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113 Cards in this Set
- Front
- Back
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Define diabetes mellitus
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Group of metabolic diseases characterized by hyperglycemia, resulting from defect in insulin secretion/action.
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Types of diabetes mellitus
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Type 1- Dog
Type 2- Cat Type 4- Gestational diabetes Other: Secondary to disorders of exocrine pancreas (Pancreatitis, neoplasia), endocrinopathies, insulin antagonists. |
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Characterize type 1 diabetes m.
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Insulin-dependent
Absolute deficiency of insulin secretion due to autoantibodies (autoimmune destruction of beta-cells) Dogs |
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Characterize type 2 diabetes m.
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2 defects:
- insulin resistance - secondary a beta-cell destruction Cats |
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Diabetes mellitus in dog
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Type 1
Permanent hypoinsulinemia (irreversible) Autoimmune mechanism (auto Ab) Genetic factors, congenital disorders, environmental factor (insulin-antagonist diseases/drugs, obesity, pancreatitis, chronic insulin resistance) |
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Diabetes mellitus in cat
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Type 2. Possible remission, Stress hyperglycemia
Reasons: - OBESITY→aberration in glucose transport→lower expression of insulin signaling genes→decreased secretion of adiponectin→INSULIN RESISTANCE - GLUCOTOXICITY →chronic hyperglycemia impairs insulin secretion (contributing to insulin res.) →Amyloid deposition→Beta-cell dysfunction→disrupts insulin secretion |
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Insulin deficiency causes what?
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↓ Glucose uptake + ↑ Gluconeogenesis → Polyphagia, glucosuria, loss of electrolytes, hyperglycmia
↑ Protein catabolism → Weight loss, weakness ↑ Lipid catabolism → ↑ NEFA, production of ketonbodies, weightloss, hpatic lipidosis |
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How does the glucose work in insulin deficiency? (simple explanation, see more in Q "Carbohydrate metabolism in i.d.")
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Normally the satiety center inhibits the feeding center after ingestion of food.
Insulin deficiency → Glucose doesn't reach satiety center→ failure to inhibit f. center → polyphagia (Increased catabolic activity→ weight loss) |
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Lipid metabolism in insulin deficiency?
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Lipolysis→ ↑ NEFA → Hypertriglycridemia
↑ levels NEFA will be transported to liver, where it undergoes beta-oxidation→ Excess Acetyl CoA→ Ketone body production→ketoacidosis (vomiting, anorexia, dehydration, lethargy) ↑ levels NEFA transported to liver → ↑ Hepatic synthesis of triglycerides →: - Hepatic stenosis - Hyperlipidemia - Hepatomegaly |
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Carbohydrate metabolism in Insulin deficiency? (Glucose)
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Insulin deficiency→ ↓ glucose to muscle/adipose/liver
→ ↑ Gluconeogenesis/glucogenolysis in liver → Hyperglycemia→Renal capasity for glucose reabsorption is exceeded→Glucose is lost in urine→ Glucosuria→Polyuria→Polydipsia |
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Chronic complications of insulin deficiency in diabetes mellitus?
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Cataracts, uveitis =mostly dog
Diabetic neuropathy=mostly cat Diabteic nephropathy ↑ susceptibility to infection (sp. urinary tract) Micro/macroangiopathy |
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Diabetes mellitus: Cataracts and uveitis as chronic complication of i.d.
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Mostly in dog.
C: Accumulation of sorbitol/fructose in lens → Influx of water to lens → Altered osmotic relationship in lens → Swelling, rupture of lens fibers → cataract U: Consequence of exposure to cataract lens proteins to local ocular immune system |
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Diabetes mellitus: Diabetic neuropathy as chronic complication of i.d.
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Vascular/metabolic factors
Demyelination/Remyelination Asaxonal degen./regen. Myelinated fibers lost → Diabetic neuropathy: Hundlimb weakness, ↓ ability to jump, plantigrade posture |
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Lab tests to confirm diabetes mellitus
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CBC: mild anemia, stress leukogram
Biochem.: hyperglycemia, hypercholesterolemia, lipemia Urineanalysis: Glucosuria, variable ketonuria, urine specific gravity (1,025), possible bact. infections |
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Hyperadrenocorticism (Cushing's) in dog
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Spontaneous, chronic, iatrogenic
Primary: Arenal-Dependent H. Secondary: Pituitary-Dependent H. |
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Primary hyperadrenocorticism in dog
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ACTH-independant increased cortisol secretion in adrenal gland.
Due to: Functional adrenal tumor Unilateral enlarged adrenal gland→ high cortisol concentration in blood→ ↓ secretion of CRH & ACTH→ Atrophy of gland and atrophy of non-tumor dells Diagnosis: at age of 11 years, Predisposed breeds: G. shepherd, dachhound, labrador Occurance: 10 % in dogs/ 50% in large dogs |
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Secondary hyperadrenocorticism in dog
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Increased secretion of ACTH by pituitary gland → bilateral hyperplasia of adrenal cortex→ ↑ synthesis of glucocorticoids.
Due to: Pituitary adenoma/adenocarcinoma secreting ACTH Develops slowely, in animals over 6 years. Diagnosis: at age of 10 years Predisp.: poodle, dachshound, beagle, g. shepherd, small terriers, boxers Occurance: 90% in dogs/ 75% in small dogs |
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Iatrogenic hyperadrenocorticism in dog
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Due to long term treatment of glucocorticoids.
↓ secretions of CRH and ACTH → bilateral atrophy of adrenal cortex. |
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Symptoms of hyperadrenocorticism in dog
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Clinical signs result from longterm influence of excessive levels of glucocorticoids.
Physiology: ↑ Gluconeogenesis in liver ↓ Glucose utilization in muscle/adipose (→ insulin resistance) ↑ Protein catabolism ↓ Protein synthesis ↑ Lipolysis Immunosuppressing action |
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Clinical signs + anamnesis of hyperadernocorticism in dog
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A: polyuria, polyphagia, polydipsia
C: Exercise intolerance Panting (abd. presses on diaphr.) Pendulous abdomen- muscle atrophy/weakness, hepatomegaly, permanently filled bladder, adipose disposition Symmetrical alopecia Hyperpigmentation Seconday lesion Skin atrophy Pyodermatitis |
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Results from radiological examination of Cushing's
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Foci of dystrophic calcification
Hepatomegaly Distended bladder vertebral osteoporosis |
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Lab test results of Cushing's
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CBC: Stress leukogram
Urine analysis: isothenuria, urinary tract infection hyperglycemia Hyperlipidemia- increased hepatic enzyme activity |
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Cushing's syndrome in cats
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Cats express 2 times less cotisol than dog and therefore need 2 times the dosage.
Strictly ass. with refractory diabetes mellitus. Polyuria/dipsia/phagia due to d.b. Pendulous abdomen, hepatomegaly, muscle atrophy |
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Hypoadrenocoticism (Addison's)
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Deficiency of adrenal cortex hormones
Chronic or acute(life-threatning) Clinical signs do not appear until 90% of adrenal gland stops working. |
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Hypoadrenocorticism forms
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Primary:
autoaggressive, infectious, neoplastic process Costisol/aldosterone deficiency Secondary: Neoplasia, inflammation, trauma to hypothalamus Lack of ACTH stimulation of adrenal gland Glucocorticoid deficiency only Iatrogenic: Incorrect treatment: Longterm drug abruptly withdrawn→ glucocorticoid deficiency Inadequate drug management of Cushing's After bilateral removal of functioning adrenal tumor→ gluco/mineralocorticoid deficiency |
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Explain primary addison's disease
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Gluco/mineralocortisoid deficiency
Aldosterone effect: - Hyponatremia→ polyuria, dehydration, vomiting - Hyperkalemia→ bradycardia, metabolic acidosis - Hyperchloremia Glucocorticoid def.: - Impaired glycogenesis - ↑ sensitivity to insulin→↑ tissue glucose utilization - ↓ glycogen synthesis - hypoglycemia |
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Clinical signs of chronic addison's
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appear and resolve
- apathy, weakness, anorexia - weight loss - polyuria, polydipsia - vomiting, diarrhea Resolved after rehydration and glucocorticoid administration |
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Clinical signs of acute addison's
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Hypovolemic shock- adrenal crisis
- dehydration, pale mucous m., slow crt - bradycardic, weak pulse - exercise intolerance - diarrhea with blood and abdominal pain - shock, hypoglycemic seizures |
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Lab test result for addison's
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CBC: Lack of stress leukogram, mild nonregenerative anemia
Urine: isothenuria Biochem.: Hypoglycemia/kalemia/natremia/chloremia, prerenal azotemia, metabolic acidosis |
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Humoral regulation of vascular tone in inflammation
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Vasodilators: histamine, bradykinin, NO, PGI2, PGE2, PGD2, PDE1
Vasoconstrictors: TXA2, leukotrienes |
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Define hyperemia
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Increased and excessive amount of blood in blood vessel
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Hyperemia: forms
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Active: due to increased flow of arterial blood in dilated capillaries. (also called arterial/fluxionary hyperemia)
Congested: Passive hyperemia resulting from an obstruction in the flow of blood from a body part. (also called venous hyperemia) |
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Active hyperemia- define
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Due to increased blood flow of area of active dilation of both arterioles and capillaries.
Associatedwith neurogenic, hormonal, metabolic function. Physiological: in working muscles, in skin following exertion, in dig. tract after feeding |
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Active hyperemia- Pathological (when?)
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Early face of inflammation
Decrease of fever Epilepsy |
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Active hyperemia- Manifestation/signs
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Redness
increased temp. Organ may be enlarged |
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Active hyperemia- consequenses
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No conseq. or hypertrophy
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Passive hyperemia- define
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Due to decreased outflow of blood from area.
Localized: pressure from mechanical/physical obstruction. Generalized: cardiac/pulmonary disorders |
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Passive hyperemia (localized)- manifestation
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Cyanosis, decreased temp., organ may be edematous.
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Ischemia (malperfusion)- define
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Insuff. supply of blood to an organ, inadq. to meet metabolic demand of tissue.
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Ischemia (malperfusion)- causes
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Blocked/constricted artery: cold, chemical stimulus, torsion, thrombosis, embolism.
Hypertension: shock |
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Ischemia (malperfusion)- adaptation
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Vasodilation- adenosine
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Ischemia (malperfusion)- what consequenses depend on.
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Depend on:
- degree of arterial obstruction - functional conditions of circulation - metabolic activity of tissue, resistance to ischemia - magnitude and length of decreased blood flow |
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Ischemia (malperfusion)- consequences
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Ischemic Infarct
Ischemic Necrosis Atrophy Ischemic-reperfusion |
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Ischemia-reperfusion injury- define
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Occurs after restitution of blood flow.
Results from: - Generation of ROS (reactive oxygen species), dysfunction of mitochondria - Epithelial injury - Neutrophil influx and activation |
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Ischemia-reperfusion injury- Generation of ROS
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Xanthine oxidase combines with oxygen and hypoxanthine= Superoxide anion is generated→ converted to other radicals (hydroxyl radical)
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Ischemia-reperfusion injury- Mitochondrial dysfunction
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Changes in membrane permeability
Inactivation of respiratory chain Increased production of ROS |
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Ischemia-reperfusion injury- Endothelial injury
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XO- mediated damage by ROS
Impaired endothelial functions: - Upregulated transcription of endothelin - Decreased NO release - No- reflow phenomenon - Vasoconstriction promoted by PAH, TxA2. Important cause of transplantation failure |
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Ischemia-reperfusion injury- inflammatory response
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Neutrophil infiltration and activation
Tissue injury due to ROS generation and release of proteolytic enzymes Increased NO & ONOO production Eicosanoid generation |
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Prolonged Ischemia
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1. Breakdown of ATP→ Hypoxanthine
2. Xanthine hydrogenease acts in REVERSE to xanthine oxidase 3. Oxidation leads to formation of ROS XO-mediated damage by ROS. |
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Thrombus- define
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Intravascular clot
Clotted mass of blood attached to interior wall of vein/artery Thrombosis: Abnormal vascular condition. clots develop in blood vessels and remain. |
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Thrombi vs coagulum
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Thrombi:
- Platelets and fibrin - solid, friable, firm - attached to interior vessel wall Coagulum: - Fibrin and blood cells - rubbery, gelatinous - loosely in lumen |
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Thrombi formation
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Due to changes in blood flow/vessel wall/blood.
Endothelial injury critical for thrombi formation: - trauma, inf. agents, immune complexes, parasites, toxins Changes in blood composition: - activates clotting factors - thrombophilia - dehydration - acidosis - polycythemia |
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Fate of thrombi
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Progression or shrinkage
Dissolution or emollition Organisation Replacement by CT Recanalization Calcification |
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Thrombi - consequences
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Ischema, congestion, thromboembolism
Depend on: type of blood vessel, dysfunction of blood flow, collateral circulation |
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Embolism- define
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Obstruction in blood vessel due to blood clot/foreign matter stuck in vessel while traveling.
ex.: detached thrombi, bacteria, neoplasm, parasite, amniotic fluid, air bubbles |
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Embolism with clinical importance (veterinary)
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Equine: Thromboembolism (colic due to aortic-iliac thombosis) ass. with S. vulgaris infection.
Carnivore + equine: Fibrocartilaginous embolism Dog + cat: In thyroid disorders After surgery |
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infarction- define
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Local are of necrosis caused by occlusion of arterial supply/venous drainage.
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Infarction- types
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Ischemic: white, pale, anemic
Hemorrhagic: red |
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Ischemic Infarct
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Coagulative necrosis
Arterial insufficiency Anemic infarct White and pale |
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Hemorrhagic infarct
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Hemorrhagic necrosis
venous insufficiency Dual blood supply Usually in tissues of loose consistency (lugns) Red infarct |
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Fate of infarcts
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Organisation→ Scar
Sequestration Emollition Calcification Regeneration |
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Hemorrhagic infarct- clinical importance (veterinary)
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Lungs
Calf- ass. w. bronchopneumonia Dog- ass. w. D. immitis, A. vasorum infections and endocrine disorders (Cushing/Addison) |
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Ischemic infarct- clinical importance (veterinary)
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Kidney
Equine- ass. w. S. vulgaris Bovine- ass. w. nephritis Suis- ass. w. endocarditis and erysipelas Canine- unknown Heart Suis Canine- ass. w. hypothyroidism Rats- following chronic ischemia Salivary glands: dogs and cats |
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Cerebral stroke- define
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Cerebrovascular
Life-threatening Brain is deprived of adequate oxygen |
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Cerebral stroke- forms
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Ischemic: blood supply to brain is interrupted (blood clot in carotid arteries)
Hemorrhagic: bleeding around or into brain |
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Cerebral stroke- human
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(rare in domestic animals)
Stroke: clinical signs of cerebral damage persist for more than 24h Usually a consequence of artherosclerosis |
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Cerebral stroke- Cat
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Feline ischemic encephalopathy
Hemorrhagic stroke results from head trauma (intracerebral/subarachnoid hem.) Peracute onset of signs |
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Cerebral stroke- Dog
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Cerebral vascular accidents
Due to:thrombosis or embolism in hypothyroidism/idiopathic hyperlipidemia Hemorrhagic stroke results from head trauma Intraparenchymal hem. can occur with hypertension secondary to hyperthyroidism/renal disease/cushing's |
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Cerebral stroke- symptoms in dog
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Change in behavior, activity, personality
Sudden collapse Disorientation, loss of balance Loss of urine control or bowel habits Loss of recognition of owner Head tilting Paresis, seizures Blindness |
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Cerebral stroke- symptoms in cat
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Loss of balance, walking in circles
Head tilting Ataxia Temporary blindness Behavioral changes, aggression Lethargy Hemiparesis, seizures Upper resp.problems (sneezing, nasal discharge) |
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Cerebral stroke- symptoms in human
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Numbness, weakness on one side of body
Confusion, trouble to speak impaired vision Trouble walking, dizziness, loss of balance/coordination Severe headache |
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Circulatory failure- define
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Inability of cardiovascular system to supply the organs of the body with enough oxygenated blood to meet metabolic demands.
Results from decreased cardiac output. Depend on: - myocardial contractability - preload/afterload - heart rate/rhythm |
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Circulatory failure- adaptations
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Neural and humoral mechanisms to maintain the proper blood flow.
Maintain perfusion in CNS and heart at cost of other organs. Adrenergic stimulation Activation of RAA system Increased cardiac output: - by increasing myocardial contractability - by increasing cardiac rhythm - maintain proper blood pressure |
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Circulatory failure- Adrenergic stimulation
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Emotional excitation
Cardiac failure results from decreased cardiac output→ ischemia Stimulus of beta-receptors ↑ myocardial contractions and frequency of beats. Stimulus of alpha-receptors→ contraction of renal/skin/visceral vessels→↑ preload/afterload. |
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Circulatory failure- Activation of RAA system
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↓ cardiac output + adrenergic stimulation:
-↓ renal flow -↑ synthesis/release of renin - renin stimulates gen.of angiotensin I and conversion to angiotensin II. - Angiotensin II stimulates release of aldosterine and vasopressin→ stimulates adrenergic pathways Stimulants: Aldosterone, vasopressin, ACE inhibitors, Diuretics, drugs used in cardiac failure |
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Circulatory failure- Activation of RAA system (aldosterone and vasopressin)
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They stimulate:
- Renal sodium and water retention → ↑ blood and EC fluid volume. - Vasoconstriction |
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Circulatory failure- Activation of RAA system - effects/consequenses
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There will be only temporary improvement (increase in cardiac output), then it becomes an additional load for the heart.
→ Myocardial hypotrophia → Congestion → ↑ cardiac pathology |
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Cardiac circulatory failure- causes
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Hypertension + ↑ blood volume
Morphological changes in myocardium Changes in heart rhythm Valve insufficiency Metabolic diseases Neural/endocrine diseases |
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Cardiac failure- valve insufficiency
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75% cardiovascular disorders in dog
Most often mitral valve Degeneration/thickening/deformation - often occur with CT changes Predisposed: Dog- king charles cavalier spaniel, poodle, yorkie, tax, pekingese Eq.- worse in young, risk of faint |
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Cardiac failure- myocardiopathia
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Degeneration on cardiomyocytes
Changes in ventricular volume and contractability Unknown cause Important factors: - congenital defects - infections, toxins - nutritional (cat- taurine) - autoimmune disease, metabolic disease Predisposed breeds: Dog- Doberman, boxer, greatdane Cat- Maine coon, ragdoll, norwegian forest |
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Cardiac failure- Congenital malformations
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Rare
Patent ductus arteriosus Ventricular/Atrial septal defect Aortic/pulmonary stenosis |
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Cardiac failure- Types
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Right: Chronic
-peripheral edema, lesions on organs Left: Acute, Chronic -pulmonary congestoin, ventricular hypetrophy/dilation |
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Cardiac failure- consequenses
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Congestion
Hypoxia- cyanosis Cough, catarrhal inflammation Transudateaccumulation Secondary lesions |
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Cardiac failure- Transudate
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Fluid circulates due to pressure gradient
- colloid osmotic pressure - hydrostatic pressure - filtration/reabsorption No/low protein content <2,5% total nucleated cell count |
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Cardiac failure- edema
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Abnormal accumulation of fluid in interstitial fluid
Accumulation of fluid in body cavities - ascites (fluid accumulation in abdominal cavity) - hydrothorax (Pleural effusion) - hydropericardium |
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Cardiac failure- edema causes
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Increased hydrostatic pressure
Decreased plasma colloid osmotic pressure Sodium retention Lymphatic obstruction Inflammation |
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Cardiac failure- Acute left
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Oedema pulmonum
Results from rapid accumulation of blood in pulmonary circulation - congestion/pulmonary hypertension - rapid transudate accumulation in alveoli/bronchioli |
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Cardiac failure- Chronic left
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Pulmonary hypertension → Cough, shortness of breath
- risk of lung edema Brown induration of lung- "Induratio fusca" |
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Cardiac failure- Chronic right
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Secondary to left heart failure
Consequence of congenital malformation - chronic congestion in pulmonary ciculation →pulmonary hypertension → increased pulmonary resistance |
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Cardiac failure- Chronic right- cause and consequence
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Cause: Pulmonary stenosis, valve insufficiency
Consequences: Secondary lesions in organs due to congestion - liver: swelling, degenerative lesions, cirrhosis - spleen, kidney |
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Cardiac failure- Peripheral- cause
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Decreased blood volume→vasodilation
Due to neural/humoral disregulation |
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Circulatory shock- definition
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Organs/tissue of body are not receiving an adequate flow of blood
Disproportion between circulating blood volume and vascular space Loss of blood/massive vasodilation - decrease in blood pressure |
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Circulatory shock- types
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- hypervolemic
- septic - anaphylactic - cardiogenic - neurogenic |
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Circulatory shock- Aim
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Maintain perfusion of CNS and heart
- redistribute blood due to adrenergic stimulation |
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Circulatory shock- clinical signs
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Tachycardia, tachypnoe, Pale, decreased temperature, oliguria, anuria, loss of consiousness
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Ciculatory shock phase 3
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Tissue ischemia
Metabolic acidosis Decreased coronary flow Release of kinins/enzymes from damaged pancreas |
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Circulatory shock phase 4
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Critical decrease of blood pressure
Vasodilation due to metabolic acidosis, DIC Necrosis of renal tubular epithelium Damage of interstitial mucosa and release toxins to circulation |
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Macrocytes
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Larger than normal RBC
Polychromatophils Codocytes Heinz body Macrocytosis: Increased MCV, Polychromasia, hypochromasia(macrocytic anemia) |
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Microcytes
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Smaller than normal RBC
Echinocytosis Poikilocytosis Fragmented RBC Spherocytes (immune mediated hemolytic anemia) Microcytosis: Decreased MCV |
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Dehydration
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↑ HCT, RBC, HGB (Erythrocytosis)
↑Total protein |
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Erythrocytosis types
(Polycythemia) |
Absolute: Primary, Secondary (appropriate/inapp.)
Relative: App./inapp. |
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Erythrocytosis Absolute
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↑ Erythropoiesis→↑ total RBC mass in body
Primary- Polycythemia vera - rare neoplatic myeloproliferation disorder independant of erythropoietin production - EPO normal or decreased Secondary - App.: Adaptive, ↑ RBC in response to severe hypoxia, severe chronic circulation/pulmonary system diseases, ↑ EPO - Inapp.: ↑ RBC without evidence of hypoxia, cause: tumors, mainly renal, ↑EPO |
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Erythrocytosis Relative
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The total RBC mass in the body is normal
- Appropriate (adaptive) - Inapp. (pathogenic) ↑ RBC count, PCV, HGB conc. Due to: - Plasma fluid loss: secondary to dehydration, ↑ total protein - Catecholamine-induced splenic contraction: (white coat syndrome), normal total protein Total RBC mass normal. |
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Anemia
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↓ HGB, HCT, RBC
RBC loss bigger than production → Hypoxia Normal/mild/moderate/marked/severe Regenerative: - hemorrhagic(acute/chronic blood loss) - hemolytic(destruction of immune origin, oxidative damage, microangiopathies) - reticulocytosis Nonregenerative: primary/secondary bone marrow disease, abnormal production |
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Erythron
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Total mass of RBC in body + precursor in bone marrow
Reflects production, release, destruction |
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Erythrogram- Size
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Normocytosis: Erythrocytes are normal in size
Aniocytosis: Variation in size -macrocytosis -microcytosis |
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Erythrogram- Stain
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Normochromia: normal color of RBC
Polychromasia: Irregular staining, macrocytes with less HGB Hypochromasia: Presence of RBC that stain less due to decreased HGB |
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Erythrogram- Shape
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Microcytes:
- Poikilocytosis/cythemia- abn. shaped RBC - Echinocytosis - Fragmented RBC - Spherocytes Macrocytes: - Polychromatophils - Codocytes - Heinz bodies, eccentrocytes Spherocytes(dog)/Macroagglutination→immunemediated hemolytic anemia→massive extravascular hemolysis |
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MCV
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↓ - microcytosis
↑ - macrocytosis |
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MCHC
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↓ - hypochromasia
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HCT
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Evaluates changes in plasma apperance
Determination of total protein concentration Estimation of leukocyte nr. - less than 0,5% leukopenia - more than 1,5% leukocytosis |
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Total protein
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Lab indicator showing body fluid condition
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Hyperhydration
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in cats
hempdilution→ ↓ HCT/HGB/RBC/Total protein |
