Anesthesia
Which drugs are reversible and what are the reversibles?
alpha 2 agonist - atipamezole
Benzodiazepines - flumazenil
Opioids - naloxone
What is GP mycosis and how is it treated
Mycotic plaques form in gutural pouch
Erode mucosa and damage nerves and arteries
Unilateral mucopurulent nasal discharge
Epistaxis (unilateral) from erosion of the carotid artery
Dysphagia from cranial nerve
Diagnosis: Endoscopy, Gross lesion is diagnostic, Histology of plaque biopsy
Treatment: Topical and systemic antifungals, embolize carotid, ballon tipped catheter
What are the clinical signs of pericardial effusion and what do you expect to see in a physical exam? (Bonus what is the difference in rhythm when pericardial effusion is accompanied by cardiac tamponade vs when it is not)
Clinical signs
Reduced cardiac output, exercise intolerance, syncope
Elevated filling pressure (edema, congestion systemic veins, ascites)
HR increases due to a compensatory mechanism
Physical examination
1. Muffled heart sounds
2. Weak femoral pulses
3. Venous congestion = jugular pulses
4. Pulsus paradoxus: dec systolic pressure while diastolic stays the same
bonus: PE + cardiac tamponade = sinus tachycardia, PE + NO cardiac tamponade = sinus rhythm
What is the difference between progressive vs nonprogressive atrophic rhinitis? How is it treated and prevented?
Non-progressive: Bordetella bronchiseptica (toxigenic strains). Progressive: Pasteurella multocida
Treatment: tetracyclines
Prevention: Ventilation, dust/ammonia control, vaccines (Bb + Pm toxoid)
Which diseases are reportable?
African horse sickness, classical/african swine fever, Equine viral arteritis,
Bovine anaplasmosis,
Newcastle disease, avian influenza, fowl cholera, marek's disease, Avian chlamydiosis
how does hypothermia,hyperthermia affect vasodilation/vasoconstriction and heart rate
Hypothermia (↓ body temp)
Vessels: Causes peripheral vasoconstriction (to conserve core heat).
Heart rate: Typically bradycardia. Cooling slows the SA node’s pacemaker activity and conduction.
Overall cardiovascular effect: Increased systemic vascular resistance, but reduced cardiac output due to lower HR and contractility. Severe hypothermia may cause arrhythmias.
Hyperthermia (↑ body temp)
Vessels: Causes peripheral vasodilation
Heart rate: Typically tachycardia. The body increases HR to maintain cardiac output despite vasodilation and to support heat loss.
Overall cardiovascular effect: Decreased systemic vascular resistance, possible hypotension; HR rises to compensate. Severe hyperthermia (e.g., malignant hyperthermia, heat stroke) → can cause arrhythmias and high HR
What is exercise induced pulmonary hemorrhage? What is the signalment? What is the cause? How is it treated?
Signalment: racing through breds and barrel racers (performance animal)
Cause
Pulmonary pressures > 100 mmHg during exercise
Alveolar pressure drops = increased pressure gradient
Pressure between the capillary and alveoli causes blood vessels to rupture the alveoli
Tx:
Short term: Lasix (diuretic → ⬇️ blood volume and pressure) and corticosteroid thErapy (diminish inflammation)
Long term: rest but lesions take a long time to resolve
Which congenital diseases cause Left vs Right heart volume overload AND pressure overload. (bonus where are the murmurs heard)
Left heart volume overload: PDA (left axilla), VSD (right sternal border), MVD (left apical)
Right heart volume overload: TVD (right CCJ), ASD (none or PS murmur)
Pressure over load: SAS (left base) and PS (left base)
What are the 2 small ruminant retroviruses? Discuss their similarities and differences.
Sheep - OPP
Clinical signs: lymphoproliferative pneumonia, meningeal arteritis with encephalitis, non-suppurative arthritis, and lymphocytic mastitis. fatal pneumonia, physical weakness, dyspnea, emaciation
Necropsy – the lungs are firm and don’t collapse, and are grey-brown in color.
Goats = CAE
Kids: neuro
Adults: arthritis
They are both transmitted by colostrum and milk. They both could have a secondary bacterial infection leading to the thickening of the interalveolar septa and lymphoid hyperplasia.
Describe interstitial emphysema in ruminants.
Forced expiration → bronchiolar collapse → air trapped distally in alveoli → alveolar rupture → leakage of air into interlobular septa
No collateral ventilation = necropsy lung looks like it has grey lines
What are the causes of hypoxemia and their associated treatments?
1 - low FiO2 / decreased inspired O2 = supplemental O2
2 - Hypoventilation = mechanical/manual ventilation
3 - diffusion impairment = treatment of underlying disease
4 - R to L shunt = treatment of underlying disease (supplemental O2 does not work)
5 - V/Q mismatch = postive-end expiratory pressure, alveolar recruitment maneuvers, albuterol, increase cardiac output
What is the clinical signs, etiology and treatment of equine inophore toxicity?
Clinical signs:
-Colic, sweating, ataxia, arrhythmias
-Acute death or development of CHF over time due to poor contractility
Etiology:
-Disrupts cell membrane causing necrosis and poor contractility
Treatment:
-gastric lavage, charcoal, anti-fibrotics and anti-arrhythmics
Which heart defects are differentials for cyanosis and describe the flow of blood for each.
rPDA
(deoxygenated blood shunts from the MPA to the descending aorta when Ppa > Pa.
only the lower extremities will be cyanotic since the PDA is after the aortic arch. They will look pink in the mouth
R to L VSD (or R to L ASD)
Deoxygenated blood shunts from RV to LV and out of the aorta when RV pressure > LV pressure
TOF
Blood shunts from RV to systemic circulation due to high RV pressure (secondary to PS) and overriding aorta
Aorta outflow for RV and LV
Describe high altitude disease in cattle - what are the clinical signs, etiology, and treatment?
Primary clinical signs
-PAP > 41; > 48 do not breed
-R CHF: Ventral edema, pleural, pericardial, abdominal effusion, distended jv
Etiology
- Hypoxia causes pulmonary hypertension and cor pulmonale
Treatment:
-Remove to lower altitude, administer O2, drain pleural/pericardial fluid
What is caval syndrome?
Most severe manifestation of heartworm disease
> 40 worms: migrate into RV → RA → CdVC
Interfering with valvular function and blood flow
Acute clinical syndrome: DIC
A 4-month-old pig is anesthetized with halothane for a diaphragmatic hernia repair. 20 minutes into surgery, you note a rapid rise in ETCO₂, tachycardia, muscle rigidity, and the rectal temperature is climbing quickly. What is the most likely diagnosis and best immediate treatment?
Malignant hyperthermia – Stop halothane, give 100% O₂, administer dantrolene
The rapid ↑ ETCO₂ despite ventilation, rigidity, tachycardia, and temperature spike are classic MH signs.
Triggered by inhalants (esp. halothane in pigs, also iso/sevo).
Treatment = immediate cessation of inhalant, O₂, dantrolene, supportive cooling/fluids.
How is African horse sickness transmitted? What is the pathogenesis? What are the 4 types of clinical syndromes?
Non contagious
Transmission: Culicoides spp.
Pathogenesis: Infects endothelial cells causing edema
📢Reportable
Clinical syndromes
Peracute pulmonary form
Depression and nasal discharge
Progresses quickly to severe respiratory distress
100% mortality
Subacute cardiac form
Edema of the periorbital fossa and conjunctiva
50% mortality
Mixed pulmonary and cardiac form
Approximately 70% mortality
Mild subclinical form
zebras and donkeys
What are the clinical signs associated with canine nasal aspergillosis and how is it diagnosed? (Bonus: how is it treated)
Clinical signs
Nasal pain, ulceration, and depigmentation of the nares
Sneezing/reverse sneezing
Unilateral or bilateral sanguinopurulent nasal discharge and/or epistaxis
Culture results alone not definitive
Imaging is highly indicative
Debullk + topical tx
Antifungal treatment
Multiple relapse episodes
Hacking cough
Clear nasal discharge
Joint infection
severe swelling and lameness of one or more leg joint
Lameness is severe enough to cause the calf to starve to death
Most calves will recover if given enough time (weeks to months)
DO NOT CULL
Will recover → uncharacteristic of septic arthritis
Ear infection
drooped ear or ears
Mycoplasma = single droop ear
Head tilt
EAR INFECTION < lameness.
large amounts of cheesy waxy exudate
Which parasites are diagnosed via the baermann test vs facal float vs sedimentation
Baermanns: Dictyocalus spp., Muellerius capillaris, eucolles spp, aelurostrongylus abstrusses
fecal float: Paracaris spp., Ascaris suum
sedimentation: paragonimus kellicoti
What is MAC and what are some things that can increase and decrease it?
MAC = minimum alveolar concentration
Increase in MAC = need more anesthetic
ex - young age, hyperatremia, stress/pain/catecholamines, hyperthermia
Decrease in MAC = need less anesthetic
ex - hypoatremia, IV anesthetics, alpha-2 agonist, benzodiazepines, opioids, geriatric age, pregnancy, hypoxia, hypotension, anemia, hypothermia
What is the difference between A, B, and C lines
A lines = horizontal reverberation from waves traveling through air. Indication of air-filled lung
B lines / comet tails = abnormal = defect on pleural surface
Normal horses have a few as they age
Multiple = disease
Causes:
Pleuritis
Fibrin tags
Superficial abscesses (R.equi)
C lines = pleural fluid and lung consolidation
Fluid = ⬆️ space
Causes: inflammation, infection, and/or hemorrhage
What are the differences in clinical signs of histo vs blasto and how do you diagnose it?
Histo:
Weight loss, fever, anorexia, pale mm
Pulmonary involvement
Tachypnea, abnormal lung sounds
Splenomegaly, hepatomegaly
Panophthalmitis
Dogs: GI signs predominate
Cats: respiratory and others
Bone marrow infection: anemia, thrombocytopenia, neutropenia/philia
Blasto
Lungs, Lymph nodes, skin, eyes, bone infected
Weight loss, inappetance, cough, respiratory distress
Fever, abnormal lung sounds, chorioretinitis, anterior uveitis, draining skin lesions, lymphadenomegaly, osteomyelitis
Cats rarely have clinical disease
leukocytosis
diagnosis: urine antigen test, demonstrate organisms
treatment: azole antifungal, amphotericin B
What agent causes swine pleuropneumonia, what is the treatment, and key lesion?
agent: Actinobacillus pleuropneumoniae
Treatment: injectable antibiotics ( cefitofur, penicillin,) and antibiotics in feed
Lesion: caudodorsal lung effected
What is the difference between avian infectious laryngotracheitis and avian infectious bronchitis? AND which one is reportable
Causative agent:
IB: Infectious Bronchitis Virus (IBV), a gammacoronavirus with many serotypes.
ILT: Herpesvirus, antigenically uniform but variable in virulence.
Host range:
IB: Chickens only (all ages).
ILT: Chickens, pheasants, peafowl; similar disease in Amazon parrots.
Transmission:
IB: Explosive spread via aerosols and feces; can persist in the environment (~4 weeks) and via carriers.
ILT: Slow lateral spread; transmitted through secretions and fomites; may recur with stress due to latency.
Clinical signs:
IB: Primarily respiratory + reproductive + renal signs.
Chicks: depression, nasal discharge, huddling.
Adults: coughing, ↓ egg production, misshapen/wrinkled eggs, soft shells, watery albumen.
Some strains → kidney damage or false layer syndrome.
ILT: Respiratory and conjunctival disease.
Severe dyspnea, bloody mucus, coughing, “blood on walls.”
Mild forms: conjunctivitis, nasal discharge, ↓ egg production.
Lesions:
IB: Catarrhal to caseous tracheitis, cloudy air sacs, swollen kidneys (nephropathic strains).
ILT: Caseous/bloody plugs in trachea, severe laryngotracheitis, sinusitis.
Diagnosis:
IB: PCR, virus isolation, serology, or sentinel birds.
ILT: Histopath with intranuclear inclusions, PCR.
Treatment:
IB: No antiviral; supportive care, antibiotics for secondary infections.
ILT: No treatment; may vaccinate unaffected birds during outbreak
Prevention
IB: Live + killed vaccines, must match local strains; given early and before lay.
ILT: TCO vaccine (eye drop) after 4 weeks; strict biosecurity
ILT IS REPORTABLE