Poorly Flashcards
Anorexia
Diagnostic approach to anorexia
Anorexia treatment
Dysphagia and clinical signs
Dysphagia history
Dysphagia causes
Dysphagia diagnostic approach
Dysphagia treatment
Orbital disease
Orbital disease diagnostic approach
Orbital disease- causes
Orbital disease treatment
Oral tumours
Oral tumours- staging
Oral tumours symptomatic care
Canine oral tumours
Algorithm for staging and treatment of oral masses
Canine oral malignant melanoma
Canine oral squamous cell carcinoma
Canine- oral fibrosarcoma
Canine- tumours of odontogenic origin
Canine oral lymphoma
Canine tongue tumours
Canine tonsillar tumours
Canine salivary gland tumours
Feline oral tumours
Idiopathic trigeminal neuritis
Masticatory muscle myositis
Weight loss
Recognition of weight loss
Weight loss with normal or increased appetite DDX
Weight loss with a decreased appetite
Approach to weight loss
Weight loss not following the norm
Diagnostic algorithm for weight loss
Feline hyperthyroidism
Hyperthyroidism history
Hyperthyroidism physical exam
Hyperthyroidism clinical pathology
Concurrent problems with Hyperthyroidism kidneys
Concurrent problems cardiac
Hyperthyroidism diagnosis
Hyperthyroidism treatment options
Considerations of choosing Hyperthyroidism treatment
Radioactive iodine therapy
Medical treatment hyperthyroidism
Oral Carbimazole
- available, no GA or surgery
- drug absorption decreased if GI disease/ vomiting
- side effects, compliance, optimal dosing can be difficult
- most side effects within 3 months: 10-15% anorexia, vomiting, depression within 3 weeks; facial/neck excoriations within 6 weeks (stop Rx); <5% neutropenia, thrombocytopenia (rare IMHA); <2% hepatopathy: increase liver enzymes, increase bilirubin (stop Rx)
- Stop 5-7 days prior to I-131
- Atenolol BID PO- control HR prior to Sx or I-131
Other medical options tx hyperthyroidism
Transdermal methimazole hyperthyroidism
monitoring hyperthyroidism therapy
How do I judge the adequacy of therapy? The TT4 needs to be in the lower half of the reference range for adequate control
How do I adjust medical treatment with hyperthyroidism?
What else should I be checking- hyperthyroidism?
Hyperthyroidism- most cost effective long term treatment
Who lives longer with what hyperthyroidism treatment?
Risks of hyperthyroidism treatment
Thyroidectomy in hyperthyroidism
Dietary therapy- hill’s y/d
Does unmasking CKD by treating hyperthyroidism affect prognosis?
CKD + hyperthyroidism diagnosis
Do I need to do a treatment trial before definitive therapy?
* To establish underlying renal status? Only if you have advanced renal disease (IRIS stage 3-4)
- Perhaps if you suspect other concurrent disease
- tendency is to do I- 131 earlier now
Do I need to worry about iatrogenic hypothyroidism?
How do I adjust therapy in light of iatrogenic hypothyroidism concerns?
Canine nutrition in pregnancy and lactation
Supplementation
Feline nutrition in pregnancy and lactation
Weight loss with decreased appetite
Signs of GI disease
Signs of cardiac disease
Signs of liver disease
Renal disease & reduced appetite & weight loss
Cachexia
Cachexia scoring
Cancer cachexia
Hypoadrenocorticism signalment
History hypoadrenocorticism
History/ Physical exam of hypoadrenocorticism
Clinical pathology- hypoadrenocorticism
Hypoadrenocorticism - imaging
Hypoadrenocorticism ECG
HypoA the great pretender
HypoA diagnostic testing
HypoA Treatment
HypoA maintenance therapy
Feline hypoA
Urinalysis- urine grossly clear pH 7
USG 1.012
Dipstick and sediment: negative/normal
* ECG
- bradycardia, no P waves, spiked T waves
- atrial standstill due to hyperkalaemia
- risk of ventricular fibrillation/asystole
Fever v. hyperthermia
True fever
Purpose of fever
The bad parts of a fever
True fever or not?
Fever of unknown origin
So what are we looking for with an fever of unknown origin?
Potential origins of a fever
Bacterial FUO how to treat?
Non-suppurative bacteria causing FUO
Organisms that could cause FUO
Vector borne causes of FUO
Systemic fungal causes of FUO
Non-infectious inflammatory causes of FUO
Immune mediated and neoplastic causes of FUO
History of PUO
Approach to physical exam PUO
In house cytology:
Filamentous rods (Actinomyces or Nocardia) + short rods and cocci
Culture: Streptococcus, Actinomyces, mixed anaerobes
Treatment:
* No money for CT or surgery, bilateral thoracostomy tubes, IV amoxicillin- clavulanate, enrofloxacin + metronidazole
* Feeding tube
* IVF, anti-emetics, analgesia (opiate/NSAID)
* 7 days in hospital
Months of oral antibiotics, serial radiographs, treated 2 weeks beyond RG resolution, thoracic rads 1 and 3 months later all clear
Dogs v. Cats PUO approach
Antibiotic trial PUO
Antipyretics in PUO?
When to consider prednisolone with PUO?
When not to give empiric therapy
Approach to PUO dos and don’ts?
Investigation of PUO
First round diagnostics PUO
Second round diagnostics PUO
Third round diagnostics: screening PUO
Client communication with PUO
How about that 10% in PUO
DDX: Immune mediated polyarthritis +/- meningitis, primary causes, pyometra- too young?
Investigation:
RG carpi, hocks, spine: mild tarsal effusion, no joint erosion
Abdominal U/S: large pyometra and MILN, LN cytology reactive
CSF analysis and culture: normal/negative
** Arthrocentesis hocks, carpi, and stifles: non-degenerate neutrophils; lack of windrowing; no organisms, culture -ve: bacterial (blood culture medium), mycoplasma (erosive, Greyhounds)
Poppy Diagnosis: Immune mediated polyarthritis (IMPA):
- Type I Idiopathic (50-65%)
- Type II Reactive (Infectious or inflammatory conditions remote from joint (13-25%)
- Type III: Enteropathic (GI/heaptic disease) 4%
- Type IV: Neoplasia remote from joint (2%)
Treatment:
Ovariohysterectomy, potentiated amoxicillin 7 days, NSAIDs and tramadol, complete recovery 4 weeks
key points FUO
Generally QAR
CVS
–
MM
injected, CRT <
1s
–
HR 150
–
Grade 3/6 murmur
–
Pulses
tall, narrow
–
Warm extremities
–
BP 110/55 (70)
–
Prolonged skin tent,
tacky
What is sepsis?
Sepsis: The clinical syndrome caused by infection and the host’s systemic inflammatory response to the infection
Severe sepsis: Sepsis complicated by organ dysfunction
Septic shock: Acute circulatory failure and persistent hypotension (despite volume resuscitation) associated with sepsis
Pathogenesis of sepsis
What we see in sepsis is the result of infection and the host’s response to it
Refer to previous notes/ lecture
LPS (lipopolysaccharide) in G(-) cell wall – one of the most potent stimuli of the host immune response – potent stimulus for release of TNF-alpha
TNF-alpha- early central regulator of interactions among cytokines
Cytokines – eg TNF, IL, chemokines
Cytokines activate inflammatory cells & chemokines attract them to the site of inflammation
Neutrophil responses to cytokine signalling can lead to extensive host tissue damage secondary to release of products like ROS, proteases, lysozymes… like an inflammatory soup!
Host response to insult
A controlled inflammatory response is beneficial to the host
Such a response is localised & represents a balance btw activation of the inflammatory cascade & host CARS
An excessive inflammatory response results from disproportionate activation of the proinflammatory mediators or lack of regulatory counterparts
The other extreme: “immune paralysis” with excessive anti-inflammatory activity
There can be regional & temporal differences in pro-inflammatory and anti-inflammatory activity
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Generation of counter-inflammatory mediators e.g. IL-4, IL-10, transforming growth factor beta, glucocorticoids
Excessive activation of the pro-inflammatory mediators with inadequate production of counter-inflammatory mediators leads to an excessive inflammatory response
Loss of homeostasis
Altered sympathetic and vagal regulation of heart function
Gives rise to reduced heart rate variability, tachycardia, impaired diastolic fn, tachyarrhythmias, myocardial ischaemia
Loss of vasomotor tone
Dysregulation of inflammation and coagulation
Dysregulation of inflammation and coagulation
There is upregulation of TF which combines with FVIIa to initiate the coagulation cascade
TF-fVIIa complex and its downstream products (i.e. thrombin) can also trigger elaboration of inflammatory cytokines and platelet activation
This, together with inhibition of natural anticoagulant and fibrinolytic processes, leads to a hypercoagulable state
Initially the homeostatic balance in septic patients favours procoagulation and antifibrinolysis
This may progress over time to a hypocoagulable state
Two points – homeostatic balance between pro- and anti-coagulant properties is lost
Considerable cross talk between coag and inflamm mediated by1. Protein C has anti-inflammatory properties
Protein S can bind to receptors that mediate an antiinflammatory regulatory loop
Thrombomodulin prevents excessive complement activation
Endothelial, microcirculatory and mitochondrial dysfunction
Endothelial, microcirculatory and mitochondrial abnormalities
Endothelial dysfn leads to increased vascular permeability – capillary leak
There is dec functional capillary density, increased diffusional distance for oxygen, heterogenous microvascular blood flow – all lead to alterations in tissue oxygen extraction and tissue hypoxia
Possible to have microcirculatory disturbance in the face of normal macrohaemodynamic variables
This disconnect btw the systemic and microcirculatory perfusion is known as cryptic shock
Mitochondrial changes can occur independently of microcirculatory dysfn – cytopathic hypoxia
Normal flux of ions, water and small molecules (and even cells!)
Abnormal flux of all of the above in abnormal amounts
Causes interstitial edema, can even happen with intravascular hypovolemia!
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- functional capillary density
- diffusional distance
- Heterogenous blood flow
Clinical signs of sepsis
Infection is documented or suspected and some of the following:
In general, sepsis is more difficult to identify in cats than it is in dogs.8 Dogs classically present with signs similar to those in people: fever, tachypnoea, tachycardia, and leukocytosis. Dogs are more likely to have a hyperdynamic response and present with hyperaemic MM and a brisk CRT. Cats, on the other hand, are frequently afebrile or hypothermic.8 Severe sepsis in cats can result in bradycardia rather than the expected tachycardia. Abdominal pain was a common physical examination finding in cats with severe sepsis but, curiously, not consistent in cats with septic peritonitis.
Late clinical signs of sepsis
Infection is documented or suspected and some of the following:
In general, sepsis is more difficult to identify in cats than it is in dogs.8 Dogs classically present with signs similar to those in people: fever, tachypnoea, tachycardia, and leukocytosis. Dogs are more likely to have a hyperdynamic response and present with hyperaemic MM and a brisk CRT. Cats, on the other hand, are frequently afebrile or hypothermic.8 Severe sepsis in cats can result in bradycardia rather than the expected tachycardia. Abdominal pain was a common physical examination finding in cats with severe sepsis but, curiously, not consistent in cats with septic peritonitis.
How are cats different?
Resuscitation therapeutic goals & safety limits
To recap…
ScVO2 ≥70%, SVO2: ≥65%
Monitoring these parameters should also be part of ongoing monitoring plan; things can change!
- Fluid balance – CVP, urine output
- Oxygenation and ventilation – SpO2, PaO2, PvCO2
- Blood pressure
Alongside with:
Clinical parameters: major body system assessment, body temp
Bloodwork: PCV, ALB, BG…
Organ function: GIT motility (V+, regurg?), urine output… (paired with bloodwork)
Drug dosage & metabolism
Level of comfort/ pain
Nursing care, TLC!
Initial resuscitation bundle in sepsis
Early antibiotic administration in sepsis
Administration of an antimicrobial effective for isolated or suspected pathogens within the first hour of documented hypotension was associated with a survival rate of 79.9%. Each hour of delay in antimicrobial administration over the ensuing 6 hrs was associated with an average decrease in survival of 7.6%.
Figure 1. Cumulative effective antimicrobial initiation following onset of septic shock-associated hypotension and associated survival. The x-axis represents time (hrs) following first documentation of septic shock-associated hypotension. Black bars represent the fraction of patients surviving to hospital
discharge for effective therapy initiated within the given time interval. The gray bars represent the cumulative fraction of patients having received effective antimicrobials at any given time point.
What are your considerations when choosing antibiotics in sepsis?
Antibiotics in septis shock, sepsis, infection?
Identifying the source of sepsis
Not an exhaustive list! Initial diagnostic tests in cases of septic cats generally consist of a complete blood count, a serum chemistry profile, a urinalysis and culture, thoracic and abdominal radiography, and abdominal ultrasonography. Additional diagnostic tests may include blood bacterial cultures, an endotracheal wash and culture, echocardiography, a cerebrospinal fluid tap, or diagnostic peritoneal lavage G(-) enteric bacteria are the most commonly implicated organisms in sepsis in dogs and cats Also G(+) and mixed infections
Septic peritonitis – abdo effusion
Effusion gluc conc < blood gluc conc
Effusion lactate conc > blood lactate conc - ≥ 2mmol/L – predictive of septic peritonitis in dogs, less useful in cats
These parameters have been shown to be unreliable indicators of septic peritonitis in the evaluation of post-op cases in which closed suction drains have been placed
Generalised hepatic microabscessation/ infectious suppurative hepatitis – extension of biliary tract infection, GIT
Culture?
Initial resuscitation bundle in sepsis
monitoring plan should include monitoring Blood Glucose
Collect samples for culture
Fresh Frozen Plasma use in patients with sepis?
What is your assessment?
Comment on use of FFP:
“The use of FFP in critically ill patients remains controversial. In the absence of clinical bleeding or a risk for clinical bleeding associated with a planned procedure, treatment use of FFP is not recommended in human patients. There are insufficient data in critically ill animals to enable formulation of recommendations. Further research is warranted in dogs and cats to establish evidence-based guidelines.”
“While guidelines for the use of FFP in human patients suggest that it should be reserved for patients with active bleeding or prior to surgery in coagulopathic patients, no such guidelines exist for veterinary use.” (jvecc 2015 – controversies in the use of FFP in critically ill small animal patients)
Multiple organ dysfunction syndrome (MODS)
2 recent vet studies have examined organ dysfn in dogs with sepsis/ SIRS – show positive correlation btw mortality and the degree of organ sys dysfn
Immune dysregulation that results in disordered systemic inflammatory processes – “one-hit” theory
Initial immune dysfunction may be augmented by ongoing inflammation in the GIT – “sustained-hit” theory
Other factors that have been implicated, through activation of previously primed inflammatory cells
Surgical trauma, drug reactions, vent-induced lung injury, hospital-acquired infections
End result: production of various soluble mediators & activation of immune effector cells
Critical illness related corticosteroid insufficiency
The definition of critical illness-related corticosteroid insufficiency is controversial and has been for years. It is probably best described as better pressor-responsiveness and faster pressor weaning seen in some human patients with septic shock who are treated with low doses of hydrocortisone. Consensus definitions don’t exist in veterinary medicine but the syndrome is recognised.
Key points in sepsis
Canine activities
Greyhounds
* seek 2nd opinions from experienced vets
Reference Texts:
–
Bloomberg, Dee and Taylor
“Canine Sports medicine and surgery”
•
Australian Greyhound Veterinarians annual
conference
p
roceedings
–
AGV is a SIG with in the AVA
Greyhound Idiosyncrasies
Canine exercise physiology
Haematology and performance
Greyhound and Whippet Haematology
* greyhounds can race successfully with haematocrits as low as 50%
* These dogs are best suited to shorter distances up to 450 meters
* Dogs which compete successfully over 500-700 meters (stayers) usually have high red cell parameters
Hyperfibrinolysis
What is Epsilom aminocaproic acid (EACA)?
Urinary tract disease and performance
Greyhound urinalysis
Greyhound Biochemistry
* Serum enzymes
- ALT: often slight elevation up to double upper normal but is of no clinical significance
- AST: often slight elevation post running indicating muscle injury
- CPK: should be < 200 IU 48 hours post run. Muscle damage indicator
- Glucose: rarely a significant parameter
Greyhound Endocrinology
Progesterone: high levels are important in false pregnancy– level above 6 nmol/L indicate taht a bitch has had a recent oestrus period
Prolactin: high levels are important in false pregnancy. Prolactin is an important luteotrophic hormone.
Anoestrus? Proestrus?
Oestrus? Dioestrus?
Oestrus cycle and performance?
Dioestrus and Greyhounds
* the period from the end of the bitch’s oestrus period until she either whelps or her progesterone level falls below 6 nmol/L
* It is usually 9 weeks in duration. Some non pregnant bitches may experience a dioestrus period longer than 9 weeks
* In the prengnat bitch Progesterone levels fall at the time of whelping. This fall to a level < 6 nmol/L and is associated with the temperature drop
Oestrus Postponement
Progestagens
Oestrus postponement with GnRH agonists and GnRH antagonists?
Suppressing false pregnancy
* Serotonin Inhibitors- Metergolic (Contralac): BID, given 7-8 weeks from the end of oestrus.
- Anabolic steroids: give a poor response
Prostaglandins for Greyhounds
Diet and poor performance
Overweight dogs
Racing dog diet
* Suggested:
600-1000 grams meat
Vegetables, Kibble, Rice, Pasta
Fats and oils (40-50% of energy)
Calcium
Multivitamin Supplements
Electrolytes
* Premium foods provide a good base diet
* Knackery “pet shop” meat may have drug residues (Procaine, Xylazine and Barbiturates)
Weight loss diet
Dietary Allergies Greyhounds
Colitis Greyhounds
Gastro Enteritis Greyhounds
Cardiac in Greyhounds
Greyhound Adoption Program
Greyhounds and stress
Stress is involved in the aetiology of several greyhound medical problems
Response to stress
- An increased secretion of cortisone which predisposes to
- PU/PD weight loss and dehydration
- Low grade infections: UTI and tonsilitis
- Ill thrift - Increased response of the autonomic nervous system
- Sympathetic: Dysuria, Barking, Panting, and dilated pupils
- Parasympathetic: diarrhoea, salivation, and coughing
Water diabetes syndrome
Clinical signs:
PU/PD, weight loss and dehydration, panting and distress
Clin Path: USG 1.001-1.010, Haemoconcentration, PCV > 70% (57-62%), TP > 70 g/l (46-60 g/L)
Aetiology of Water Diabetes Syndrome
Acute Water Diabetes Syndrome Treatment
Chronic Water Diabetes Syndrome Clinical signs and clinical pathology?
Chronic water diabetes syndrome treatment
Post Racing Dysuria
Pathophysiology: high levels of cortical stimulation increase bladder sympathetic tone and reduces parasympathetic tone
* Treatment:
- alpha adrenergic blockers. Phenoxybenzamine 10-15 mg TID
- Diazepam 5-10 mg TID
- Hyoscine Butylbromide (Buscopan) 10 mg bid
- Reduce stress
- Antibiotics
- Catheterise, may need GA
Dysuria
Canine Exertional Rhabdomyolysis
Aetiology of Canine Exertional Rhabdomyolysis
Canine Exertional Rhabdo Treatment
Cramping in Greyhounds
Respiratory Tract Disease Greyhound
Acute Kennel Cough in Performance Dogs
Canine Haemorrhagic Pneumonia in Performance Dogs
Chronic Respiratory Disease
Exercise Induced Asthma
Eye Abnormalities in Performance Dogs
Treatment of Pannus in Performance Dogs
Dominant Dogs Greyhounds
Timid, Nervous and Excitable Dogs
Papillomas
Musculoskeletal injury Greyhounds
Intra-articular injections performance dogs
Nutraceuticals and Joint disease, stem cells
Hip, elbow, stifle, and lumbar problems in working dogs
Medical treatment of joint problems
Back Pain Greyhounds Treatment
Chronic muscle injuries treatment
Photobiomodulation
Multi Wave Locked System– treatment? In performance dogs
Stifle: Medial Collateral Ligament
•
How do we treat that injury
???
•
Rest
•
Pentosan
•
NSAIDs
•
Local cortisone injections
•
Laser therapy
•
Massage
Vets role in Greyhound industry
Greyhound don’t miss list
Exam!!!
SG > 1.025 in a Greyhound!!!
*Impossible to differentiate between proestrus and dioestrus except to measure progesterone
Proestrus < 6 nmol/L because she hasn’t ovulated
