ABVP List of conditions Flashcards
Dental Caries (106 cards)
1
Q
What is a mesioversion?
A
When persistent deciduous teeth can cause permanent teeth to erupt in an abnormal position resulting in a malocculsion. In this case, maxillary canine teeth erupt mesial (rostral) to retained deciduous teeth this can result in a diastema (space) that is too narrow to accomodate the crown.
2
Q
Linguoversion is what?
A
When the mandibular canine teeth erupt lingual to the persistent deciduous teeth, this can result in a narrow space between the lower canines resulting in impingement on the soft tissue of the hard palate
3
Q
What is a rostral crossbite?
A
All permanent incisors erupt lingual to persistant deciduous incisors
4
Q
What is a long term complciation from a linguoversion of permanent teeth?
A
When mandibular teeth form a liguoversion it can result in trauma and an oronasal fistula
5
Q
Why are dental radiographs important when considering planning of removal of deciduous roots?
A
If the deciduous root has undergone resorption, it may not require extraction of the full root. However, if the permanent tooth has erupted in an abnormal position, it will require extraction.
Also, can identify between permanent and deciduous teeth, can identify dental abnormalities prior to extraction, such as persistent deciduous tooth with no successor, retained root with rown missing, unerupted permanent tooth
6
Q
Retained deciduous teeth are more common in:
A
Dogs than cats, and more common in small breed dogs vs large breed dogs
7
Q
What is a dentrigerous cyst?
A
Cyst formation originating from tissue surrounding the crown of an unerupted tooth.
8
Q
How is this treated?
A
If cystic formation is present, surgical extraction, complete debridement of cyst lining and histological evaluation is indicated
9
Q
Complications of dentigerous cyst?
A
Pathological fracture if not treated, fracture of mandible at time of extraction due to compromised supporting bone, root resorption or devitalization of neighboring teeth
10
Q
What is diabetes insipidus?
A
Disorder of water metabolism characterized by PU, urine of low specific gravity or osmolality. Central DI (CDI) is caused by a deficiency in the secretion of antidiuretic hormone (ADH). This form can be secondary to a pituitary tumor. Nephrogenic DI is caused by renal insensitvity to ADH.
11
Q
How is renal insensitivity to ADH caused?
A
Congenital defect in aquaporin, secondary to drugs (lithium, demeclocycline), secondary to endocrine disorders such as hyperadrenocorticism, hypercalcemia, secondary to renal disease or infection.
12
Q
How is diabetes incipidus diagnosed?
A
MRI or CT if pituitary tumor is suspected, ADH supplementation trial, modified water deprivation test. Rule out all other causes of PUPD prior to considering primary central diabetes incipidus. Classically, the urine specific gravity is less than <1.006
13
Q
Diabetes mellitus with hyperosmolar hyperglycemia is caused by/criteria:
A
Hyperosmolar hyperglycemic state is a complicated form of diabetes mellituscharacterized by severe hyperglycemia and dehydration that produces a marked elevation in serum osmolarity. Unlike DKA, ketone production and metabolic acidosis are not major features of HHS. serum effective osmolarity >320, glucose >300, bicarbonate >18 with minimal ketonuira are criteria in humans.
14
Q
A
15
Q
How do you claculate serum osmolarity?
A
2(NA + K) + (BUN/2.8 + Glucose/18)
16
Q
Diabetic ketoacidosis is what?
A
A medical emergency that is secondary to absolute or relative insulin deficiency characterized by hyperglycemia, ketonemia, metabolic acidosis and electrolyte depletion.
17
Q
What is the pathophisology of diabetes mellitus in cats.
A
The most common form in cats resembles type II or non insulin dependent diabethes mellitus of humans. Insulin resistance impairs the ability of tissues to use carbohydrates, fats and proteins. Impaired systemic glucose utilization coupled with ongoing hepatic gluconeogenesis causes persistent hyperglycemia, which directly impiars insulin secretion by reducing function beta cell mass (glucose toxicity) Beta cell dysfunction progresses to irreversible failure of insulin production as reactive oxidative sypecies, inflammatory cytokines and amyloid deposition perpetuate beta cell injury and loss.
18
Q
What diet is appropriate for a feline diabetic?
A
Ultra low carbohydrate (<12% metabolizable energy) and high protein (>40% metabolizable energy) canned diets may improve glycemic control and increase the liklihood of diabetic remission in newly diagnosed diabetic cats
19
Q
True or False:
In tact female cats should be spayed when diagnosed with DM as progesterone secreted during diestrus can make management of DM challenging.
A
True
20
Q
What insulin formulations are best in cats?
A
(U-40 for both) PZI which is protamine zinc and porcine zinc lente insulin
21
Q
What is feline diabetic remission?
A
Some cats may recover inuslin-secreting ability (diabetic remission) typically if glycemic control is achieved within 6 months. However, relapse is common (30%). Reported remission varies greatly, from 25%to 30% is a reasonable expectation. (reported ranges from 0-100%)
22
Q
Cataracts are a common finding in dogs with DM. What percent of dogs will have cataracts in >12 months of DM management?
A
80%
23
Q
Pathophysiology of canine DM
A
Generally canine DM is characterized by loss of insulin-secreting ability through presumed immune mediated destruction of pancreatic beta cells. Far less frequently, canine DM can develop as a result of combination of relative insulin-deficient state with concurrent peripheral insulin resistance.
24
Q
What should obese diabetic dogs be fed?
A
High fiber low calorie food, however this has no role in improving diabetic control (may improve patient satiety and owner satisfaction)
25
Canine insulin recommendations:
Vetsulin (porcine-origin lente) needs to be U-40 dosed, Humulin N, Novolin N are intermediate acting human insulins. PZI is rarely used in dogs.
26
Diaphragmatic hernia definition and types:
Protrusion of an abdominal organ through an abnormal opening in the diaphragm, can be an acquired injury or as a congenital defect. Can be acute, subacute or chronic. Can be pleuroperitoneal or peritonealpericardial diaphragmatic hernia.
27
Exam findings on an animal with diaphragmatic hernia:
Tramatic: cna be acute, subaute or chronic. History of blunt trauma. Difficulty breathing, evidence of shock (tachycardia, pale mm, weak pulses) GI sounds in thorax, empty abdomen- signs may be progressive
28
Prognosis with diaphragmatic hernia surgery is:
If animal survives first 12-24 hours post operatively, prognosis is excellent. 80-90% survival rate. Death is most often due to concurrent injury however respiratory distress, pneumothorax and reperfusion injury are all potential complications
29
Feline diarrhea is considered chronic at what point?
3 weeks, or with a pattern of episodic recurrence
30
Small bowel diarrhea is typically:
-normal to increased volume, normal to moderately increased defecation frequency, weight loss, polyphagia, melana, flatulence, vomiting is variable.
31
Large volume diarrhea:
Smaller volume, frequency of defecation is increased >4 x a day, hematocheia, mucus, tenesmus, urgency, dyschezia, flatulence, borborygmus variable
Body condition unremarkable
32
Feline chronic diarrhea- feeding an elimination diet (in tact novel protein source of hydrolyzed protein) will resolve diarrhea in what percent of cats with chronic enteropathy?
How long before there should be a response?
40-60% of cats respond, should see improvement in 2-3 weeks following dietary implementation. Repeated changes of diet made in order to maintain a symptom free situation indicates that further testing is needed
33
What percent of dogs are shown to have chronic diarrhea shown to be diet responsive? What kind of food is best?
Up to 75% Feeding lowerfat, novel (for the patient) protein source, highly digestible, or fiber supplemented diets for 3–4 weeks may resolve diarrhea due to dietary intolerance or allergy; repeated changes of diet to maintain symptom free situation suggests further testing needed.
34
Digotin toxicity
Patients are often on digoxin, it has a narrow therapeutic range. Renal disease impairs elimination, obseity can be a risk factor if not factored into disage, ingestion of owners medication is possible. For patients on it, check level 8-10 hours post oral dose. AV block, arrhythmias and ST depression
-Treat bradycardia with atropine or temp pacemaker
-Ventricular arrhythemias with lidocaine or phenytoin
-Digoxin binding antibiodies (expensive and limited)
Check thyroid level, supplement if low
35
What happens when a dog ingests diisocyanate glue?
-Includes wood glue, construction glue, gorilla glue
-Ingestion as small as 2 oz almost always requires surgical removal
-Expand rapidly in moist environment of stomach, causing bloat and FB obstruction
36
Tooth discoloration can have different causes, if the underlying dentin is effected what kind of discoloration is it?
Intrisinic, if it effects the surface is it extrinsic
37
If a dog has hyperbilirubinemia during development?
Affects all teeth during dentin formation bilirubin accumulates in dentin from excess red blood cells. Extent of discoloration depends on length of hyperbilirubinemia
38
What is the condition that results in developmental alteration in the structure of enamel affecting all teeth; chalky appearance with a pinkish hue; problem in the formation of the organic matrix, mineralization of the matrix, or the maturation of the matrix?
Amelogenesis imperfecta
39
What is developmental alteration in dentin formation; enamel separates easily from the dentin, resulting in grayish discoloration?
Dentinogenesis imperfecta
40
What can an infection such as parvovirus or distemper virus do to the teeth?
Parvovirus, distemper virus, or any agent that causes a sustained body temperature rise; affects the formation of enamel; a distinct line of resolution is visible on the teeth; affects all teeth developing at the time of the insult; results in enamel hypoplasia or hypocalcifica- tion where the abnormal enamel can have black edges and the dentin is brownish.
41
What is the key difference between extrinsic and intrinsic stain in discolored teeth?
Extrinsic stain removal is mainly cosmetic, intrinsic stain treatment is functional and pain relieving.
42
Simple way to start with extrinsic stain removal in discolored teeth?
Polishing the teeth with 3% hydrogen peroxide
43
Definition of discospondylitis
A bacterial, fungal and rarely algal infection of the intervertebral end plates, discs and adjacent vertebral bodies
44
What is the most common bacterial cause of discospondylitis?
Staphylococcus pseudintermedius, others include streptococcus, brucella canis, e coli
45
What fungal infections can cause discospondylitis?
spergillus, Paecilomyces, Scedosporium apiospermum, and Coccidioides immitis.
46
Grass awn migration can cause discospondylitus, what specifically are you concerned about and what disc spaces would you examine closely?
Actinomyces L2-L4
47
How can you differentiate vertebral neoplasia vs discospondylitis radiographically?
Vertebral neoplasia does not usually affect adjacent vertebral end plates
48
Risk factors for discospondylitis?
UTI, reproductive tract infection, periodontal disease, bacterial endocarditits, pyoderma, immunodeficiency, recent steroid administration, in tact males
49
What kind of culture would you send out for discospondylitits?
Aerobic, anaerobic, and fungal blood cultures (this will give you an answer in 35% of cases)
Urine culture- this is positive in 30% of cases
Serologic testing for brucella canis
50
Imaging to consider for discospondylitis:
Spinal radiography—usually reveals lysis of vertebral end plates adjacent to the affected disc, collapse of the disc space, and varying degrees of sclerosis of the end plates and ventral spur formation; may not see lesions until 3–4 weeks after infection (therefore normal radiographs do not rule out).
* Myelography—indicated with substantial neurologic deficits; determine location and degree of spinal cord compression, especially if considering decompressive surgery; spinal cord compression caused by discospondylitis typically displays an extradural pattern.
* CT or MRI—more sensitive than radio- graphy; indicated when radiographs are normal or inconclusive.
51
What treatment choice would you select for discospondylitis if there is a negative culture?
Assume its staphylococcus and treat with cephalexin 22 mg/kg for 8-12 weeks
Treat with IV antibiotics initally if clincial signs are acutely progressive (cefazolin 22 mg/kg IV q 8 hours)
**Remember, this condition can be surgical if there is spinal cord compression or if there is no improvement with antibiotic therapy- most of the time clinical improvement is noted after 5 days
52
What organisms causes ear mites and how do you treat them?
Otodectes cynotis, ears should be thoroughly cleaned. Selamectin per label instructions or repeated in two weeks, imidacloprid/moxidectin (advantage multi) isoxazolines
Caution with ivermectin in ABCB-1 mutant dogs
53
Describe eclampsia, when it commonly occurs and CBC abnormalities
Postparturient hypocalcemia, usually occurs 1-4 weeks post partum, life-threatening tetany and convolusions (normally seum calcium <9 in bitches, <8 in queens)
Inoinized calcium is the form important for neuromuscular function
54
Treatment of eclampsia
-Treat hyperthermia, remove puppies from the dam and hand raise, if not possible remove them until calcium is stable and supplement calcium/monior
Calcium gluconate 10% 0.22 ml/kg
Calcium carbonate or calcium gluconate until lactation ends (if magnesium is low, supplement)
-CALCIUM SUPPLEMENTATION not during gestation- calcium phos ratio should be 1.1 :1 or 1.2 to 1 - avoid high phyate foods like soybeans
-Likely will occur with litters in future
55
Ectropion
Eversion or rolling out of the eyelid margin, resulting in exposure of the palpebral conjunctiva.
* Can be conformational/congenital (primary) or acquired (secondary).
* Exposure and poor tear retention/ distribution may predispose patient to irritation, recurrent infections, and sight- threatening corneal disease.
Surgical treatment—eyelid shortening or radical facelift; necessary for severely affected patients that have chronic ocular irritation.
56
What is the predominant species of ehrlichia and how is it transmitted?
Ehrlichia canins, canine monocytic ehrlichiosis
obligate intracellular pathogens
Rhipicephalus sanguineus (brown dog tick) tick vector; infects mononuclear cells; 1–3-week incubation period; three stages of canine disease: ◦ Acute (2–4 weeks)—spread to spleen, liver, lymph nodes; causes endothelial cell and perivascular inflammation, thrombocytopenia (possible antiplatelet antibodies), mild anemia; infections may be subclinical. ◦ Subclinical (months–years)—organism persists; hyper- globulinemia; mild thrombocytopenia; dogs may eliminate infection, others remain persistently infected or develop chronic disease. ◦ Chronic—myelosuppression; pancytopenia. *
57
Ehrilchia ewingii is transmitted by what and how is it different?
Amblyomma americanum (lone star tick) tick vector; infects granulocytes; dogs can be persistently infected and asymptomatic; acute clinical signs include fever, neutrophilic polyarthritis, neutrophilia, reactive lymphocytes, and proteinuria; bleeding disorders uncommon.
58
Anaplasma, what are the two types?
Anaplasma phagocytophilium and anaplasma platys. A. phagocytophillium is granulocytic anaplasmosis, a. platys is thrombocytic.
A. Phagocytophiliu Ixodes tick vector, a platys is tick vector likely r. sanguineus
59
Ehrlichia historical findings and PE exam findings
Historical Findings
* Fever, lethargy, anorexia, weight loss. Spontaneous bleeding—sneezing, epistaxis, petechia, ecchymosis. * Ocular discharge/ pain. * Lameness. * Ataxia, head tilt
Acute
* Bleeding diathesis. * Fever. * Generalized lymphadenopathy. * Organomegaly (spleen, liver). * Ocular discharge. * Lameness. * Ticks.
Chronic E. canis
* Pale mucous membranes (anemia).
* Ulcerative stomatitis. * Hind limb or scrotal edema. * Uveitis, hyphema, retinal hemorrhages. * Ataxia, vestibular dysfunction, cervical pain.
60
Describe testing for erhlichiosis.
Antibodies present ~3 weeks postinfection. * Immunofluorescent antibody test (IFAT)— sensitive; cross-reactivity between Ehrlichia species; use same laboratory to compare acute and convalescent titers; fourfold increase paired in convalescent titer indicates active infection; detection at one time-point may represent past exposure or active infection.
PCR testing is also recommended. Detects pathogen DNA; sensitive indicator of active or recent infection. * Whole blood or tissue (spleen, lymph node, liver, bone marrow); identifies species; detect as early as 7 days postinfection. * Negative PCR result cannot rule out VBD infections; false negative can occur due to low organism load; genetic variations can prevent PCR detection. * Combining serology and PCR optimal for accurate diagnosis.
61
Ehrlichiosis and anaplasmosis prognosis:
Acute—prognosis excellent with appropriate therapy. * Chronic—prognosis guarded; cytopenia resolution may take >6 months; prognosis poor if hypoplastic bone marrow.
62
Ehrlichiosis and anaplasmosis treatment
Doxycycline—5 mg/kg PO q12h or 10 mg/kg PO q24h for 3–4 weeks; clinical response usually in 1–2 days; slower response in chronic ehrlichiosis or neurologic disease Prednisolone or prednisone, use with antibiotics; anti-inflammatory (0.5–1 mg/kg PO q12–24h for 3–5 days) for polyarthritis; immunosuppressive (1–2 mg/kg PO q12h for 5 days; rarely exceed 60 mg/dog/day) when immune-mediated disease suspected. *
63
What is elbow dysplasia?
A group of developmental abnormalities that lead to malformation, degeneration and secondary OA of the elbow joint.
1. Un-united anconeal process (UAP)
2. Osteochondrosis dissecans
3. Fragmented medial coronoid process
4. Incongruity
64
Elbow dysplasia: Most common documented medial compartment disease pathologies?
Fragmented medial coronoid process and incongruity
65
Describe united acondeal process in elbow dysplasia
The delayed closure of the anconeal process and proximal ulnar metaphysis (olecranon) by 5 months of age may result in abnormal mechanical stress on anconeal process
66
In elbow dysplasia, where do OCD lesions occur?
Medial aspect of humeral condyle. It is a disturbance in the endhochondral ossification that casues retention of the articular cartilage and subsequent mechanical stress leads to a cartilage flap lesion
67
FMCP in elbow dysplasia is:
Chondral or osteochondral fragmentation or fissure of medial coronoid process of ulna; possibly manifestation of osteochondrosis of coronoid process; coronoid does not have separate ossification center; may be result of abnormal mechanical stress on medial coronoid process considered to be due to incongruity.
68
What is incongruity in reference to elbow dysplasia?
Incongruity is the asynchronous growth between radius and ulna which may lead to abnormal loading, wearing and erosion of cartilage in the humeroulnar compartment. Malformation of trohlear notch of the ulta will lead to decreased curviture of the notch, resulting in points of contact between the anconeal process, coronoid process and medial humoral condyl
69
Age of onset of clinical signs of elbow dysplasia?
Age at onset of clinical signs—typically 4–10 months.
* Age at diagnosis—generally 4–18 months. * Onset of symptoms related to degenerative joint disease (DJD)—any age.
70
You are examining a 10 month old lab who is resisting flexion, what are your thoughts?
Any resistance at all in flexion in immature dog should raise suspicion of elbow dysplasia. * Not all patients are symptomatic when young. * Intermittent episodes of elbow lameness due to advanced DJD changes in mature patient—common.
71
Describe clinical signs you look for when evaluating a dog for elbow dysplasia.
Pain—elicited on elbow hyperflexion or extension; elicited when holding elbow and carpus at 90° while pronating and supinating carpus and applying pressure to medial compartment.
* Affected limb—tendency to be held in abduction and supination.
* Joint effusion and capsular distension— especially noted between lateral epicondyle and olecranon.
* Crepitus—may be palpated with advanced DJD.
* Diminished range of motion.
72
What should you keep in mind when evaluating radiographs for elbow dysplasia?
1. Radiograph both elbows, often disease is bilateral
2. UAP—best diagnosed from mediolateral hyperflexed view; may see lack of bony union. Comparison to contralateral elbow may be helpful, although high incidence of bilateral disease should be kept in mind.
3. OCD—best diagnosed from craniocaudal and craniocaudal-lateromedial oblique views; reveals radiolucent defect or flattening of medial aspect of humeral condyle.
4. FMCP may or may not be visualized. DJD trochear sclerosis
73
How do you treat UAP in a dog?
4 options:
Removal, dynamic proximal ulnar osteotomy, lag screw fixation, dynamic proximal osteotomy plus lag screw fixation
74
How do you deal with OCD and fractured medial coronoid process?
Medial approach to elbow, removal of loose fragments
75
What is the most common signalment for electric cord injury?
Young animals, 5 months to 1.5 years.
76
What are some common clinical signs?
* Burns associated with gingiva, tongue, palate. * Singed hair or whiskers. * Most common clinical signs are related to acute dyspnea. * Coughing. * Tachypnea.
* Orthopnea. * Increased respiratory effort. * Cyanosis. * Crackles during pulmonary auscultation. * Tachycardia. * Muscle tremors. * Tonic–clonic activity. * Collapse.
77
You have a 1 year old animal that has burns in their mouth, and has mild increased in respiratory rate and effort. What are next important diagnostics steps and what are you looking for:
* Thoracic radiographs may help distinguish between cardiogenic and noncardiogenic causes of pulmonary edema. * Radiographic pattern is usually a generalized, mixed alveolar bronchial pattern; edema is often most notable in caudal dorsal lung fields.
* Pulmonary venous congestion is absent with noncardiogenic pulmonary edema.
* Echocardiography may help identify or rule out underlying cardiac disease.
Check ECG
If you can get an arterial blood gas, it may support hypoxemia
78
How do you treat electrical shock in a dog or cat?
If in shock, treat with fluid bolus, treat anxiety and pain. Oxygen support as indicated. Check ECG, may need antiarrhythymic therapy
79
A young patient has been shocked by an electric wire. Describe prognosis.
Prognosis based on response to therapy.
* Pulmonary edema can develop as soon as
1 hour and as late as 36 hours after incident. * Pulmonary edema associated with electro- cution is associated with high mortality (38.5%). * If patient survives first 24 hours, prognosis improves. * Resolution of pulmonary edema may take 3–5 days. * Most oral lesions resolve. * Inappetence related to oral lesions resolves.
80
What breeds are predisposed to GME VS NECROTIZING granulomatous meningoencephalitis vs Neocrotizing leukocephalitis vs eosinophilic meningioecephalitis?
GME: toy poodle and terrier
NGME pug and chihuahua
NLE yorkie and frenchie
EME golden and rottie
81
Entropion definition
Inversion or rolling in of eyelid margin, resulting in frictional irritation of cornea and/ or conjunctiva from contact with outer surface of eyelid.
* May result in keratitis, corneal ulceration, or corneal perforation.
* Can be conformational/congenital (primary) or acquired (secondary).
82
Entropion breeds:
Common in dogs—seen in chow chow, Chinese Shar-Pei, Norwegian elkhound, sporting breeds (e.g., spaniel, retriever), brachycephalic breeds, toy breeds, and giant breeds; age—puppies as early as 2–6 weeks old; usually identified in dogs <1 year old.
* Cats—usually in brachycephalic breeds,in young cats due to chronic ocular surface disease, and older animals due to retrobulbar fat loss.
83
Treatment of entropion
* Do not initially perform skin resection surgery.
* If cornea ulcerated—topical antibiotic (e.g., neomycin/polymyxin B/bacitracin) ointment q6–8h.
* If mildly entropic and cornea not ulcerated, lubricate with artificial tear ointment q8–12h. * If moderate to severe entropion with or without corneal ulceration, temporarily evert eyelid margins with sutures to break the irritation–spasm cycle; if successful, permanent procedure is unnecessary; may need to be repeated every 2–4 weeks until adult facial conformation is achieved.
* Semi-permanent eyelid eversion with hyaluronic acid filler injection—lasts up to several months, often until adult facial conformation is achieved.
* Permanent skin resection technique— postponed until patient’s facial conformation matures (usually 1.5–2 years).
84
Hotz-Celsus procedure
Entropion treatment, which removes a sliver of tissue under eyelid margin - often combined with lid shortening procedures
85
What makes up eosinophilic granuloma complex in cats?
Eosinophilic plaque, eosinophilic granuloma, and indolent ulcer; grouped primarily according to their clinical similarities, their frequent concurrent (and recurrent) development, and their positive response to corticosteroids
86
Eosinophilic granuloma complex in dogs
Rare
Dogs <3 years of age 72% males
ulcerated plaques and nodules; green/ orange color; most often affects the tongue and palatine arches; uncommon cutaneous lesions on the abdomen, cheek, digits, prepuce, and flanks. * Cavalier King Charles spaniels—lesions on the soft palate or near the tonsils.
87
88
Most commonly, where are eosinophilic lesions located on a cat?
Single or multiple, alopecic, erythematous, eroded/ulcerated well demarcated and flat topped ± white necrotic foci; most commonly seen on the abdomen and medial thighs, but may also see in mucocutaneous junctions and other areas of the skin; frequently moist or glistening; may appear oval or linear due to pattern of licking.
89
Where are eosinophilic granulomas located on a cat?
Caudal thigh (linear granuloma)—distinctly linear orientation on the caudal thigh; chin (“pouting cats”)—lip margin and chin swelling; paw pads—footpad swelling, pain, and lameness; oral cavity—ulceration common (especially on the tongue, palate): cats with oral lesions may be dysphagic, have halitosis, and may drool; can be located anywhere on the body; spontaneous regression— especially in young cats with the inheritable form.
90
Describe an indolent ucler in a cat
Indolent ulcer—classically concave and indurated ulcerations with a granular, orange yellow color, confined to the upper lips near philtrum or upper canine teeth.
91
What are potential causes of eosinophillic granuloma complex?
* Hypersensitivity—flea or insect (mosquito bite), food hypersensitivity, and atopy; a heritable dysfunction has been proposed.
* Idiopathic. * EGD—unknown; genetics in susceptible breeds; a hypersensitivity reaction often suspected (insect bite) in nongenetically susceptible breeds.
92
A dog comes in with epididymititis/orchitits of one testicle. What is the first disease you test for and how do you test for it?
B. Canis.
Serology—tests identifying B. canis antibodies or antigens may take up to 12 weeks to become detectable: perform immediate testing in any dog with scrotal enlargement (see Brucellosis). * Rapid slide agglutination test (RSAT)—screening test; sensitive but not specific. * Due to occurrence of false positives with RSAT, retest all positives for B. canis with a more specific test method: modified rapid slide agglutination test (MERSAT), agar gel immunodiffusion test (AGID), tube agglutination test (TAT), PCR, or bacterial culture of whole blood or lymph node aspirate.
93
Genetic epilepsy (previously known as idiopathic)- what is the mean age and range?
Mean age 10 months–3 years. * Range 6 months–5 years.
94
What is the most efficacious antiepileptic drug in a dog?
Phenobarbital Most efficacious antiepileptic drug (AED) in the dog. * Traditional first-line drug; initial dosage 3–5 mg/kg PO q12h; steady state reached at 12–15 days, but levels decrease significantly in first 6 months owing to activation of lysosomal enzymes. * Optimal therapeutic serum levels—100–120 μmol/L or 23–28 μg/mL. * Oral loading dose (if needed)—6–10 mg/kg PO q12h for 2–3 days to reach therapeutic range rapidly.
95
What is a first-line drugs when seizure frequency is less than <1 a week?
Zonisamide: First-line drug when seizure frequency allows steady state 4 days; therapeutic range in human 10–45 μg/mL.
Levetiracetam: First-line drug when seizures have focal onset; <1 seizure/week; 20–70 mg/kg (smaller breeds require higher dosage) PO q8h; must be given q8h to reach adequate levels; no hepatic metabolism; safe; steady state 3 days;
Potassium Bromide
* Traditional first-line drug; varies with salt concentration in diet; bioavailability differs between dogs.
96
What antiepileptic drug should not be used with dogs that have had concerns with pancreatitis?
Phenobarbital or KBr
97
98
What toxicity has the highest mortality rate of all poisons?
Ethylene glycol toxicosis , cats have a higher fatality rate vs dogs
99
PE findings in dogs and cats with ethylene glycol toxicosis.
Early—from 30 minutes to 12 hours post ingestion in dogs: nausea and vomiting; mild to severe depression; ataxia and knuckling; muscle fasciculations; nystagmus; head tremors; decreased withdrawal reflexes and righting ability; polyuria and polydipsia.
Dogs—with increasing depression, patient drinks less but polyuria continues, resulting in dehydration; CNS signs abate transiently after approximately 12 hours, but recur later. * Cats—usually remain markedly depressed; do not exhibit polydipsia. * Oliguria (dogs: 36–72 hours; cats: 12–24 hours) and anuria (72–96 hours post ingestion)—often develop if untreated. * May note severe hypothermia. * Severe lethargy or coma. * Seizures.
* Anorexia. * Vomiting. * Oral ulcers.
* Salivation. * Kidneys—often swollen and painful, particularly in cats.
100
Lab work abnormalities with ethylene glycol toxicosis:
Stress leukogram— common. * High blood urea nitrogen (BUN) and creatinine—dog: 36–48 hours post ingestion; cat: 12 hours post ingestion. * Hyperphosphatemia may occur transiently 3–6 hours post ingestion, owing to phosphate rust inhibitors in antifreeze; hyperphosphatemia is also seen with azotemia owing to decreased glomerular filtration. * Hyperkalemia if oliguric or anuric. * Hypocalcemia—occurs in approximately half of patients, owing to chelation of calcium by oxalic acid; clinical signs infrequently observed because of acidosis.
* Hyperglycemia—occurs in approximately half of patients, owing to inhibition of glucose metabolism by aldehydes, increased epinephrine and endogenous corticosteroids, and uremia. * Isosthenuria—by 3 hours post ingestion, owing to osmotic diuresis and serum hyperosmolality-induced polydipsia
***Calcium oxalate crystalluria—consistent finding; as early as 3 hours post ingestion in cats and 6 hours in dogs; monohydrate form more common.
* Serum osmolality and osmole gap—high by 1 hour post ingestion, in parallel with serum EG concentrations; dose related; usually remain high for approximately 18 hours post ingestion; EG toxicosis most common cause of high osmolal gap. * EG serum concentration— peaks 1–6 hours post ingestion; usually not detectable in serum or urine by 72 hours. * Commercial kits—PRN Pharmacal REACT EG measures concentra- tions at >50 mg/dL; estimate by multiplying osmole gap by 6.2. ◦
101
Describe what causes exercise induced collapse in a dog, what breeds are predisposed, and describe a classic collapse episode.
Genetic disorder—inherited as an autosomal recessive trait.
* Symptomatic dogs are homozygous for a mutation in the dynamin 1 gene. Dynamin 1 (DNM1) is a protein important in neuro- transmission in the brain and spinal cord during high-level neuronal activity. There is evidence that the DNM1 mutation associated with EIC has its most profound effect on DNM1 function when body temperature is elevated, as normally occurs with exercise.
Labradors, also other breeds (less common)
* Weakness occurs after 5–20 minutes of intense exercise with excitement or stress. * Rear limbs become weak and unable to support weight.
* Rear limb muscles are flaccid during collapse and there is a loss of patellar reflexes. * Dogs may continue to run, dragging their rear limbs in a crouched posture.
* During a severe episode, all four limbs can be affected; rarely the dog may become recumbent and unable to move its limbs or raise its head.
* Dogs remain conscious and fully alert during episodes.
elevated temp (mean 107)
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Describe exocrine pancreatic insufficiency and note a breed that is predisposed.
* Most commonly caused by insufficient synthesis and secretion of pancreatic enzymes by the exocrine pancreas. * In rare cases can be caused by an obstruction of the pancreatic duct or isolated lipase deficiency.
* Insufficient synthesis of pancreatic digestive enzymes can be due to destruction of acinar cells resulting from chronic pancreatitis (approximately 50% of cases in dogs and almost all cases in cats) or can be due to idiopathic pancreatic acinar atrophy (PAA; most common cause of exocrine pancreatic insufficiency in German shepherd dogs).
* Deficient exocrine pancreatic secretion results in maldigestion and nutrient malab- sorption, leading to weight loss and loose stools with steatorrhea. * Malabsorption contributes to small intestinal dysbiosis.
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Describe clinical signs and exam findings associated with exocrine pancreatic insufficiency.
Historical Findings
* Weight loss with normal to increased appetite. * Chronically loose stools or diarrhea. * Fecal volumes are larger than normal and may be associated with steator- rhea. * Flatulence and borborygmus are commonly reported, especially in dogs.
* May show coprophagia and/or pica. * May be accompanied by polyuria/polydipsia with diabetes mellitus as a sequel to chronic pancreatitis.
Physical Examination Findings
* Thin body condition. * Decreased muscle mass. * Poor-quality hair coat. * Cats with steatorrhea may have greasy “soiling” of the hair coat in the perineal area, but this is seen in the minority of cases.
104
Describe testing for exocrine pancreatic insufficiency.
Trypsin-Like Immunoreactivity (TLI)
* Diagnostic test of choice in both dogs and cats. * Principle of test—serum TLI can be measured by an assay that detects trypsinogen and trypsin that is directly released into the blood from pancreatic acinar cells; serum TLI is detected in the serum of all normal dogs and cats with a functional exocrine pancreatic mass. * Serum TLI concentrations are dramatically reduced with EPI—dogs: cTLI ≤2.5 μg/L; cats: fTLI ≤8.0 μg/L. * The TLI tests are species specific. * Advantages—simple; quick; single serum specimen (fasted); highly sensitive and specific for EPI in both species.
Fecal assays for proteolytic activity exist, false positives and negatives, only use in exotics not in dogs or cats
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