
    Cells are largely uncoupled and mainly produce heat and very little ATP
74
Q

What is the main type of heat transfer from the tissues

A

circulatory convection
allows preferential redistribution of heat to conserve core temperature (this can protect the brain and major viscera)
- Alternatively heat can be preferentially directed to the skin to promote cooling by:
1. Dilation of the arterioles of the skin vascular beds
2. Opening the arteriovenous anastomoses in the limbs, ears and muzzle in distal extremities

75
Q

What occurs when hot and cold in terms of circulation on limbs and what other counter current exchanges are there in the body

A
  • When environmental temperature is high, superficial veins are used for venous return
  • When it is cold, deep veins are used
    1. The carotid Rete (spider web of arteries) - the carotid artery forms a rete bathed in a venous sinus that drains the nasal cavity
  • This cools the blood going to the brain and is especially important during exercise - camels
    2. Air filled guttural pouches - surround the internal carotid artery and are believed to have a similar function
76
Q

Convection when important and how reduced

A

Important with juveniles/small animals in a breeze or current can rapidly lose heat

  1. Piloerection
  2. Thickness of the hair coat
  3. Reducing the exposed surface area by curling in a ball or huddling together
77
Q

Evaporation when is it the only effective heat loss

A

if ambient temperature approaches body temperature =- depends on air humidity as well
Panting or sweating
sweating - sympathetic control - horses, cattle
panting - movement of small tidal volumes over respiratory dead space through the nasal turbinates - avoid resp alkalosis - dogs, sheep
Rabbits smear saliva or water over fur

78
Q

Temperature regulation, where in the brain, what sensors predominate and what occurs with small and large changes in temp

A

central receptors in Hypothalamus premodinate over peripheral
cold sensors in viscera predominate
- Small changes are handed by vaso-motor mechanisms such as piloerection and skin blood flow
- Large changes require evaporative cooling or thermogenesis (shivering and non-shivering)

79
Q

List the 4 temperature derangement

A
  1. Fever
  2. Heat stroke
  3. Exercise induced hyperthermia
  4. Malignant hyperthermia (pathologic and pharmacologic)
80
Q

Fever how occurs, why present and types of pyrogens

A

How - part of actue phase response to injury or infection - initiated by exogeous pyrogen that activate endoegenous pyrogens - enter hypothalamus and produce metabolites that rest body’s set-point
why - enhance leukocyte activity, reduce morbidity and mortality form infection, viruses are heat sensitive
pyrogens
exogenous - infectious and nonmicrobal (bile acid)
endogenous - cytokines

81
Q

Heat stroke how occurs and possible causes

A

1) temp increase above 41-42 cellular function impaired - organ damage - alteration of heat shock proteins - denaturing and inflammatory cascade activation
2) Inflammatory mediators cascade throughout the whole body, whole body starts reacting - vasodilation and holes in blood vessels leading to the multi-organ dysfunction
3) Hallmark of heat stroke is severe CNS derangement

82
Q

Heat stroke how occurs

A

1) temp increase above 41-42 cellular function impaired - organ damage - alteration of heat shock proteins - denaturing and inflammatory cascade activation
2) Inflammatory mediators cascade throughout the whole body, whole body starts reacting - vasodilation and holes in blood vessels leading to the multi-organ dysfunction
3) Hallmark of heat stroke is severe CNS derangement

83
Q

List possible causes and cosequences of heat stroke and treatment

A

causes - inadequate heat dissipation
consequences - renal failure, metabolic acidosis, DIC, gastro-intestinal failure, hepatic failure, myocardial failure
Treatment - total body cooling immediately and supportive care

84
Q

What occurs with exercise induced hyperthermia

A
  • Similar pathway as heat stroke
  • Causes include inappropriate amounts of exercise and secondary to seizures including seizures from eclampsia (low calcium)
85
Q

Malignant hyperthermia what is it, what associated with and causes

A
  • A rapid and often relentless progressive increase in body temp
  • Is associated with metabolic heat production due to disturbed intracellular calcium metabolism
  • The calcium is released from the sarcoplasmic reticulum
  • rare
    Causes
  • Triggered by drugs
  • Pathologic lesions affecting the hypothalamus - include neoplasia
86
Q

What is primary and secondary hypothermia

A
  • Primary hypothermia is caused by excessive exposure to low environmental temperature - occurs at lower temperature than secondary
  • Secondary hypothermia is a result of disease, trauma, surgery or drug-induced heat production and thermoregulation - generally have more profound clinical signs at higher temperature
87
Q

List some cardiovascular and respiratory responses to hypothermia

A

cardio
- increased HR and BP from catecholamine release but lose affinity - vasodilation - decrease CO and peripheral hypoxia
also left shift in oxygen dissociation curve - more O2 bound
Respiratory
- decreased cellular metabolism, decrease CO production, decrease stimulus to breath - decrease respiratory rate - pulmonary oedema, bronchopneumonia

88
Q

Neurological and metabolic effects of hypothermia

A

neurological
- unconsciouness, cereabral metabolism decreased
- if core temp 19-20 can still have brain function
metabolic
- acidosis from respiratory depression and tissue hypoxia, also shivering
- primary immune function impaired
- coagulation altered

89
Q

initial treatment of heat stroke and what not to do

A
  • No ice bath - leads to vasoconstriction which results in no heat exchange which is what is needed to cool down the patient
  • Spray water onto the patient and use a fan to promote evaporative cooling
  • Cold intravenous fluids are given to reduce core body temperature
90
Q

Describe the following abnormailites from a blood sample from a patient with heat stroke

1) increased lactate
2) icnreased glucose
3) low pCO2
4) low HCO3

A

1) using anaerobic pathways within metabolism, not getting enough oxygen within blood or due to seizues of the animal
2) stress response
3) respiratory alkalosis due to panting but also compensatory method
4) metabolic acidosis - common

91
Q

What can result from severe heat stroke, treatment and prognosis

A

1) SIRS - systemic inflammatory response syndrome
- Global inflammation - can happen from infection, major trauma and heat stroke
- Heat shock proteins don’t work above 42o
2) DIC - Disseminated intravascular coagulation
- Presence of petechial and ecchymotic haemorrhages
Treatment
Normalise every body system - intensive monitoring

DVM 2 - 1 (31 decks)

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