Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
20 Cards in this Set
- Front
- Back
|
What is meant by the following terms: haemorrhage by rhexis and haemorrhage by
diapedesis? |
HEMORRHAGE = escape of blood from the cardiovascular system
HEMORRHAGE BY RHEXIS - a substantial tear in a blood vessel or a tear in a heart chamber rapid escape of a substantial volume of blood HEMORRHAGE BY DIAPEDESIS - escape of red blood cells one by one through minute or microscopically imperceptible defects in vessel wall |
|
|
What is meant by the following terms: haemothorax, haemopericardium,
haemoperitoneum, haemarthrosis, haematuria, haemoptysis, haematemesis, haematochezia, epistaxis, dysentery, melaena and hyphaema? |
HAEMOTHORAX = haemorrhage into the pleural cavity
HAEMOPERICARDIUM = haemorrhage into the pericardial sac HAEMOPERITONEUM = haemorrhage into the peritoneal cavity HAEMOARTHROSIS = haemorrhage into a synovial joint HAEMATURIA = haemorrhage into urine HAEMOPYTSIS = coughing of blood HAEMATEMESIS = vomiting of blood HAEMATOCHEZIA = passage of fresh blood in faeces (typically over the surface of stools) EPISTAXIS = bleeding from the nose DYSENTERY = diarrhoea containing blood MELAENA = diffuse, dark red-black discolouration of faeces due to upper alimentary tract haemorrhage or swallowing of blood from the respiratory tract HYPHAEMA = haemorrhage into the anterior chamber of the eye |
|
|
What is meant by the following terms: petechiae, purpura, ecchymoses, paintbrush or
suffuse haemorrhages? |
PETECHIAE = tiny, pinpoint foci of haemorrhage, 1-2 mm in diameter
- petechiae are typically found in skin and on mucosal membranes and serosal surfaces PUPURA = slightly larger haemorrhages > or equal to 3 mm in diameter ECCHYMOSES = larger foci of haemorrhage, 2-3 cm in diameter; usually blotchy and of irregular shape PAINTBRUSH OR SUFFUSE HAEMORRHAGES = linear or streaky haemorrhages, especially over serosal or mucosal membranes, as if a brush dipped in red paint has been hastily splashed across the tissues *all of these are not palpable |
|
|
What is a haematoma?
|
HAEMATOMA = a palpable, discrete, space-occupying mass of clotted blood within tissues
- small haematomas are common at sites of venipuncture |
|
|
How do bruises and haematomas resolve?
|
- extravasated blood cells and coagulated fibrin are removed by lysis and especially by
phagocytosis - erythrophagocytosis by macrophages commences within a few hours of onset of haemorrhage - in the acute phase, bruises appear red-blue due to the presence of poorly oxygenated haemoglobin - in the subacute phase, bruises appear blue-green due to the formation within macrophages of biliverdin and bilirubin (derived from the porphyrin component of haemoglobin) - in the chronic phase, bruises appear gold-brown due to the formation of haemosiderin and, to a lesser extent, haematoidin +/- lipofuscin pigments - from 5-7 days after onset, haematomas become enveloped by granulation tissue - following phagocytosis of the extravasated blood, the cavity of a haematoma is ultimately filled in by scar tissue |
|
|
What is the most common cause of haemorrhage in domestic animals?
|
The most common cause of haemorrhage is physical trauma to blood vessels
|
|
|
What are other potential causes of haemorrhage?
|
· active inflammation (hyperaemic phase) haemorrhage by diapedesis
· passive congestion increased hydrostatic pressure in capillary beds haemorrhage by diapedesis · severe tissue inflammation with secondary damage to local blood vessels · erosion/ulceration of a mucous membrane to the level of underlying vessels · invasion of a vessel by a malignant neoplasm · inflammation, degeneration or necrosis of a blood vessel - e.g. vasculitis, bacteraemia, viraemia, endotoxaemia, uraemia (renal failure) · rupture of a weakened vessel wall - e.g. vascular aneurysm, copper deficiency, scurvy (vitamin C deficiency) · defects in primary and/or secondary haemostasis |
|
|
What factors determine the clinical significance of haemorrhage?
|
- the clinical significance of haemorrhage depends on its location and the rate and volume
of blood loss LOCATION: -fatal in brain (stroke or cerebrovascular accident) or if intra-cranial (e.g. subdural hematoma) -in hemopericardium may lead to cardiac tamponade RATE: -the more rapid the blood loss, the smaller the volume of blood necessary to induce shock VOLUME: -rapid removal of 20% of total blood volume = little impact -loss of 20-40% blood volume = hemorrhagic (hypovolemic) shock -loss of 50% = death |
|
|
What are the haemorrhagic diatheses?
|
- haemorrhagic diatheses are clinical disorders of haemostasis characterised by a bleeding
tendency |
|
|
What clinical signs would make you suspicious that an animal has a defect in primary
haemostasis? |
- because the primary haemostatic platelet plug is short-lived and ultimately enveloped by
fibrin, disorders of primary haemostasis provoke multiple short-lived bleeds that cease once the coagulation cascade generates fibrin - bleeding commences immediately after venipuncture or other trauma and is prolonged but is ultimately terminated by formation of fibrin - multiple, small volume, superficial, petechial, purpural, ecchymotic and/or paintbrush haemorrhages are typical over the skin, mucous membranes and serosal surfaces - epistaxis is common and bleeding from other mucous membranes may cause haematuria, melaena and/or haematochezia - haematomas may develop but are more commonly seen in animals with disorders of secondary haemostasis |
|
|
What clinical signs would make you suspicious that an animal has a defect in secondary
haemostasis? |
- animals with disorders of secondary haemostasis can form short-lived, primary
haemostatic platelet plugs but cannot generate (or, rarely, maintain) the fibrin plug - bleeding after venipuncture or other trauma is usually delayed by the platelet plug but, once it commences, it may be prolonged and severe - deep haematomas are common - severe haemorrhage into body cavities, joints and skeletal muscles may occur - haemorrhage from mucous membranes (e.g. melaena, epistaxis) occurs occasionally |
|
|
List the four major mechanisms responsible for defects in primary haemostasis.
|
1. Thrombocytopenia
2. Thrombocytopathies 3. Von Willebrand's Disease 4. Damage to Small vessels |
|
|
What are the major mechanisms responsible for thrombocytopenia in domestic animals?
Which of these mechanisms are most likely to cause a clinically significant thrombocytopenia? |
♦Decreased Platelet Production:
✤myelophthisis - replacement of bone marrow by neoplastic tissue (e.g. leukemia), collagen (myelofibrosis), bone (osteosclerosis) or inflammatory exudate (e.g. chronic granulomatous osteomyelitis in systemic fungal infections) ✤marrow aplasia or panhypoplasia -due to injury to haematopoietic stem cells or their progeny and/or marrow stromal cells (with decreased production of growth stimulant factors or increased production of growth suppressor factors) eg. drug cytotoxicity - chemotherapeutic agents, estrogen (dogs & ferrets) e.g. toxins - bracken fern e.g. ionizing radiation e.g. viral infection e.g. other infectious agents ✤megakaryocytic hypoplasia -dogs, autoantibody directed against megakaryocytes -begins with neutropenia, followed by thrombocytopenia, and non-regenerative anemia ♦Increased Platelet Destruction: ✤immune mediated destruction 1) Primary immune mediated thrombocytopenia - autoantibodies against platelet autoantigens -can also target megakaryocytes -common in dogs 2) Secondary immune-mediated thrombocytopenia - secondary to another disease e.g. Systemic lupus erythematosus (SLE), viral infections, drug administration (e.g. penicillins) -may be triggered by exposure of hidden or altered antigenic epitopes on platelet surfaces by the non-specific binding of antigens, drug haptens, or antigen-antibody complexes to platelets, or by drug-induced formation of autoantibodies directed against a normal platelet membrane antigen e.g. neonatal alloimmune thrombocytopenia - piglets & foals with immune mediated destruction of platelets due to maternal antibodies against them in colostrum ✤non-immune-mediated destruction e.g. infectious agents e.g. Anaplasma platys ♦Consumption of Platelets -DIC -or if there is significant vascular endothelial injury: *heartworm (Dirofilaria immitis) infection *haemangiosarcoma *endotoxaemia *severe liver necrosis *vasculitis ♦Platelet sequestration -in health 30-40% of platelets are located in the spleen -hypothermia can cause sequestration in the liver -sequestration of platelets in lung capillaries can occur with endotoxemia and in other causes of "shock lung" -MILD THOMBOCYTOPENIA, NO OVERT BLEEDING ♦Massive Acute Hemorrhage: -MILD & SUBCLINICAL because of large splenic resevoir |
|
|
What is the most common mechanism responsible for clinically significant
thrombocytopenia in cats? What are the most common underlying conditions in cats? |
Descrease platelet production
-largely due to retroviral infection (especially feline leukemia virus (FeLV) and/or myeloproliferative or lymphoproliferative disease |
|
|
What is the most common mechanism responsible for clinically significant
thrombocytopenia in dogs? What can trigger this condition in dogs? |
Increased platelet destruction
♦Immune mediated destruction -autoantibodies against platelet autoantigens |
|
|
What is meant by the following terms: thrombocytopathy, thrombopathy and
thrombopathia? What are some causes of these conditions in domestic animals? |
It means platelet dysfunction.
✤Inherited Platelet Dysfunction: -rare, but reported in dogs, cats, cattle, horses & pigs e.g. Chediak Higashi Syndrome - Persian cats, Hereford cattle -platelets lack discernible dense granules and are deficient in adenin nucleotides, serotonin, and divalent cations e.g. Glanzmann thombasthenia - Great Pyrenees dogs, Otterhounds, Thoroughbred horses -platelets are deficient in surface glycoproteins GPIIb-IIIa complexes ✤Aquired Platelet Dysfunction -drugs e.g. barbituates e.g. cyclooxygenase inhibitors e.g. aspirin irreversibly acetylates COX in platelets & megakaryocytes - impairs TXA2 synthesis - impaired platelet function for 5 days -diseases e.g. SLE .e.g. chronic liver disease e.g. DIC |
|
|
What role does von Willebrand factor play in primary haemostasis?
|
it mediated platelet adhesion to exposed subendothelial collaged
-under low sheer strss platelets can adhere to vollagen via GpIa/IIa and GpVI ie. in capillaries -in high sheer stress e.g. arteries, vWF is essential for adhesion -platelets attach to vWF via GPIb receptors -once attached to vWF platelets can anchor to collagen via GpIa/IIa receptors |
|
|
Which species of domestic animal is most commonly affected by von Willebrand’s
disease? Which breeds are most often affected in Australia? How is the condition inherited in these breeds? |
-most common disorder of dogs
Type I vWD -most common form in dogs (>90%) -all of various multimer chains of vWF are present but in reduced concentrations (<50%) of all the chains -autosomal recessive inheritance -doberman pinschers Type 2 vWD -autosomal recessive -German short-haired and wire-haired pointers -decreased plasma concentrations of vWF is associated with a disproportionate loss of high m.w. multimers Type 3 vWD -negligable vWF in plasma, all multimers are absent -Scottish terriers -autosomal recessive |
|
|
What clinical signs would you expect to see in a dog with von Willebrand’s disease?
|
Type I vWD
-subclinical or cause mild to moderate bleeding Type II vWD -severe hemorrhage Type III vWD -trauma in homozygotes - severe hemorrhage -dogs with vWD do not bleed spontaneously -excessive hemorrhage may be triggered by hair clipping, venipuncture, surgery or other trauma -can occur during tooth eruptions or estrous -if spontanous hemorrhage does occur, it is often as diffuse oropharyngeal bleeding -epistaxis, GI bleeding and hematuria may also occur -petechia are infrequently seen on these dogs -if there is a concurrent reduction in plasma factor VIII:C activity, dogs may develop hematomas -perinatal mortality (including abortions & stillbirths) may be high in affected litters of puppies (especially with type II or type III) |
|
|
What are some of the blood vessel disorders that can manifest as petechiae and
ecchymoses in the skin and/or mucous membranes? |
e.g. toxemia - bacterial endotoxins or exotosins
e.g. immune mediated vasculitis e.g. feline infectious peritonitis virus e.g. fragility of blood vessels - scurvy in guinea pigs |
