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Last updated 12:37 AM on 4/17/26
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75 Terms

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caseous lymphadenitis

chronic contagious disease of sheep and goats that effects lymph nodes and lymphatic tissue resulting in significant economic losses to producers

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caseous lymphadenitis etiology

gram + intracellular bacteria that releases an endotoxin that damages the cell wall of the host. two biotypes exist, one infecting sheep/goats and another infecting horses

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caseous lymphadenitis resistance and zoonotic

live on surfaces for 2 mo and soil up to 8 mo. highly resistant. zoonotic

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caseous lymphadenitis enter host

trough damaged skin or via mucous membranes. once in host bacteria invades lymph nodes or other internal organs

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caseous lymphadenitis incubation

1-3 mo. internal and external abceses develop and drain

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external caseous lymphadenitis symptoms

draining lymph nodes! draining abscess heal w scar tissue but purulent material contaminates env.

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common lymph nodes for caseous lymphadenitis

submandibular, prescapular, parotic, prefemoral

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internal caseous lymphadenitis symptoms

chronic weight loss, failure to thrive, variable due to what organ is involved

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caseous lymphadenitis diagnosis

clinical signs, culture and sensitivity of purulent material, extensive workup to diagnose internal

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caseous lymphadenitis treatment

aimed at limiting transmission, recurrence is common. antibiotic therapy if cull is not an option. draining abscess and isolation

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biosecurity for caseous lymphadenitis

isolation, disinfection, cull infected once draining abscess heals, vaccinate, pasteurize milk

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lamb body temp normal

102.2-104 F

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mild hypothermia in lamb

98.6-102.2

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severe hypothermia in lamb

less than 98.6

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risk factors for hypothermia

increased body surface, small lambs, thin coat, drafty env, poor mothering

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prevent hypothermia

indoor lambing, observation, short lambing season, excellent maternal nutrition to improve lamb birthweight, ensure colostrum intake

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brown fat stores

lamb uses them to generate energy to maintain body temp (initiated by oxygen and colostrum intake. brown fat is laid down in pregnancy. poor ewe nutrition means small lamb with little brown fat reserves. a small weak lamb will be slow to nurse and so no start of brown fat metabolization. once brown fat is utilized, lamb must get energy from milk to provide heat.

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hypothermia timeline

brown fat used within 5-12 hr post birth. if lamb doesn’t get energy from milk, then risk for hypothermia and hypoglycemia

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hypoglycemia

low blood glucose

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clinical signs of hypothermia/hypoglycemia

weakness, lethargy, decreased or absent suckle reflex, seizures from hypoglycemia from decreased glucose delivery to the brain

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treatment for hypothermia/hypoglycemia

provide warmth and nutrition. tube feed colostrum if can swallow. if lamb cant swallow, warm first and glucose via injection before tube feeding. warm with circulating air

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orogastric intubation

proper training necessary before attempting procedure. ensure in stomach not lungs

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diabetes mellitus

disease associated w absolute or relative insulin deficiency in both dogs and cats. due to destruction of islet of Langerhan cells in pancreas

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diabetes mellitus predisposing factors

glucocorticoid admin, pregnancy in dogs, obesity

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pancrease

near duodenum. endocrine component contained in clumps of cells called pancreatic islets or islets of langerhans. alpha cells produce glucagon, beta cells produce insulin

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insulin

essential for life. causes absorption of glucose, AA, fatty acids into cells. overall effect is to lower blood glucose levels.

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hyperglycemia

results from insulin deficiency. insulin decreases blood glucose by increasing cellular uptake of glucose and storage in the form of glycogen and fat. when no insulin, body cannot use glucose so it breaks down fat or protein

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diabetes mellitus etiology

occurs when pancreas cant produce sufficient amounts of insulin or when the cells are resistant to insulin

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type i

insulin dependant

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type ii

non insulin dependent. results from resistance of tissue to the activation of insulin

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diabetes mellitus clinical signs

polyuria, polydipsia, polyphagia, weight loss, diabetic ketoacidosis if left untreated

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diabetic ketoacidosis

life threatening emergency. if cells can’t use glucose, they begin fat metabolism. ketones are byproduct

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diabetes mellitus diagnosis

persistent hyperglycemia and glucosuria, fructosamine

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diabetes mellitus treatment

dietary management, insulin therapy (multiple types and twice daily dosing)

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diabetes mellitus dietary management in dogs

high fiber diet

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diabetes mellitus dietary management in cats

high protein low carb

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insulin types

must be given parentally usually SQ. types: long acting, intermediate acting, short acting. concentration is measured in units of insulin per mL

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use of insulin products

must be refrigerated, given at time fed, site rotation to prevent scar tissue, roll don’t shake bottle, twice daily, only use insulin syringes twice, owner edu, too much insulin can cause hypoglycemia

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hyperthyroid

due to excessive secretion of thyroid hormone from the thyroid gland, results in increased metabolic rate, primarily a disease of cats

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thyroid gland

two lobes on either side. produce thyroid hormone after stimulation by TSH from pituitary gland and produces calcitonin

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thyroid hormone

helps regulate the body’s metabolic rate, growth and development, body temp, skin conditions, etc. T4 is circulating reservoir converted to T3 in peripheral tissues and is active form in body.

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calcitonin

helps lower blood calcium levels

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hyperthyroid clinical signs

weight loss, increased appetite, unthrifty appearance, polyuria, polydipsia, palpably enlarged thyroid gland, tachycardia, hypertension, vomiting and diarrhea

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hyperthyroid diagnosis

high circulating thyroid hormone levels in blood - free T4 is most common

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hyperthyroid treatment

radioactive iodine (of choice), thyroidectomy has potential to damage parathyroid gland and can lead to hypothyroidism, antithyroid meds need lifelong treatment and can effect WBCs

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hypothyroidism

primarily a disease of dogs but can be seen in cats. due to destruction of thyroid gland. results in overall decrease of metabolic rate. (in cats usually secondary to treatment for hyperthyroidism)

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hypothyroidism clinical signs

lethargy, weight gain without increase in appetite, exercise intolerance, alterations in haircoat like dry skin and alopecia

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hypothyroidism diagnosis

measuring T4, free T4, and or TSH. commonly over diagnosed. non thyroid issues can lower thyroid hormones and mimic (such as euthyroid sick syndrome)

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hypothyroidism treatment

treated by supplementation w thyroid hormone. easily treated but requires lifelong therapy. levothyroxine sodium is treatment of choice

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cushing’s syndrome

any disease causing increased cortisol concentrations in the blood

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cushings disease

elevated cortisol due to pituitary dependent hyperadrenocorticism or adrenal dependent hyperadrenocorticism. PDH is most common cause due to an adenoma of pituitary gland

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adrenal gland

small gland lives adjacent to kidneys. cortex produced cortisol, aldosterone, and androgens. medulla produced epinephrine and norepinephrine. controlled by ACTH which is produced by pituitary gland

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adrenal cortex

develops from glandular tissue. outer gland. produces steroid hormones stimulated by ACTH from anterior pituitary

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glucocorticoid hormones

includes cortisol and corticosterone. hyperglycemic effect. catabolism of proteins and lipids, breakdown products converted to glucose in liver. help maintain BP and help body resist the effects of stress

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hyperadrenocorticism

common endocrine disease of dogs caused by excessive circulating cortisol. two types (pituitary dependent and adrenal dependent)

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pituitary dependent hyperadrenocorticism

benign tumor of the pituitary gland causes gland to produce too much ACTH resulting in excess cortisol

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adrenal dependent hyperadrenocorticism

tumor of one of the AGs and it produces a large amount of cortisol

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cortisol

function to help body prepare for fight or flight

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hyperadrenocorticism signs

polyuria, polydipsia, polyphagia, muscle wasting, poor skin condition, pendulous abdomen, chronic infection

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hyperadrenocorticism treatment

meds available to decrease amount of cortisol from adrenal gland. meds vary depending on if patient has PDH or ADH. requires lifelong therapy and regular monitoring

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hypoadrenocorticism

addison’s disease. due to insufficient aldosterone production by adrenal gland. these dogs usually present as an emergency case, in shock, but they can present w chronic GI symptoms, anorexia, PU/PD, hypoglycemic

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mineralocorticoid hormones

aldosterone. regulates levels of some important electrolytes. target organ is the kidney where it causes Na ions to be reabsorbed from urine in exchange for K and H ions. water accompanies Na back into bloodstream

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hypoadrenocorticism symptoms

dehydration, sodium depletion, potassium excess

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heartworm disease etiology

dirofilaria immitis nematode parasite transmitted by mosquitoes

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heartworm lifecycle

microfilaria are ingested by mosquitoes - molt several times in mosquito to L3 stage - L3 larvae enter tissues of host when mosquito bites - L3 mature to L4 in tissues of host in 3-12 d - L4 develop into immature adults about 50-70 days - immature adults migrate to heart and develop to sexually mature worms about 70-120 d - mature worms produce microfilaria about 6 mo post infection

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heartworm pathogenesis

adult worms live in pulmonary vasculature. symptoms result from inflammation in the lungs, increased blood pressure, and R heart failure

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wolbachia pipiens

intracellular endosymbiotic bacteria who lives within the heartworm. releases endotoxins and worsens symptoms of disease. bacteria appears to be necessary for normal maturation and repro of worm

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heartworm clinical signs in dogs

cough, decreased activity, unthrifty appearance, dyspnea, cyanosis, syncope, collapse, ascites

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heartworm clinical signs in cats

cough, dyspnea, vomiting, diarrhea, weight loss. associated w respiratory disease w asthma like symptoms from a secondary allergic response to the worm

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heartworm diagnosis in dogs

ELISA antigen test detects infection 5-6 mo post infection. tests for a protein from mature female worm. microfilaria test in blood test like smear. radiographs to determine stage of disease

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heartworm diagnosis in cats

harder to diagnose bc small worm burdens and male only infections. symptoms, radiographs, ultrasounds. antigen tests have high false negatives, antibody tests indicate exposure but not a definitive test

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heartworm treatment in dogs

curative treatment w injectable meds. treatment of 3 injections over 2 mo period, each followed by strict exercise restriction for 30 days. antibody therapy to remove wolbachia. staging is performed prior to therapy to determine safest approach.

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heartworm treatment in cats

no curative treatment. symptomatic for clinical signs

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heartworm prevention

year round prevention recommended for cats and dogs regardless of housing

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heartworm prevention macrocyclic lactones

ivermectin, moxidectin, milbemycin oxime, selemectin, also target GI nematodes