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Teaching and learning about veterinary diagnostic imaging.

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4 p's:

PU/PD

Polyphagia

PantingPanting

-Pendulous abdomen

-Thin skin

3 types of the disease:

>Pituitary Dependent Hyperadrenocorticism (PDH)

>Adrenal Dependent Hyperadrenocorticism (ADH)

>Iatrogenic

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-Sago palm: acute hepatotoxicity, hepatic necrosis, neurologic signs

-Marijuana: Prolongued sedation, hypotension, bradycardia, hypothermia, mydriasis, hyperexcitability. Rarely lethal

-Foxglove: Cardiac glycosides, arrhythmias, lethargy, GI upset, hyperkalemia. Highly lethal

-Oleander: Cardiac glycosides, arrhythmias, lethargy, GI upset, hyperkalemia. Highly lethal

-Yew: Vomit, diarrhea, hypotension, bradycardia, tremors, seizures. Potentially lethal

-Cholecalciferol (Vit D3): Hypercalcemia and hyperphosphatemia lead to metastatic mineralization of soft tissues, following signs of renal, cardiac, and GI damage

-Raisins and grapes may cause acute renal failure

-Griffonia simplicifolia: Can cause serotonin syndrome. It is used as an antidepressant in Africa, contains 5-hydroxytryptophan causes seizures, tremors, hyperesthesia, ataxia, vomiting, diarrhea, hyperthermia, transient blindness.

-Ma Huang: Hyperthermia, tachycardia, tremors

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-Arsenic toxicosis: Ant baits. GI hemorrhages (check renal damage). Tx. Succimer or penicillamine as chelator

-Amitraz: Component of tick prevention collar. Reverse with Atipamezole

-Tricyclic antidepressants: Treat with Sodium bicarbonate.

-Ethylene glycol: Antifreeze. TX 4-methilpirazole (fomepizole 4-MP). Acute renal failure

-Zinc oxide: is a component of baby diapers. Normal attitude but vomit and diarrhea due to GI irritation

-Zinc toxicosis: By ingesting US pennies, batteries, car parts, paint, zinc-oxide sunscreen creams, screws, galvanized metals

-Chocolate: Methylxanthines caffeine and theobromine are the toxic components in chocolate, the darker the more harmful. Tx Methocarbamol, anticonvulsants, anti arrythmics. Decontaminate (emesis, activated charcoal)

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-Doxycycline: Leptospirosis (acute initial indication, and for clearing renal infection). If concurrent hepatic disease a Beta-Lactam can be used initially to address LEPTOSPIREMIA, but Doxycycline MUST be finally used to clear renal Leptospira infection. Also to treat vector-borne disease

-Doxorubicin: Nephrotoxic for cats, cardiotoxicity for dogs. Be aware of age and chronicity.

-Fenbendazol: Whipworm, Trichuris

-Imidocarb: Babesia spp (parasite anticholinergic)

-Levetiracetam: Anticonvulsant indicated when portosystemic vascular liver disease, is not metabolized by liver

-Phenobarbital: Anticonvulsant

-Finasteride: Androgen inhibitor, used in prostatic hypertrophy to decrease prostate size

-Selegiline: To treat Cognitive dysfunction syndrome

-Oclacitinib: FDA-approved for allergic skin diseases, such as atopic dermatitis. Increases risk of infection as it inhibits proinflammatory cytokines

-Pimobendan: common to treat heart disease and myxomatous Mitral Valve Disease MMVD. Vasodilator. Contraindicated with arrhythmias

-Sulfa trimethoprim: Relation with keratoconjunctivitis sicca

-Timolol (Beta blocker): Glaucoma. Adverse effects: eye discomfort dryness irritation, systemic lower pressure, bradycardia, allergic

-Dorazolamyde (carbonic anhydrase inhibitor): Glaucoma, decreases aqueous humor production

-Misoprostol: Prostaglandin E1 analog, decreases the risk of GI ulceration associated with NSAIDs

-Latanoprost (prostaglandin): Glaucoma, increase aqueous humor drainage

-Carprofen: NSAID commonly for arthritis, side effect GI upset, hepatopathy (rare)

-Apomorphine in conjunctival sac: to induce emesis with hypotension risk, when xylazine is not indicated since causes first brief hypertension but results in hypotension

-Vitamin K (Phytonadione): for coagulopathy secondary to decreased enteric absorption

-Alprazolam: For noise-related phobias

-Diltiazem: Atrial fibrillation

-Lidocaine: IV anti-arrhythmic

-Ivermectin

-Atropine: To treat organophosphate intoxication

-Benazepril: ACE inhibitor, can be used to treat protein loosing nephropathy

-Desmopressin acetate (vasopressin): To enhance surgical hemostasis in a patient with types I and II von Willebrand disease

-Clotrimazole: topical tx of nasal aspergillosis

-Lokivetmab: Tx of atopic dermatitis, a dog-specific monoclonal antibody, neutralizes interleukin 31

-Cephalexin: first choice Ab for acute mastitis pending culture results

-Amitraz: has been discontinued as causes sedation, hypothermia, hypotension, bradycardia, hyperglycemia, and GI stasis. Antagonist Atipamezole

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-Low dexa test

-ACTH stimulation test

-High dexa test (differentiate PDH from ADH

-PDH: 75% will suppress

-ADH won`t suppress

Treatment:

Medical:

> Trilostane

>Mitotane

>Lysodren (cause neoplastic adrenal glands necrosis)

Surgical:

>Adrenalectomy

Prognosis:

Fair to Poor

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Typical signs: obesity, rat tail, cold, “tragic face”

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Typical signs: obesity, rat tail, cold, “tragic face”

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Aditional sx: estibular signs, facial paralysis, laryngeal paralysis (stridor)

DX: Total T4

Free T4 (most accurate as single test)

TSH normal doesnt rule out, high: highly supportive

TX: Levothyroxine

Euthyroid syndrome: Thyroid not underlying problem. Rule out other diseases

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Acute:

>Hypovolemic shock

>Weakness

>Vomiting

Chronic:

>Non-specific

>Can be mistaken (GI disease/renal disease/pancreatitis)

>PU/PD

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SX: puppies 7 weeks - 12 months old / Vomit, diarrhea

DX: parvo fecal ELISA (false +: vaccination, false -: Fecal sample taken out of shedding time)

Blood chemistry: Leukopenia neutropenia, hypoalbuminemia, hypokalemia, pre-renal azotemia

TX: FLUID THERAPY-KLC/dextrose, additives colloid betstarch

ABS: Ampicilline, cephalosporines, metronidazol

ANTI EMETICS: ondansentron, maropitant

PX: Vaccination

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CAUSE: ⬆️ Fat diet

SX: Vomit, diarrhea, abdominal pain, anorexia

DX: Pancreatic lipase immunoreactivity

US: Enlarged hypoechoic pancreas with periferal hyperechoic fat

TX: Fluid therapy

Antiemetics: Ondansentron, maropitant

Pain control: Fentanyl, hydromorphone

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ETHIOLOGY:

Congenital: Persistent right aortic arch

Acquired: Myastenia gravis, addison (muscle tone loss)

DX: XR-esophagus distention

ACTH stimulation test: Addison

Acethylcholine receptor antibody titer: Myastenia gravis

TX: ADDISON- glucocorticoid & mineralocorticoid

MYASTENIA GRAVIS: Pyridostigmine (anticholinesterase)

*Prevent aspiration pneumonia

*Prokinetics: help speed gastric emptying

*Proton pump inhibitors: lower gastric acid

*Gastrotomy tube: lower regurgutation

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Soft-tissue sarcomas are poorly characterized despite being common tumors. It can be difficult to determine their biologic behavior and if they are benign or malignant. Generally, benign soft-tissue sarcomas have a superficial location, small size, slow rate of growth, and low vascularity.

Tx: Surgical excision with wide margins; Obtain as wide as possible margins.

If the tumor is in an area with limited tissue, consider adjunctive radiation therapy or amputation.

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Old dog, anemic, large-breed with collapse, mass in the cranial abdominal cavity, organomegaly, cavitated splenic mass(the spleen is the most common site), and free abdominal fluid.

Tx: Stabilize the patient and consider exploratory laparotomy with splenectomy and chemotherapy.

Px: Guarded to poor

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It is thought to be inherited in German shepherds (has also been described in rough-coated collies and other breeds)

Maldigestion, weight loss/failure to gain weight, diarrhea, and polyphagia are caused by insufficient secretion of pancreatic digestive enzymes by the exocrine pancreas (acinar atrophy).

Concurrent small intestinal dysbiosis and cobalamin deficiency are common. Dogs with EPI frequently have loose stools that are “antibiotic-responsive” due to small intestinal bacterial overgrowth.

Diagnosis: Measure serum trypsin-like immunoreactivity concentration (<2.5 µg/L)

Tx: Oral enzyme replacement and cobalamin supplementation if deficient

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Predisposición: non spayed female

Clinical signs: Depression, anorexia, fever, lethargic, PU/PD

Dx: US (image like multiple bladders)

Tx: Ovariohysterectomy

Prognosis: Depend on clinical signs or other organs involved (kidney disease).

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Platelet count and buccal mucosal bleeding time (BMBT)

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Hemostasis is a complex physiological process involving cells (platelets, especially but also fibroblasts), and soluble (coagulation factors and inhibitors) and insoluble proteins (extracellular matrix proteins). The hemostatic system is usually activated upon injury to the blood vessels, which disrupts endothelial cells exposing thrombogenic (or procoagulant) substances in the extravascular space. Once activated, the hemostatic system serves to seal off the injury through platelet plug and fibrin clot formation. This allows time for the injured endothelium to heal. Once healed, the clot must be dissolved (fibrinolysis) to restore blood flow.

The hemostatic system is really a delicate balance of pro- and anticoagulant forces and can be thought of a pendulum that swings between these forces. Initially on vessel injury, procoagulant forces dominate resulting in a fibrin/platelet clot, which seals off the injured blood vessel. Once the endothelium has healed, the pendulum swings in favor of anticoagulant and profibrinolytic forces, allowing clot lysis and restoring blood vessel patency.

Alterations in this delicate balance can result in hemostatic abnormalities, which can manifest as either hemorrhage or thrombosis. Most animals with hemostatic disorders present with clinical signs of excessive hemorrhage. In contrast, thrombosis is far more difficult to detect clinically or by laboratory tests, particularly when it occurs in internal microvessels. When any animal presents with clinical signs of a hemostatic disorder (hemorrhage or thrombosis), it is essential to do a complete diagnostic evaluation, including performing a thorough physical examination and taking a detailed history. Vital clues as to the underlying cause of the hemostatic disorder are obtained from the signalment (age, breed and sex), history (e.g. access to toxins or drugs, evidence of multiple hemorrhagic episodes) and clinical signs (e.g. type and location of hemorrhage).

This section is organized as follows

Physiology: Information on how hemostasis works, distinguishing processes of primary hemostasis, secondary hemostasis, fibrinolysis and inhibitors.

Diagnostic approach: How to work up a patient with a hemostatic disorder.

Clinical signs: Expected clinical signs associated with hemostatic disorders.

Sample collection: Crucial!! How not to mess up hemostatic test results, which are majorly affected by preanalytic (sample collection and storage) variables.

Tests: Different tests of hemostasis, separated into sections based on

Disorders affecting hemostasis.

Test summary: Table summarizing changes in hemostasis test results with various disorders.

Primary hemostasis: Vessel wall defects, thrombocytopenia, thrombopathia, von Willebrand disease.

Secondary hemostasis: Inherited factor deficiencies, vitamin K deficiency/antagonism

Inhibitors

Global disorders: Disseminated intravascular coagulation, underlying disease, drugs.

Transfusion medicine

Blood collection for transfusion purposes.

Blood components used for transfusion, e.g. whole blood, packed red blood cells, cryoprecipitate.

Blood types: The different blood groups in animals.

Cross-matching: How and when this test is performed.

Transfusion therapy: What and how to administer transfusions, with dose guidelines.

Adverse reactions: Immune and non-immune mediated reactions to transfusions.

Related links

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Hemostasis is a complex physiological process involving cells (platelets, especially but also fibroblasts), and soluble (coagulation factors and inhibitors) and insoluble proteins (extracellular matrix proteins). The hemostatic system is usually activated upon injury to the blood vessels, which disrupts endothelial cells exposing thrombogenic (or procoagulant) substances in the extravascular space.

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Multifactorial: tumors, vaccination, sepsis, medications

: May trigger an autoimmune response against erythrocites

Sx: icterus, hepatomegaly, splenomegaly, discolored urine

Dx: blood smear: spherocytes, anisocytosis, poikylocitosis

Saline slide agglutination: differentiates rouleux

Urine: hemoglobinuria, bilirubinuria

Coombs: aglutination +

Tx: immunosupressors: prednisone, azathioprine, cyclosporine, mycophenolate

Anticoagulants: clopridogel, low dose aspirin

Blood transfussion

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Is seen most commonly in older dogs (median age eleven years) with a history of pollakiuria, stranguria, dysuria, and hematuria. Scottish terriers have a 20-fold increased risk.

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Congenital and Inherited Spinal Cord Disorders in Animals - Nervous System - Merck Veterinary Manual

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Learn about the veterinary topic of Congenital and Inherited Spinal Cord Disorders in Animals. Find specific details on this topic and related topics from the Merck Vet Manual.

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Clinical signs:

PU/PD

Increased appetite

Weigh loss

If ketoacidosis: vomiting, inappetence, lethargy

Diagnosis:

Serum chemistry profile: Hyperglycemia , hypercholesterolemia

UA: Glucosuria, ketonuria, low USG

Treatment:

Insuline (NPH, Vetsulin)

Diet change: Higher fiber diet, prescription diabetic diet

If ketoacidotic: Hospitalization for IV fluids, anti-emetics, other supportive care for symptoms.

Prognosis:

Fair to good