Veterinary Physiology phase 1 test

What are the 5 main functions of the skeleton?

Support the soft cells and tissues that comprise the rest of the body.
Protect delicate organs.
Attachment and leverage for skeletal muscles.
Reservoir or storage area for minerals; mainly calcium.
Haemopoeisis \= in particular erythropoiesis, all bones in young animals, sternum, ribs, pelvis, proximal ends of femurs etc in adults, neonates; liver and spleen.

What is the importance of skeletal anatomy?

Skeletal anatomy is used every day in practice.
-Cat spey positioning.
-X-ray positioning and appraisal.
-Fracture support.
-Points of the horse.

What is topography?

The study of superficial anatomy.
Anatomy that is palpable.
We can use the bone of the skeleton as reference points.
Much of the skeleton has knobbly ridged bits that can be felt through the skin.
These topographical landmarks can help us navigate around the external body.
Any species can be palpated. Often this will give us clues about what might be wrong with the animal before doing anything invasive.
We can use the surface anatomy to help us navigate e.g. locating a tumour.

What is the topographical anatomy for a chest right lateral?

Right lateral recumbency, extended forelimbs, pad placed under sternum to reduce rotation. Centering on the caudal border of the scapula midway between the skin surfaces. Colimation includes the front shoulder and diagphram.

What is the topographical anatomy for pelvis: ventrodorsal?

Dorsal recumbency, hindlimbs extended and rotated internally so the femurs lie parallel and the patella is centred over the stifle joint. Centre on the midline, level with the greater trochanters. Collimation includes the upper thirds of the femur and the wings of the ilium.

What is the x-ray appraisal?

Important to know your anatomy to help you interpret radiographs (both topography and internal).
Bone is white.
Air is black.
Everything else shades of grey.
X-rays travel in straight lines.
The denser the object the more the x-ray wave will be stopped (radiopaque \= white on x-ray).
Less denser tissue won't stop as many of the x-rays (radiolucent \= black/shades of grey on x-ray).
The higher the atomic number the more absorption.

Why does bone appear white on an x-ray?

Bone is composed of calcium.
Calcium has an atomic number of 20.
Tissue of comprised of a high amount of air.
Oxygen has an atomic number of 8.

What is arthiritis?

Broad and loose term to describe any condition affecting the synovial joint.
Arthr \= joint.
Itis \= inflammation.
Most common form of the lameness in dogs.

What are the different types of arthritis?

Degenerative
Traumatic
Septic
Immune mediated
Neoplastic
Polyarthritis
Metabolic
Haemoarthrits

What is degenerative arthritis?

DJD.
A disease process secondary to an initiating event. AKA osteoarthritis.

What is immune mediated arthritis?

There is two types:
Systemic
-Systemic lupus erythematosus (SLE) is the most common form of non-erosive arthritis.
Idiopathic
-Rheumatoid arthritis, Greyhound polyarthritis, and feline progressice polyarthritis are examples of erosive arthritis.

What is neoplastic arthritis?

Synovial cell sarcoma is the most common malignant tumour involving the joints.

What is polyarthritis?

Affects multiple joints.
Classified as either infectious or non-infectious.
So septic arthritis affecting multiple joints is an infectious polyarthritis.
Immune mediated can also be type of non-infectious polyarthritis.

What is metabolic arthritis?

AKA grout.
Sodium urate crystals are deposited in joints.
Never accurately documented in animals, even in Dalmatians that have a high uric acid serum level.

What is haemoarthritis?

Some coagulant conditions can cause bleeding into the joint space.
An animal on anticoagulant therapy may experience this or an animal with Von WIllebrand's disease.

What is oesteoarthritis?

DJD.
Further division:
-Primary.
-Secondary.
Osteoarthritis may be a secondary complication of an existing disease process e.g. due to hip dysplasia or trauma.
Or a normal aging process.
DJD is a non-inflammatory condition although there is an inflammatory component.

What is the pathophysiology of arthritis?

Loading ability of joint is altered.
Damaged chondrocytes secrete enzymes that cause collagen degradation.
-Chondrocytes are found in healthy cartilage. They maintain the main cartilage matrix.
Collagen breakdown alters synthesis of new collagen.
Nitric oxide is released breaking down cartilage and supports inflammation.
Synovial membrane inflammation decreases viscosity of synovial fluid.
-Decreased viscosity reduced lubrication.
Poor synovial fluid reaches oxygen and nutrient supply to the chondrocytes.
Bone becomes sclerotic.
-Sclerotic means hardening of tissue and bone. This worsens the loading capabilities of the bone.
Continuation of these processes leads to tears in the cartilage.
Pain comes from the stimulation of receptors in tendons, ligaments, bone and joint capsule.
Fibrosis of the joint will occur.
-Fibrosis is formation of excess fibrous connective tissue.
Reduced functionality and ankylosis.
-Ankylosis is stiffening of a joint due to abnormal adhesion and ridgidity.

What are the cruciate ligaments?

These are intracapsular ligaments.
They extend between articular surfaces of femur and tibia and wind round each other in a spiral fashion.
Named according to attachment to tibia \= cranial cruciate, caudal cruciate.
Important in limiting movement in cranial and caudal directions and also maintaining rotational stability.

The cruciate ligaments functions as constraints of joint motion.
Specifically, the cranial crucial ligament functions to prevent cranial displacement of the tibia on the femur, limit excessive internal rotation of the tibia on the femur by twisting on the caudal cruciate ligament and prevent hyperextension of the stifle joint.
The caudal cruciate ligament functions to prevent caudal displacement of the tibia on the femur and, in conjunction with the cranial cruciate ligament, limits excessive internal rotation of the tibia on the femur.

What is the patellar ligament?

Actually the tendon of insertion of the quadriceps femoris to muscle.
Inserts on the tibial tuberosity.
There is only one patella ligament present in the dog.
Problems associated with the ligaments of the stifle joint.

What is the mensical ligament?

Attach cranial and caudal horns of menisci to femur and tibia.
Also present (only in the dog and ox) is a transverse (intermeniscal) ligament uniting the two cranial tibial ligaments.

What are the medial and lateral femoropatellar ligaments?

Extend from femoral epicondyles (and the fabellae (sesamoid bone) in the dog) to the medial and lateral borders of the patella.
Fused with the fibrous layer of the joint capsule.
Help hold the patella in the trochlea of the femur.

What is the pathophysiology of acute ruptures of the cranial cruciate ligament?

Relates to the cruciate ligament function.
Sudden rotation of the stifle \= acute.
-An acute rupture occurs when the leg rotated 20-50 degrees whilst in partial felxion.
Cruciates wind around each other.
CrCL wound tight.
Rubs against lateral femoral condyle.
Hyperextension.
Caudal ligament rupture are:
-Severe trauma.
-Dislocation.
-Protected by other structures.
Repetitive injury due to neuromuscular incoordination, aging, conformational abnormalities, poor muscle tone.
Related to size.

What is the treatment/management of CCLD?

Surgery vs non surgery\= dependent on weight.
-

What are osteoblasts?

Cells that synthesise new bone.

What are osteoclasts?

Cells that destroy or remodel bone.

What are osteocytes?

Formed from osteoblasts.
Involved in turnover of bony matrix.

What is diaphysis?

Shaft of bone.

What is epiphysis?

End of bone.

What is epiphyseal plate?

Growth plate.

What is endochondral ossification?

Most bones in the animal develop in this manner.
Bones at the base of the skull and long bones are formed via endochondral ossification.
Embyronic connective tissue forms cartilage template.
Bone develops by replacing hyaline cartilage, cartilage does not become bone.
Begins with cartilage template.
Central part of template dehydrates.
Cartilage cells degenerate: enlarge, die and calcify.
Primary ossification centres in diaphysis.
Blood vessels bring bone forming cells.
A collar bone is formed around the shaft.
Collar is within perichondrium (layer of dense irregular connective tissue that surrounds the cartilage of developing bone).
Vascular, cellular, fibrous membrane that surrounds the collar known as periosteum.
Bone collar of periosteal bone is supportive.
Creates a tubular shaft for the cartilage.
Core of degenerating calcifying cartilage.
Blood vessels from the periosteum penetrate the collar.
These then proliferate.
Osteoblasts can now enter the cartilage model.
Osteoblasts line up along the diaphysis and secrete new bone.
Calcified cartilage is absorbed.
Cavity of tubular shaft becomes filled with gelatinous red marrow.
Secondary centres of ossfication begin at the epiphysis.
Cartilage that remains between epiphysis and diaphysis is known as epiphyseal plate.

What is dyschondroplasia?

Inherited abnormalities of development of cartilage and bone.
Bones of the limb, trunk and head may be underdeveloped or deformed.
-Dwarfism.
-Short bent legs, dolichocephalic heads, disproportionate, short thick limb bones, short vertebrae.
Characteristics produced by this disorder are an important feature in some breeds.
-Short legs and long bodies.
Osteochondrodysplasia: OCD is a similar disease seen in Scottish Fold cats giving them folded ears and stumpy legs with a curly tail.

What are growth plate fractures?

Weak link in growing skeleton of animal.
20-50% as strong.
Usually due to trauma.
Damaged cells can then no longer function normally.
NWB (non-weight bearing) (generally 10/10 lame).
Swelling.
Pain.
Angulation in distal part of leg.
Radiography.
Salter-Harris Classification.
Higher the classification the less likely the prognosis for uncomplicated growth.

What is Queen Ann Legs: Carpal Valgus?

Premature closure of the distal ulnar growth plate.
-Can also happen due to trauma to the growth plate.
3-4 months of age.
Radius grows longer as ulna stays the same length.
Long limbed and short limbed.
Surgery.

How does nutrition affect bone development?

Low calcium \= development of osteochondrosis (interruption of blood supply to bone).
High phosphorus \= decreases calcium absorption \= poorly calcified bones.
Vitamin D deficiency \= inadequate mineralisation of bone, no calcification of growth plate.
High energy (fat or proteins) \= weaker growth plates and bone.
Copper deficiency \= impair bone metabolism.
Zinc deficiency \= impaired growth and skeletal development.

What is hip dysplasia?

Poor fit between femoral head and acetabulum (hip socket).
Interferes with normal development.
Irregularly shaped acetabula and femoral heads.
Overloading of the articular cartilage.
Genetic inheritance.

What are the clinical signs of hip dysplasia?

Lameness.
SAR (stiffness after rest).
HW (hindquarter) wobbliness.
Swaying gait.
Pain.
Exercise intolerance.
Crepitus in hips (bone grinding on bone).

What is the treatment for hip dysplasia?

Surgical:
-Pelvic osteotomy (as long as there is no osteoarthritis/usually in juvenile patients).
-THR (total hip replacement).
-FHNE (Femoral head and neck incision).

Non-surgical:
-Weight control.
-Exercise control.
-Hydrotherapy.
-NSAIDS (non-steroidal anti-inflammatory drugs).
Nutraceuticals.

What is a fracture?

A dissolution of bony continuity with or without displacement of the fragments.
A fracture will always be accompanied by soft tissue damage.

How does a fracture occur?

Bone is rigid but are able to 'give' a little.
If a force is applied that exceeds the ultimate strength and elasticity of a bone, then a fracture will occur.
Causes:
-Indirect trauma.
-Pathological.
-Direct trauma.

What is indirect trauma in a fracture?

Force is transmitted in a specific fashion.
Avulsion fractures and bony prominences.
-Fractures caused by violent contraction of a muscle are called avulsion fractures.
-They may occur because of violent isometric contraction but are associated more commonly with trauma that results in forceful muscular shortening.
-These fractures frequently occur in immature animals while the physeal plate remains open.
-Such muscular forces are more likely to separate a cartiliganous union then the eventual bony union of mature animals.
-Avulsion fractures affecting bony prominence that serve as the major origin or insertion of a muscle seen routinely.
Greater tubercle, olecranon, ischial tuberosity, tibial tuberosity, calcaneous etc.

What are the pathological causes of fractures?

Due to underlying bony or systemic disease that causes abnormal bone.
Neoplasia, osteomyelitis, nutritional hyperparathyroidism.
DIagnosis of underlying pathology more important that fixation.
Correction of pathology, then treat fracture.

What are the direct trauma causes of fractures?

RTA's, falls etc.
Outcome unpredictable.
The amount and direction of force will vary from accident to accident so type of fracture can vary.

What is a greenstick fracture?

Incomplete fracture, result of bending force, immature animals with elastic supple bones.

What is a fissure fracture?

Incomplete fracture, application of direct trauma (long and flat bones), Periosteum intact, simple or multiple, single cortex, no defromity or over riding occurs.

What is a depression fracture?

Incomplete fracture, multiple fissure fracture lines, entire area depresses in direction of force, cranium, maxilla, frontal bone.

What is a transverse fracture?

Complete loss of bony continuity, over riding, deformity, transverse to long axis of bone, smooth or rough surface, most caused by bending, rough surface improves reduction, once reduced should not over ride.

What is a oblique fracture?

Complete fracture, oblique to long axis, two cortices on same plane, rough or smooth edges, bending or axial compression, over ride and rotate unless traction maintained throughout healing.

What is a spiral fracture?

Complete fracture, spiral along long axis of bone, sharp points and edges, fracture with over ride or rotate unless constant traction or external fixation maintained throughout healing process, torsional, twisting, rotating forces.

What is a comminuted fracture?

Complete fracture, at least three fracture fragments, interconnecting fracture lines, caused by high energy trauma e.g. RTA, very common in animals, difficult to fix external contraction and alignment or internal traction required throughout healing process.

What are multiple/segmented fractures?

Complete fracture, three or more fragments in a single bone, fracture lines do not interconnect, completely independent fractures of the same bone, requires two separate reduction and fixation techniques.

What are compression/impacted fractures?

Complete fracture, cancellous bone collapses and compresses on itself, common in vertebral body, non-reducible, stable and heal in place, shortening occurs as a result of compression.

What are avulsion fractures?

Complete fracture, occurs when a fragment of bone tears away from the main mass of bone as a result of physical trauma, this can occur at the ligament due to the application forces external to the body (such as a fall or pull) or at the tendon due to a muscular contraction that is stronger than the forced holding the bone together, generally muscular avulsion is prevented due to the neurological limitations placed on muscle contractions.

What is the initial nursing care for fractures?

Pain relief.
Correction of underlying pathology if required (get a thorough history from owner).
Bandage vs leave.
-RJ (Robert Jone's bandage).
-Splint.
-Cage rest.
-Dependent on where the fracture is.
Open fractures require immediate intervention.
-KY jelly.
-Clip.
-Lavage (flush the wound).
-Sterile wound dressing.
-Doughnut bandage.
Animals prognosis will be significantly poorer if the fracture is not treated ASAP, fracture usually heavily contaminated.

What is reduction when repairing a fracture?

The fracture fragments must be brought together into alignment.
Closed reduction or open reduction.
-Open reduction \= no incision needed. We're able to re-align the bones under anaesthesia without doing surgery. So we may be applying a dressing support or splint.
-Open reduction \= surgical fixation where internal fixation (plate or pin) is needed.

What is fixation when repairing a fracture?

Immobilisation in the correct alignment until clinical union occurs.

Why is blood supply important when repairing a fracture?

Preservation of blood supply to the bone fragments is essential: healing will only occur with adequate blood supply.
Reduction and fixation must be done to maintain the blood supply.
If we don't maintain the blood supply, the fracture will not heal.

What is primary healing of a fracture?

Direct healing.
Occurs after rigid internal fixation.
No gaps at fracture sites.
Bone forms directly between the cortices.
Little or no bridging callus may be visualised on radiographs.

What is secondary healing within a fracture?

Fracture heals by production of fibrous of fibrocartilaginous-osseus callus.
Relies on stability and viable biological tissue.

What are the 4 stages of bone healing?

Inflammatory.
Proliferate.
Maturation/modelling.
Remodelling.

What is involved in the inflammatory stage of bone healing?

Periosteum, surrounding muscles and blood vessels are torn.
Haemorrhage for 6-8 hours until haematoma formation.
Vasodilation.
Oedema.
Osteocytes are deprived of nutrition and die.
Ends of fracture site effectively dead and turn necrotic.
Acute inflammatory cells migrate to the area.
Removal of necrotic tissue by phagocytosis.

What happens in the prolferative stage of bone healing?

Haematoma organised.
Stem cells invade area.
Granulation tissue and cartilage replaces haematoma.
New blood vessels grow down from periosteum and medulla.
Results in soft callus.
Soft callus appears 4-5 days past fracture.
Cannot be seen on x-ray until 10-12 days post fracture.

What happens in the maturation/modelling phase of bone healing?

Hard callus formation.
Created by fibrous tissue, cartilage and immature bone.
High proportion of osteocytes.
Stability arrives when callus envelope bone ends.
Eventually fibrous tissue replaced by more cartilage and bone.
Clinical union occurs when bone fragments are rigidly united by callus (12-16 weeks).

What happens in the remodelling phase of bone healing?

In humans this has shown to last for 6-9 years.
Follows clinical union.
Initial soft callus and extra bone removed by scavenger cells.
Woven bone replaced by stronger lamellar bone.
Correct alignment of fragments allows restoration of original shape.

What factors influence the rate of a fracture healing?

Patients age \= geriatrics are slower to heal, juvenile/paediatric quicker to heal.
Damage to soft tissues \= fractures with major soft tissue damage are more likely to become infected due to reduced blood supply.
Osteomyelitis \= Inflammation of bone delays healing.
Debilitation and systemic illness \= slow rates of repair.
Biological factors will affect the healing time of fractures.
Movement at the fracture site will also play a role \= an unstable, displaced fracture compare to a stable reduced fracture.
Good blood supply \= improves rate of healing.
Oblique fractures heal more rapidly than transverse \= larger surface area to promote tissue regrowth.

How does nutrition affect bone healing?

Bones are affected by nutrition as well as mechanical forces.
Any sort of healing created an extra nutritional demand.
For bone healing animals require adequate amounts of:
-Vitamin D.
-Calcium.
-Phosphorus.
Hormones regulate levels of calcium and vitamin D in the body.
-Parathyroid.
-Calcitonin.

What is the interaction between hormones and calcium?

Vitamin D.
-Helps with calcium metabolism.
-Regulates absorption of calcium and phosphorus.
Parathyroid hormone (PTH).
-Increases plasma calcium.
-Increases calcium release from bone.
Calcitonin.
-Decreases plasma calcium.
Low plasma calcium leads to an increase in secretion of PTH.
PTH increases the resorption of calcium from the bone, so more PTH \= an increase in the amounts of calcium resorbed from the bones.
PTH also increases the levels of Vitamin D which enables less calcium and phosphorus to be lost by the kidney and more to be absorbed through the intestine.
However, if the animal is not being fed enough calcium in their diet, the animal will depend on the calcium being released from bones as there isn't sufficient amounts being absorbed via the intestine.

What happens if there is loss of bone mineral?

If the animal does not have enough dietary calcium it can cause problems with the healing and growth of bones.
Rickets is a disease where the animal has a bone mineral deficiency.
To cause this the diet could be deficient in either calcium and/or phosphorus and also be lacking in Vitamin D.
A lack of sunlight may also play a role as sunlight is needed to metabolise vitamin D.
Animals affected are usuallt young, have stunted growth and have a bowlegged appearance.

What is metabolic bone disease?

A disorder of calcium metabolism that can lead to a variety of clinical signs including weak, brittle bones.
It is mainly seen in rapidly growing herbivores and insectivorous reptiles because they have very high calcium demands to grow strong bones.
This is a disease that can be prevented by creating the conditions they would have in the wild.
Inadequate calcium in the diet, and inverse Ca:P ration, no provision of UVB light and suboptimal temperatures all play a role in causing this disease.
It is these factors that lead to a low calcium level (hypocalcaemia) which can lead to a variety of clinical signs including weak, brittle bones.

What is the pathophysiology of MBD?

The action of UVB light produces pre-vitamin D3 in the reptiles skin. Active Vitamin D3 is created with the correct skin temperature.
The vitamin D produced is needed for calcium absorption in the intestine.
Correct levels of calcium \= healthy strong bones.
Commonly kept reptiles come from regions where they will be exposed to high levels of UVB irradiance most days of the year.
The UVB can come from normal sunshine, however it will not pass through glass therefore the reptile needs access to an appropriate UVB lamp with access to sunshine whenever possible.
Appropriate levels of calcium consumed in the diet is also extremely important.
The reptile must be at the preferred optimum temperature zone so that their digestive system works at optimum level, so they can absorb calcium effectively.

What are the consequences of MBD?

Clinical signs include:
-Abnormal gait.
-Lethargy.
-Skeletal deformities.
-Bone fractures.
-Weight loss.
-Twitching and muscle tremors with adult onset.
If these reptiles do not receive adequate dietary calcium, are fed a diet with an incorrect Ca:P ration and are not exposed to UVB light with the correct temp, then their calcium becomes low.
This is known as hypocalcaemia. In this situation PTH secretion increases releasing calcium from the bones to help increase blood calcium levels.
This causes the bones to become weak and brittle.

What are the prevention methods for MBD?

Nutrition \= getting the correct Ca:P ratio in the diet and supplement.
UVB lighting \= providing the appropriate fluroescent tube and avoiding the mistakes made.
Temperature \= providing the preferred optimum temperature zone for the species of reptile you are keeping.

What are the three types of muscle tissue?

Skeletal \= voluntary, striated.
Smooth \= involuntary, non-striated.
Cardiac \= Involuntary, striated (intercalated discs).

What is skeletal muscle?

Muscle 'fibres' rather than cells.
Multiple nuclei.
Stripy appearance histologically (light and dark bands \= striated appearance).
Voluntary control (walking, biting, facial expressions, tail wagging etc).
Stimulated by affected nerve fibres.
Importance of nervous system.
3 layers to the muscles:
-Epicycium \= outer layer, collagen fibres, protective.
-Perimycium \= contains blood vessles and nerves.
-Endomycium \= surrounds individual muscle fibres.

What is smooth muscle?

Small cells.
Spindle shaped.
One nucleus.
No striations.
Involuntary (peristalsis, vasoconstriction, urination, uterine contraction).
Nerve regulates movement.

What is cardiac muscle?

Found only in the heart.
Small cells.
One nucleus.
Branched.
Striated.
Cells connected via intercalated discs (found only in cardiac muscle).
Involuntary.
No nervous stimulation required.

What are the components of muscle cells?

Proteins that make up myofilaments.
-Actin \= thin, I band.
-Myosin \= thick, A band and M band.
Sacromeres \= make up the myofilaments.
Myofilaments \= make up the myofibrils.
Myofibrils \= make up the muscle fibres.
Muscle fibres \= muscle cell (myocyte).

What are the myofilaments in the sarcomere?

There is a binding site for each of the myosin heads on the globulin actin molecule.
The myosin heads bind to the actin molecules and exert a force.
Dark bands are known as A bands.
Light bands are known as I bands.

What is the neuromuscular junction?

Connection between nerve (carrying impulse) and muscle.
Muscle must receive impluses to move.
No impulse \= atrophy.
Actually a gap \= synaptic cleft.
Acetylocholine bridges the gap.
Muscle can't keep being stimulated (Acetylcholinesterase breaks up the acrtylcholine bridge).
Impulse causes depression.
-Amount of Ca2+ (calcium ions) in cells increases.
-Acetylcholine released.
Acetylcholine binds to receptors on the sarcolemma (muscle cell membrane) which stimulates the impulse.
Travels along the sarcolemma and reaches T-tubules.
Eventually reaches sarcoplasmic reticulum.
Ca2+ released into sarcoplasm.
Ca2+ diffuses into myofibrils.
Turns on contraction process.

What is the sliding filament theory?

When relaxed actin and myosin overlap a little.
When Ca2+ floods the myofibrils it binds to troponin.
This exposes the binding site for the myosin by moving the tropomyosin.
ATP stimulated.
-ATP splits into ADP.
-Splitting creates energy.
Myosin filaments ratchet over actin filaments so sarcomere is shortened.
Contraction.
Importance of calcium.

What is milk fever/Parturient paresis?

A metabolic disorder caused by insufficient calcium, commonly occuring around calving.

What is Puerperal hypocalcaemia?

Life threatening drop in blood calcium levels. Most commonly occurs when the puppies are one to four weeks of age and the mother is producing the most milk.

What is blood?

"A suspension of cells in extracellular fluid."
Specialised extracellular fluid.
Cells constitute 30-60% of blood volume.

What are electrolytes?

Ionised constituents of blood.
Dissolved in the water of the plasma.
Concentration limits are narrow.
Numerous control systems accomplish regulation e.g. urinary.
Diffuse easily across capillary walls.
Interstitial fluid and plasma have typically similar electrolyte concentration.

What are plasma proteins?

Carried whole in the solution.
Golbulin and albumin important in the immune response.
Fibrinogen important for clotting.
Synthesised in the liver and added to the bloodstream.

What is hypoalbuminaemia?

A condition where your body doesn't produce enough albumin protein that's responsible for keeping fluid in your blood vessels.

What are eryhthrocytes?

Formed erythropoiesis.
Contain haemoglobin.
Oxygen + haemoglobin \= oxyhaemoglobin.
The RBC surface contains glycoproteins.
Specific to the individual and potentially antigenic (toxin).
Plasma contains 'antibody-like' substances known as agglutinin.
Transfusion reaction.
Other blood type abnormalities:
-Neonatal isoerythrolysis in horses.
-Fading kitten syndrome.

What is haemoglobin?

Oxygen binding protein.
Responsible for the transport of oxygen from the lungs to the tissues.
Responsible for the transportation of carbon dioxide from the tissues to the lungs for elimination.
There are 3 types of haemoglobin:
-Embryonic.
-Foetal.
-Adult.

What is immune mediated haemolytic anaemia?

An autoimmune disease in dogs in which the body attacks its own red blood cells. This can lead to very low red blood cell counts that require multiple blood transfusions. Can predispose dogs to forming blood clots, mostly in the lungs or in the brain.

What are leukocytes?

White blood cells.
5 major types:
-Neutrophils.
-Eosinophils.
-Basophils.
-Lymphocytes.
-Monocytes

What are platelets?

AKA thrombocytes.
No nucleus.
5-9 days.
Functions in the maintenance of haemostasis.
Normal dogs and cats should have platelet counts close to or of \>20,000.
Too little can result in thrombocytopaenia.
Too many can result in thromboembolism.

What is haemostasis?

The stopping of a flow of blood.

What is thrombocytopaenia?

Vessels undergo micro-injury hundreds of times a day.
Insufficient numbers of platelets.
30,000-50,000 \= mild bleeding.

What is thromboembolism?

A blood clot that travels and lodges in a bessel.
Often form in the heart and migrate (trauma when introducing catheters.
Pulmonary thromboembolism.
Iliac thromboembolism.
Management:
-Pain management.
-Anticoagulants.
-Physiotherpay.

What is the clotting cascade?

Contraction of the injured blood vessel.
Formation of the platelet plug.
Coagulation of the blood.
Contraction of injured blood vessel.
-Smooth muscle contraction.
-Reduces blood flow.
-Greater the injury the greater the contraction.
Formation of the platelet plug.
-Platelets attach to the damaged endothelial layer of the blood vessel.
-Facilitated by Von Willebrand factor, a plasma protein.
-VW forms bridges between platelets and collagen in connective tissue.
-Platelets swell and become sticky.
-FIbrin threads reinforce the plug.
-After 1-1.5 hours clot shrinks, pulling edges of vessel together.
-Serum squeezed out.
-Platelet plug cannot bridge gap when serious injury occurs to artery or vein.
Coagulation of blood.
-Fibrinogen is a soluble plasma protein, produced in the liver.
-When conveted to fibrin, coagulation can occur (Prothrombin, Factor X, Thrombin).
-Activation of factor X depends on intrinsic or extrinsic pathways (tissue factors, blood contact with surfaces different to normal).
-Activation of coagulation factors is a chain reaction.
-Vitamin K required by the liver to form prothrombin and other coagulation factors.

What is warfarin toxicity?

Anticoagulant rodenticides.
-Brodifacoum, diphanconcone, warfarin, bromadiolone.
Effects may not appear for several days.
Warfarin inhibits action of vitamin K.
-The anticoagulant rodenticides abolish Vitamin K recycling.
-As soon as the body's active vitamin K reserves are depleted there can be no meaningful blood clotting.
Decrease in vitamin K:
-Decrease in prothrombin formation.
-Less thrombin can synthesized.
-Less fibrinogen can be converted into fibrin.
-Less fibrin available to stabilise platelet plug.
-Haemorrhage able to continue.

What is immunity?

The resistance possessed by the body to infectious diseases and substances.
Immunity to a disease means that the animal is resistant to the threat of a particular disease.

What is innate immunity?

First line of defence against microorganisms.
Examples \= skin, gastric acid, secretions, cilia.
Non-specific \= reacts to all antigens.
No memory \= only simplistic response, so no need for recall.
Rapid response \= sneezing, coughing etc some are instantaneous, others can take a few hours.
Basic response to pathogens.
Found even in lower organisms e.g. insects, crabs, starfish.
At a cellular level things are a little more complicated.
Functions:
-Kill microorganisms.
-Phagocytosis.
-Stimulate further immune responses.
If pathogen breaches initial barriers then cellular components of innate immunity begin to act.
Cells in the cardiovascular system which are involved in the innate immune response \= white blood cells, dendritic cells, mast cells

What is a monocyte?

Kidney shaped nucleus.
Phagocytic cells.
Produce toxic oxygen species.
Also an antigen-presenting cells.

What is a macrophage?

Highly phagocytic.
Kill microorganisms by production of toxic oxygen radicals and enzymes.
Scavenge dead cells and debris occurring during wound healing.
Good antigen presentation to lymphocytes (therefore have a role in stimulating adaptive immunity).

What is a neutrophil?

Commonest white blood cell (may represent 50-70% of the WBC population).
Phagocytic cells.
-Rapidly migrate into tissue in response to bacterial and fungal infection (die in tissue).
Pus \= dead bacteria and neutrophils.
The ability to phagocytose microorganisms, dead cells and debris is an important feature of the innate immune system.