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213 Cards in this Set
- Front
- Back
What are the primary lymphoid organs? |
Thymus and bone marrow- where the sites of the immune system are formed |
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What are the secondary lymphoid organs? |
Spleen, lymph nodes and lymph nodules responsible for immune responses |
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If the lymphoid organs are abnormally functioning, what disorders or things can result? |
1. Hypersensitivity or Allergic reactions 2. Immune-mediated disease 3. Immunodeficiency |
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Describe the maturation cycle/style of both the B lymphocytes and the T lymphocytes |
B lymphocytes- 2 phases, antigen independent and antigen-dependent phases. First phase is in the bone marrow, second phase is in the secondary lymphoid tissues T lymphocytes- originate in the bone marrow, mature in the thymus and then migrates to the secondary lymphoid tissues |
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If an animal dies from bone marrow failure? What is the death actually a result of? |
Lack of blood cells, NOT a lack of lymphoid cells |
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When evaluating the thymus histologically, in a general sense, what kind of things are you looking for? |
Inflammation of the thymus, decreased size, decrease in lymphocytes, increased cellularity within the medulla, areas of asymmetry, etc. |
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What are the 6 things that cause a decrease in the size of the thymus? |
1. Congenital immunodeficiency disorders (Ex. SCID in foals, and in Jack Russell Terriers) 2. Infectious agents, bacteria, viruses (Ex. Parvo, BVD) 3. Drugs or immunotoxins 4. Severe Stress 5. Irradiation 6. Starvation/malnutrition |
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What is the most common cause of an enlarged thymus? What are the two different types? |
Neoplasia- 1. Thymoma- neoplastic epithelial cells, non-neoplastic lymphocytes. Older animals, invasive, myasthenia gravis associated (dogs) 2. Lymphoma- neoplastic proliferation of lymphocytes- T cell neoplasm of young cattle and cats (less so in dogs) |
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What are the three more uncommon causes of an enlarged thymus? |
1. Hyperplasia of unknown significance 2. Hematoma/Hemorrhage- can cause acute death of unknown cause, may be anti-coagulant toxicity? 3. Inflammation- porcine circovirus 2 infection and occasionally bacterial septicemias |
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What are the functions of the spleen? |
1. Lymphocyte production and immune response to blood-borne particles 2. Storage of RBCs and platelets 3. Filtration and Phagocytosis (foreign antigens, aged cells) 4. Extramedullary Hematopoiesis |
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What is found in the red pulp of the spleen? The white pulp? |
White- germinal centers, lymphocytes Red- monocytes, macrophages, red blood cells |
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How do you diagnose splenomegaly? |
Physical Exam Diagnostic Imaging (can't be done definitively on serum chemistry) |
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What are the causes of splenomegaly?
(uniform spleens that ooze when you cut into it) |
Acute or chronic congestion- obstruction of blood flow from spleen
(From drugs (euthanasia), acute/chronic right sided heart failure, portal hypertension from liver disease, splenic torsion, splenic vein thrombosis, anthrax) |
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Splenomegaly with Nodules is most commonly caused by what? |
Hematomas, commonly confused with neoplasia (hemangioma, hemangiosarcoma) *histology to diagnose |
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What changes are seen in a kidney due to extramedullary hematopoeisis? |
Diffuse or nodular enlargement, due to the increased demand for blood cells (can be due to many conditions) Look for increased precursor cells on cytology/histology |
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If you had hyperplasia from an increased need of normal resident cells in the spleen, where would you expect the spleen to enlarge if you needed more; B cells? T Cells? Macrophages? Other reasons it may be grossly expanded? |
B cells- nodules in white pulp T cells- expansion of periarterial sheaths in white pulp Macrophages- expansion of red pulp Other bloodborne antigens, particulate material- infections, immune-mediated, hemolytic anemia, neoplasia |
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Splenitis causes what kind of changes in the spleen? |
Diffuse to nodular enlargement, hyperemia, necrosis, lymphoid cell lysis, influx of non-lymphoid inflammatory cells Abscess or granuloma formation Seen when systemic infections occur |
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Nodular lymphoid hyperplasia of the spleen means what as far as a diagnosis? |
Incidental, not a precursor to lymphoma, unknown cause Seen in older dogs NOT neoplasia! *histopath is the only way to diagnose definitively, neoplasia will lose architecture. Nodular hyperplasia will maintain normal architecture |
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Neoplasia in the spleen causes what kind of gross and histologic changes? |
Diffuse or nodular enlargement Hemangioma/hemangiosarcoma- endothelial cell origin, presenting with acute hemorrhage into the abdomen (need histopath to differentiate between) |
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If lymphoma was the diagnosis, what changes would you expect in the spleen? |
Diffuse* sometimes nodular splenomegaly |
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What are the causes of a decreased splenic size? |
Splenic contraction Atrophy- old age or CWD Immunosuppressive drugs or toxins Congenital immunodeficiency syndromes |
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What are the things that would cause a spleen to rupture? |
Physical trauma May lead to the seeding of splenic fragments in the abdominal cavity |
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Define Siderotic Plaques |
Yellow to tan dry plaques on the surface of the spleen that are in older dogs as an incidental finding. May be areas of old hemorrhage |
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What are the functions of the lymph nodes? |
Filtration of lymphatic fluid- phagocytosis and immune response to antigens |
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in a germinal center of a lymph node, what type of immune cell predominates? The paracortical area? |
B cells paracortical area- T cells |
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Define the medullary sinuses of lymph nodes Medullary cords? |
Sinuses- enlarges spaces with lymph and a few lymphocytes Cords- masses of lymphocytes |
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What is the histology seen with lymph node hypoplasia? |
Overall decreased lymphocyte density with normal architecture. (cannot find hypoplasia on PE or on cytology) |
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What signs within a lymph node would make you suspicious of a congenital immunodeficiency (such as SCID in arabian foals and jack russel terriers) |
Follicles- poorly developed/absent B cells (also seen in spleen) Paracortical zones- hypocellularity (also seen in periarteriolar sheeths in spleen) Blood- decreased immunoglobulins, lymphopenia Thymus- atrophy |
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What are some causes of acquired atrophy of the lymph nodes? |
Infections- viruses that target lymphoid cells Immunosuppressive/immunotoxic drugs or toxins (cancer drugs) Malnutrition/cachexia Age |
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What is the cause of lymphadenopathy/hyperplasia of the lymph nodes? |
Response to immune stimulation. Can be either localized (draining a specific area of infection) or systemic in response to a systemic disease/neoplasia *RARELY idiopathic Associated with an increase in B cells in germinal centers, T cells in paracortical areas, macrophages in sinuses. RETAINED ARCHITECTURE |
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What is lymphadenitis? |
Influx of inflammatory cells into the lymph node. Can be systemic or local, depending on disease. Often accompanied by hyperplasia but can be seen alone |
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What are the causes of lymphadenitis? |
Infections! Simple bacteria = neutrophillic response Complex organisms = histiocytic or mixed neutrohilic/histocytic response Eosinophilic due to allergies, parasites, some neoplasias (ex, mast cell tumors) *look for a mixed healthy population of cells, rather than neoplastic cells |
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Corynebacterium Pseudotuberculosis causes what lesions in the lymph nodes? |
caseous Lymphadenitis, onion like accumulation of necrosis in the lymph nodes of sheep |
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What does TB look like in the lymph nodes? |
Multifocal caseous abscesses with mineralization, with a gritty texture *look for lesions in mediastinal, retropharyngeal, hepatic, mesenteric, etc. (12 lymph nodes that are examined) Definitive diagnoses with Ziehl-Neelson stain for the TB organisms |
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Define lymphoma |
Malignant proliferation of neoplastic lymphocytes outside the bone marrow (inside the bone marrow would be leukemia) One or more lymphoid organs are enlarged, either diffuse or nodular Most common hematopoietic neoplasm- highest prevalence in dogs and cats |
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What clinical signs are presented with a case of lymphoma? |
Depends on where it started- dyspnea, vomiting, diarrhea, polyuria/polydypsia, etc. Most cats- ill with no lymphadenopathy Dogs- completely fine except for lymphadenopathy Difficult diagnosis to make if the small lymph nodes are the neoplastic lymph nodes |
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What are the ways that lymphoma can be classified grossly? |
Multicentric- peripheral lymph nodes +/- internal organ systems Alimentary- intestine, mesenteric LN +/- internal organ systems Thymic/mediastinal Cutaneous Solitary, regional or extranodal (depending on site(s) involved) |
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What histology would you expect to find with lyphoma? |
Disruption of normal architecture* Loss of cellular heterogeniety increased mitosis Immunophenotyping- tells you if it's B cell or T cell tumor |
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What are the etiologic causes of lymphoma? |
Viral associations- FeLV, FIV, BoLV Others- tobacco smoke, herbicides/environmental pollutants, magnetic fields, hereditary predisposition *no known viral association in dogs |
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What things are associated with a poorer prognosis in lymphoma? |
T cell lymphomas bone marrow involvement Clinical signs seen upon presentation Incomplete initial response to chemotherapy |
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What is the most common form of lymphoma in horses? |
Multicentric- spleen and liver involvement (alimentary form brings about profound weight loss) (cutaneous form is chronic without blood or internal organ involvement) |
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In adult cattle, the most likely cause of lymphoma is what? |
BLV infection, between 5-8 years old In young animals, the thymic, cutaneous and multicentric forms are not BLV associated |
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What forms of lymphoma are found in cats? |
FeLV associated- leading to mediastinal and multicentric forms of lymphoma In FeLV negative cats- Alimentary form in cats 10 years old or older is the most common |
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In general, what is the normal heart weight to body weight percentage? What is the species that we often use this comparison to determine if the heart is enlarged or not? |
0.3%-1.25% of body weight is normal. In cats, 17g is the magic number of heart weight, any higher, we start to think hypertrophy (pigs, smallest heart, athletic dogs, largest, neonates larger than adults) |
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Compare/contrast the growth of the heart in neonates and adults |
Neonates- hyperplasia occurs in first few months, regeneration is limited Adults- hypertrophy only Regeneration does NOT occur in "higher vertebrates", limited regeneration in some species |
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In acute situations, how does the heart compensate? Chronic? |
Acute- increased HR, increased peripheral resistance, redistribution of blood flow Chronic- myocardial hypertrophy, cardiac dilation |
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Define hypertrophy of the heart cells. |
Increase in mass of the cardiac mycotes but NOT number. (An increased number would be hyperplasia.) Due to an increase in work load in the heart Seen as a normal physiologic process or can be pathologic or idiopathic *physiologic is reversible, pathologic is usually not reversible |
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What are the two reversible morphologic changes seen in the heart muscle? |
Hypertrophy of myocardium Atrophy of the myocardiaum |
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What is the most common lethal injury of the heart cells? |
Injury to the myocytes, leading to necrosis Will see increased interstitial stroma and vessels, collapsed sarcolemma and fibrosis/collagen deposition *fibosis is the most common end-stage response of the heart |
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What are the syndromes associated with cardiac failure? |
Congestive heart failure Acute heart failure L sided heart failure-acute and chronic R sided heart failure- acute and chronic Cardiac hypertrophy Cardiac dilation |
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Define Congestive Heart Failure. What two things are commonly associated with it? |
Gradual loss of cardiac pumping efficiency leading to forward or backward heart failure. Impaired pump function and increased workload (increased hypertension) both associated with it. *valvular disease is most common |
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What is the pathophysiology that ties the kidneys to congestive heart failure? |
Decreased renal blood flow = renal hypoxia = activation of RAAS = Na/H2O retention in DCT = fluid retention = increased fluid in body cavities = hypervolemia = increased workload on the heart = continued compensation = eventual heart failure |
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Acute Forward heart failure would be associated with what clinical signs? |
Intermittent weakness/syncope Sudden/unexpected death Minimal gross/histologic lesions would point you to this |
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What are the causes of left sided heart failure? Clinical signs? |
Loss of myocardial contractility (second most common) Dysfunction of mitral* most common cause or aortic valves Congenital heart disease Dyspnea, Cough |
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Gross lesions of left sided heart failure would be what? |
Pulmonary congestion, Edema Tan hue of the lungs due to hemosiderin laden macrophages in the alveoli (associated with a chronic left sided heart failure) |
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What are the causes of right sided heart failure? |
Cardiomyopathy* most common Pulmonary hypertension (2nd common) Tricuspid and pulmonary valve disease Leads to increased right atrial pressure and systemic venous congestion (backward failure) |
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What clinical signs are associated with right sided heart failure? Gross lesions? |
Clinical signs- jugular distension, hepatomegaly and splenomegaly Gross lesions- nutmeg liver (hepatic congestion), edema (ascites in dogs, hydrothorax in cats, ventral SQ in horses and ruminants) |
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What is concentric hypertrophy? |
thickening of the wall, chamber gets smaller Afterload problem, pressure load causes it Most commonly due to restricted outflow- valvular stenosis, systemic hypertension, pulmonary disease |
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What is eccentric hypertrophy? |
The wall gets thicker but the chamber gets larger (wall appears thinner) Caused by volume/preload overload Commonly due to incomplete emptying of the chamber from septal defects, valvular insufficiencies*most common |
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Whatis cardiac dilation? |
There is an increase in the size of the chamber but there is no hypertrophy of the wall seen This is compensatory to an increased workload, causing increased stretching that eventually will be detrimental to the heart (usually end-stage cardiac failure) |
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What are the common causes of circulatory failure? |
Acute internal or external hemorrhage Dehydration Endotoxic shock (can lead to heart failure) |
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Describe how you perform a necropsy examination of the heart. |
1. Incise pericardial sac- nature of volume and quality of the pericardial fluid 2. Remove heart and lungs together "pluck" 3. Examine great vessels 4. Examine gross appearance/shape of heart 5. open heart as if the blood was going through it (right atrium, right ventricle, apex, pulmonary outflow tract). Then flip it over and cut through left atrium, left ventricle, apex, and finally, aorta *right side, follow the septa. Left side, don't. |
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If you want to take histologic sections of the heart, which sections do you want to take? |
Left ventricular papillary muscle Right and left ventricular free wall Interventricular septa |
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What is the pathophysiology behind rigor mortis in the heart? |
Lack of ATP, cannot keep the myofibrils relaxed so they contract and then autolysis of the myocytes occurs Happens 15-30 min. after death *if there is clotted blood in the left ventricle, suspect myocardial disease, this should empty out |
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What are the other post-mortem changes you can see in the heart? |
1. Dark red mottling of the myocardium (uneven blood distribution) 2. Diffuse red staining of endo and epicardium (lysis of erthrocytes/imbibition of hemoglobin 3. Flabby ventricles (after rigor) 4. Crystalline deposits (intracardiac barbituates) 5. "currant jelly" clot not attached to the endocardium (no muscle to expel the clot) 6. "chicken fat" clot not attached (coagulation cascade pieces- indicative of anemia or prolonged agonal period, or found in horses due to rapid erythrocyte sedimentation) |
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What are the two very important shunts that get blood past the lungs in the fetus? |
Foramen ovale- between the two atria Ductus arteriosus- between aorta and pulmonary artery |
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The stimuli for the closure of foramen and ductus ateriosus is what? |
The animal breathing- changes in oxygen tension and intracardiac pressure |
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Define valvular insufficiency Valvular stenosis |
Insufficiency- failure to close *preload increases with insufficiency Stenosis- narrowing/failure to open *afterload increases due to restricted outflow *preload decreases |
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If the fetal shunts fail to close properly, what three anomalies will develop? |
1. PDA 2. ASD 3. VSD |
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In a PDA, blood is abnormally shunted where? What is the biggest change seen because of this abnormality? |
From the aorta to the pulmonary artery, never reaching the body where the oxygenated blood should go Biggest change is increased pulmonary arterial pressure! Increased afterload of the right ventricle, leading to concentric hypertrophy (less common, increased blood returning from pulmonary system, increased preload of atria and ventricle, eccentric hypertrophy of both |
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What abnormality is seen in this image? |
Patent Ductus Arteriosus |
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Atrial septal defect is caused by what? What changes are seen with this abnormality? |
Failure of foramen ovale to close Blood flows from left to right atrium, increasing the preload (eccentric hypertrophy) of the right ventricle, increased volume them causes pulmonic stensosis In late stage, pulmonary hypertension may develop, resulting in reverse shunt |
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What is abnormality seen in this image? |
Atrial septal defect |
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Ventricular septal defects are seen in what species of animals? What is the pathophysiology? |
Horses, cattle and dogs *most often by the AV valve leaflets, under the aorta or within membranous portions of the septa Left to right shunt, increasing both preload and afterload in the right ventricle, increased preload in left atrium and ventricle, eccentric hypertrophy and bilateral dilation results |
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What is the abnormality in this image? |
VSD *most common a higher abnormality but can also be lower |
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What are the three classifications? What is the pathophysiology of this? |
Supravalvular, valvular, subvalvular pulmonic stenosis (this would be post-stenotic in this image) Leads to increased afterload on the right ventricle (concentric hypertrophy), and poststenotic dilation of the pulmonary artery |
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What is the defect seen with tetralogy of Fallot? |
1.*Hypoplasia and malpositioning of the conotruncal septum 2. Overriding (dextroposition) of aorta (covers the VSD) 3. High VSD 4. Pulmonic stenosis 5. Hypertrophy of right ventricle is secondary defect |
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As a result of Tetralogy of Fallot, where does blood flow? What changes result? |
The degree of the disease determines how much blood bypasses the lungs and goes into the aorta. Leads to cyanosis and right ventricular hypertrophy because of the increased afterload |
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What compensatory changes are seen in a heart with aortic/subaortic stenosis? |
A malformation of the aortic valve leads to increased afterload and left ventricular hypertrophy Myocardial necrosis is also seen due to ventricular dysrhythmias |
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What is the most common cardiac anomaly in cats? What gross changes are seen with this abnormality? |
Mitral valve insufficiency/stenosis Leads to an enlarged mitral valve opening, short, thickened valve leaflets and short, thickened chordae tendinae |
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What is the lesion seen in this image? What is the significance? |
Congenital valvular cysts (can be blood or lymph filled), common in young ruminants. There is no functional significance and they will regress spontaneously |
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What is the abnormality seen in this image? What causes this lesion? |
Endocardial fibroelastosis Caused by a heritable defect (or secondary to increased ventricular turbulence) in cats/foals where there is thickening of the endocardium with collagen and elastin, leading to restrictive cardiomyopathy |
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What is the lesion in this image? What developmental thing happens to lead to this? |
Persistent right aortic arch develops (instead of left)- the left goes on to form ligamentum arteriosum The esophagus and trachea get caught in a vascular ring, obstructing the esophagus |
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What is the most common non-lesion of the heart? |
Hemorrhage on the surface of the heart |
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What etiologies can lead to hemorrhage in the heart? |
Agonal (horses) Anoxia Septicemia Toxemia (Clostridial enterotoxemia) Nutritional Deficiency (Se, Vit. E) |
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What is hydropericardium? |
Accumulation of normal straw colored fluid Can cause sudden death if it rapidly fills, stretches out with a chronic slow fill. *Fibrin in the fluid if associated with vascular injury |
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What are the causes of hydropericardium? |
Congestive heart failure** Systemic disease with vascular injury Renal failure Salt poisoning (poultry) Anemia/hypoproteinemia Generalized edema |
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What is hemopericardium? What causes it? |
Whole blood in the pericardium, death may occur from cardiac tamponade Causes: iatrogenic puncture, foreign body, ruptured vessel/chamber, rupture of neoplasm* |
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What is seen in this image? What causes it? |
Metabolic alteration, associated with anorexia, starvation and cachexia or parasites, should normally be fat in that pericardial groove |
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What abnormality is seen in this heart? What causes it? |
Fibrinous exudate in the pericardium- gray/yellow/shaggy projections
Longstanding- granulation tissue superficial, fibrosis deep Caused by bacterial infection! (causes death) |
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What abnormality is seen in this heart? What are the possible causes? |
Suppurative pericarditis Thick, yellow pus, bread and butter lesions Pyogenic bacterial agents present adjuct to pleuritis or bronchopneumonia |
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What is the classification scheme for endocardial disease? |
Degeneration- mineralization, fibrosis, endocardiosis Inflammation- endocarditis |
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If someone said it was "mural endocardium", what endocardium do they mean? |
The endocardium lining the walls of the chambers |
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What are the portals of entry into the endocardium? |
Hematogenous Parasitic migration Intravenous and intracardiac catheters in place for a long time Uremia-induced vascular damage |
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Uremia induced endocardial mineralization is a pattern found where? |
In the left atrium (and possibly other areas) |
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What are the overall causes of endocardial mineralization and fibrosis? |
Increased intake of Vitamin D Ingestion of plants containing Vitamin D Chronic cardiac dilation Cachexia Healed uremic lesions Chronic trauma from turbulent blood flow through diseased valves "jet lesions" |
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What is seen in the left atrium of this heart? What is the most likely cause? |
This is endocardial mineralization, most likely caused by uremia Would have gritty feel |
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What is the most common cause of congestive heart failure? What kinds of animals is it seen in? |
Endocardiosis, degeneration of the valvular collagen *mitral valve being the most common Seen most in middle aged to older small and toy breed dogs |
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Grossly, what lesions are seen with endocardiosis? What can endocardiosis lead to? |
Shortened, thickened valves Nodular free margins Thick chordae tendinae Opaque-white, smooth/shiny appearance Jet lesions in atria due to regurgitation Sequelae- atrial dilation and CHF |
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What is this image showing? |
Endocardiosis and "jet lesions" |
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What is the proposed pathogenesis of endocarditis? |
Inflamatory process associated with adherence of bacteria and bacteremia. Bacteria, with turbulent blood flow results in focal endothelial disruption, inflammation and dibrin deposition |
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What gross lesions are associated with endocarditis? What are the sequelae to this disease? |
Large, friable adherent vegetations Rough edges Fibrin, that can be peeled off Mitral > aortic > triscupsid > pulmonary Septic emboli in the myocardium, kidneys- infarction, abscesses, inflammation Death due to effects of bacteremia and cardiac failure from valve dysfunction |
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What is this a picture of? |
Endocarditis in the valves |
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What are the portals of entry into the myocardium? What kind of things can lead to disease in the myocardium? |
Hematogenous, embolic Disturbances of growth (physiologic and pathologic hypertrophy), fatty infiltration, degeneration, necrosis, cardiomyopathies, inflammation |
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Fatty infiltration in the myocardium is a result of what disease processes? |
Obesity (normal in these cases) Hypothyroidism Cardiomyopathy |
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What are the important causes of myocardial necrosis? What gross lesions are associated with necrosis of the myocardium? |
Ionophores Catecholamines Vitamin E-Selenium deficiency Pale patches/streaks, gritty/mineralization throughout the myocardium, subendocardial or within the papillary muscles (may be scattered, harder to find) |
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What toxicity leads to this necrosis (but no fibrosis) of muscle? |
Ionophore toxicity, most likely a toxicity from feed additives *very toxic to horses Leads to this streaking of muscles but no mineralization |
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Vitamin E-Se deficiency is associated with what gross lesions? |
Focal to extensive pale white streaks with mineralization (tongue, larynx, other larger muscles, heart) Disease of young animals Without these compounds, it reduces the free radical injury to cell membranes |
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If this was seen in the heart of a dog, what disease would you be suspicious of? |
"Brain-heart syndrome", associated with a catecholamine excess when there is neurologic disease, post-trauma, etc. Gross lesion- multi-focal necrosis |
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What are the causes of cardiomyopathy? |
Primary- idiopathic, progressive cardiac disease THREE FORMS: hypertrophic, dilated, restrictive Secondary- generalized myocardial disease of nown cause *associated with right or left sided heart failure |
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What are the gross lesions associated with hypertrophic cardiomyopathy in cats? Sequelae? |
Enlarged heart Prominent concentric hypertrophy of the left ventricle Left atria may be dilated Sequelae- CHF and sudden death, left atrial thrombosis- saddle thrombi |
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What are the gross lesions associated with dilated cardiomyopathy? Causes? |
Round, enlarged heart Thin walled, flabby chambers Cats- taurine deficiency |
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What are the sequelae of dilated cardiomyopathy? |
CHF, nutmeg liver Decreased contractility of myocardium Decreased systolic contraction and cardiac output Valvular regurgitation |
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what are the two types of restrictive cardiomyopathy? Sequelae? |
Fibrosis of left ventricular endocardium Excessive moderator bands in left ventricle Impaired filling, signs of heart failure -> death *primarily in cats |
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What is myocarditis? Cause? |
Inflammation of the heart muscle Hematogenous spread of infection to the myocardium |
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What are the different categories of myocarditis? What causes each? |
Suppurative- bacteria, abscesses with localized inflammation Nonsuppurative- necrotizing, hemorrhagic, lymphocytic (viral, protozoa, toxic, immune-mediated) Eosinophilic (look for green tissue) |
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What are the different neoplasms in the heart? |
Primary- HEMANGIOSARCOMA, most common. Rhabdomyoma and rhapdomyosarcoma Metastatic- hemangiosarcoma, lymphosarcoma Heart base tumors (second most common) |
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Hemangiosarcomas are most commonly found in where in the heart? |
Right atrium! |
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The most common metastatic disease to the heart is what? |
Lymphosarcoma *especially in BLV with cattle Seen in uterus, abomasum May produce heart failure |
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The most common heart base tumor is what? |
Aortic body tumor "chemodectoma" May cause vascular obstruction/rupture |
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What are the reactions when each part of the vessel gets damaged? Endothelium damage Endothelium necrosis |
Damage to endothelium- seperation from the underlying basement -> increased permeability to plasma protein movement into subendothelium Necrosis- activate coagulation cascade -> thrombus formation *endothelium can migrate and repair defects |
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What most likely caused this congenital malformation? |
Congenital hereditary lymphadema- caused by malformation of lymphatics Can also be delayed development in which it will resolve itself postnatally Causing stillbirth with generalized subcutaneous edema, edema in the ear tips, symmetrical swelling of head, neck, tail |
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What mineral deficiency can lead to rupture of vessels? |
Copper deficiency - leads to abnormal development of elastic tissue (seen in turkeys and pigs) |
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Equine vascular rupture of the aorta is caused by what? Sequelae? Of the internal carotid artery? |
Spontaneous or extreme exertion, parasites, trauma/falls with thoracic injury Hemopericardium and cardiac tamponade (rapid death) Internal carotid- guttural pouch mycosis, sees epistaxis clinically |
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In the dog, the parasite that lives in the wall of the aorta and can cause vascular rupture is what? |
Spirocerca lupi |
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Idiopathic rupture of vessels can be caused by what condition in cats and dogs? |
Chylothorax |
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The layer of the arteries that thickens in hypertrophy is what? |
The tunica media- the smooth muscle in the middle layers |
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Pulmonary arterial hypertrophy is seen with what cardiac condition? Normal in what types of animals? Parasitic cause? |
Left to right shunts Normal in cattle in high altitudes Aelurostrongylus abstrusus*, toxocara, dirofilaria immitis in cats |
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Define Aneurysm How is this different from a false "dissecting aneurysm? |
Localized dilation, thin-walled outpouching in the artery False "dissecting aneurysm"- fracture in tunica media, splits the tissue into two layers and the blood flows between two tubes |
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What are the causes of aneurysm? |
Copper deficiency Lathyrism Parasites Verminous arteritis in horses- strongylus vulgaris infection causes cranial mesenteric artery dilation and rupture |
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What is the cause of varicose veins (varicosities)? Sequelae? |
Dilation of the vein for many reasons- can be an insufficiency of the valve, leading to more dilation and twisting in the valves Seen most in the pampiniform plexus but relatively uncommon Sequelae- thrombosis or sclerosis |
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Define telangiectasis What tissues are these found on? |
Foci of abnormally dilated capillaries, sinusoids, arterioles, or venules Skin/mucous membranes most common Dilated sinusoids in liver are common incidental finding in cats and cattle** |
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Define Arteriosclerosis What gross signs are associated with this? |
Intimal fibrosis of large elastic arteries, chronic degeneration and proliferation of arterial wall, narrowing the lumen Gross lesions- slightly raised, firm, white plaques, branching sites, *Abdominal aorta being the most common site |
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Define Atherosclerosis What gross lesions are associated with it? |
Intimal and medial lipid deposits in elastic and muscular arteries. Chronic accumulation of lipid, fibrous tissue and calcium Dogs with hypothyroidism and hypercholesterolemia Thickened, firm, yellow-white arteries |
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What are the common causes of arterial medial calcification? Gross lesions? |
Calcinognic plant toxicity Vitamin D toxicosis Renal insufficiency Severe debilitation Spontaneous lesion in rabbits Solid, dense, white, pipelike vessels Raised, white, solid intimal plaques |
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What is fibrinoid necrosis? |
Lesion of acute degeneration and inflammation of small arteries and arterioles *Important diagnostic feature of selenium-Vitamin E deficiency |
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What are some common causes of thrombosis? |
Aortic thrombosis in feline cardiomyopathy Thromboembolic colic in horses TEME in cattle, histophilus somni In dogs with dirofilariasis DIC |
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What are the sequelae of thrombosis? |
Occlusion of blood supply, infarction, death, recanalization and restored blood flow |
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What are some of the specific examples of arteritis? |
Erysipelothrix rhusiopathiae in pigs Dirofilariasis in dogs Strongylus vulgaris in horses |
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What are the causes of phlebitis? |
Neonatal umbilical infection Systemic infection- salmonellosis in pigs Faulty intravenous infection FIP |
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What gross lesions are seen with lymphangitis? |
Thick, cordlike structures within the distal limbs, may be nodular and ulcerative (suppurative discharge) |
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What are the four layers of skin? |
Stratum corneum (+/- stratum lucidum), granulosum, spinosum, basale Thickness = spinosum + corneum |
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What is responsible for the regrowth of hair? |
The hair bulge |
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e basement membrane is made up of what three structures? |
Basal surface of basal keratinocytes Basal lamina Reticular lamina |
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is the hair growth cycle? |
Anagen (growing phase), Catagen (transition phase), telogen (resting phase), exogen (shedding of hair) |
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What are the three things that can cause alopecia? |
Hair cycling disorders Dystrophy/dysplasia of hair follicle Atrophy/miniaturization |
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Define Tylotrich hairs |
Rapid-adapting mechanoreceptors, scattered among normal hair |
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What is the function of sebaceous glands? Where are they located? |
They provide the sheen to the coat by secreting a lipid component They are located all over the body but are more numerous at mucocutaneous junctions, chin, lip, extremities Modified structures: Meibomian glands, hepatoid glands |
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Where are the apocrine sweat glands located? Eccrine? |
Apocrine- throughout haired skin, responsible for sweating in horses Eccrine- footpads, frog region of ungulates, carpus of pigs, nasolabial region of ruminants and pigs |
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What is different histologically between the footpads of cats and the footpads of dogs? |
Cats- have smooth compacted skin layers in their digital pads Dogs- conical papillae |
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What are the three vascular plexuses of the dermis, what do each supply? |
Superficial- superficial follicles and epidermis
Middle- sebaceous glands, mid follicles, arrector pili muscles Deep- subcutis and deep portion of follicles and apocrine glands |
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Whatare the four barrier functions of the skin? |
Structural- stratum corneum (keratin protein is the brick, lipid between cells is the mortar)
Metabolic- stratum spinosum, detoxification Immunologic- keratinocytes of stratum corneium, langherhan cells Photoreceptive- hair, melanocytes, keratinocytes |
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Innate immunity of the skin is caused by what? Adaptive immunity? |
Innate- statum corneum with macrophages and neutrophils Adaptive- langerhan cells and dendritic cells, T-lymphocytes and stimulated lymphocytes |
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What term is used to describe the changes seen on these skin samples? |
This is a macule/patch Flat/flush with surface, color of the skin, most common changes due to blood or melanin Macule <1cm Patch >1cm |
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What term is used to diagnose these bumps on the skin? |
This is a papule, <1cm solid elevation of the skin. usually a hyperplastic process due to inflammatory infiltrates (insect bite, papilloma, superficial folliculitis) |
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What term is used to describe these lesions? |
These are plaques, flat, slightly elevated solid large lesions that are "plateau-like" From coalescing papules or from eosinophils |
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What is the lesion seen here? |
These are wheels. Raised, solid, sharply demarcated with steep sides Result from edema in the dermis, they will pit on pressure (insect bites, urticaria, allergic reaction) |
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How would you describe these grossly? |
These are nodules, round, solid elevated 3D structures that are more than 1cm in size Can be inflammatory or neoplastic |
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What are these most likely? |
These are neoplasms, abnormal masses of tissues that exceed and is uncoordinated with that of normal tissue. |
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What are these lesions? |
These are vesicles/bulla. These are well circumscribed and contain serum. These result from separation of normally adherent tissues When these rupture, they can lead to erosion or ulceration Vesicle <1cm, bulla >1cm Examples: burns, viral infection, immune-mediated disease |
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What are these lesions? |
This is a pustule, a vesicle or bulla that contains purulent contents From bacterial infections, pemphigus foliaceous *acantholytic cells = pemphigus |
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What are these lesions called? |
Papillomas, fingerlike projections above the skin surface Associated with a hyperplastic dermis |
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What is this secondary lesion? |
This is a secondary lesion, a scale. This is an accumulation of the cornified layer of skin. Will appear white, yellow and dry |
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What are these lesions called? |
These are epidermal collarette, flat regions of scale that grow in circular rings Ex, superficial bacterial infection, *ringworm, insect bite, fungal infection |
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These lesions are known as what? |
This is a crust, composed of keratin, dried serum, blood, bacterial debris Resulting from a transudative/exudative process, chronic stage of pustular disease Erosion or ulceration of epidermis is beneath |
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What are these lesions? |
These are vegetations, multiple crusts on top on each other. |
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What are these lesions? |
These are erosions, superficial defects of the epidermis *basement membrane and dermis is in tact Surface trauma or from a prior vesicle/pustule rupture |
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What are these lesions? |
These are ulcers, complete defects of the epidermis into the dermis. Ex. Indolent ulcer, surface trauma, ischemia |
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What is this lesion? |
This is lichenification, thickening of the skin due to chronic rubbing, scratching, irritation Ex. chronic superficial pruritic dermatitis |
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What are these lesions? |
These are fissure, cracks in the epidermis or through the epidermis and into the dermis secondary to loss of elasticity and moisture Ex. footpad fissures, necrolytic dermatitis, digital hyperkeratosis |
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What is hyperkeratosis? Orthokeratotic hyperkeratosis? |
Increase in the thickness of the stratum corneum (Orthokeratotic hyperkeratosis is excess of the normal type of keratin), NO nuclei Primary lesion- vitamin A deficiency Usually secondary* to trauma and inflammation |
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What is parakeratotic hyperkeratosis? |
Retention of nuclei in the stratum corneum, abnormal cornification as a result of increased epidermal turnover Primary lesion- zinc responsive dermatosis Secondary lesion*- chronic trauma or sun exposure |
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What is hyperplasia/acanthosis of the dermis? |
Increased thickened of the epidermis, usually stratum spinosum A result of chronic irritation NOT the same as acantholytic! |
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Intracellular edema in the skin is due to what change? Intercellular? |
Intracellular- degenerative change of keratinocytes (cell swelling) Intercellular- inflammation, accompanied by exocytosis (spongiosis) |
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What is dyskeratosis? |
Premature keratinization of individual keratinocytes Retained, condensed nuclei Associated with benign cornification disorders of malignancies |
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What is acantholysis? |
Loss of adhesion desmosomes between keratinocytes. Usually pemphigus or bacterial dermatitis |
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What is exocytosis in the skin? |
Migration of inflammatory cells into the epidermis or adnexal epithelium, associated with spongiosis |
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What are epidermal clefts? |
Empty slit-like spaces that run parallel to the epidermis at the dermo-epidermal junction Basal cell damage or basement membrane disease |
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What is the most common pattern of inflammation in the skin? |
Perivascular dermatitis, a very nonspecific pattern of inflammation where the inflammatory cells aggregate around superficial dermal vessels Seen in hypersensitivity disorders, ectoparasitism (sarcoptes), superficial bacterial infections Early in inflammatory process, ALL are perivascular |
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hat are some things that help determine the underlying cause of perivascular dermatitis? |
Character of the infiltrates Type and degree of hyperkeratosis *be aware of secondary changes which are common and can change the diagnosis |
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What diseases of the skin are characterized by perivascular dermatitis and parakeratosis? |
zinc-responsive dermatosis Superficial necrolytic dermatitis- severe systemic disease- liver disease metabolic disease |
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What is interface dermatitis? What two things must be there for it to be interface dermatitis? |
pathology that targets basal keratinocytes and dermoepidermal junction two things: INflammatory cells obscuring the dermoepidermal junction and hydropic degeneration of basal cells Autoimmune or hereditary disease |
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Exfoliative cutaneous lupus erythematosus of the german shorthair pointer is what kind of inflammation? What kind of gross lesions are seen? |
Severe autosomal recessive disease causing interface dermatitis Causes scaling with erosions, hair loss, depigmentation |
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What is the disease dermatomyositis? |
Familial skin disease of collies, shelties and their crosses Affects the skin, blood vessels and muscles resulting in interface dermatitis |
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If you have an acute skin disease characterized by crusting, erosions, ulcers with dyskeratosis seen histologically, what disease would you be suspicious of? |
Erythema multiforme, causing interface dermatitis Caused by adverse drug reactions, infections, neoplasia, or can be idiopathic |
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What is pemphigus vulgaris? |
Autoantibody to desmoglein-3, an adhesion molecule Causes acantholytis swith suprabasilar clefting (tombstoning), BIG bulla/erosions/ulcers on the oral mucosa |
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What are the viral infections that can cause infections in the skin? |
Foot and mouth disease Vesicular stomatitis Contagious pustular dermatitis (contagious ecthyma/orf, sheep and goats, vesicles, pustules, crusts) |
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efine subepidermal vesicular dermatitis |
vesicles that form within or below the basement membrane zone Due to immune-mediated or genetics |
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What is Bullous pemphagoid? |
An acquired cause of subepidermal vesicular dermatitis, affecting hemidesmosomal proteins |
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What is epidermolysis bullosa? |
A congenital defect causing subepidermal vesicular dermatitis junctional- affecting the lamina lucida and dystrophic- affecting anchoring fibrils- look at where the cleft is forming to distinguish between |
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How is nodular to diffuse dermatitis characterized? Where are they found? |
Found scattered throughout thick skin, Characterized by predominate cell type, caused by infectious agent or they can be noninfectious |
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What are the nonifectious causes of nodular to diffuse dermatitis? |
Feline eosinophilic dermatitis complex- look for eosinophilic plaques, granuloma formation, indolent ulcers Associated with hypersensitivities Equine eosinophilic granuloma |
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The fungal diseases that have a dermatitis component are what |
Blastomyces dermatidis Cryptococcus neoformans Coccidiodes immitis |
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Define Perifolliculitis Folliculitis Furunculosis |
peri- inflammation around the hair follicle folliculitis- inflammation of and within the hair follicle Furunculosis- follicular rupture with inflammation |
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What are the three causes of folliculitis? |
Bacteria- staphylococcus pseudintermedius Dermatophytes- microsporum, trichophyton, epidermophyton Demodex mites- proliferate with immunosuppression |
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What two things must be present for it to be vascultitis? |
Inflammatory cells within or around vessel wall Evidence of vascular injury Typically part of a systemic disease |
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what is panniculitis |
Inflammation of the adiopose tissue of the hypodermis Often idiopatic and sterile, must rule out infectious agent, trauma, foreign body |
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What is atrophic dermatosis? |
Constellation of changes associated with underlying endocrine disorders- hyperadrenocorticism Epidermal atrophy, follicular atrophy, atrophy of sebaceous glands, calcinosis cutis Grossly- bilateral symmetric alopecia, dull, dry, brittle hair, hyperpigmentation |
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What is fibrosing dermatosis |
Chronic change- indicated s prior insult Ranges from fibroplasia to fibrosis (scar) Newly formed granulation tissue to mature fibrosis with connective tissue |
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What are the four disorders of hair follicles? |
Nonscarring alopecia Scarring alopecia Folliculitis Hypertrichosis |
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In non-scarring alopecia, what is unique about the hair follicle? |
The hair shaft can be made but it is weak and can break off easily Not usually associated with inflammation Endocrine, congenital, cyclical flank, frictional, post-clipping, traction, immune-mediated |
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What is sebaceous adenitis? |
Autosomal recessive mode of inheritance Inflammatory destruction of the sebaceous gland leading to scaling and alopecia Severe hyperkeratosis with follicular plugging |
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is alopecia areata? |
Targeted destruction of anagen hair follicles, usually the dark hair |
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Scarring Alopecia is associated with what? |
Destruction of the hair follicles Folliculitis or severe pyoderma Local wound/scarring that destroys adnexia Scleroderma |
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What is hypertrichosis? |
Either excessive hair and/or the hair is longer and coarser than normal Equine Cushing's Hirsutism is due to enlarged pars intermedia that regulates body temp, appetite and seasonal shedding of hair |
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fine Hamartoma |
Normal looking tissue in the right place but arranged incorrectly Epidermal hamartoma, follicular hamartoma, mesenchymal origin, vascular origin |
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What are the ectodermal neoplasms? |
squamous cell carcinoma Papilloma Infundibular keratinizing acanthoma |
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What are the neoplasms of adnexal origin? |
Sebaceous gland adenoma Hair follicle tumors Perianal gland adenoma Carcinoma of the apocrine glands of the anal sac |
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What is an infundibular keratinizing acanthoma? |
Common intracutaneous cornifying epithelioma Common benign lesions in dogs |
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Perianal "hepatoid" gland adenomas are made up of what |
Modified sebaceous glands, common in old, intact male dogs Raised nodules on the perineum or ventral tail, frequently ulcerated |
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Hair follicle tumor are usually present as what? |
Subcutaneous nodules, usually benign |
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What are the neoplasms of mesodermal neoplasms |
Mesenchymal origin- fibrosarcoma in cats, soft tissue sarcomas in dogs, equine sarcoid (viral induced), hemangioma (vascular), lipomas Leukocytic proliferations- canine cutaneous histiocytoma (langerhan's cells), mast cell tumor, lymphoma |
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What are the melanocytic neoplasms |
Melanocytoma Malignant melanoma Variable biologic behavior- need histopath |