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731 Cards in this Set
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What is the hypothalamus-pituitary-thyroid axis?
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Hypothalamus: releases TRH which acts on pituitary, Pituitary: releases TSH which acts on thyroid gland, Thyroid gland: releases T3 & T4 which acts (-) on pituitary gland
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Which three affects does T4 and T3 increase?
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1) metabolism
2) oxygen consumption 3) + ionotrope and chronotrope |
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How is thyroid hormone synthesized and released? (3 basic steps)
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1) Iodide oxidation by thyroid peroxidase
2) Formation of iodothyronines in throglobulin: DIT/DIT=T4, DIT/MIT=T3 3) Secretion: endocytosis of colloid |
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What species primarily gets primary hypothyroidism?
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Canine
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How much of the thyroid must be destroyed before clinical signs of primary hypothyroidism present?
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75%
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What are the two most common types of primary hypothyroidism? What is their prevalence?
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Lymphocytic thyroiditis and idiopathic thyroid atrophy: each about 50% of the cases
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What is the etiology of lymphocytic thyroiditis leading to primary hypothyroidism? What percent is immune mediated?
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leakage of thyroglobulin leading to fibrosis and inflammation
42-59% is immune mediated |
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What is the thyroid tissue replaced with in primary hypothyroidism due to idiopathic thyroid atrophy?
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adipose tissue
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What neoplasia is most commonly associated with primary hypothyroidism in canines?
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thyroid adenocarcinoma- non-productive
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What is the most common cause of primary hypothyroidism in cats?
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iatrogenic: due to surgery, I131 and anti-thyroid drugs
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What are the five causes of primary hypothyroidism?
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1) lymphocytic thyroiditis
2) idiopathic thyroid atrophy 3) neoplasia 4) adenomatous hyperplasia 5) Iatrogenic |
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What causes adenomatous hyperplasia leading to primary hypothyroidism?
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intrathyroidal metabolic defect
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What causes secondary hypothyroidism? Common or rare?
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pituitary malformation/neoplasia
Rare |
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What is cretinism? What causes it? Rare or common?
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congenital hypothyroidism
Iodine deficiency--> thyroid dysgenesis, dyshormonogenesis Rare |
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What is the usual signalment of hypothyroidism?
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Middle age: 4-10 (mean 7.2 yr)
Golden Retrievers Spayed and neutered dogs |
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What four breeds of dogs have inherited hypothyroidism?
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Beagle
Danes Borzoi OESD |
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Tragic expression is a classic sign of what endocrine disorder?
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Hypothyroidism
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What are 8 clinical signs of hypothyroidism?
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1) Weight gain
2) Lethargy/mental dullness 3) Dermatological signs 4) Heat seeking/cold intolerance 5) Bradycardia 6) Constipation 7) MM weakness/atrophy 8) Edema |
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What are four additional clinical signs of hypothyroidism?
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1) Infertility
2) Ophthalmologic abnormalities 3) Neurological abnormalities 4) Myxedema (Rare) |
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What are 8 clinical signs of cretinism?
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1) Mental retardation
2) Stunted, disproportionate growth 3) Lg broad heads 4) Megaglossia 5) Hypothermia 6) Delayed dental eruption 7) Ataxia and abdominal distention 8) Derm signs |
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What are three signs of hypothyroidism and cretinism on CBC and Chem?
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1) Mild non-regenerative anemia
2) Fasting hypercholesterolemia 3) Hypertriglyceridemia |
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What causes fasting hypercholesterolemia in a hypothyroidism dog? How many hypothyroidism dogs show this sign?
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Increased concentration of HDLs
75% |
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What causes hypertriglyceridemia in hypothroidism dogs? What can this cause?
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Increased LDL, VLDL and hyperchylomicronemia
Can cause atherosclerosis |
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What is the screening test for hypothyroidism?
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Total T4
Sens: 95%, Spec: 80% |
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What are the two diagnostic tests for hypothyroidism? Which is the Dx test of choice?
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Free T4 by equilibrium dialysis: Test of Choice!!!
TSH |
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What two provocative tests are rarely done to diagnose hypothyroidism?
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1) TSH stim test
2) TRH response test |
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When will a thyroglobulin autoantibody test be positive in a hypothyroid dog?
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In lymphocytic thyroiditis: ~50% of all hypothyroid cases
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What are three procedures to follow if a total T4 comes back elevated in a dog?
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1) anti-T4 antibodies
2) RIA 3) +/- hypothyroidism |
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What syndrome must be ruled out that causes a pseudohypothyroidism?
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euthyroid sick syndrome:
systemic illness causing a decrease in tT4 Occurs in 80% of dogs with severe illness |
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What can cause an artificial low tT4 in dogs? (Iatrogenically) What four kinds?
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Drugs!!
1) steroids 2) phenobarbital 3) antibiotics 4) furosemide |
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How is hypothyroidism treated?
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L-thyroxine
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What are the three causes of feline hypothyroidism? Common or rare?
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1) non-thyroid illness
2) iatrogenic- over tx for hyper 3) congenital: DSH and abyssinian Rare |
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What is the most common endocrine disorder of cats?
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hyperthyroidism
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What is the most common cause of hyperthyroidism in cats?
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adenomatous hyperplasia/adenoma
70% bilateral |
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What disease does hyperthyroidism in cats contribute to? Why?
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Chronic kidney disease:
hypertension--> increased GFR, sclerosis |
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Why does treating hyperthyroid cats risk unmasking of pre-existing chronic kidney disease?
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increases renal hemodynamics therefore displaying clinical signs of CKD
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What is the signalment of cats with hyperthyroidism?
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middle aged to old cats: median is 13 yr
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What effect does hyperthyroidism have on cardiac? DDX?
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thyrotoxic cardiomyopathy: tachycardia, increased R wave, ventricular arrhythmias, conduction abnormalities
Big left ventricle: DDx: hypertrophic cardiomyopathy |
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What can sometimes be felt on physical examination of a hyperthyroid cat?
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thyroid slip
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What are the 5 standards of care (nursing process) by the ANA?
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Assess
Diagnosis Planning Implement Evaluate (ADPIE ) |
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What will be elevated on a Chem of a hyperthyroid cat?
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Liver enzymes (ALT, ALP, LDH, AST)
Glucose Azotemia Phosphorus Bilirubin |
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What are 7 possible ddx for hyperthyroidism in cats?
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1) DM
2) CKD 3) Cardiomyopathy 4) Hepatic insufficiency 5) maldigestion/malabsorption 6) Neoplasia 7) CNS dz |
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What will be seen radiographically on a hyperthyroid cat?
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Mild to severe cardiomegaly
pleural effusion/pulmonary edema |
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What is the diagnostic test of choice for hyperthyroidism?
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high total T4
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Besides total T4, what are five other diagnostic tests for hyperthyroidism?
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1) TSH
2) Free T4 3) T3 suppression test 4) TRH stim 5) TSH response |
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Which test can be done to identify a treatment plan in cats suspected of hyperthyroidism but with no thyroid slip?
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pertechnetate scan
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When is surgery okay to perform on a hyperthyroid cat? What are the complications?
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if its unilateral
complications: hypoparathyroidism--> hypocalcema--> seizures/death |
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What are three medical treatments for hyperthyroidism?
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1) anti-thyroid medication: methimazole/tapazole
2) I-131 3) B-blockers for cardiomyopathy |
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What is the MOA of methimazole? Reversible? Effectiveness?
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blocks hormone synthesis and release: prevents iodine incorporation and inhibits coupling of DIT and MIT
Reversible >99% effective |
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What are the two types of side effects of methimazole?
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reversible and irreversible
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What are the three reversible side effects of methimazole? How are they treated?
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1) anorexia
2) lethargy 3) vomiting stop tx for a few days then reinstate at lower dose |
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What are the 5 irreversible side effects of methimazole? How are they treated?
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1) facial excoriations
2) bleeding diathesis 3) hepatopathy 4) MG 5) cold agglutinin-like disease Stop Methimazole!!!! |
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How does methimazole effect ANA?
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Causes positive ANA
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How does I-131 radioiodine therapy treat hyperthyroidism?
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selectively destroys active thyroid tissue while normal tissue is preserved do to atrophy from negative feedback
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What must occur prior to I-131 treatment for hyperthryoidism?
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methimazole trial for at least 1 month: tT4 in lower 1/2 range with USG
discontinue 2 weeks before I-131 |
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What usually causes hyperthyroidism in dogs? What is the most common type?
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thyroid tumors: large, nonfunctional, invasive follicular carcinomas
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What is the prognosis of thyroid follicular carcinomas causing hyperthyroidism? What is a common characteristic of this tumor?
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poor
BLEED (even with FNA) |
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In treating canine thyroid neoplasia, what is the usual affect?
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palliative relief
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What is the definition of diabetes mellitus (simple!)?
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starvation in the face of excess
persistent hyperglycemia |
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What are two causes of diabetes mellitus?
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1. lack of insulin
2. inability of insulin receptors to respond to simulation |
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Endocrine Pancreas: What do these cells produce?
1. beta cells 2. alpha cells 3. delta cells 4. PP cells 5. D Cells |
1. insulin
2. glucagon 3. somatostatin 4. pancreatic polypeptide 5. vasoactive intestinal peptide |
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What are the two types of diabetes mellitus?
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1. spontaneous
2. secondary |
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What type of diabetes mellitus are usually in skinny dogs and cats?
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Type I spontaneous: IDDM/juvenile onset
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What type of diabetes mellitus are usually in fat cats?
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Type II spontaneous: NIDDM/adult onset
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What causes secondary diabetes mellitus?
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insulin antagonists
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What two dog breeds are predisposed to getting diabetes mellitus? Age? Sex?
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dachshunds and poodles: middle aged to older
Females 4x more likely |
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What may be the initial sign of diabetes mellitus in dogs?
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cataracts
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In cats what may be the initial sign of diabetes mellitus?
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peripheral neuropathy: plantigrade stance
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What are four causes of diabetes mellitus in dogs?
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1. chronic pancreatic inflammation
2. pancreatic atrophy 3. immune mediated destruction of the b cells 4. transient: pregnant and diestrus |
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What are five causes of DM in cats?
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1. chronic insulin resistance w/ beta cell exhaustion
2. pancreatic amyloidosis 3. increased basal hepatic glucose production 4. obesity 5. glucose toxicity |
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What clinical signs will be seen in a non-ketotic stable DM? (4)
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weight loss
polyphagia PU/PD cataracts: dogs |
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What clinical signs will be seen in a ketoacidotic DM? (5)
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weight loss
PU/PD dehydration labored breathing lethargy/collapse/stupor |
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What clinical signs will be seen in a non-ketotic hyperosmolar DM?
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all signs of ketoacidotic DM
decreased GFR blood glucose is high chronically |
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What will happen if fluids are given too fast to a non-ketotic hyperosmolar DM animal?
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hydrocephalus
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What BG will be seen on a dog with DM?
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BG> 200mg.dL
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What BG will be seen on a cat with DM? Why may cats have a false positive?
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BG > 300mg/dL
cats can have a severe stress hyperglycemia-- must do repeat measurements |
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What thyroid test should be done to all cats >6?
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total T4
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What thyroid test should be done to dogs? Why may dogs have low T4?
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free T4 and TSH
Due to euthyroid sick syndrome |
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What is really important when treating DM and giving fluids?
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Must give potassium: normal K and P on chemistry but total body stores are usually low
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What test should always be done on urine with DM?
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urine culture
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What two ketoacids are detected on a urine dipstick? What one ketoacid is not detected on urine dipstick?
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acetone and acetoacetate
B hydroxybutrate |
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Why do neutrophils have decreased function with DM?
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persistent hyperglycemia neutralizes neutrophils
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What diagnostic test can be used instead of glucose curves on stable DM? How long does it take?
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Serum fructosamine: 2-3 weeks
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What is the draw back of glucotest?
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can only be used in a single cat household- tests urine in litter box
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What is the mainstay management for all dogs and most cats with DM? What are the goals?
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insulin therapy
decrease c/s, decrease BG |
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What species does bovine insulin work with? Porcine?
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cats/cows
puppies/pigs |
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What species does NPH insulin work with?
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economical for large dogs: intermediate acting
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What insulin should be used on cats?
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glargine/lantus: ultra long acting
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What insulin should be used for emergency treatment of ketoacidosis?
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regular insulin
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What are changes in NPH insulin doses based on?
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nadar (low point) of the blood glucose curve
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What is the best way to determine effectiveness of insulin in treating DM?
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glucose curves
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What are adjustments of glargine/lanutus based on in DM patients?
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pre-insulin BG levels: ACME (NOT nadar)
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What insulin can possibly cause remission of DM?
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glargine/lantus: after a minimum of 2 weeks of therapy
pre insulin BG is <180 decrease to Q24h, if stay below 180 discontinue and monitor |
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What is glucose toxicity? What will lead to a better prognosis?
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persistent hyperglycemia that inhibits release of insulin from B cells
hyperglycemia resolves quickly enough B cells can regain function: CATCH QUICKLY |
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What diet is important for DM dogs? cats?
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dogs: high fiber
cats: low carbs/high protein |
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What will oral hypoglycemics in cats do? What are four types of oral hypoglycemics?
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make hyperglycemic cats LESS hyperglycemic- NOT normal
sulfonylureas, biguanides, thiazolidinediones, transition metals |
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What is important to remember when mixing insulin?
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roll dont shake
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How are DM initially evaluated following insulin treatment?
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Monitor BG Q2-4 hr for first 12-24 hrs
BG curve in 1 wk Curve 5-6 days after any changes in insulin dosage |
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When is insulin decreased or discontinued in cats with DM?
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BG <70 at anytime OR pre-insulin BG <180 mg/dL
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What three behavioral changes will be seen in a DM patient gone hypoglycemic?
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1. ataxia
2. pyrexia 3. ptyalism |
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How are blood glucose curves performed? What are the glucose nadirs for dogs and cats?
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BG Q2h for 12-24 hrs: if BG <125 d Q1h measurements
dogs: 120-300, cats: 70-180 |
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What is an indication of insulin resistance in DM?
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> 2 U/kg and still unregulated
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What are three concurrent diseases dogs get with DM?
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1. hyperadrenocorticism
2. hypothyroidism 3. chronic pancreatitis |
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What are three concurrent diseases in cats with DM?
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1. hyperthyroidism
2. acromegaly 3. hypoadrenocorticism |
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What is the Somogyi effect in animals with DM?
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If the body has periods of hypoglycemia, you will see rebound HYPERglycemia
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What causes the somogyi effect in DM animals?
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the glucose gets so low that the body activates every anti-insulin hormone: cortisol, growth hormone, ACTH, epinephrine
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In typical hypoadrenocorticism, what are the deficiencies? What is atypical?
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both mineralcorticoid and glucocorticoid
Glucocorticoid only |
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Hypoadrenocorticism: what is the usual signalment?
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young (<4 yrs), females, poodles
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Hypoadrenocorticism: What is a major ddx?
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Renal disease: Low sodium, high potassium- "the great pretender"
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Hypoadrenocorticism: What are mineralcorticoids controlled by?
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renin-angiotensin-aldosterone
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Hypoadrenocorticism: What are the cardinal chronic clinical signs?
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waxing and waning, vomiting and diarrhea
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Hypoadrenocorticism: What will be ABSENT on the CBC?
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a stress leukogram
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Hypoadrenocorticism: What do mineralcorticoids normally do? Glucocorticoids?
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Mineral: Keep Na, Ca and water and dump K
Gluco: Deals with stress |
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Hypoadrenocorticism:What can be seen on a sodium potassium ratio on a positive case? What type will this be suggestive of?
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<27:1
Typical: seen with mineralcorticoid deficiency, will miss atypical |
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Hypoadrenocorticism: Is sodium potassium ratio a diagnostic test?
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NO- only suggestive
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Hypoadrenocorticism: What parasite causes pseudohypoadrenocorticism?
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whipworms
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Hypoadrenocorticism: What three clinical signs will be seen on radiographs?
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1. microcardia
2. hypocirculation 3. esophageal dilation |
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Hypoadrenocorticism: What three signs will be seen on ECG? What causes these changes?
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1. tall tented Ts
2. Absent Ps 3. Prolonged QRS Hyperkalemia |
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Hypoadrenocorticism: What is the diagnostic test of choice?
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ACTH stimulation
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Hypoadrenocorticism: What test differentiates between primary and secondary and atypical?
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Endogenous ACTH concentration
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Hypoadrenocorticism: What are two medications to treat chronic cases?
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oral steroids and mineralcorticoid supplementation
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Hypoadrenocorticism: What oral steroid is used?
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Low dose prednisone: will not suppress endogenous hormone levels
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Hypoadrenocorticism: What are two types of mineralcorticoid supplements?
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1. Fludrocortisone: both MC and GC
2. DOCP: MC only |
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What causes secondary hypoadrenocorticism? How does this present?
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acute glucocorticoid withdrawal: rapid steroid withdrawal
presents with signs of HYPERadrenocorticism |
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Why does secondary hypoadrenocorticism present with small adrenals?
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negative feedback: causes ACTH to stop which shrinks the adrenals
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Secondary hypoadrenocorticism: How will the electrolytes present? Endogenous ACTH concentration?
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Electrolytes: Normal- b/c they do not have the mineralcorticoid issue
ACTH: Low |
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Secondary hypoadrenocorticism: Treatment?
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glucocorticoids
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Secondary hypoadrenocorticism: Prognosis?
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adrenal glands will most likely recover
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What do pheochromocytomas produce? Where will these tumors present?
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excessive catecholemines: epinephrine and norepinephrine
medullary tumor of adrenal glands |
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What is the primary diagnostic tool for pheochromocytomas? What is the ultimate diagnosis?
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repeated BP measurements
histopath |
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What is the treatment for pheochromocytomas?
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adrenalectomy: if bilateral must treat for hypoadrenocorticism
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What is the most common endocrinopathy of dogs?
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hyperadrenocorticism
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What are the three types of hyperadrenocorticism? What do 85% of dogs get?
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1. pituitary dependent
2. adrenal tumor 3. Iatrogenic pituitary dependent |
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Hyperadrenocorticism: What percent of adrenal tumors are benign?
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50/50 benign malignant
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Hyperadrenocorticism: What percent of overall cases are iatrogenic?
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50%
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Hyperadrenocorticism: What is the most important clinical sign that could potentially cause renal failure?
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proteinuria
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Hyperadrenocorticism: What skin condition can be a clinical sign? When will this be seen?
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calcinosis cutis: appear after steroid cessation in iatrogenic
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Hyperadrenocorticism: What will be seen on a CBC?
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stress leukogram and thrombocytosis
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Hyperadrenocorticism: What four values will be elevated on a chemistry?
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1. glucose
2. ALT 3. cholesterol 4. SLP |
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Hyperadrenocorticism: What are the two screening tests?
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1. chemistry: high ALP
2. urine cortisol/creatinine ratio- if normal NOT cushings, if positive: could be anything! |
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Hyperadrenocorticism: What are the two diagnostic tests?
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1. ACTH stimulation test
2. Low-dose dexamethasone suppression test |
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Hyperadrenocorticism: What are the two differentiation tests?
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1. high-dose dexamethasone suppression test
2. endogenous ACTH concentration |
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Hyperadrenocorticism: What is the only test that can diagnose iatrogenic?
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ACTH Stimulation test
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Hyperadrenocorticism: How do you interpret LDDST?
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Look at 8hr
Normal: 4hr: >50% suppression, 8hr: <40nmol/L PDH: 4hr: >50% suppression, 8hr: >40nmol/L PDH/AT: 4hr: <50% suppression, 8hr: >40nmol/L |
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Hyperadrenocorticism: How is the ednogenous ACTH concentration interpreted? What must be in tube to run a eACTH concentration?
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eACTH: normal to high= PDH
eACTH: low= AT aprotinin to prevent breakdown |
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Hyperadrenocorticism: How will PDH appear on U/S? AT?
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PDH: bilateral adrenal enlargement
AT: unlilateral mass near kidney: liver metastasis, caval invasion |
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Hyperadrenocorticism: What are four drugs used to treat?
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1. mitotane/lysodren
2. trilostane/vetoryl 3. ketoconazole 4. selegeline/L-Deprenyl |
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Hyperadrenocorticism: What is a possible complication for doing neurosurgery on a PDH?
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ADH problems: diabetes insipitus: usually transient because hypothalamus makes ADH
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Hyperadrenocorticism: What is the MOA of mitotane/lysodren? Side effects
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selectively destroys zonae fasciculata and reticularis
Side effects: vomiting, anorexia, aldosterone effected |
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Mitotane/lysodren: How long is the loading dose? What are the signs of a response?
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maximum of 8 days or until response
decreased appetites, vomiting, diarrhea, listlessness, PU/PD |
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Mitotane/lysodren: What do you do following a loading dose?
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Do an ACTH stimulation test then start on maintenance dose
Recheck ACTH at 1 mo, 3 mo, 6 mo |
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Mitotane/lysodren: What is it best used to treat? What is the goal?
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adrenal tumors
Goal is to destroy adrenals |
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Mitotane/lysodren: How do you treat differently if patient concurrently has DM with cushings?
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Lower dose and concurrent treatment with pred
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Trilostane: MOA?
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Competitively inhibits 3-B hydroxysteroid dehydrogenase: inhibit cortisol and aldosterone synthesis
Does NOT destroy adrenal gland |
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Trilostane: reversible?
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YES
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Trilostane: When should you recheck ACTH? How does this effect serum electrolytes?
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In 14 days- 4-6 hrs post pill
interferes with aldosterone: check potassium |
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Ketoconazole: MOA
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inhibits numerous steps in steroid biosythesis
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Ketoconazole: When should this drug be used?
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Dogs that cannot handle mitotane or trilostane AND pre-surgically for AT pts to stabilize
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Selegilene/Anipryl: MOA
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increases dopamine from the hypothalamus to the intermediate lobe: decrease ACTH
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Selegilene/Anipryl: What patients will this work on?
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Animals with an intermediate lobe tumors
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Hyperadrenocorticism: When is radiation therapy indicated? Prognosis?
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if neurological signs are present
33% worsen, improve short term, improve long term |
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Hyperadrenocorticism: What three things will be in excess in adrenocortical tumors?
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1. glucocorticoid excess
2. mineralocorticoid excess: Conn's syndrome 3. Sex hormone excess: feminization |
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Hyperadrenocorticism: In adrenocortical tumors, what species commonly has feminization?
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ferrets
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Hyperadrenocorticism: Adrenocortical tumors: Treatment?
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surgical removal and Mitotane
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Hyperadrenocorticism: In felines, what is a unique clinical sign?
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markedly thin skin
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Feline Hyperadrenocorticism: What types of diabetic are these usually?
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insulin resistant diabetic w/o acromegaly
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Feline Hyperadrenocorticism: What are two diagnostic tests that can diagnose? Treatment?
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1. ACTH stimulation test
2. serum chemistry: NO ALP elevation Adrenalectomy |
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What species normally gets insulinomas?
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ferrets
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Insulinomas: What are three clinical signs?
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1. weakness
2. good appetite 3. seizures: drooling |
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Insulinomas: What will be apparent on a chemistry?
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fasting hypoglycemia, severely low glucose: insulin levels measured with a BG of <40mg/dL
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Insulinomas: Are tumors visible on U/S?
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NO
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Insulinomas: What are the treatment options? Best option?
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Surgical and medical: pred, diazoxide, streptozotocin
Pred and surgery |
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Insulinomas: Prognosis?
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guarded to poor: often have metastasized at time of diagnosis
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What is zollinger-ellison syndrome?
|
gastrinomas
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Gastrinomas: What is elevated on serum?
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gastrin levels
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Gastrinomas: What are the treatments? (3)
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1. proton pump inhibitors: omeprazole
2. sucralfate: band-aid to ulcers 3 surgery: tumor removal +/- gastrectomy |
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What three hormones are released from the parathyroid?
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1. parathyroid hormone: produced by chief cells and stimulated in response to low Ca
2. Calcitonin: Produced by C cells: lowers Ca 3. Vit D |
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Where is cholecalciferol originated? 25-hydroxycholcalciferol? 1,25, dihydroxycholecalciferol?
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Dietary vitamin D3
Liver Kidney |
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What causes primary hyperparathyroidism?
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benign adenoma
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What clinical sign can be seen in the urinary tract when a patient has hyperparathyroidism?
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Ca urolithiasis
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Hyperparathyroidism: Diagnosis?
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elevated PTH is the face of elevated Ca
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Hyperparathyroidism: What should be always be evaluated?
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ionized Ca
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Hyperparathyroidism: What should be ultrasounded?
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neck: can often ID the affected glands
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Hyperparathyroidism: Treatment?
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surgical excision
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Hyperparathyroidism: What is important on post operative management?
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Make them hypocalcemic until remaining parathyroid escape suppression: monitor Q2-4 hrs
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What is the first sign of hypocalcemia? How do you treat if this happens?
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itchy face!!!
IV calcium gluconate |
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Hyperparathyroidism: When should calcitriol be given in relation to surgical excision?
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the day of or one day before surgery
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Renal Secondary Hyperparathyroidism: What usually causes this disease?
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chronic kidney disease: Low calcium triggers elevated PTH
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Renal Secondary Hyperparathyroidism What is a clinical sign?
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Demineralized bone: teeth falling out
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Renal Secondary Hyperparathyroidism: Treatment?
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1. treat CKD
2. Normal Ca/Phos: <70 3. Calcitriol therapy: if Pho <6 |
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Hypoparathyroidism: What causes this?
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immune mediated destruction of parathyroids: lymphocytic parathyroids
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Hypoparathyroidism: What are the c/s?
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Related to hypocalcemia: muscle fasciculation and cramps, seizures, itchiness, cataracts, diaphragm contractions concurrent with heartbeat- "thumps"
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Hypoparathyroidism: How is this diagnosed? (3)
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1.decreased total and ionized calcium
2. increased phosphorus 3. decreased iPTH |
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Hypoparathyroidism: Treatment?
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IV calcium, oral calcitriol, oral calcium supplements
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Diabetes Insipidus: What are the characteristics of this disease?
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1. decrease in ADH/VP: secondary to pituitary tumor
2. decrease in receptors |
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Diabetes Insipidus: What is the quantified water intake usually seen?
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>100 ml/kg/day
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Diabetes Insipidus: Can this be diagnosed easily?
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NO: Cannot diagnose until all other excluded: final 3 rule outs: CDI, NDI, psychogenic polydipsia
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Diabetes Insipidus: What are the two diagnostic tests?
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1. DDAVP response test
2. Water deprevation test |
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Diabetes Insipidus: DDAVP Response test: How are the results interpreted?
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-Decrease in water intake and >50% increase in USG= CDI and PP
-moderate response= partial CDI -No response= NDI |
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Diabetes Insipidus: Two types? (should have been said earlier....)
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1. Central= CDI
2. Nephrogenic= NDI |
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Nephrogenic Diabetes Insipidus: What are the three ways to treat primary?
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1. thiazide diuretics: increase Na reapsorption
2. low salt diet 3. decreased water intake to only 2x normal |
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What is SIADH?
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syndrome of inappropriate ADH release
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What are the usual C/S of chemistry of SIADH?
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severe hyponatremia: normal renal and adrenal function
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What are the catabolic actions of growth hormone? This causes what three actions?
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insulin antagonist: three actions
1. stimulates gluconeogenesis 2. promotes lipolysis 3. hyperglycemia and ketogenesis |
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What are the anabolic actions of growth hormone? (2)
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1. IGF-1
2. stimulate protein synthesis and growth promotion |
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What canine species normally gets dwarfism?
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german sheperds
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How is dwarfism diagnosed? (3)
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1. basal IGF-1
2. thyroid testing: (diffferentiate from creatinism) 3. open epiphysis in older dogs |
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How is dwarfism treated?
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hGH
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What causes Acromegaly?
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GH excess
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What is the usual signalment of acromegaly?
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Cats: Male older
Dog: Intact female, older |
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What disease will 100% of acromegaly cats have?
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DM- uncontrollable
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What conformational alterations will acromegaly patients have?
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big heads, big interdental spaces, prgnathism
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What clinical signs will acromegaly patients have? (2)
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1. gaining weight in face of DM
2. inspiratory stridor |
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How do are acromegaly patients treated? (2)
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1. Spay
2. radiation therapy: if pituitary disease |
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Oncology
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Oncology
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When normal cells are subjected to stress signals, DNA damage, or oxygen depletion, what occurs?
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1. undergo cell cycle arrest in G1, S, G2
2. undergo programmed cell death |
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What are the three steps in the carcinogenic cascade of cells?
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1. initiation
2. promotion 3. progression |
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What is initiation of the carcinogenic cascade of cells?
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Rapid step: application of a carcinogen to tissue
If cell DOES NOT repair the damage then promotion may occur, if cell DOES repair the damage then no further consequence |
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What occurs in the promotion step in the carcinogenic cascade of cells?
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2nd mutation that adds to the cells ability to "out-compete" its neighbor= expansion of the cell line
VERY SLOW STEP |
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What occurs in the progression step of the carcinogenic cascade of cells?
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Reinforces the cell's malignant potential allowing invasion, tissue destruction and metastasis
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What is responsible for controlling cell prliferation in cells wild-type state?
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cancer genes: oncogenes and tumor suppressor genes
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What is proto-oncogenes?
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oncogenes that do NOT have the potential to form tumors in their normal state but if altered can lead to malignancy
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What are proto-oncogenes usually involved in controlling? Examples?
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cell growth and proliferation
growth factors, growth factor receptors: c-kit, protein kinases. etc |
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What type of mutations produce oncogenes?
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Involve a dominant gain of function- only one allele is required to cause effect
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What is the overall effect of oncogenes?
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OVERSTIMULATION of cell growth
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In normal cells, what are tumor suppressor genes responsible for?
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inhibiting cell growth
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What does loss of function of tumor suppressor genes via mutation leads to what?
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loss of inhibitory signals= uncontrolled cell grwoth
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What is the overall effect of tumor suppressor gene mutation?
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loss of INHIBITORY function on cell growth
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What are the siz alterations in cell physiology that collectively cause malignancy, AKA "hallmarks of cancer"?
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1. self sufficient growth
2. insensitive to anti-growth signals 3. evading normal cell death 4. limitless potential to divide 5. sustained angiogenesis 6. tissue invasion and metastasis |
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What are the three routes by which metastasis can occur?
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1. hematogenous
2. lymphatic 3. peritoneal seeding |
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Is tumor growth rate constant?
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NO
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What is tumor growth characterized by?
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Gompertzian growth kinetics: tumor growth fraction is not constant and growth increases exponentially over time, then plateaus
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What does the response of the tumor to radiation and chemotherapy dependent on?
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where the tumor is on the growth curve:
-growth fraction is low= fraction of cells killed is small |
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What is skipper's log kill hypothesis?
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A constant FRACTION of cells are killed by a given dose of chemotherapy and proliferation of surviving cells will take place between treatments
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What are the three tumor cell types?
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1. mesenchymal
2. epithelial 3. round |
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Mesenchymal cell type:
1. nucleus? 2. cytoplasm? 3. exfoliate? 4. cancer type? |
1. round to ovoid
2. spindle or fusiform- wispy tails 3. poorly- individually 4. sarcoma |
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Epithelial cell type:
1. nucleus? 2. cytoplasm? 3. exfoliate? 4. cancer type? |
1. round
2. round, ovoid, angular 3. well- sheets and clumps 4. carcinoma, adenocarcinoma **may form ducts or acini |
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Round cell type:
1. nucleus? 2. cytoplasm? 3. exfoliate? 4. cancer type? |
1. round
2. round, scant to moderate 3. well- individually "discrete"-- mast cell 4. lymphoma, transmissible venereal tumor, plasmacytoma, histiocytoma, mast cell tumor |
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What are 7 criteria for malignancy? What is more reliable?
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1. pleomorphism of cell size, shape
2. high or variable nuclear to cytoplasmic ratio 3. anisokaryosis 4. coarse nuclear chromatin clumping 5. nuclear molding 6. multinucleation 7. abnormal mitotic figures or increased numbers of mitotic figures ** Nuclear more reliable than cytoplasmic |
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What is the only type of tumor that gets biopsied from the center? Where are all other tumor biopsies taken from?
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osteosarcoma
the edge |
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Where are the three sites of bone marrow biopsies?
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1. proximal humerus
2. proximal femur 3. ileal wings |
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When is bone marrow examination indicated?
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pursue causes of unexplained
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What are the two advantages of bone marrow aspirate?
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1. critically differentiate and evaluate individual cells and cell pipilations
2. cheaper |
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What are the two disadvantages of bone marrow aspirate?
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1. cannot assess tissue architecture
2. may be hard to differentiate poorly cellular BM vs poor sample |
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What are the two advantages of bone marrow core biopsy?
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1. assess tissue architecture, necrosis, infiltrative patterns, myelofibrosis
2. better assessment of BM cellularity and megakaryocyte number |
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What are the two disadvantages of bone marrow core biopsy?
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1. more expensive
2. more difficult to differentiate cells |
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What must also be submitted along with a bone marrow sample?
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CBC
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What are three types of bone marrow hyperplasia?
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1. erythrocyte
2. granulocytic 3. megakaryocytic |
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What are three causes of effective erythropoesis leading to erythrocyte hyperplasia?
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1. secondary to blood loss
2. appropriate erythrocytotic disorders: right to left shunts, chronic pulmonary dz, hyperthyroidism 3. inappropriate erythrocytotic disorders: renal neoplasms, cysts, other dz |
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What are two causes of ineffective erythropoiesis leading to erythrocyte hyperplasia?
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1. immune mediated non-regenerative anemia
2. nutritional deficiency: iron, coper, folate, vit B12 |
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What are two types of animals that get cyclic hematopoiesis leading to erythrocyte hyperplasia?
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1. grey collies
2. FeLV infected cats |
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What are two mechanisms that could lead to granulocytic hyperplasia?
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1. effective granulopoiesis
2. ineffective granulopoiesis |
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What are five causes of effective granulopoiesis leading to granulocytic hyperplasia?
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1. inflammatory
2. paraneoplastic 3. neutrophilia of leukocyte adhesion deficiency 4. early estrogen toxicity 5. cyclic hematopoiesis |
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What are two causes of ineffective granulopoiesis leading to granulocytic hyperplasia?
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1. immune neutropenia
2. chronic idiopathic neutropenia |
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What are two causes leading to megakaryocytic hyperplasia?
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1. recovery from thrombocytopenia: IMHA
2. inflammation |
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What are the recommendations of chemotherapy if a dog tests positive as a double mutant for WSU?
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25% dose reduction of vincas
50% dose reduction of doxorubicin |
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What are the GI side effects of chemotherapy?
|
damage to intestinal epithelial cells- crypt cells: inappetence, nausea, vomiting, diarrhea
3-5 days post tx Efferent nervous stimulation of the CTZ: during or immediately after treatment= cisplatin |
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What is the treatment for chemotherapy induced nausea?
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1. supportive care
2. metaclopramide 3. ondansetron 4. maropitant: cerenia 5. mirtazapine 6. prednisone |
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How is chemotherapy induced diarrhea treated?
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1. supportive care
2. fluid therapy 3. bland diet 4. metronidazole 5. loperamide |
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How does chemotherapy cause myelosuppression?
|
damage to rapidly dividing bone marrow stem cells= cells with short lifespan most susceptible
neutropenia/thrombocytopenia |
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How is chemotherapy induced myelosuppression treated? When should you treat neutropenia?
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hospitalization, fluids inappetance
Tx for neutropenia: concurrent fever, lethargy, inappetance |
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Chemotherapeutics: Alkalating agents: MOA?
|
bind to DNA strands-> inserts alkyl group= changes structure of DNA to interfere w/ transcription, replication, repair machinery= inhibits DNA, RNA, and protein synthesis
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Chemotherapeutics: Alkalating agent: What are the four types?
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1. chlorambucil (leukeran)
2. cyclophosphamide (cytoxan) 3. melphalan 4. CCNU (lomustine, Cee-NU) |
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Chemotherapeutics: Alkylating agents: What is the most common side effects?
|
myelosuppression
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Chemotherapeutics: Cyclophosphamide: What is the unique toxicity?
|
sterile hemorrhagic cystitis
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Chemotherapeutics: CCNU: What is the common toxicity?
|
delayed BM- esp. in cats
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Chemotherapeutics: CCNU: What is the unique toxicity?
|
Dog: hepatotoxicity
Cat: pulmonary toxicity |
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Chemotherapeutics: CCNU: What is the unique characterisitc?
|
crosses the BBB
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Chemotherapeutics: Platinum agents: MOA
|
heavy metal, binds within and btwn DNA strands= inhibits protein synthesis
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Chemotherapeutics: Platinum agents: What are the two types?
|
1. cisplatin
2. carboplatin |
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Chemotherapeutics: Cisplatin: What is the unique toxicities?
|
acute emesis, nephrotoxicity, ototoxicity, neurotoxicity
CATS: FATAL PULMONARY EDEMA ***Dogs: require saline diuresis to prevent renal toxicity |
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Chemotherapeutics: Cisplatin: What species should you not use this on?
|
Cats
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Chemotherapeutics: Carboplatin: How does it compare with cisplatin?
|
less nephrotoxic and safe to use in cats- does nto require saline diuresis
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Chemotherapeutics: Antimetabolites: MOA? Cell cycle phase?
|
structurally similar to natural compounds required for synthesis of purines, pyrimidines, and nucleic acids= interfering with DNA synthesis
*** S |
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Chemotherapeutics: What are the three types?
|
1. cytosine arabinoside
2. 5-fluorouracil 3. azathioprine |
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Chemotherapeutics: Cytosine arabinoside: What is a unique characteristic?
|
short 1/2 life, crosses BBB
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Chemotherapeutics: 5-fluorouracil: What is a unique toxicity?
|
Fatal neurotoxicity in CATS
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Chemotherapeutics: Azathioprine: What is this agent used for?
|
immunosuppression
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Chemotherapeutics: Antitumor antibodies: MOA
|
causes DNA damage by free radical formation and/or interference with topoisomerase II
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Chemotherapeutics: Antitumor antibodies: What are the three types?
|
1. doxorubicin
2. mitoxantrone 3. actinoycin-D (dactinomycin) |
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Chemotherapeutics: Doxorubicin: What are four unique toxicities?
|
1. Cumulative dose= cardiotoxicity (DCM)= DOGS
2. Nephrotoxicity= CAYS 3. Mast cell degranulation and anaphylaxis 4. severe tissue vesicants |
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Chemotherapeutics: Actinomycin-D: What is a unique toxicity?
|
tissue vesicant
|
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Chemotherapeutics: Vinca alkaloids: MOA? Cell cycle phase?
|
inhibits formation of microtubules- prevents microtubule assembly
M |
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Chemotherapeutics: Vinca alkaloids: What is the main toxicity?
|
Nephrotoxicity
vincristine>vinblastine>vinorelbine |
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Chemotherapeutics: VInca alkaloids: What are the three types?
|
1. vinblastine
2. vincristine 3. vinorelbine |
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Chemotherapeutics: Vinblastine: What is the three unique toxicities?
|
1. tissue vesicant
2. autonomic dysfunction 3. neurotoxicity |
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Chemotherapeutics: What can cure TVT?
|
vincristine
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Chemotherapeutics: Vincristine: What is three unique toxicities?
|
1. tissue vesicant
2. neurotoxicity: peripheral neuropathy 3. autonomic neuropathy |
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Chemotherapeutics: Paclitacel: MOA? Cell cycle phase? Unique toxicity?
|
prevents microtubule DISASSEMBLY
M hypersensitivity reaction |
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Chemotherapeutics: L-asparaginase: MOA? Cell cycle phase?
|
bacteria derived enzyme that degrades the amino acid asparagine, depriving growing cells of asparagines and inhibiting protein synthesis
G1 |
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Chemotherapeutics: L-asparaginase: What are the two unique toxicities?
|
1. hypersensitivity
2. pancreatitis: RARE |
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Chemotherapeutics: palladia: MOA?
|
inhibits receptor tyrosine kinase c-kit which is frequently mutated in higher grad II and III MCTS- also inhibits PDGFR and VEGFR
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Chemotherapeutics: Palladia: What is the primary toxicity?
|
GI
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Chemotherapeutics: Kinavet: MOA?
|
inhibits receptor tyrosine kinase c-kit which is frequently mutated in higher grade II and III MCTs, also inhibits PDGFR
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Radiation Therapy: What is teletherapy?
|
external beam radiation therapy: deliver radiation from machine to patient
|
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Radiation Therapy: What is brachytherapy?
|
shallow penetration, implanted: delivers high doses to very localized areas
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Radiation Therapy: What is systemic therapy?
|
systemic radioactive substances
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Radiation Therapy: What is the most radiosensitive part of the cell that is susceptible to ionizing radiation?
|
DNA
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Radiation Therapy: Ionizing radiation: What is the MOA?
|
direct: electron interacts directly with DNA
indirect: free radical formation |
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Ionizing radiation: What is the goal?
|
destory reproductive capability of tumor cells, w/o excessive damage to normal tissues
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Radiation Therapy: What are the four factors that influence tumor control?
|
1. repair
2. redistribution: most sensitive- M, most resistant- late S 3. reoxygenation 4. repopulation |
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Radiation Therapy: Why are small doeses per fraction given?
|
allows for higher total dose w/o increasing late side effects
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Radiation Therapy: Early Effects: When does this occur? What tissues are effected?
|
During/shortly after therapy
rapidly proliferating tissues: oral mucosa, intestinal epithelium, epithelial structures of eye and skin |
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Radiation Therapy: Late Effects: What tissues are effected? What are the possible effects to these tissues?
|
slow proliferating tissues: bone, lung, heart, kidneys, spinal cord
fibrosis, necrosis, loss of fxn, death |
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What are the four types of canine oral tumors?
|
1. melanoma
2. SCC 3. fibrosarcoma 4. epulis |
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Canine Melanoma: How common? Metastasis? Chemo response? Radiotherapy response?
|
Most common canine oral tumor
90% metastasis Does not respond to chemo RT: good response rate |
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Canine SCC: Metastasis? RT response?
|
Uncommon: unless tonsillar
72% respond to RT |
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What are the two types of feline oral tumors?
|
1. SCC
2. fibrosarcoma |
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Feline SCC: RT response?
|
Poor- difficult to excise due to extensiveness
|
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What are the three main types of canine nasal tumors?
|
1. adenocarcinoma (ACA)
2. carcinoma (CA) 3. sarcoma (SC) |
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Canine nasal tumors: metastasis? Which one has the worst prognosis?
|
Uncommon- locally invasive
Sarcomas |
|
|
What is the main types of feline nasal tumor?
|
lymphosarcoma (LSA)
|
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|
What is one of the most common canine malignancies and the most common hematopoietic tumor in dogs?
|
canine lymphoma
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Canine lymphoma: What are five high risk breeds? Two low risk breeds?
|
boxer, bassets, scottie, airedale, bulldog
dachshund, pomeranian |
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Canine lymphoma: What is the most common anatomic form?
|
multicentric
|
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Canine lymphoma: What is the most common sign of abdominal organ involvement with the multicentric form?
|
hepatosplenomegaly
|
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Canine lymphoma: What is the most common paraneoplastic syndrome?
|
anemia: nonregenerative, normocytic, normochromic
|
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Canine lymphoma: What abnormality is normally seen on a biochemistry?
|
hypercalcemia
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Canine lymphoma: What clinical signs may be seen (4)?
|
1. monoclonal gammopathies
2. neuropathies 3. fever 4. cachexia |
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Canine lymphoma: What are the five stages? What are the two substages?
|
I: single node or lymphoid tissue in a single organ (not BM)
II: LNs in regnial area (cr or ca to diaphragm) III: generalized lymphadenopathy (both cr and ca to diaphragm) IV: liver and/or spleen involvement V: blood/BM or other organ systems Substages: a= no clinical signs b= clinical signs |
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Canine lymphoma: What clinical signs will be seen in a substage b?
|
PU/PD, lethargy, anorexia, intolerance to exercise
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Canine lymphoma: What substage has the better prognostics?
|
a
|
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Canine lymphoma: What are the four locations that are thought to have a worse prognosis?
|
1. cutaneous (diffuse)
2. alimentary 3. mediastinal 4. CNS |
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Canine lymphoma: What immunophenotype has a better prognosis?
|
B cell better than T cell
|
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Canine lymphoma: What two other factors lead to a better prognosis?
|
1. prior glucocorticoid therapy- development of MDR
2. response to treatment |
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Canine lymphoma: What are the two ways to treat?
|
1. glucocorticoids
2. combination chemotherapy |
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Canine lymphoma: Why is combination chemotherapy a good treatment?
|
different mechanisms or action so tolerable to the dog. Together used at maximum tolerable doses and do not have overlapping toxicities
|
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Canine lymphoma: What are the two combination chemotherapy protocols?
|
1. CHOP
2. COP |
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Canine lymphoma: What does CHOP chemo mean?
|
C: cyclophosphamide
H: hydroxyldaunorubicin O: oncovin P: prednisone +/-asparaginase |
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Canine lymphoma: What does CNS location cause in clinical signs? Treatment?
|
multifocal or solitary leading to seizures, paresis, paralysis
Chemotherapeutics that cross the BBB |
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Canine lymphoma: What are the clinical signs of the mediastinal location?
|
respiratory distress: due to mass or effusion
regurgitation precaval syndrome enlargement of craniomediastinal LNs, thymus or both |
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Canine lymphoma: How common are is mediastinal LSA?
|
43% of all dogs with hypercalcemia and LSA
|
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Canine lymphoma: What is the more common immunophenotype for mediastinal LSA? Treatment?
|
T cell
standard chemo and palliative RT |
|
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Feline lymphoma: What virus plays a direct role in tumor formation?
|
FeLV
|
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Feline lymphoma: How is FeLV transmitted?
|
Queen to kitten or in saliva and milk
|
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Feline lymphoma: How much more of a risk are FeLV + cats are to developing LSA than FeLV-?
|
60 fold increase risk in + more than -
|
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Feline lymphoma: What age group is more commonly diagnosed?
|
Younger cats
|
|
|
Feline lymphoma: What three locations are most common?
|
1. mediastinal
2. multicentric 3. spinal |
|
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Feline lymphoma: What virus plays an indirect role in tumor formation?
|
FIV
|
|
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Feline lymphoma: How does FIV increase the risk of lymphoma? By how much more?
|
Causes immunosepression
5x higher risk of developing |
|
|
Feline lymphoma: Where are the four most common sites of FIV lymphoma?
|
1. kidney
2. GI 3. liver 4. multicentric |
|
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Feline lymphoma: FIV lymphoma is more likely to be what immunophenotype?
|
B cell
|
|
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Feline lymphoma: What is the typical presentation?
|
FeLV -
median age 11 years |
|
|
Feline lymphoma: What is the most common form?
|
alimentary
|
|
|
Feline lymphoma: How is the overall incidence changing?
|
increasing despite drop in FeLV + cats
|
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Feline lymphoma: Alimentary: What is the most common immunophenotype? Signalment?
|
B cell
older cats, FeLV - |
|
|
Feline lymphoma: Alimentary: How do the tumors usually appear?
|
solitary or diffuse through the intestinal muscle layers and submucosa
can cause complete or partial obstruction |
|
|
Feline lymphoma: Alimentary: What are the four most common clinical signs?
|
1. anorexia
2. weight loss 3. anemia 4. palpable abdominal mass or thickened bowel loops |
|
|
Feline lymphoma: Alimentary: What is the prognosis with therapy?
|
complete remission
|
|
|
Feline lymphoma: Alimentary: What are two positive prognostic factors?
|
1. feLV-
2. addition of doxirubicin |
|
|
Feline lymphoma: Alimentary: Is the immunophenotype prognostic?
|
Not as prognostic as dogs
|
|
|
Feline lymphoma: Alimentary: Lymphocytic lymphoma CR and MST?
|
CR: 70%
MST: 16 mos |
|
|
Feline lymphoma: Alimentary: What is the response of large granular lymphoma to chemotherapy?
|
poor response
|
|
|
Feline lymphoma: What three areas are affected by mediastinal lymphoma?
|
1. thymus
2. mediastinal LNs 3. sternal LNs |
|
|
Feline lymphoma: Mediastinal: Is hypercalcemia common? Pleural effusion?
|
RARE
COMMON |
|
|
Feline lymphoma: Mediastinal: Age? FeLV? Immunophenotype?
|
Young
FeLV + T cell |
|
|
Feline lymphoma: Mediastinal: 7 Differentials?
|
1. thymoma
2. chylothorax 3. cardiomyopathy 4. pyothorax 5. FIP 6. Mesothelioma 7. diaphragmatic hernia |
|
|
Feline lymphoma: Mediastinal: How is it diagnosed?
|
cytology of pleural fluid or mass
|
|
|
Feline lymphoma: Mediastinal: What is the MST w. CHOP if young and FeLV +?
|
2-3 months
|
|
|
Feline lymphoma: Renal: Where does this usually extend to?
|
CNS- 40-50%
|
|
|
Feline lymphoma: Renal: How will the kidneys appear? Renal insufficiency?
|
Bilateral and uniformly enlarged
50% will have renal insufficiency |
|
|
Feline lymphoma: Nasal/paranasal: Does this metastasize? Exceptions?
|
No- usually localized- unless FeLV+
|
|
|
Feline lymphoma: Nasal/paranasal: Prognosis in cats?
|
Best of the LSA- MST 1.5-2 yrs w/ RT alone and FeLV-
|
|
|
Feline lymphoma: What is the difference in prognosis between the different types? (from best to worst)
|
Nasal-> alimentary-> mediastinal, multicentric, renal hepatic
|
|
|
Feline lymphoma: Protocols with which drug provides longer remission and survival times?
|
doxorubicin
|
|
|
Feline lymphoma: How does FeLV effect prognosis?
|
FeLV- is better than FeLV+
|
|
|
Soft tissue sarcomas: What is a possible parasitic etiology?
|
spirocerca lupi
|
|
|
Soft tissue sarcomas: What tissues does this normally originate from? What is the most common?
|
Connective tissues: muscle, adipose, neurovascular, fascial, fibrous
May arise from any site Most common: skin and subcutaneous tissue |
|
|
Soft tissue sarcomas: Are these capsulated? ***TQ
|
Appear pseudocapsulated: may look well encapsulated but histologically have poorly defined margins and infiltrate through and along fascial planes
|
|
|
Soft tissue sarcomas: Are these invasive?
|
LOCALLY INVASIVE
|
|
|
Soft tissue sarcomas: Will they reoccur after conservative surgery?
|
Yes- commonly
|
|
|
Soft tissue sarcomas: Metastasis?
|
20%- hematogenous route
|
|
|
Soft tissue sarcomas: What predicts metastasis? Recurrence?
|
Histopathologic grade
Histologic margins |
|
|
Soft tissue sarcomas: What size of tumor has a poor response to chemotherapy and radiation therapy b/c they are too bulky?
|
>5cm
|
|
|
Soft tissue sarcomas: What are the three grades based on mitoses and necrosis?
|
I: M: 0-9, N: none
II: M: 10-19, N: <50% IIl: M: >20, N: >50% |
|
|
Soft tissue sarcomas: What is a paraneoplastic syndrome of tumors of smooth muscle? ***TQ
|
HYPOGLYCEMIA
|
|
|
Soft tissue sarcomas: What kind of false result is common on cytology?
|
False negative b/c sarcomas do not exfoliate well
|
|
|
Soft tissue sarcomas: What are the recommended minimum margins for surgery? What should be done after excision to tumor?
|
3cm lateral and 1 fascial plane deep
formalin fixation, ink lateral and depp margins |
|
|
Soft tissue sarcomas: What is the best opportunity for local control?
|
1st surgery
|
|
|
Soft tissue sarcomas: What should be done if surgical margins are clean but close or dirty?
|
follow-up therapy: radiation and/or second surgery
|
|
|
Soft tissue sarcomas: What are three poor prognostic factors for local control?
|
1. large tumor size
2. incomplete surgical margins 3. high histological grade |
|
|
Soft tissue sarcomas: What are the three poor prognostic factors for systemic control?
|
1. high histological grade
2. number of mitotic figures/% necrosis 3. local tumor recurrence |
|
|
Soft tissue sarcomas: Cats: What is the time to tumor development post vaccination?
|
4 weeks to 10 years
|
|
|
Soft tissue sarcomas: Cats: Vaccine associated v non-vaccine associated: Which is more aggressive? Why? (3)
|
Vaccine associated: marked nuclear/cellular pleomorphism, increased tumor necrosis, high mitotic activity
|
|
|
Soft tissue sarcomas: VAS in Cats: What type of diagnostic method is not recommended? Why?
|
Excisional biopsy: increases risk of recurrence and both disease free interval and survival times will decrease
|
|
|
Soft tissue sarcomas: VAS in Cats: What tool is recommended for local staging and to plan surgery?
|
CT scan
|
|
|
****TQ*********Soft tissue sarcomas: VAS in cats: When do you investigate a mass at a vaccination site?
|
3-2-1
1. Mass still present >3 MONTHS after vaccination 2. Mass is >2cm in DIAMETER 3. Mass is INCREASING IN SIZE >1 MONTH after vaccination |
|
|
Soft tissue sarcomas: VAS in cats: What is important not to do in surgery?
|
NO MARGINAL EXCISION
|
|
|
Soft tissue sarcomas: VAS in cats: Who should perform the 1st surgical attempt?
|
By a referral surgeon to increase chances of success
|
|
|
Soft tissue sarcomas: VAS in cats: What size should the surgical margins be?
|
Historically: 3cm, NOW: 5cm
|
|
|
Soft tissue sarcomas: VAS in cats: Where should vaccinations NOT be given?
|
Interscapular region
|
|
|
Mast cell tumors in dogs: Common?
|
MOST COMMON canine cutaneous tumor
|
|
|
Mast cell tumors in dogs: What mutation is associated with higher grade?
|
C-kit
|
|
|
Mast cell tumors in dogs: What are the four clinical signs? Why?
|
1. Darier's sign: manipulation-> degranulation; erythema and wheal formation in surrounding tissues
2. GI ulceration: Histamine acts on parietal cells via H2 receptors-> increased HCl 3. Hypotension: Histamine H1 4. Local irritation: histamine H1 |
|
|
Mast cell tumors in dogs: How does the diagnostic cytology appear?
|
small to medium round cells
+/- basophilic cytoplasmic granules (undifferentiated MCTs will not have granules) |
|
|
Mast cell tumors in dogs: How can you tell grade?
|
cytology
|
|
|
Mast cell tumors in dogs: What predicts behavior?
|
histologic grade
|
|
|
Mast cell tumors in dogs: What is the patnaik grading scale?
|
l: well differentiated: clearly defined cytoplasmic boundaries, regular nuclei, lg deep staining cytoplasmic granules, rare to absent mitotic figures
ll: intermediate differentiation: infrequent mitotic figures, lower N:C, indistinct cytoplasmic boundaries III: anaplastic, undifferentiated, high grade: irregular nuclei size and shape, low # to no granules, frequent mitotic figure |
|
|
Mast cell tumors in dogs: What are five positive prognostic factors?
|
1. low histologic grade
2. WHO clinical stage 1 or 2 3. slow growth 4. boxer breed 5. low AgNOR count (black spots in nucleus |
|
|
Mast cell tumors in dogs: What are the seven negative prognostic factors?
|
1. high histologic grade
2. location: preputial, subungual, perianal, oral/mucocutaneous, muzzle 3. visceral/BM involvement 4. fast growth rate 5. recurrence 6. systemic signs 7. high AgNOR count |
|
|
Mast cell tumors in dogs: What is the treatment of choice in tumors localized to skin or subQ tissues?
|
surgery
|
|
|
Mast cell tumors in dogs: What should the surgical margins be?
|
2-3 cm margins and extensive deep margins- evaluate margins histologically for completeness
|
|
|
Mast cell tumors in dogs: What are the four indications for chemotherapy treatment?
|
1. metastatic dz
2. high grade (III) mast cell tumor 3. high grade II mast cell tumor 4. not surgically resectable |
|
|
Mast cell tumors in dogs: What is the gold standard chemotherapy treatment?
|
vinblastine/prednisone
|
|
|
Mast cell tumors in dogs: Besides vinblastine/prednisone chemo, what two other plans are used?
|
1. lomustine: CCNU
2. prednisone single agent |
|
|
Mast cell tumors in dogs: What are two adjuctive treatments?
|
1. diphenhydramine
2. famotidine |
|
|
Mast cell tumors in dogs: What are the three indications for adjuctive treatment?
|
1. systemic signs
2. manipulation: surgery or FNA 3. treating gross/microscopic dz: risk of degranulation |
|
|
Mast cell tumors in cats: Common?
|
Second most common cutaneous tumor in the cat
|
|
|
Mast cell tumors in cats: Two forms? What breed is predisposed?
|
1. mastocytic: mean age 10 yrs
2. histiocytic: mean age 2.4 yrs siamese |
|
|
Mast cell tumors in cats: Visceral MCTs more common?
|
More common in cats than dogs
|
|
|
Mast cell tumors in cats: Associated with viruses?
|
No association with FeLV, FIV, FIP
|
|
|
Mast cell tumors in cats: What is the treatment of choice for cutaneous, well differentiated form? Recurrence?
|
Surgical excision
0-22%- usually w/i 6m of surgery |
|
|
Mast cell tumors in cats: What is the treatment for cutaneous anaplastic form? Recurrence? Metastasis?
|
Aggressive surgery, wide margins
High rates of recurrence and metastasis Metastasis: w/i 2 months |
|
|
Mast cell tumors in cats: What is the treatment for splenic form? Survival?
|
Splenectomy: even w/ BM involvement may see regression
12-19 months |
|
|
Hemangiosarcoma in dogs: Accounts for how many splenic malignancies?
|
50%
|
|
|
Hemangiosarcoma in dogs: What three breeds are overrepresented?
|
1. GSD
2. goldens 3. labs |
|
|
Hemangiosarcoma in dogs: What is the most common primary site? What are the four other sites?
|
spleen---- DERRRRRRR
1.right atrium 2. skin 3. subQ 4. liver |
|
|
Hemangiosarcoma in dogs: What is the only form that where metastasis is less common?
|
pure cutaneous or dermal HSA w/o any clinical or histological evidence of subdermal infiltration
|
|
|
Hemangiosarcoma in dogs: How does metastasis usually occur?
|
hematogenous route or seeding of the abdomen after rupture
|
|
|
Hemangiosarcoma in dogs: Most common metastatic sarcoma to what organ?
|
brain
|
|
|
Hemangiosarcoma in dogs: What are the clinical signs? (6)
|
1. lethargy, lack of appetite
2. abdominal swelling 3. waxing and waning lethargy 4. weight loss 5. acute weakness or collapse 6. death secondary to hemorrhage/hypotensive shock |
|
|
Hemangiosarcoma in dogs: What are the three findings on CBC?
|
1. anemia: schistocytes, acanthocytes, regenerative or non-regenerative
2. neutrophilic leukocytosis 3. thrombocytopenia |
|
|
Hemangiosarcoma in dogs: What does the coagulation panel appear on 50% of cases?
|
Meet criteria for DIC
|
|
|
Hemangiosarcoma in dogs: Is cytology of effusion diagnostic?
|
rarely
|
|
|
Hemangiosarcoma in dogs: What is the primary method of treatment?
|
surgery
|
|
|
Hemangiosarcoma in dogs: What is the prognosis for splenectomy alone?
|
MST 20-80 days, <10% alive at 1 year
|
|
|
Hemangiosarcoma in dogs: What is teh prognosis for splenectomy + doxorubicin?
|
140-180 dats, <10% alive at 1 year
|
|
|
Hemangiosarcoma in dogs: Cutaneous: Prognosis of dermal w/o subdermal invasion and surgery alone?
|
780 days
|
|
|
Hemangiosarcoma in dogs: Cutaneous: Prognosis with invasion into SC tissue?
|
MST 172 days w/ sx alone
|
|
|
What is the most common primary bone tumor?
|
osteosarcoma: 85% of all cancers in the skeleton
|
|
|
Canine Osteosarcoma: What is the usual signalment?
|
median age 7 ys
large to giant breeds |
|
|
Canine Osteosarcoma: What are the 7 higher risk breeds?
|
1. st. bernard
2. great dane 3. irish setter 4. doberman 5. rottweiler 6. GSD 7. golden |
|
|
Canine Osteosarcoma: What is the most common primary site?
|
metaphyseal region of long bones
front limbs are more often than rear limbs Distal radius and proximal humerus |
|
|
Canine Osteosarcoma: Is it common for it to cross the joint surface? Where is it aggressive?
|
no its RARE
locally |
|
|
Canine Osteosarcoma: Is metastasis common?
|
Yes- 90% will die of metastatic disease
|
|
|
Canine Osteosarcoma: How does it usually metastasis? What is the most common sites?
|
hematogenous route
LUNG, bone, other soft tissue sites |
|
|
Canine Osteosarcoma: Is hypercalcemia common?
|
NO- its very rare
|
|
|
Canine Osteosarcoma: What signs will be seen on radiographs? (4)
|
1. cortical lysis
2. soft tissue extension, soft tissue swelling 3. new bone- tumor or reactive bone 4. codman's triangle |
|
|
Canine Osteosarcoma: What are the six differentials for the radiographic changes?
|
1. other bone tumors: CSA, FSA, HSA
2. metastatic cancer to bone 3. MM or LSA of bone 4. systemic mycosis w/ bone localization 5. bacterial osteomyelitis 6. bone cysts |
|
|
Canine Osteosarcoma: Where should a biopsy be taken?
|
center of the lesion
|
|
|
Canine Osteosarcoma: With lymph node metastasis. what is the prognosis?
|
MST 59 days compared to 318 in dogs w/o lnn involvement
|
|
|
Canine Osteosarcoma: With amputation treatment alone, what is the prognosis?
|
4-5 mos MST
|
|
|
Canine Osteosarcoma: Why is radiation therapy used?
|
for palliation of bone pain
|
|
|
Canine Osteosarcoma: What does pamidronate do?
|
-inhibit bone resorption by binding to hydroxyapatite crystals, inhibiting further calcium and phosphorus dissolution
-block osteoclastic activity and induces apoptosis of osteoclasts ***RESULT: inhibition of bone resorption |
|
|
Canine Osteosarcoma: Why is chemotherapy used to treat?
|
extends median survival time in amputees and limb spares
MST: 8-12 mos |
|
|
Feline Osteosarcoma: Common? Where?
|
Rare
long bones>axial skeleton |
|
|
Feline Osteosarcoma: Can amputation cure the patient?
|
yes- if no metastasis present
|
|
|
Feline Osteosarcoma: What is the prognosis for axial sites?
|
Poorer prognosis
|
|
|
Clinical Immunology
|
Clinical Immunology
|
|
|
What are the four hypersensitivity reactions?
|
l: immediate, mediated by IgE attached to mast cells
ll: cytotoxic, destruction of normal cells by antibiotics lll: immune complex deposition in lg amts of tissue leading to inflammation lV: delayed, cell mediated, mediated by T cells and NK cells |
|
|
What is immune mediated hemolytic anemia?
|
life threatening hematologic dz in which RBCs are destroyed by a TYPE II HYPERSENSITIVITY reaction--> extravascular or intravascular hemolysis
|
|
|
IMHA: When does extravascular hemolysis occur?
|
immunoglobulin or complement coated RBCs are removed by phocytosis
|
|
|
IMHA: When does intravascular hemolysis occur?
|
If RBCs are coated with enough IgG or IgM molecules to fix complement
|
|
|
What is primary IMHA?
|
A TRUE autoimmune reaction against RBCs
60-75% of cases |
|
|
What is secondary IMHA? What species most commonly has this
|
RBCs are destroyed in an immune rxn against foreign proteins that may be adherent to the RBC
Most common form in Cats |
|
|
What are the clinical signs of IMHA? (7)
|
1. anorexia
2. lethargy 3. weakness 4. icterus 5. tachycardia 6. pallor 7. hepatosplenomegaly |
|
|
Class I IMHA: What is the optimal temp? What is the predominant Ab? Type of hemolysis?
|
Room temp
IgG>>>>>>>>>IgM Extravascular hemolysis |
|
|
Class II IMHA: What is the optimal temp? What is the predominant Ab? Type of hemolysis?
|
body temp
IgM Intravascular hemolysis |
|
|
Class III IMHA: What is the optimal temp? What is the predominant Ab? Type of hemolysis?
|
body temp
IgG Extravascular hemolysis |
|
|
Class IV and V IMHA: Optimal temp? Ab?
|
4C
IgM |
|
|
IMHA: What lab results will be seen?
|
Anemia
Spherocytosis Strong regenerative response: polychromasia, anisocytosis, nRBCs, macrocytosis +/- microscopic agglutination Thrombocytompenia AUTOAGGLUTINATION |
|
|
IMHA: What will be seen on a urinalysis?
|
Bilirubinuria
Hemoglobinuria if intravascular |
|
|
IMHA: What does a direct coomb's test detect? Is a positive test result diagnostic?
|
detects presence of antibodies and/or complement on RBC surface
+= consistent with but not diagnostic |
|
|
IMHA: What is the three treatments?
|
1. supportive care
2. blood transfusion 3. immunosuppressive therapy |
|
|
IMHA: What are the five possible complications?
|
1. refractory anemia
2. hemorrhage 3. bacterial/fungal infections 4. acute renal failure 5. PTE |
|
|
IMHA: What are the four causes of inherited IMHA?
|
1. pyruvate kinase deficiency
2. phosphofructokinase deficiency 3. chondrodysplasia/anema 4. nonspherocytic hemolytic anemia |
|
|
IMHA: What are the four immune mediated causes?
|
1. primary idiopathic IMHA
2. IMHA assoc. w/ systemic lupus erythematosus 3. neonatal isoerythrolysis 4. incompatible transfusion |
|
|
IMHA: What is the metabolic cause?
|
hypophosphatemia
|
|
|
IMHA: What is the neoplastic cause?
|
microangioapthic anemia assoc with hemangiosarcoma or lymphoma
|
|
|
IMHA What are the eight infectious causes?
|
1. bebesia canis or gibsoni
2. mycoplasma haemominutum, haemofelis or haemocanis 3. dirofilaria immitis 4. bacterial endocarditis 5. FeLV 6. leptospirosis 7. cytauxzoon felis 8. Ehrlichia canis |
|
|
IMHA: What are the nine toxin or drug related causes?
|
1. onion toxicity, 2. zinc toxicosis, 3. methylene blue, 4. copper toxicity, 5. propylthiouracil, 6. methimazole, 7. sulfa drugs, 8. penicillins and cephalosporins, 9. quinidine
|
|
|
Immune mediated thrombocytopenia (IMT): What is primary? Common?
|
Idiopathic
Most common form in dogs |
|
|
IMT: What is secondary?
|
antibody targets non-self antigens absorbed onto the surface of platelets or when immune complexes become bound to platelet surfaces
|
|
|
IMT: Diagnostics?
|
-thrombocytopenia: blood smear
-stippled blue morulae w/i platelets during clinical episodes= confirms anaplasma pltys |
|
|
IMT: Is jugular catheterization contraindicated?
|
In thrombocytopenic patients: due to hemorrhage complications
|
|
|
hIMT: Where is the most common site of significant bleeding from thrombocytopenia?
|
GI
|
|
|
IMT: What is the treatment?
|
Immunosuppressive therapy: corticosteroids +/- corticosteroids
splenectomy as a last resort |
|
|
Systemic Lupus erythematosus (SLE): What are the 7 canine overrepresented breeds?
|
1. shetland sheepdog
2. OESD 3. afghan hound 4. beagle 5. GSD 6. irish setter 7. poodle |
|
|
SLE: What are the three feline overrepresented breeds?
|
1. persian
2. siamese 3. himalayan |
|
|
SLE: What are the three underlying pathologies?
|
1. immune complex formation induces tissue damage: type III hypersensitivity
2. Direct antibody mediated cytotoxicity: Type II hypersensitivity 3. Cell mediated autoimmunity: Type IV hypersensitivity= less common |
|
|
SLE: Inflammatory lesions caused by antigen-antibody complexes not specific for organ systems but can lead to four clinical signs?
|
1. vasculitis
2. glomerulonephritis 3. polyarthritis 4. dermatitis |
|
|
SLE: What are underlying events involved in the development of SLE? These can be triggered by what?
|
abnormal immune activation and loss of self tolerance and the expansion of an autoreactive B cell population--> autoantibody producing cells as well as memory B cells
endogenous factors or exogenous factors |
|
|
SLE: What is the most common C/S complaint?
|
shifting leg lameness= polyarthritis/polymyositis
|
|
|
SLE: Diagnosis? (2)
|
1. 2 major signs and + serology
2. 1 major sign, 2 minor signs, + serology |
|
|
SLE: What are seven major signs? ****TQ*****
|
1. skin lesions
2. polyarthritis 3. hemolytic anemia 4. glomerulonephritis 5. polymyositis 6. leukopenia 7. thrombocytopenia |
|
|
SLE: What are six minor signs? *****TQ******
|
1. fever of unknown origin
2. CNS signs- seizures 3. oral ulceration 4. lymphadenopathy 5. pericarditis 6. pleuritis |
|
|
SLE: What are two serological diagnostic tests? Other diagnostic tests?
|
1. ANA
2. Lupus erythematosus preparation synovial fluid analysis and culture and skin biopsy of lesions, synovial biopsy= confirm diagnosis |
|
|
SLE: What is the treatment?
|
prednisone/prednisolone
If no improvment in 7-10 days= add azathioprine (DOGS) and chlorambucil (CATS) |
|
|
Immune mediated arthritis (IMA): What is the most important rule out? ****TQ*****
|
infectious arthritis- esp if a single jt b/c classically IMA effects multiple jts
|
|
|
IMA: What is the initial treatment? ****TQ*****
|
prednisolone
|
|
|
Hemostasis and Coagulation
|
Hemostasis and Coagulation
|
|
|
What are the five main functions of platelets?
|
1. adhesion
2. aggregation 3. secretion 4. facilitate coagulation 5. clot retraction |
|
|
What are four clinical signs of platelet dysfunction?
|
1. cutaneous ecchymoses
2. bleeding from mucosal surfaces: gingival hemorrhage, epistaxis, melena, hematuria 3. prolonged/excessive bleeding at sx site or trauma 4. petechiae |
|
|
What are the five screening tests for platelet dysfunction?
|
1. Platelet count
2. coagulation assays 3. vWF 4. BMBT 5. antithrombin. fibrin degradation products. D-dimer |
|
|
What is a test of platelet function?
|
BMBT
|
|
|
What causes prolonged BMBT? (4)
|
1. marked thrombocytopenia
2. drugs: NSAIDs 3. Hereditary platelet defects 4. Van Willebrand disease |
|
|
What is the most common cause of canine hereditary hemostatic defect?
|
von willebrand disease
|
|
|
What is von willebrand factor?
|
a plasma glycoprotein that bridges platelets to injured vessel walls and contributes to platelet-platelet bridging
|
|
|
Where are all coagulation factors and cofactors are synthesized where? How do they circulate in plasma?
|
Liver
inactive form |
|
|
What coagulation factor has the shortest half life?
|
Factor VII
|
|
|
What is the initiating event for clotting and activation occurs when tissue factor is present?
|
Factor VII activation
|
|
|
What is the most important inhibitor of coagulation?
|
antithrombin III
|
|
|
What is fibrinolysis?
|
degradation of clot and scar tissue formation
|
|
|
Degradation of fibrin is mediated by what?
|
plasmin: generated by the action of plasminogen activators on plasminogen
|
|
|
What are six tests of coagulation?
|
1. ACT
2. aPTT 3. OSPT 4. Thromboelastography 5. Fribrin or Fibrinogen degradation products 6. D-dimer |
|
|
What does the ACT evaluate?
|
Intrinsic and common pathways
|
|
|
What does aPTT evaluate?
|
Intrinsic and common pathway
|
|
|
What does OSPT evaluate?
|
extrinsic and common pathway- especially factor VII
|
|
|
What does thromboelastography evaluate?
|
all steps of hemostasis
|
|
|
What does fibrin or fibrinogen degradation products detect?
|
detects increased fibrinolysis assoc. w/ excessive coagulation and increased fibrinogenolysis
|
|
|
What causes increased fibrin or fibrinogen degradation products?
|
Localized or disseminated intravascular coagulation, decreased FDPs by the liver
|
|
|
What does d-dimer detect? What does it NOT detect?
|
Detects increased fibrinolysis secondary to excessive coagulation
Fibrinogenolysis |
|
|
What is hemophilia A?
|
Deficiency in functional factor VII
|
|
|
What is hemophilia B?
|
Factor XI deficiency
|
|
|
What is hageman trait? Inherited?
|
Factor XII deficiency: incidental prolongation of aPTT in cats- w/o a bleeding tendency
Autosomal recessive |
|
|
What is factor XII important for?
|
contact activation in vitro
|
|
|
What is the most common cause of vitamin K deficiency?
|
antagonism of vit K- ingestion of anticoagulant rodenticides
|
|
|
What are the three alterations of Virchow's triad?
|
1. vascular endothelial damage
2. stasis of blood flow 3. hypercoaguable state |
|
|
What are the four signs of vascular endothelial damage?
|
1. vasculitis
2. sepsis 3. trauma 4. neoplasia |
|
|
What are the four causes of stasis of blood flow?
|
1. hypertrophic cardiomyopathy
2. increased blood viscosity 3. recumbency 4. shock |
|
|
What are the four causes of hypercoaguable state?
|
1. glomerular disease
2. GI disease 3. DIC 4. Cushing's disease |
|
|
What five diseases in thrombosis associated with?
|
1. IMHA
2. hyperadrenocorticism 3. PLE 4. systemic amyloidosis 5. canine parvovirus |
|
|
What is a clinical sign of pulmonary thromboembolism?
|
acute dyspnea
|
|
|
What is a clinical sign of renal arterial thromboembolism?
|
acute renal failure
|
|
|
What is the end result of systemic thrombosis?
|
DIC
|
|
|
What is the pathogenesis of DIC?
|
primary dz--> widespread thrombosis--> consumption of clotting factors--> uncontrolled fibrinolysis--> massive hemorrhage, tissue hypoxia, organ failure, death
|
|
|
GI
|
GI--- FUCK
|
|
|
What is motility controlled by?
|
ANS + ENS
|
|
|
What is reduced activity of segmental contractions?
|
D
|
|
|
What is the reduced activity of peristatic contractions?
|
Ileus
|
|
|
What controls the "housekeeping" of the GI?
|
MMC
|
|
|
What are the dysphagia rule-outs? (5)
|
1. foreign bodies
2. ulceration, inflammation or infection 3. dental disease 4. fractures 5. sialodenitis |
|
|
What neuromuscular diseases cause dysphagia? (4)
|
1. masticatory muscle myositis
2. oropharyngeal dysphagia: oral phase, pharyngeal phase, cricopharyngeal phase 3. circopharyngeal achalasia and asynchrony 4. tetanus/botulism/rabies |
|
|
What cranial nerves can cause dysphagia when they are dysfunctioning? (5)
|
V, VII, IX, X, XII
|
|
|
What masses can cause dysphagia?
|
1. abscesses
2. neoplasia |
|
|
What type of muscle is a dogs esophagus made of? Cats?
|
Dogs: all striated
Cats: distal portion= smooth muscle |
|
|
What is the clinical manifestation of esophageal disease?
|
regurgitation
|
|
|
What is the primary reason for regurgitation?
|
anesthesia- w/i one week of surgery
|
|
|
What signs will you see with regurgitation? Vomiting?
|
Regurg: passive process, large appetite
Vomiting: active process, retching, bile, nausea, +/- digested, +/- appetite |
|
|
What is the most common vascular ring anomaly? Breed predilection?
|
persistent right aortic arch
GSD |
|
|
What are regurgitation rule-outs? (12)
|
1. megaesophagus/esophageal weakness
2. secondary acquired: MG, addisions, etc 3. vascular ring anomaly 4. esophageal FB 5. stricture, diverticula, fistulas 6. esophagitis 7. LES achalasia 8. esophageal masses 9. hiatal hernia 10. GE intsussusceptions 11. lead poisioning 12. canine distemper |
|
|
What are three causes of esophagitis?
|
1. post anesthesia
2. GERD: gastro-esophageal relfux disease 3. excessive acidity |
|
|
What are two types of esophageal masses?
|
1. Neoplasia: esophageal or extraesophageal
2. granulomas: spirocerca lupi |
|
|
What does contrast radiography help to diagnose?
|
1. defects
2. FB |
|
|
What is a possible problem with using contrast radiography on esophageal problems?
|
aspiration
|
|
|
What should be used with contrast radiography if suspected perforation?
|
iodinated agent
|
|
|
What are the benefits of endoscopy used as a diagnostic test? (3)
|
1. Direct visualization
2. Assess severity of disease 3. Therapeutic intervention: FB removal, balloon dilatation |
|
|
How will an animal with congenital idiopathic megaesophagus present? Prognosis?
|
regurgitation and poor growth after weaning
fair to guarded |
|
|
What is acquired idiopathic megaesophagus?
|
neuronal dysfunction in esophageal motility
|
|
|
What is the usual age of acquired idiopathic megaesophagus?
|
middle aged to older
|
|
|
Acquired idiopathic megaesophagus: Prognosis? Why?
|
Poor due to high incidence of aspiration pneumonia
|
|
|
What are the five treatments for megaesophagus?
|
1. elevated feeding and water: during and 15-20 mins post
2. Experiment with food 3. +/- motility drugs: metoclopramide/cisapride 4. feeding tubes: PEG 5. treat pneumonia if present |
|
|
What are two ways to treat PRAA? Prognosis?
|
1. surgical: remove vascular band
2. PEG tube Good if caught early enough: cranial esophagus may remain dilated, motility will usually return |
|
|
What are the three most common signs for esophageal foreign bodies?
|
1. thoracic inlet
2. heart base 3. LES |
|
|
What happens due to a FB being in the esophagus and secondary peristalsis continue?
|
pressure necrosis
|
|
|
What are two possible options to treat esophageal foreign bodies with an endoscopy?
|
1. Retrieval- make sure not to manipulate if FB penetrates full thickness
2. Advance into stomach- digestion or sx removal |
|
|
What are five complications of esophageal foreign bodies?
|
1. hemorrhage
2. perforation 3. esophagitis 4. stricture 5. diverticulum |
|
|
How do you treat perforation if small? Large?
|
Small: PEG tube, sucralfate and metaclopramide
Large: Surgical management |
|
|
What are owners advised to watch for after treatment of a foreign body?
|
Regurgitation which will be an indication of esophageal stricture
|
|
|
What are three causes of esophageal stricture secondary to injury?
|
1. esophagitis
2. FB 3. DOXYCYCLINE: CATS****** |
|
|
What is the most common cause of esophagitis?
|
recent anesthesia
|
|
|
What is the usual cause of esophageal perforation?
|
Traumatic- post FB or esophagitis
|
|
|
What is a common sequelae of esophageal perforation?
|
esophageal stricture
|
|
|
hat two possible sequelae does spirocerca lupi lead to?
|
1. sarcoma
2. aortic aneurysms |
|
|
What is the autonomic control of the stomach? Enteric?
|
Autonomic: vagus and ciliac plexus
Enteric: myenteric and submucosal plexus |
|
|
Stomach: What do the parietal cells produce? (4)
|
1. HCl
2. Gastrin 3. ACh 4. Histamine |
|
|
Stomach: what do the chief cells produce?
|
pepsinogen
|
|
|
Stomach: What do the mucous cells produce?
|
bicarbonate
|
|
|
Stomach: What are the two phases of secretion?
|
1. cephalic: PNS and ACh
2. Gastric: gastrin |
|
|
Vomiting: What controls the vomiting center? (3)
|
1. Dopamine
2. histamine 3. ACh |
|
|
Vomiting: What is the usual contents?
|
gastric and duodenal contents
|
|
|
Vomiting: What is usually lost? What does this lead to?
|
Bicarbonate- leads to metabolic acidosis****
|
|
|
What does high GI obstruction lead to? (think electrolytes)
|
Hypochloremic metabolic alkalosis*******
|
|
|
Vomiting: What usually is NOT given? Why?
|
Anti-emetics- b.c it hides the important clinical signs
|
|
|
Vomiting: What is the usually cause of unproductive vomiting, distended abdomen +/- shock/collapse? Treatment?
|
gastric dilatation and volvulus
Emergency stabilization and surgery |
|
|
What is the primary sign of Heartworm disease in cats?
|
Vomiting
|
|
|
What should be done first to treat chronic vomiting?
|
therapeutic de-worming
|
|
|
Vomiting: Treatment?
|
1. fluids
2. NPO/bland diet/TPN/PPN/feeding tubes 3. gastric protectants 4. prokinetics |
|
|
Vomiting: What gastric protectants are used?
|
1. H2 blockers/proton pump inhibitors
2. sucralfate 3. misoprostal: inhibit NSAID ulceration |
|
|
Vomiting: What prokinetics are used?
|
1. metoclopramide
2. cisapride 3. erythromycin |
|
|
Vomiting: When are prokinetics contraindicated?
|
Obstruction: will cause perforation
|
|
|
When are antiemetics contraindicated? (3)
|
1. GI infection
2. toxicity 3. obstruction |
|
|
What are three antimetics that can be used?
|
1. metoclopramide, ondansetron/dolasetron, maropitant
2. Anticholinergics: atropine, scopolamine, aminopentamide/centrine, isopropaminde 3. Phenothiazines |
|
|
Why are anticholinergics bad?
|
cause ileus and cramping
|
|
|
Why is pepto bismol contraindicated?
|
Turns poo black- may mask melena
|
|
|
What causes acute gastritis? (3)
|
1. dietary: indiscretion, caustic substances, FBs
2. Drugs: NSAIDs 3. Infectious: helicobacter |
|
|
What clinical signs will be seen with hemorrhagic gastroenteritis?
|
1. hematemesis
2. hematochezia 3. elevated PCV, normal TP: due to severe dehydration |
|
|
Hemorrhagic Gastroenteritis: What type of breeds are overrepresented?
|
small breed dogs
|
|
|
Hemorrhagic gastroenteritis: Treatment? Prognosis?
|
Tx: Fluids, GI protectants, +/- Ab
Prognosis: Good if caught early |
|
|
Hemorrhagic gastroenteritis: What are the four complications?
|
1. DIC
2. thromboembolism 3. renal failure 4. shock |
|
|
How will gastritis appear with histopath?
|
L/p, eosinophilic, granulomatous, atrophic
|
|
|
Definitive diagnosis of gastritis requires what?
|
Biopsy
|
|
|
What parasites can cause gastritis?
|
1. helicobacter
2. physaloptera- tx= pyrantal 3. Ollulanus- CATS- tx= fenbendazole |
|
|
What usually causes pyloric stenosis?
|
benign muscular pyloric hypertrophy
|
|
|
How will pyloric stenosis present?
|
persistent vomiting- esp right after eating
|
|
|
What animals are predisposed to pyloric stenosis?
|
brachycephalic dogs and siamese cats
|
|
|
What are possible complications to pyloric stenosis? (3)
|
1. esophagitis
2. ME 3. regurgitation |
|
|
What is the treatment for pyloric stenosis?
|
pyloroplasty
|
|
|
What is antral hypertrophy? Cause?
|
Excessive mucosa
Idiopathic |
|
|
Antral hypertrophy: Diagnosis? Treatment?
|
Dx: Biopsy
Tx: pyloroplasty and mucosal resection |
|
|
GDV: Diagnosis?
|
unproductive retching, PE, lg cranial abdomen, tympany
Radiographs: right lateral abdominal**** |
|
|
GDV: How does lactate affect prognosis?
|
6= bad prognosis
|
|
|
GDV: Treatment?
|
1. Shock rate fluids
2. Gastric decompression and lavage: tube or trochar |
|
|
GDV: What are four possible complications?
|
1. electrolyte abnormalities
2. Lactate 3. ECG abnormalities 4. reperfusion injury |
|
|
GDV: What causes the ECG abnormalities? Treatment?
|
Splenic involvement--> decreased PCs
Lidocaine |
|
|
What is gastric atony?
|
Idiopathic gastric hypomotility
|
|
|
What are the four primary ruleouts for gastric atony?
|
1. obstruction
2. IBD 3. Hypercalcemia 4. Hypocalcemia |
|
|
How is gastric atony diagnosed? Treatment?
|
Dx: fluoroscopy
Tx: Prokinetics: metoclopramide, cisapride, erythromycin |
|
|
What are the five causes of GI ulceration?
|
1. Stress: hypovolemia, septic, extreme exertion
2. Drugs: NSAIDS and corticosteroids 3. Neoplasia: MCT!!! & gastrinomas 4. Hepatic Dz 5. Uremia: secondary to increased gastrin |
|
|
How do you treat GI ulceration?
|
Eliminate predisposing cause
GI protectants: sucrophate |
|
|
What neoplasia will be found in the pylorus? Cardia? Anywhere?
|
gastric adenocarcinoma= metastatic
Leiomyosarcoma lymphoma |
|
|
How do patients with pythium insidiosum present?
|
vomiting and diarrhea
|
|
|
What kind of infection is Pythium insidiosum? What kind of histopath is found?
|
Fungal
purulent, eosinophilic, granulomatous, submucosal inflammation |
|
|
What is the treatment for P. insidiosum? Contingencies?
|
Sx resection
Itraconazole -MUST be caught early |
|
|
What do enterocytes do in the intestines?
|
Get nutrition form the food in the lumen
|
|
|
What happens if a dog is put on NPO?
|
kills enterocytes- especially cats
|
|
|
What do goblet cells do?
|
mucous and trefoil peptides
|
|
|
What virus is indicated if the tops of the crypts are damaged? Low?
|
Corona virus
Parvo virus |
|
|
What is a possible complication of increased segmental motility?
|
increased absorption= possible constipation
|
|
|
What are the ruleouts for acute diarrhea? (5)
|
1. dietary: allergies/changes/indiscretion
2. Parasites: helmiths, protozoa 3. Infectious disease: parvo, corona, FeLV/FIV, rickettsia, bacterial overgrowth 4. intussusception 5. hypoadrenocorticism |
|
|
Besides acute reasons, what are the ruleouts for chronic diarrhea? (7)
|
1. neoplasia
2. fungal infections: pythiosis, histoplasma 3. lymphangectasia 4. Breed specific enteropathies 5. systemic diseases 6. Malabsorptive diz: ARE/SIBO, Dietary, IBD 7. Maldigestive dz: EPI |
|
|
What are the ruleouts for chronic LARGE intestinal diarrhea?
|
1. dietary
2. fiber responsive 3. parasites: giardia, whips 4. bacteria: clostridium 5. histiocytic ulcerative colitis 6. fungal 7. IBD 8. Neoplasia 9. FeLV/FIV |
|
|
What is ARE?
|
antibiotic responsive enteropathies
|
|
|
What are two breed predisposed to histiocytic ulcerative colitis? Clinical sign?
|
Boxers and frenchies
Bloody diarrhea, scope= red dots in colon |
|
|
What will the signs of small bowel diarrhea?
|
lg volume, melena, steatorrhea, undigested food, variable color
|
|
|
What will the signs of small bowl diarrhea when it comes to defecation (freq, tnesmus, dyschezia, urgency)?
|
Frequency: 5x normal
Urgency: rare Tenesmus/dyschezia: absent |
|
|
What will "other signs" of small bowel diarrea be? (weight loss, flatulence, halitosis)
|
WL: usually present
Flatulence: possible Halitosis: present |
|
|
What will the signs of large bowel diarrhea?
|
Mucus, hematochezia, normal color
|
|
|
What will the signs of large bowel diarrhea be when it comes to defecation? (Freq, tenesmus, dyschezia, urgency)
|
Frequency: >3x normal
urgency: present Tenesmus: frequent Dyschezia: present |
|
|
What are the "other signs" of large bowel diarrhea? (WL, flatulence, halitosis)
|
WL: Rare
Flatulence: Absent Halitosis: Absent |
|
|
What are three types of fecal flotations that can be performed?
|
1. Sheather's- normal sugar float
2. Sinc sulfate or Giardia AG 3. Baermann: lung worms |
|
|
What will be the top DDx if on smear lots of spore forming rods are observed?
|
clostridium
|
|
|
What is the DDx for globulins and albumin seen?
|
PLE/PLN
|
|
|
What is on a Texas A&M GI panel?
|
PLI, TLI, cobalamin, folate
|
|
|
On a GI panel, what does low cabalamin diagnostic of?
|
malabsorptive diseases
|
|
|
On a GI panel, what does high folate diagnostic of?
|
interstitial bacterial overgrowth- ARE
|
|
|
GI: What is a possible problem with antibiotic treatment?
|
bacterial translocation
|
|
|
What species is important to use probiotics?
|
rabbits
|
|
|
Why is feeding better than NPO?
|
B/c enterocytes need nutrition
|
|
|
What are two sources of fiber?
|
1. metamucil
2. canned pumpkin |
|
|
T/F: Anti-diarrheals are usually indicated for diarrhea therapy? Two types?
|
False: rarely indicated
Opiates, bismuth subsalicylate |
|
|
Parvo: What cells are effected?
|
rapidly dividing cells: crypt epithelium and bone marrow
|
|
|
Parvo: What five breeds are predisposed?
|
1. dobies
2. rotties 3. pits 4. Labs 5. GSD |
|
|
Parvo: Diagnostic tests?
|
1. PE and history
2. Neutropenia 3. ELISA |
|
|
Parvo: Tx fluids?
|
Crystalloids +/- colloids
Glucose- young puppies K+ supplementation |
|
|
Parvo: Abx?
|
Newer IV beta-lactams
Ampicillin/enrofloxacin combo |
|
|
How do you increase efficacy with ampicillin?
|
Time depending= give more frequent
|
|
|
How do you increase efficacy with enrofloxacin?
|
Concentration dependent= give more than 1x/day
|
|
|
What are side effects of enrofloxacin?
|
seizures and vomiting, blindness in cats (instead use marbofloxacin)
If given too little= resistence to all drugs |
|
|
Parvo: complications?
|
intussusception: denuded entire gut= slippery
|
|
|
What kind of virus causes feline parvoviral enteritis?
|
panleukopenia virus
|
|
|
How is feline parvoviral enteritis diagnosed?
|
1. Canine ELISA- early
2. Presumptive w/ PE, Hz and CBC |
|
|
T/F: Very little changes will be seen on CBC with feline parvoviral enteritis
|
FALSE- drastic changes will be seen
|
|
|
Geographically, where is histoplasmosis?
|
mississippi and ohio river valleys
|
|
|
Histoplasmosis: Type of diarrhea?
|
chronic large bowel diarrhea
|
|
|
Histoplasmosis: What are the three other systems that are most commonly affected after LI?
|
1. eyes
2. respiratory 3. lymph nodes |
|
|
Histoplasmosis: Describe disease....
|
diffuse, severe, granulomatous, ulcerative mucosal disease
|
|
|
Histoplasmosis: What two clinical signs will be seen?
|
1. Melena and hematochezia
2. hypoproteinemia= ascites |
|
|
Histoplasmosis: Diagnosis? (3)
|
1. Rectal scrapes
2. Tap 3. Urine Ag test |
|
|
Histoplasmosis: Treatment?
|
Itraconazole: 4-6 mos.
|
|
|
Prototheca: Most common?
|
Algae- P. zopfi
|
|
|
Prototheca: Three areas affected?
|
1. skin
2. colon 3. eyes |
|
|
Prototheca: What breed is overrepresented?
|
Collies
|
|
|
Prototheca: What is the usually disease that is caused?
|
colitis with hematochezia
|
|
|
Prototheca: Treatment?
|
Not really
Liposomal amphotericin B- renal failure is common |
|
|
Prototheca: Prognosis?
|
poor
|
|
|
Whipworms: C/S? (4)
|
1. chronic diarrhea
2. PLE 3. Hematochezia 4. pseudoaddisonian: hyperkalemia, hyponatremia |
|
|
Roundworms: C/S? Tx?
|
inflammatory SI infiltrates
Tx: fenbendazole or pyrantel |
|
|
Hookworms: C/S? Tx?
|
severe anemia
Fenbendazole or pyrantel |
|
|
Tapeworms: Tx?
|
praziquantal
|
|
|
Strongyloides: tx?
|
fenbendazole
|
|
|
Coccidiosis: Tx? Should be used in caution in what dogs?
|
Sulfadimethoxine or TMS
Dobies/rotties= black and tan dogs |
|
|
Cryptosporidia: Tx?
|
no known treatment
|
|
|
Giardia: tx?
|
fenbendazole
|
|
|
Trichomoniasis: Tx?
|
+/- ronidazole
+/- tylosin |
|
|
Heterobilharzia: Tx?
|
fenbendazole + praziquantal
|
|
|
Histocytic Ulcerative Colitis: Two breeds predisposed?
|
1. boxers
2. frenchies |
|
|
Histocytic Ulcerative Colitis: Type of diarrhea?
|
Recurrent large bowel diarrhea
|
|
|
Histocytic Ulcerative Colitis: Tx?
|
enrofloxacin/batril
|
|
|
Histocytic Ulcerative Colitis: T/F Can easily see the bacteria
|
False: Can't find bacteria- responds to Ab
|
|
|
IBD: Type of inflammation?
|
idiopathic intestinal inflammation
|
|
|
IBD: What part of the GI does this affect?
|
any part- mucosal cellular infiltrates, inflammatory mediators, intestinal dysmotility
|
|
|
IBD: Response to normal fauna or dietary antigens?
|
exaggerated response
|
|
|
IBD: What other disease can this look like?
|
lymphoma- lymphocytic/plasmacytic
|
|
|
IBD: Dx?
|
Diagnosis of exclusion
|
|
|
IBD: What type of deficiency is this associated with?
|
cobalamin deficiency
|
|
|
IBD: Tx? (5)
|
1. hypo/low allergen diets
2. Antibiotics for ARE 3. Cobalamin supplementation 4. anti-inflammatory to immunosuppressive doses of corticosteroids 5. additional immunosuppressive drugs: azathioprine, cyclosporine |
|
|
Lymphangectasia: Three breeds predisposed?
|
1. yorkies
2. wheaten 3. lundehunds |
|
|
Lymphangectasia: C/S?
|
1. diarrhea/PLE
2. ascites/transudate 3. dilation and leakage of lacteals: protein, lumph, chylomicrons |
|
|
Lymphangectasia: Tx?
|
1. ultra low fat diet
2. prenisone 3. +/- additional immunosuppressive |
|
|
GI Neoplasia: What are the four types?
|
1. lymphoma
2. adenocarcinoma 3. leiomyoma/sarcomas 4. polyps |
|
|
Tenesmus/Dyschezia: Five causes
|
1. inflammation
2. infection 3. obstruction 4. urethral obstruction 5. constipation/obstipation |
|
|
Tenesmus/Dyschezia: What are the three cuases of inflammation?
|
1. anal sacculitis
2. perianal fistulas 3. tumors |
|
|
Tenesmus/Dyschezia: What are the two causes of infection?
|
1. pythiosis
2. histoplasma |
|
|
Tenesmus/Dyschezia: What are four causes of obstruction?
|
1. neoplasia
2. granulomas/abscesses 3. prostatic dz 4. pelvic fractures |
|
|
Tenesmus/Dyschezia: What species are predisposed to urethral obstruction?
|
Cats
|
|
|
Tenesmus/Dyschezia: What are two drug causes?
|
opiods and barium
|
|
|
Tenesmus/Dyschezia: What are two dietary causes?
|
fiber and indiscretion
|
|
|
Tenesmus/Dyschezia: What are two stool softeners?
|
DSS and lactulose
|
|
|
What is the cause of perianal fistula? Predisposed breed?
|
idiopathic immune mediated dz
GSD |
|
|
Perianal fistula: C/S?
|
painful draining tracts around anus
|
|
|
Perianal fistula: tx?
|
1. daily cleaining
2. topical tacrolimus 3. oral prednisone 4. cyclosporine 4. abx |
|
|
What will be seen on biochemistry: Anal sac adenocarcinoma?
|
hypercalcemia
|
|
|
CARIO
|
FUUUUCKKK MYYYYY LIIIIFE
|
|
|
Exocrine
|
Seconday to last.....
|
|
|
What does the exocrine pancreas produce? (2)
|
1. Digestive enzymes
2. bicarbonate production- neutralizes acid |
|
|
What does exocrine pancreas facilitate? (3)
|
1. nutrient absorption
2. mucosal cell turnover 3. enzyme activation |
|
|
What does exocrine pancreas inhibit? (2)
|
1. autodigestion via enzyme inhibitors
2. bacterial proliferation |
|
|
What causes pancreatitis?
|
Inflammatory dz: activation of digestive enzymes within the pancreas- maintained and exacerbated by inflammatory cytokines and free radial prodiction
|
|
|
Pancreatitis: What are the causes?
|
Unknown: diet/malnutrition, stress, low protein w/ high fat, hyperlipidemia, drugs, duct obstruction, trauma, hyperadrenocorticism, DM, previous GI dz, hypothyroidism
|
|
|
Pancreatitis: What breed is predisposed to hyperlipidemia causing pancreatitis?
|
miniature schnauzers
|
|
|
Pancreatitis: Acute dz?
|
necrotizing
hemorrhagic leakage of digestive enzymes into serum and surrounding tissues systemic inflammation |
|
|
Pancreatitis: What is the triaditis?
|
1. pancreatitis
2. cholangiohepatitis 3. IBD |
|
|
Pancreatitis: Signalment?
|
middle aged: females and yorkies
Obese Hx of high fat meal or garbage invasion |
|
|
Pancreatitis: Clinical signs? (7)
|
1. depression
2. anorexia 3. vomiting 4. diarrhea 5. shock 6. abdominal pain 7. +/- icterus |
|
|
Pancreatitis: Acute: What will the chemistry show? (7)
|
1. hyper/hypoglycemia
2. hypocalcemia 3. elevated liver enzymes 4. hypercholesterolemia/hyperglyceridemia/hyperlipidemia 5. bilirubinemia 6. renal or pre-renal azotemia |
|
|
Pancreatitis: Acute: What will be seen on the CBC? (4)
|
1. hemoconcentration
2. anemia 3. thrombocytopenia 4. neutrophilia w/ left shift |
|
|
Pancreatitis: Acute: What will be seen on the UA? (3)
|
1. bilirubinuria
2. hemoglobinuria 3. concentrated USG |
|
|
Pancreatitis: What are the diagnostic tests? (2)
|
1. TLI
2. PLI- test of choice |
|
|
Pancreatitis: Acute: Treatment? (7)
|
1. fluids
2. pain meds 3. +/- NPO... controversial 4. anti-emetics 5. plasma 6. H2 blockers or proton pump inhibitors 7. Abx |
|
|
Pancreatitis: Acute: Prognosis?
|
Depends on severity of dz- severe dz are often fatal (4)
1. MODS 2. ARDS 3. thromboembolism 4. DIC |
|
|
Pancreatitis: Chronic: Signalment?
|
middle aged to older: CKCS, Cockers, Collies, Boxers, DSH cats
|
|
|
Pancreatitis: Chronic: C/S? (6)
|
1. smoldering
2. waxing and waning GI signs/EBDO 3. no serum abnormalities 4. malabsorption/maldigestion 5. acute exacerbations: eventual insufficency, fibrosis 6. progression to DM or EPO |
|
|
Pancreatitis: Chronic: Diagnosis? (5)
|
1. CS and Hx
2. U/S 3. TLI 4. cPLI 5. Biopsy- GOLD STANDARD |
|
|
Pancreatitis: Chronic: Tx?
|
1. Low fat diet
2. cobalamin supplement 3. symptomatic tx for acute exacerbations: GI and liver protectants 4. +/- abx |
|
|
Hyperlipidemia: What are the two types?
|
true vs. post prandial
must do a > 12 hr fast |
|
|
Hyperlipidemia: What are the clinical syndromes? C/S?
|
pancreatitis and hyperviscosity syndrome
severe illness and seizures |
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Hyperlipidemia: idiopathic hyperchylomicronemia: signalment? Causes?
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Small breed dogs
< lipoprotein lipase activity or < aproprotein |
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Hyperlipidemia: What is idiopathic hyperlipidemia of Mini schnauzers?
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elevation in VLDL and depressed LDL due to a defect in LPL or Apo C-II
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Hyperlipidemia: C/S?
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Acute pancreatitis: vomiting, abdominal pain, lethargy
seizures: hyperviscosity |
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Hyperlipidemia: diagnosis?
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1. fasting lipemia
2. triglycerides > 500 mg/dL |
