Immunology/Hematology/Derm/Special Senses Flashcards
(161 cards)
1
Q
According to ACVIM (2018), what is the definition of primary IMHA in dogs and cats?
A
Primary (idiopathic) IMHA refers to an autoimmune process where antibodies are directed against the animal’s own red blood cells in the absence of an identifiable underlying cause.
2
Q
According to ACVIM (2018), what are the three key diagnostic criteria for IMHA in dogs?
A
Evidence of hemolytic anemia (e.g., spherocytosis, hyperbilirubinemia), positive Coombs’ test or in-saline agglutination, and exclusion of underlying causes.
3
Q
What are the hallmark CBC findings in IMHA as per the 2018 ACVIM consensus?
A
Regenerative anemia, spherocytosis, autoagglutination, thrombocytopenia (if concurrent Evan’s syndrome), leukocytosis.
4
Q
According to ACVIM (2018), what is the role of a saline agglutination test in IMHA diagnosis?
A
A positive macroscopic saline agglutination test supports IMHA if true agglutination (not rouleaux) is confirmed with saline dispersion.
5
Q
What is the role of the Coombs’ test in IMHA diagnosis according to the consensus?
A
A positive direct antiglobulin test (Coombs’) supports a diagnosis of IMHA but has variable sensitivity and specificity; negative results do not rule out IMHA.
6
Q
What are common underlying causes of secondary IMHA in dogs and cats? (ACVIM 2018)
A
Infectious diseases (e.g., Babesia, Mycoplasma), neoplasia, drug-induced (e.g., sulfonamides), vaccine reactions, systemic inflammation.
7
Q
According to the ACVIM 2018 consensus, how should diagnostic workup for IMHA be approached?
A
Full diagnostic workup should include CBC, chemistry, UA, thoracic and abdominal imaging, infectious disease testing based on geography and risk.
8
Q
According to ACVIM (2018), what are the recommended first-line immunosuppressive therapies for canine IMHA?
A
Prednisone or prednisolone at 2 mg/kg/day PO divided or once daily.
9
Q
What adjunct immunosuppressants are recommended in dogs with severe or refractory IMHA (ACVIM 2018)?
A
Mycophenolate mofetil, cyclosporine, or azathioprine (dogs only) may be added based on clinical judgment, side effect profile, and patient status.
10
Q
What is the recommended duration of immunosuppressive treatment for IMHA according to the ACVIM?
A
Tapering over months is recommended, with gradual reduction after clinical and hematologic remission (PCV normalization, resolution of hemolysis).
11
Q
What is the evidence-based approach to anticoagulation in IMHA per ACVIM (2018)?
A
Anticoagulant prophylaxis is recommended due to high thromboembolic risk; options include clopidogrel, low-dose aspirin, or LMWH.
12
Q
What blood products are recommended for IMHA patients with severe anemia?
A
Packed red blood cells (PRBCs) are recommended; whole blood can be considered in concurrent coagulopathies or massive hemolysis.
13
Q
What does the ACVIM consensus recommend regarding transfusion triggers for IMHA?
A
Transfusions should be based on clinical signs of poor oxygen delivery (e.g., tachycardia, collapse), not strict PCV thresholds.
14
Q
What prognostic indicators are identified in ACVIM 2018 for IMHA in dogs?
A
Negative prognostic factors include hyperbilirubinemia, autoagglutination, elevated BUN, thrombocytopenia, and need for multiple transfusions.
15
Q
What is the definition of Evan’s Syndrome per the ACVIM 2018 IMHA guidelines?
A
Evan’s Syndrome is the concurrent immune-mediated destruction of red blood cells and platelets (IMHA + ITP).
16
Q
What is the pathophysiologic mechanism of red cell destruction in IMHA as described by the ACVIM 2018 statement?
A
Destruction occurs via extravascular hemolysis (macrophage-mediated in spleen/liver) and intravascular hemolysis (complement-mediated RBC lysis).
17
Q
How does complement contribute to IMHA pathophysiology? (ACVIM 2018)
A
Complement activation leads to membrane attack complex formation and direct intravascular lysis of RBCs, contributing to acute hemoglobinemia and hemoglobinuria.
18
Q
What mechanisms lead to a hypercoagulable state in IMHA, according to the 2018 ACVIM consensus?
A
Endothelial injury, exposure of phosphatidylserine on RBCs, circulating microparticles, and systemic inflammation increase thrombosis risk.
19
Q
What are potential complications of immunosuppressive therapy in IMHA patients (ACVIM 2018)?
A
Secondary infections, gastrointestinal upset, hepatotoxicity (esp. azathioprine), bone marrow suppression, and poor wound healing.
20
Q
How should relapse of IMHA be managed according to ACVIM (2018)?
A
Reintroduction or escalation of immunosuppression, reassessment for new underlying triggers, and prolonged taper once remission is achieved.
21
Q
Define ‘input sensor’ in the context of immune-mediated disease as it applies to IMHA.
A
The immune system’s antigen-presenting cells act as input sensors, detecting self-antigens on RBCs and initiating an inappropriate autoimmune response.
22
Q
Define ‘controller algorithm’ in the IMHA pathophysiology framework.
A
The controller algorithm is the adaptive immune response (primarily T-helper cells) that determines the strength and type of immune activation.
23
Q
What is the ‘actuator’ in IMHA pathophysiology?
A
The effector arms of the immune system, including B cells (antibody production), macrophages (phagocytosis), and complement activation pathways.
24
Q
What is the ‘target setpoint’ concept in immune tolerance, and how is it disrupted in IMHA?
A
The immune system’s setpoint is self-tolerance. In IMHA, this is lost or lowered, allowing recognition of RBC antigens as foreign.
25
How does the feedback loop in IMHA worsen disease progression?
Ongoing RBC destruction leads to inflammatory cytokine release, increased antigen presentation, and further loss of tolerance—a positive feedback loop.
26
What biomarkers are useful in monitoring IMHA treatment response (ACVIM 2018)?
PCV/hematocrit, bilirubin, reticulocyte count, autoagglutination status, and inflammatory markers (e.g., CRP if available).
27
According to O’Marra et al. (2011), what was the primary objective of their retrospective study on ITP?
To identify clinical features, treatment strategies, and predictors of outcome in dogs diagnosed with primary immune-mediated thrombocytopenia (ITP).
28
What was the median presenting platelet count in dogs with ITP in this study?
The median platelet count was 6,000/μL (severe thrombocytopenia).
29
What percentage of dogs with ITP survived to discharge according to O'Marra et al. (2011)?
86% of dogs survived to discharge.
30
What clinical signs were most commonly observed in dogs with ITP in this study?
Petechiae, ecchymoses, melena, epistaxis, and hematuria.
31
What was the most common initial immunosuppressive therapy used in O'Marra et al. (2011)?
Prednisone alone (2 mg/kg/day) or in combination with azathioprine or cyclosporine.
32
According to O'Marra et al., what factor was significantly associated with increased mortality in dogs with ITP?
Higher initial BUN concentration was associated with increased mortality.
33
What was the median time to platelet count normalization in surviving dogs (O’Marra 2011)?
Median time was 6 days (range 2–20 days).
34
What proportion of dogs with ITP required a second immunosuppressive agent?
49% of dogs received a second agent (usually azathioprine or cyclosporine) due to poor initial response.
35
What role did vincristine play in the treatment of ITP in O’Marra’s study?
Vincristine (0.02 mg/kg IV once) was used in 27% of dogs and was associated with shorter time to platelet recovery.
36
What adverse effects were observed in dogs receiving immunosuppressive therapy (O’Marra 2011)?
Gastrointestinal signs (vomiting, diarrhea), hepatotoxicity (azathioprine), and secondary infections were noted.
37
What does the pathophysiology of primary ITP involve according to established veterinary ECC understanding?
Autoantibody-mediated destruction of platelets occurs primarily via macrophage clearance in the spleen and liver (Fc receptor-mediated phagocytosis).
38
What compensatory mechanisms occur in early ITP?
Megakaryocyte hyperplasia and increased thrombopoiesis in the bone marrow attempt to offset peripheral platelet destruction.
39
What is the major 'input sensor' abnormality in ITP pathogenesis?
Breakdown in immune tolerance allows B cells to recognize normal platelet membrane antigens as foreign.
40
What is the 'controller algorithm' dysfunction in ITP?
Dysregulated helper T cell activity supports autoreactive B cell survival and antibody production against platelets.
41
What is the 'actuator' in ITP’s immune destruction process?
Autoantibodies, particularly IgG, act as effectors, opsonizing platelets and facilitating phagocytosis by splenic/liver macrophages.
42
How does the feedback loop contribute to ongoing platelet destruction in ITP?
Continuous destruction leads to increased antigenic exposure and further activation of autoreactive lymphocytes.
43
Why does thrombopoietin (TPO) remain normal or low in ITP despite thrombocytopenia?
TPO levels are regulated by platelet mass, but the immune system clears platelets too quickly for TPO to rise effectively.
44
What is the utility of bone marrow evaluation in ITP diagnosis according to standard ECC guidelines?
Bone marrow exam is helpful in atypical cases to confirm increased megakaryocytes and rule out marrow failure or neoplasia.
45
When is splenectomy considered in ITP cases?
Considered in refractory ITP cases where immune-mediated destruction persists despite immunosuppression, as the spleen is the major site of clearance.
46
What is Evan’s syndrome in relation to ITP?
Evan’s syndrome refers to concurrent immune-mediated thrombocytopenia and immune-mediated hemolytic anemia (IMHA + ITP).
47
How does extravascular hemolysis predominate in IMHA, and what organs are involved?
Antibody-coated RBCs are phagocytosed by macrophages in the spleen and liver via Fc and complement receptors, leading to extravascular hemolysis.
48
What is the primary immunoglobulin class involved in extravascular hemolysis?
IgG is the predominant immunoglobulin mediating extravascular hemolysis by opsonizing erythrocytes.
49
What is the primary immunoglobulin class associated with intravascular hemolysis in IMHA?
IgM is more efficient at activating complement, leading to MAC (membrane attack complex)-mediated RBC lysis in circulation.
50
How does hemoglobinemia develop in IMHA?
In intravascular hemolysis, free hemoglobin is released into plasma, exceeding haptoglobin binding capacity and leading to hemoglobinemia.
51
What causes bilirubinemia in IMHA, and what is its significance?
Excess breakdown of hemoglobin from RBC destruction produces unconjugated bilirubin, overwhelming hepatic conjugation and leading to hyperbilirubinemia, which correlates with disease severity.
52
How does systemic inflammation contribute to IMHA pathogenesis?
Inflammatory cytokines (e.g., TNF-α, IL-6) promote endothelial activation, hypercoagulability, and amplification of autoimmune responses.
53
What is the role of phosphatidylserine exposure on RBCs in IMHA?
Damaged or antibody-bound RBCs expose phosphatidylserine, a procoagulant signal that contributes to thrombin generation and thrombosis.
54
How does RBC oxidative injury contribute to pathogenesis in IMHA?
Oxidative stress may alter RBC membranes, enhancing recognition by the immune system and accelerating clearance.
55
What is the relationship between anemia severity and tissue oxygen delivery in IMHA?
Reduced RBC mass lowers oxygen-carrying capacity, prompting compensatory responses such as tachycardia, vasodilation, and increased cardiac output.
56
What compensatory mechanisms occur in response to anemia in IMHA?
Increased erythropoietin production stimulates reticulocytosis; splenic contraction may transiently improve PCV; 2,3-DPG shifts hemoglobin-oxygen curve rightward to enhance tissue oxygenation.
57
What is the role of haptoglobin in IMHA pathophysiology?
Haptoglobin binds free hemoglobin from lysed RBCs; depletion indicates ongoing intravascular hemolysis.
58
How does thrombosis occur mechanistically in IMHA?
Endothelial activation, exposure of RBC-derived microparticles, increased tissue factor, and platelet hyperreactivity contribute to a prothrombotic state.
59
Why are dogs with IMHA at risk of pulmonary thromboembolism (PTE)?
The combination of endothelial injury, hypercoagulability, and reduced fibrinolysis predisposes to PTE — a major cause of death in IMHA patients.
60
What pathophysiologic features differentiate acute vs. chronic IMHA?
Acute IMHA presents with sudden-onset hemolysis and clinical deterioration, while chronic cases may show waxing and waning anemia with lower-grade immune destruction and compensation.
61
What are the consequences of persistent autoagglutination in IMHA?
Agglutinated RBCs may be prematurely sequestered and destroyed in the microvasculature, worsening anemia and impairing perfusion.
62
What is the mechanism of hyperlactatemia in IMHA?
Inadequate oxygen delivery due to anemia leads to anaerobic metabolism and lactic acid production. Hyperlactatemia is a poor prognostic marker.
63
How does splenic macrophage activity contribute to both destruction and immune perpetuation in IMHA?
Macrophages not only phagocytose RBCs but also present antigen and secrete inflammatory cytokines, driving further immune activation.
64
What is the effect of ongoing hemolysis on renal function in IMHA?
Hemoglobinuria may cause tubular damage and acute kidney injury, particularly in intravascular hemolysis.
65
What was the goal of the Hillier et al. (2014) ISCAID guidelines on SBF?
To provide evidence-based guidelines for diagnosis, antimicrobial selection, and treatment of superficial bacterial folliculitis (SBF) in dogs, emphasizing antimicrobial stewardship.
66
What is the most common bacterial organism associated with SBF in dogs?
Staphylococcus pseudintermedius is the most frequently isolated pathogen in SBF.
67
According to Hillier et al. (2014), what are the typical clinical signs of SBF in dogs?
Papules, pustules, crusts, epidermal collarettes, alopecia, and sometimes pruritus. Lesions are typically localized to the trunk and limbs.
68
What diagnostic tests are recommended to confirm SBF?
Cytology (tape, slide, or impression smears), bacterial culture and susceptibility testing, and skin scrapings to rule out other causes.
69
When is bacterial culture and susceptibility testing indicated for SBF?
For recurrent infections, poor response to empiric therapy, or history of recent antibiotic use.
70
What are the three recommended categories of topical therapy in Hillier et al. (2014)?
Antiseptic shampoos (e.g., chlorhexidine), sprays or mousses, and wipes containing antibacterial agents.
71
What is the first-line topical agent for superficial bacterial folliculitis?
2–4% chlorhexidine (alone or with miconazole) is most frequently recommended due to broad activity and safety.
72
When should topical therapy be used alone in SBF?
In cases with localized or mild disease, or to avoid systemic antimicrobial use in appropriate patients.
73
What systemic antimicrobials are recommended as first-line options for SBF (Hillier et al. 2014)?
Clindamycin, first-generation cephalosporins (cephalexin), or amoxicillin-clavulanate.
74
What are the recommended second-line antimicrobials for SBF if culture is pending or resistance suspected?
Doxycycline, chloramphenicol, or potentiated sulfonamides (based on susceptibility and clinical context).
75
Which antimicrobials are considered third-line and should only be used based on culture results?
Fluoroquinolones, rifampin, aminoglycosides, and vancomycin — due to importance in human medicine and risk of resistance.
76
What is the minimum recommended duration of systemic antimicrobial therapy for SBF?
Treat for at least 3 weeks and continue for 1 week beyond clinical resolution of lesions.
77
Why is antimicrobial stewardship emphasized in the treatment of SBF?
Overuse or misuse of antimicrobials contributes to resistance, including MRSP (methicillin-resistant Staphylococcus pseudintermedius), a serious zoonotic and therapeutic challenge.
78
What strategies can reduce recurrence of SBF in dogs?
Identifying and addressing underlying causes (e.g., allergies, endocrinopathies), using topical therapies, and minimizing systemic antibiotic use.
79
What does the presence of methicillin resistance imply in SBF cases?
The organism is resistant to all beta-lactam antibiotics (including penicillins and cephalosporins), necessitating alternative therapies based on susceptibility.
80
How does chlorhexidine work mechanistically in the treatment of SBF?
It disrupts microbial cell membranes and precipitates cell contents, leading to bacterial death; its activity persists in the stratum corneum.
81
How do potentiated sulfonamides work in bacterial infections like SBF?
They inhibit folate synthesis at two sequential steps (sulfonamides inhibit dihydropteroate synthase; trimethoprim inhibits dihydrofolate reductase).
82
What is the mechanism of resistance in MRSP?
Altered penicillin-binding proteins (PBPs), particularly PBP2a encoded by the mecA gene, reduce beta-lactam binding and efficacy.
83
Define 'input sensor' in the context of antimicrobial resistance in skin infections.
Clinical monitoring of treatment efficacy and cytology/culture results serve as input sensors to guide therapy adjustments.
84
What is the 'controller algorithm' in managing SBF with antimicrobials?
The clinical decision process integrates diagnostic results, severity of disease, and antimicrobial susceptibility to optimize therapy.
85
What is the 'actuator' in treatment of SBF?
Topical or systemic antimicrobials act as the therapeutic effectors that kill or suppress bacterial pathogens.
86
What is the ‘feedback loop’ in antimicrobial therapy for SBF?
Re-evaluation of clinical response, culture results, and recurrence informs therapy adjustment and helps prevent resistance development.
87
What underlying diseases often predispose dogs to recurrent SBF?
Atopic dermatitis, hypothyroidism, hyperadrenocorticism, and ectoparasite infestations.
88
How does chronic use of corticosteroids affect SBF pathophysiology?
Corticosteroids suppress innate skin immunity and barrier function, increasing susceptibility to bacterial colonization and infection.
89
Why is treatment beyond clinical resolution recommended in SBF?
To ensure complete eradication of the infection and prevent relapse due to residual bacterial populations.
90
What was the primary objective of Brauer et al. (2011)?
To characterize the clinical features and outcomes of dogs with seizures caused by metabolic or toxic etiologies.
91
What percentage of seizure cases in this study were caused by metabolic or toxic conditions?
13.2% of all seizure cases seen during the study period were due to metabolic or toxic causes.
92
What were the most common metabolic causes of seizures identified in Brauer et al. (2011)?
Hepatic encephalopathy, hypoglycemia, and electrolyte imbalances (especially hyponatremia and hypocalcemia).
93
What were the most common toxic causes of seizures in the study?
Metaldehyde, ethylene glycol, ivermectin, xylitol, and chocolate ingestion.
94
Which laboratory parameters were commonly abnormal in dogs with metabolic seizures?
Elevated liver enzymes, hyperammonemia, hypoglycemia, low serum sodium, and decreased ionized calcium.
95
What neurologic signs were frequently observed in dogs with metabolic or toxic seizures?
Altered mentation, pacing, head pressing, ataxia, tremors, and generalized tonic-clonic seizures.
96
How did the prognosis compare between metabolic and toxic causes of seizures?
Dogs with toxic causes had a worse prognosis than those with reversible metabolic abnormalities.
97
What proportion of dogs survived to discharge in this study?
77.1% of dogs with metabolic or toxic seizures survived to hospital discharge.
98
What are the primary pathophysiologic mechanisms of hepatic encephalopathy-related seizures?
Hyperammonemia crosses the blood-brain barrier, disrupting astrocyte function, increasing glutamine, causing cerebral edema, and altering neurotransmission.
99
How does hypoglycemia lead to seizures?
Glucose deprivation impairs neuronal ATP production, leading to membrane instability, excitotoxicity, and neuronal depolarization.
100
What is the role of calcium in seizure pathophysiology?
Hypocalcemia lowers neuronal membrane threshold, increasing excitability and promoting spontaneous depolarization.
101
How does hyponatremia cause neurologic signs and seizures?
Osmotic swelling of brain cells leads to cerebral edema; rapid changes in serum sodium can destabilize neuronal ion gradients.
102
What is the pathophysiologic mechanism of metaldehyde-induced seizures?
Metaldehyde interferes with GABAergic neurotransmission and causes CNS excitation, tremors, and seizures.
103
How does ethylene glycol toxicity cause neurologic signs?
Metabolites like glycolic and oxalic acid cause metabolic acidosis and calcium oxalate crystal deposition in tissues, including the CNS.
104
What are the mechanisms of ivermectin-induced neurotoxicity in dogs?
Ivermectin enhances GABA activity and crosses the blood-brain barrier in dogs with MDR1 mutations, leading to CNS depression and seizures.
105
How does xylitol cause seizures in dogs?
Xylitol induces a profound insulin release, leading to hypoglycemia; in large doses, it may also cause hepatic necrosis and encephalopathy.
106
Define the 'input sensor' in the context of metabolic seizure pathophysiology.
Chemoreceptors, glucose sensors, and osmoreceptors detect abnormal systemic states (e.g., low glucose, sodium) and signal CNS adaptation or dysfunction.
107
What is the 'controller algorithm' in metabolic seizure regulation?
Homeostatic regulation via liver, pancreas, adrenal glands, and kidneys that maintain electrolyte, glucose, and toxin balance.
108
What are the ‘actuators’ in preventing metabolic seizures?
Hepatic detoxification, insulin/glucagon release, renal filtration, and ion exchange mechanisms actively restore physiologic stability.
109
What is the consequence of a failed feedback loop in metabolic diseases causing seizures?
Persistent hypoglycemia, hyperammonemia, or electrolyte derangement overwhelms compensatory mechanisms, leading to excitotoxic injury and seizures.
110
What diagnostic tests are critical in identifying metabolic causes of seizures?
Serum chemistry, ammonia, glucose, bile acids, ionized calcium, sodium/potassium, and toxicology panels.
111
Why is rapid identification of metabolic seizure causes essential in emergency medicine?
Many metabolic or toxic seizures are reversible if treated early; delay can result in permanent CNS damage or death.
112
What was the primary objective of Charalambous et al. (2017)?
To compare the efficacy and safety of intranasal (IN) midazolam versus rectal (PR) diazepam in stopping status epilepticus (SE) in dogs.
113
What was the study design used in this paper?
Multicenter, prospective, randomized, parallel-group clinical trial.
114
What was the primary outcome measure in Charalambous et al. (2017)?
Cessation of clinical seizure activity within 5 minutes of drug administration.
115
Which drug showed superior efficacy in stopping seizures in canine SE?
Intranasal midazolam was significantly more effective than rectal diazepam (70% vs. 20% success at 5 minutes).
116
What was the dosage of intranasal midazolam used in the study?
0.2 mg/kg intranasally via mucosal atomization device.
117
What was the dosage of rectal diazepam used?
1 mg/kg rectally.
118
What was the median time to seizure cessation in the intranasal midazolam group?
1.6 minutes.
119
What major adverse effects were observed with either drug?
Mild sedation and ataxia; no severe adverse effects were reported in either group.
120
What is the proposed mechanism of action of midazolam in terminating seizures?
Enhances GABA-A receptor activity, increasing chloride influx and neuronal hyperpolarization, leading to seizure suppression.
121
What is the major benefit of intranasal administration for emergency seizure control?
Rapid absorption via the nasal mucosa and direct access to the CNS via the olfactory nerve and cribriform plate vasculature.
122
Why is rectal administration of diazepam less effective in SE?
Poor and variable absorption, especially during ongoing seizures; reduced rectal perfusion can impair drug uptake.
123
How does status epilepticus affect GABA receptor function over time?
Prolonged seizures lead to internalization of GABA-A receptors and increased resistance to benzodiazepines.
124
Why is rapid seizure control critical in veterinary SE management?
Prolonged seizures increase risk of neuronal damage, cerebral edema, hyperthermia, hypoxia, and multi-organ failure.
125
Define 'input sensor' in the neurophysiology of SE.
Seizure-activated neural networks and limbic system structures detect uncontrolled electrical activity and initiate compensatory mechanisms.
126
What is the 'controller algorithm' in pharmacologic seizure termination?
Benzodiazepine-mediated modulation of GABAergic tone regulates inhibitory control of neural firing.
127
What is the 'actuator' in benzodiazepine therapy for seizures?
Activation of GABA-A receptors on post-synaptic neurons, enhancing inhibitory neurotransmission.
128
What is the target setpoint for seizure control?
Restoration of inhibitory-excitatory balance to terminate seizure activity and prevent recurrence.
129
What defines the feedback loop failure in status epilepticus?
Persistent seizure activity leads to receptor desensitization, metabolic derangement, and perpetuation of seizures despite endogenous inhibition.
130
What clinical takeaway can be applied from this study in emergency practice?
Intranasal midazolam should be considered the first-line out-of-hospital therapy for canine status epilepticus due to superior efficacy and ease of administration.
131
Why might mucosal atomization be important in intranasal drug delivery?
It increases surface area coverage and promotes more rapid and consistent absorption into nasal vasculature and CNS.
132
What is one limitation of this study noted by the authors?
It included various etiologies of seizures and did not control for underlying cause, which may influence treatment response.
133
How does this study support translational medicine between veterinary and human neurol
134
What is the primary goal of the 2015 ACVIM seizure management consensus?
To provide evidence-based and expert consensus guidelines for the diagnosis, treatment, and long-term management of seizures in dogs.
135
How does the ACVIM define epilepsy in dogs?
A disease of the brain characterized by recurrent unprovoked seizures (≥2 seizures >24 hours apart).
136
What are the major classifications of seizures according to the consensus?
Focal, generalized, and focal-to-generalized seizures.
137
What are the three broad etiologic categories of seizures discussed?
Idiopathic epilepsy, structural epilepsy, and reactive seizures.
138
What defines a reactive seizure in this framework?
Seizure secondary to metabolic or toxic disturbances, not due to intrinsic brain disease.
139
What are the minimum recommended diagnostic tests in a dog presenting with seizures?
CBC, chemistry, urinalysis, bile acids or ammonia (if concern for HE), blood pressure, and possibly infectious disease testing.
140
What are the Tier I recommendations for seizure diagnostics per the consensus?
Minimum database testing (CBC, chem, UA), bile acids or NH3, blood pressure, and MRI/CSF if warranted.
141
When is MRI/CSF strongly recommended in seizure patients (Tier II/III)?
Age <6 months or >6 years at seizure onset, interictal neurologic abnormalities, or poor response to therapy.
142
What is the recommended first-line anticonvulsant for idiopathic epilepsy in dogs (ACVIM 2015)?
Phenobarbital is first-line based on efficacy, availability, and cost.
143
What other first-line AEDs are considered acceptable alternatives?
Imepitoin (where approved) or potassium bromide (in non-sighthounds or non-asthmatic dogs).
144
What AEDs are considered second-line or adjuncts?
Levetiracetam and zonisamide.
145
What is the target serum phenobarbital concentration for dogs with epilepsy?
15–35 µg/mL; monitoring is essential for efficacy and toxicity.
146
What are the most common side effects of phenobarbital?
Sedation, polyphagia, PU/PD, hepatotoxicity, and myelosuppression (at high doses).
147
When should antiepileptic treatment be initiated in dogs with idiopathic epilepsy?
After ≥2 seizures within 6 months, status epilepticus or cluster seizures, or prolonged postictal periods.
148
What defines status epilepticus (SE) per the ACVIM?
A seizure lasting >5 minutes or ≥2 seizures without full recovery of consciousness between events.
149
What defines cluster seizures?
≥2 seizures within a 24-hour period, separated by return to consciousness.
150
What is the first-line therapy for status epilepticus in dogs according to ACVIM (2015)?
Benzodiazepines (IV or IN midazolam, or rectal diazepam) are first-line emergent treatment.
151
What are maintenance strategies after SE stabilization?
Phenobarbital loading, levetiracetam bolus, and consideration of CRIs (e.g., midazolam, propofol) if seizures recur.
152
What is the mechanism of action of phenobarbital?
Enhances GABA-A receptor activity and inhibits glutamate excitation via AMPA receptors.
153
How does potassium bromide control seizures mechanistically?
Competes with chloride ions, hyperpolarizing neurons and raising seizure threshold.
154
What role does levetiracetam play in seizure control?
Binds SV2A vesicle protein, modulating neurotransmitter release; effective as adjunct or monotherapy.
155
What is pharmacoresistant epilepsy and how is it addressed in the consensus?
Failure to control seizures despite appropriate therapy with two AEDs; may require polytherapy, advanced imaging, or metabolic investigation.
156
Define the 'input sensor' in seizure pathophysiology.
Neuronal excitability and synaptic input via glutamate pathways act as initial signals triggering seizure activity.
157
What is the 'controller algorithm' in seizure suppression?
Endogenous GABAergic inhibition and AED-mediated enhancement of inhibitory tone modulate firing thresholds.
158
What are the ‘actuators’ in seizure management?
Anticonvulsant drugs (AEDs) that modulate neurotransmission and prevent neuronal depolarization.
159
How does the ‘feedback loop’ relate to long-term seizure control?
Seizure frequency, medication response, and therapeutic monitoring guide AED titration and drug selection over time.
160
Why is client education emphasized in the consensus?
Realistic expectations, seizure diaries, and adherence improve quality of life and long-term seizure control.
161
What is the role of therapeutic drug monitoring in seizure management?
Ensures serum levels are within therapeutic range and helps identify poor compliance, overdosage, or hepatic effects.
